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Deflating Door-to-Balloon Time

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Both the American Heart Association and the American College of Cardiology have made a special effort to shorten door-to-balloon time in patients with ST-segment elevation MI in order to decrease the mortality of this high-risk group of patients.

Improvement in the logistics and quality of hospital systems has led to a significant decrease in door-to-balloon time (DBT). Systems have been initiated to effect rapid referral of ST-segment elevation MI (STEMI) patients to primary percutaneous coronary intervention (PCI) centers, either directly or by expeditious transfer of STEMI patients from facilities without interventional capability to PCI centers.

This process has been vigorously advocated by the AHA through its program, “Mission: Lifeline” aimed at improving and shortening the arrival time of STEMI patients to PCI hospitals.

Several recent reports provide insight into the issues relative to the importance of shortening of DBT and give us reason to evaluate the nuances of our strategies. A recent report from Michigan examined the Blue Cross Blue Shield database between 2003 and 2008 that included 8,771 patients. The report indicated that the DBT decreased from an average of 113 minutes to 76 minutes over the 8-year period without any impact on mortality. The number of patients with DBT of less than 90 minutes was 28.5% in 2003 and 67.2% in 2008, with an observed hospital mortality of 4.1% and 3.8% respectively (Arch. Intern. Med. 2010;170:1842-9).

The authors suggested that the failure to affect mortality by shortening the DBT was due in part to the fact that the higher-risk patients accounted for most deaths and experienced the longest symptom-to-door time.

It has been clear for some time that although expeditious hospital therapy is important, the duration between symptom onset and eventual arrival in a medical facility represents the major delay to therapy, compared with DBT. As the patient wrestles with the significance of his or her indigestion or chest pressure, valuable minutes fly by that have critical effects on patient survival.

Major efforts have been made to acquaint patients with the importance of dealing with symptoms, to little avail. But the time from initiating contact with the emergency care system and the patient's arrival to the hospital is a time frame that we should be able to deal with, according to strategies proposed by Mission: Lifeline.

In a study of 6,209 Danish patients who were followed in a registry from 2002 to 2008 in a highly structured emergency care system – unlike that of the United States, which is a system in name only – the investigators observed that the elapsed time from the call for emergency care to the ultimate arrival in the hospital had the largest impact on patient survival, and had greater importance on survival than did DBT (JAMA 2010;304:763-71). A system delay of up to 60 minutes was associated with a long-term mortality of 15.4%, whereas a delay of up to 360 minutes doubled that risk to 30.8%.

The investigators indicated that programs focusing on the time between the first contacts with the health system to initiation of reperfusion will have the greatest impact on mortality.

The importance of the timeliness of early therapy (either PCI or fibrinolysis) was emphasized in a similar registry study carried out in Quebec in 80 hospitals during 2006-2007 (JAMA 2010;303:2148-55). PCI was the predominant mode of therapy for STEMI, either by direct transport to a PCI center or a transfer from a non-PCI center to a PCI center.

Delay in either therapy had a major effect on mortality, and was of particular importance in patients who were transferred from a non-PCI hospital to a PCI center. DBT in directly admitted patients to PCI centers was 83 minutes, compared with 123 minutes for transferred patients. The most striking observation was that regardless of the mode of therapy – fibrinolysis administered within 30 minutes or PCI within 90 minutes – the 30-day mortality benefit of early therapy was similar (3.3% with fibrinolysis and 3.4% with PCI).

Timing, therefore, trumps intervention.

These recent observations, developed exclusively from registry databases and not from randomized clinical trials, should give us pause to rethink our strategies. Registry data often can provide information that more closely represents actual community care.

The overemphasis on PCI for STEMI therapy has led to delay in treatment, when fibrinolysis could be just as effective. This pertains particularly to the patients who are transferred from non-PCI centers to PCI centers. More importantly, these studies emphasize the importance of developing better emergency care systems for the treatment of all patients, including those with STEMI.

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Both the American Heart Association and the American College of Cardiology have made a special effort to shorten door-to-balloon time in patients with ST-segment elevation MI in order to decrease the mortality of this high-risk group of patients.

Improvement in the logistics and quality of hospital systems has led to a significant decrease in door-to-balloon time (DBT). Systems have been initiated to effect rapid referral of ST-segment elevation MI (STEMI) patients to primary percutaneous coronary intervention (PCI) centers, either directly or by expeditious transfer of STEMI patients from facilities without interventional capability to PCI centers.

This process has been vigorously advocated by the AHA through its program, “Mission: Lifeline” aimed at improving and shortening the arrival time of STEMI patients to PCI hospitals.

Several recent reports provide insight into the issues relative to the importance of shortening of DBT and give us reason to evaluate the nuances of our strategies. A recent report from Michigan examined the Blue Cross Blue Shield database between 2003 and 2008 that included 8,771 patients. The report indicated that the DBT decreased from an average of 113 minutes to 76 minutes over the 8-year period without any impact on mortality. The number of patients with DBT of less than 90 minutes was 28.5% in 2003 and 67.2% in 2008, with an observed hospital mortality of 4.1% and 3.8% respectively (Arch. Intern. Med. 2010;170:1842-9).

The authors suggested that the failure to affect mortality by shortening the DBT was due in part to the fact that the higher-risk patients accounted for most deaths and experienced the longest symptom-to-door time.

It has been clear for some time that although expeditious hospital therapy is important, the duration between symptom onset and eventual arrival in a medical facility represents the major delay to therapy, compared with DBT. As the patient wrestles with the significance of his or her indigestion or chest pressure, valuable minutes fly by that have critical effects on patient survival.

Major efforts have been made to acquaint patients with the importance of dealing with symptoms, to little avail. But the time from initiating contact with the emergency care system and the patient's arrival to the hospital is a time frame that we should be able to deal with, according to strategies proposed by Mission: Lifeline.

In a study of 6,209 Danish patients who were followed in a registry from 2002 to 2008 in a highly structured emergency care system – unlike that of the United States, which is a system in name only – the investigators observed that the elapsed time from the call for emergency care to the ultimate arrival in the hospital had the largest impact on patient survival, and had greater importance on survival than did DBT (JAMA 2010;304:763-71). A system delay of up to 60 minutes was associated with a long-term mortality of 15.4%, whereas a delay of up to 360 minutes doubled that risk to 30.8%.

The investigators indicated that programs focusing on the time between the first contacts with the health system to initiation of reperfusion will have the greatest impact on mortality.

The importance of the timeliness of early therapy (either PCI or fibrinolysis) was emphasized in a similar registry study carried out in Quebec in 80 hospitals during 2006-2007 (JAMA 2010;303:2148-55). PCI was the predominant mode of therapy for STEMI, either by direct transport to a PCI center or a transfer from a non-PCI center to a PCI center.

Delay in either therapy had a major effect on mortality, and was of particular importance in patients who were transferred from a non-PCI hospital to a PCI center. DBT in directly admitted patients to PCI centers was 83 minutes, compared with 123 minutes for transferred patients. The most striking observation was that regardless of the mode of therapy – fibrinolysis administered within 30 minutes or PCI within 90 minutes – the 30-day mortality benefit of early therapy was similar (3.3% with fibrinolysis and 3.4% with PCI).

Timing, therefore, trumps intervention.

These recent observations, developed exclusively from registry databases and not from randomized clinical trials, should give us pause to rethink our strategies. Registry data often can provide information that more closely represents actual community care.

The overemphasis on PCI for STEMI therapy has led to delay in treatment, when fibrinolysis could be just as effective. This pertains particularly to the patients who are transferred from non-PCI centers to PCI centers. More importantly, these studies emphasize the importance of developing better emergency care systems for the treatment of all patients, including those with STEMI.

Both the American Heart Association and the American College of Cardiology have made a special effort to shorten door-to-balloon time in patients with ST-segment elevation MI in order to decrease the mortality of this high-risk group of patients.

Improvement in the logistics and quality of hospital systems has led to a significant decrease in door-to-balloon time (DBT). Systems have been initiated to effect rapid referral of ST-segment elevation MI (STEMI) patients to primary percutaneous coronary intervention (PCI) centers, either directly or by expeditious transfer of STEMI patients from facilities without interventional capability to PCI centers.

This process has been vigorously advocated by the AHA through its program, “Mission: Lifeline” aimed at improving and shortening the arrival time of STEMI patients to PCI hospitals.

Several recent reports provide insight into the issues relative to the importance of shortening of DBT and give us reason to evaluate the nuances of our strategies. A recent report from Michigan examined the Blue Cross Blue Shield database between 2003 and 2008 that included 8,771 patients. The report indicated that the DBT decreased from an average of 113 minutes to 76 minutes over the 8-year period without any impact on mortality. The number of patients with DBT of less than 90 minutes was 28.5% in 2003 and 67.2% in 2008, with an observed hospital mortality of 4.1% and 3.8% respectively (Arch. Intern. Med. 2010;170:1842-9).

The authors suggested that the failure to affect mortality by shortening the DBT was due in part to the fact that the higher-risk patients accounted for most deaths and experienced the longest symptom-to-door time.

It has been clear for some time that although expeditious hospital therapy is important, the duration between symptom onset and eventual arrival in a medical facility represents the major delay to therapy, compared with DBT. As the patient wrestles with the significance of his or her indigestion or chest pressure, valuable minutes fly by that have critical effects on patient survival.

Major efforts have been made to acquaint patients with the importance of dealing with symptoms, to little avail. But the time from initiating contact with the emergency care system and the patient's arrival to the hospital is a time frame that we should be able to deal with, according to strategies proposed by Mission: Lifeline.

In a study of 6,209 Danish patients who were followed in a registry from 2002 to 2008 in a highly structured emergency care system – unlike that of the United States, which is a system in name only – the investigators observed that the elapsed time from the call for emergency care to the ultimate arrival in the hospital had the largest impact on patient survival, and had greater importance on survival than did DBT (JAMA 2010;304:763-71). A system delay of up to 60 minutes was associated with a long-term mortality of 15.4%, whereas a delay of up to 360 minutes doubled that risk to 30.8%.

The investigators indicated that programs focusing on the time between the first contacts with the health system to initiation of reperfusion will have the greatest impact on mortality.

The importance of the timeliness of early therapy (either PCI or fibrinolysis) was emphasized in a similar registry study carried out in Quebec in 80 hospitals during 2006-2007 (JAMA 2010;303:2148-55). PCI was the predominant mode of therapy for STEMI, either by direct transport to a PCI center or a transfer from a non-PCI center to a PCI center.

Delay in either therapy had a major effect on mortality, and was of particular importance in patients who were transferred from a non-PCI hospital to a PCI center. DBT in directly admitted patients to PCI centers was 83 minutes, compared with 123 minutes for transferred patients. The most striking observation was that regardless of the mode of therapy – fibrinolysis administered within 30 minutes or PCI within 90 minutes – the 30-day mortality benefit of early therapy was similar (3.3% with fibrinolysis and 3.4% with PCI).

Timing, therefore, trumps intervention.

These recent observations, developed exclusively from registry databases and not from randomized clinical trials, should give us pause to rethink our strategies. Registry data often can provide information that more closely represents actual community care.

The overemphasis on PCI for STEMI therapy has led to delay in treatment, when fibrinolysis could be just as effective. This pertains particularly to the patients who are transferred from non-PCI centers to PCI centers. More importantly, these studies emphasize the importance of developing better emergency care systems for the treatment of all patients, including those with STEMI.

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CABG Volume vs. Performance

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Thanks to the joint effort of the Society for Thoracic Surgery and Consumer Reports, we can now learn about the quality of coronary artery bypass graft surgical centers both locally and throughout the United States. The report lists how each participating center is following the guidelines established by the STS.

Not all centers are participating in the Consumer Reports review, since it is voluntary. If we don't find our local center listed, we might assume that that center is either too busy doing other things or it is an outlier. Each center is rated on pre- and postoperative care and surgical mortality. Like the Michelin Guide for restaurants, each CABG center is scored on a three-star scale, with three stars for above average, two for average, and one for performance below the STS standards (N. Engl. J. Med. 2010;363:1593-5). Quality measures that are graded, in addition to surgical mortality, include postoperative renal failure, the need for reoperation, the use of beta-blockers before and after the operation and at discharge, lipid-lowering treatment at discharge, the occurrence of stroke, duration of intubations, wound infection, and the use of internal thoracic artery for bypass. Using this methodology, 29% of the centers were outliers, receiving only one star based on their performance during the last 3 years.

The volume of CABG surgery over the last few years has leveled off as a result of the wider use of percutaneous coronary intervention. According to the voluntary STS database, 163,149 isolated CABG procedures were performed in 955 operative sites in the United States in 2009 (DCRI executive summary) compared to 146,384 in 365 sites in 2000. The number of CABG centers has increased 2.5-fold in the past decade, while the CABG procedure has increased by about 11% annually. This has resulted in a significant dilution of procedures and an increase in the number of low-volume CABG centers.

Several studies have examined the relationship between volume and CABG mortality. In the most recent, Dr. David M. Shahian of Harvard Medical School, Boston, and colleagues looked at the association of CABG volume with process of care, mortality, and morbidity in the STS database (J. Thorac. Cardiovasc. Surg. 2010;139:273-82). Of the 737 centers that were included in the STS voluntary reports in 2007, 18% performed fewer than 100 procedures and 38% performed fewer than 150 procedures. The surgical mortality varied from 2.6% in the low-volume centers to 1.7% (a highly significant difference) in centers performing 450 procedures or more. Previous studies have reported a variable relationship between volume and mortality. According to the authors of this most recent study, “high volume does not guarantee a better outcome in any specific program” despite the significant difference between the high- and low-volume centers reported. It is quite possible that low-performing centers did not report their results, as only 733 of the 866 centers performing CABG surgery in 2007 were included in the study by Dr. Shahian. It is quite likely that there were more low-volume centers in action in 2007 among the 133 centers that are not included in the report, and that they could have affected the mortality rates in the low-volume centers. Because much of these data are provided on a voluntary basis, Consumer Reports' rankings may fall short in providing a complete picture of the current CABG quality.

Much of the development of new open-heart surgery programs are driven by both the perception and requirement that in some states surgical backup is needed in order to perform PCI. In many states, however, the availability of surgical back-up is no longer a requirement. In the setting of better stents and intervascular support technology, the need for the availability of open-heart surgical programs may no longer be relevant. The other driving force for the development of cardiosurgical programs is the marketing cachet for community hospitals in view of the intense competition between hospitals in many communities.

The development of improved technology and the increased skills of our interventional colleagues have led to much more aggressive PCI. As a result, patients who are referred for surgery have more complex coronary artery disease that is often associated with left ventricular failure and concomitant valvular disease. It is reasonable to question the advisability of the initiation and continuation of low-volume centers. As more low-volume centers enter the CABG surgical arena, it is possible that the marginal differences previously reported might become more significant. With the availability of almost 1,000 CABG centers nationwide, it would seem reasonable to call a halt to further expansion.

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Thanks to the joint effort of the Society for Thoracic Surgery and Consumer Reports, we can now learn about the quality of coronary artery bypass graft surgical centers both locally and throughout the United States. The report lists how each participating center is following the guidelines established by the STS.

Not all centers are participating in the Consumer Reports review, since it is voluntary. If we don't find our local center listed, we might assume that that center is either too busy doing other things or it is an outlier. Each center is rated on pre- and postoperative care and surgical mortality. Like the Michelin Guide for restaurants, each CABG center is scored on a three-star scale, with three stars for above average, two for average, and one for performance below the STS standards (N. Engl. J. Med. 2010;363:1593-5). Quality measures that are graded, in addition to surgical mortality, include postoperative renal failure, the need for reoperation, the use of beta-blockers before and after the operation and at discharge, lipid-lowering treatment at discharge, the occurrence of stroke, duration of intubations, wound infection, and the use of internal thoracic artery for bypass. Using this methodology, 29% of the centers were outliers, receiving only one star based on their performance during the last 3 years.

The volume of CABG surgery over the last few years has leveled off as a result of the wider use of percutaneous coronary intervention. According to the voluntary STS database, 163,149 isolated CABG procedures were performed in 955 operative sites in the United States in 2009 (DCRI executive summary) compared to 146,384 in 365 sites in 2000. The number of CABG centers has increased 2.5-fold in the past decade, while the CABG procedure has increased by about 11% annually. This has resulted in a significant dilution of procedures and an increase in the number of low-volume CABG centers.

Several studies have examined the relationship between volume and CABG mortality. In the most recent, Dr. David M. Shahian of Harvard Medical School, Boston, and colleagues looked at the association of CABG volume with process of care, mortality, and morbidity in the STS database (J. Thorac. Cardiovasc. Surg. 2010;139:273-82). Of the 737 centers that were included in the STS voluntary reports in 2007, 18% performed fewer than 100 procedures and 38% performed fewer than 150 procedures. The surgical mortality varied from 2.6% in the low-volume centers to 1.7% (a highly significant difference) in centers performing 450 procedures or more. Previous studies have reported a variable relationship between volume and mortality. According to the authors of this most recent study, “high volume does not guarantee a better outcome in any specific program” despite the significant difference between the high- and low-volume centers reported. It is quite possible that low-performing centers did not report their results, as only 733 of the 866 centers performing CABG surgery in 2007 were included in the study by Dr. Shahian. It is quite likely that there were more low-volume centers in action in 2007 among the 133 centers that are not included in the report, and that they could have affected the mortality rates in the low-volume centers. Because much of these data are provided on a voluntary basis, Consumer Reports' rankings may fall short in providing a complete picture of the current CABG quality.

Much of the development of new open-heart surgery programs are driven by both the perception and requirement that in some states surgical backup is needed in order to perform PCI. In many states, however, the availability of surgical back-up is no longer a requirement. In the setting of better stents and intervascular support technology, the need for the availability of open-heart surgical programs may no longer be relevant. The other driving force for the development of cardiosurgical programs is the marketing cachet for community hospitals in view of the intense competition between hospitals in many communities.

The development of improved technology and the increased skills of our interventional colleagues have led to much more aggressive PCI. As a result, patients who are referred for surgery have more complex coronary artery disease that is often associated with left ventricular failure and concomitant valvular disease. It is reasonable to question the advisability of the initiation and continuation of low-volume centers. As more low-volume centers enter the CABG surgical arena, it is possible that the marginal differences previously reported might become more significant. With the availability of almost 1,000 CABG centers nationwide, it would seem reasonable to call a halt to further expansion.

Thanks to the joint effort of the Society for Thoracic Surgery and Consumer Reports, we can now learn about the quality of coronary artery bypass graft surgical centers both locally and throughout the United States. The report lists how each participating center is following the guidelines established by the STS.

Not all centers are participating in the Consumer Reports review, since it is voluntary. If we don't find our local center listed, we might assume that that center is either too busy doing other things or it is an outlier. Each center is rated on pre- and postoperative care and surgical mortality. Like the Michelin Guide for restaurants, each CABG center is scored on a three-star scale, with three stars for above average, two for average, and one for performance below the STS standards (N. Engl. J. Med. 2010;363:1593-5). Quality measures that are graded, in addition to surgical mortality, include postoperative renal failure, the need for reoperation, the use of beta-blockers before and after the operation and at discharge, lipid-lowering treatment at discharge, the occurrence of stroke, duration of intubations, wound infection, and the use of internal thoracic artery for bypass. Using this methodology, 29% of the centers were outliers, receiving only one star based on their performance during the last 3 years.

The volume of CABG surgery over the last few years has leveled off as a result of the wider use of percutaneous coronary intervention. According to the voluntary STS database, 163,149 isolated CABG procedures were performed in 955 operative sites in the United States in 2009 (DCRI executive summary) compared to 146,384 in 365 sites in 2000. The number of CABG centers has increased 2.5-fold in the past decade, while the CABG procedure has increased by about 11% annually. This has resulted in a significant dilution of procedures and an increase in the number of low-volume CABG centers.

Several studies have examined the relationship between volume and CABG mortality. In the most recent, Dr. David M. Shahian of Harvard Medical School, Boston, and colleagues looked at the association of CABG volume with process of care, mortality, and morbidity in the STS database (J. Thorac. Cardiovasc. Surg. 2010;139:273-82). Of the 737 centers that were included in the STS voluntary reports in 2007, 18% performed fewer than 100 procedures and 38% performed fewer than 150 procedures. The surgical mortality varied from 2.6% in the low-volume centers to 1.7% (a highly significant difference) in centers performing 450 procedures or more. Previous studies have reported a variable relationship between volume and mortality. According to the authors of this most recent study, “high volume does not guarantee a better outcome in any specific program” despite the significant difference between the high- and low-volume centers reported. It is quite possible that low-performing centers did not report their results, as only 733 of the 866 centers performing CABG surgery in 2007 were included in the study by Dr. Shahian. It is quite likely that there were more low-volume centers in action in 2007 among the 133 centers that are not included in the report, and that they could have affected the mortality rates in the low-volume centers. Because much of these data are provided on a voluntary basis, Consumer Reports' rankings may fall short in providing a complete picture of the current CABG quality.

Much of the development of new open-heart surgery programs are driven by both the perception and requirement that in some states surgical backup is needed in order to perform PCI. In many states, however, the availability of surgical back-up is no longer a requirement. In the setting of better stents and intervascular support technology, the need for the availability of open-heart surgical programs may no longer be relevant. The other driving force for the development of cardiosurgical programs is the marketing cachet for community hospitals in view of the intense competition between hospitals in many communities.

The development of improved technology and the increased skills of our interventional colleagues have led to much more aggressive PCI. As a result, patients who are referred for surgery have more complex coronary artery disease that is often associated with left ventricular failure and concomitant valvular disease. It is reasonable to question the advisability of the initiation and continuation of low-volume centers. As more low-volume centers enter the CABG surgical arena, it is possible that the marginal differences previously reported might become more significant. With the availability of almost 1,000 CABG centers nationwide, it would seem reasonable to call a halt to further expansion.

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Atrial Fibrillation and ICDs

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The confluence of atrial fibrillation and an implanted cardioverter defibrillator for primary prevention of sudden death in patients with chronic heart failure is coming under increased scrutiny as a cause for inappropriate shocks. Current guidelines advise the use of an ICD or CRT-D (cardiac resynchronization therapy–defibrillator) in chronic heart failure patients with an ejection fraction of less than 35%.

It is well known that atrial fibrillation (AF) is a common occurrence in heart failure patients. AF is the most common reason for inappropriate ICD shocks, which comprise 20%–25% of all ICD discharges (J. Am. Coll. Cardiol. 2008;51:1357-65).

Inappropriate shocks have as yet been of little concern other than a cause of transitory discomfort to the patient and its impact on the patient's quality of life. However, recent follow-up examinations of patients suggest that inappropriate shocks in heart failure are more frequent in patients who also have AF, and that such patients have an increased mortality risk.

In a study of AF in ICD patients, 85% of whom were implanted for primary prevention, 27% had either paroxysmal or chronic persistent AF at the time of implantation (J. Am. Coll. Cardiol. 2010; 55:879-85). During the 3 years of follow-up, 4% developed new AF. The incidence of inappropriate shock was twice as frequent in patients with AF, compared with those with normal sinus rhythm. Patients with persistent AF experienced a significant, twofold increase in mortality, compared with patients in sinus rhythm. In the Sudden Cardiac Death in Heart Failure Trial (SCD-HeFT) using a single-lead defibrillator, appropriate shocks occurred in 48% of patients and inappropriate shocks comprised 32% of defibrillator shocks. Patients receiving either appropriate shocks for ventricular tachyarrhythmias or inappropriate shocks had an increased risk of mortality (N. Engl. J. Med. 2008;359:1009-17).

Inexpert programming may be a major cause of inappropriate shocks, according to a retrospective analysis of 89,000 patients that focused on the physiologic causes of inappropriate shocks in patients with new-onset or chronic AF presented by Dr. Bruce Wilkoff at the annual meeting of the Heart Rhythm Society. Dr. Wilkoff, of the Cleveland Clinic Foundation, suggests that the occurrence of inappropriate shocks is largely related to a low heart rate threshold for the discharge of a shock (more than 180 bpm), a rate that often encompasses the rate of AF, making it unlikely that the ICD will discriminate that rhythm from slow ventricular tachycardia or fibrillation, thus leading to inappropriate shocks. As the device comes out of the box it is preprogrammed at 180 bpm, and according to Dr. Wilkoff the implanter rarely adjusts it. This is probably more likely to occur in patients implanted by nonelectrophysiologists, which occurs in 25% of instances. He reported that in this retrospective study, increasing the rate threshold can decrease the frequency of inappropriate shocks by 17%–28%. He further makes a plea to adjust the threshold of ICD discharge to more than 200 bpm at the time of implantation (

There is some suggestion that the single-chamber ICD, the most commonly implanted ICD for primary prevention in heart failure patients, is not as sensitive to the recognition of supraventricular tachycardia as is a dual-chamber ICD, and therefore more likely to lead to an inappropriate shock (Circulation 2007;115:9-16). The MADIT-RIT trial is currently recruiting patients in a randomized trial using a dual-chamber ICD comparing standard programming to higher rate cutoff or a longer discharge delay or both on the frequency of inappropriate shocks. An additional objective of the trial will be to examine if these changes will affect mortality and morbidity.

The cause of heart failure progression in patients is uncertain and difficult to predict. It is possible that the development of AF is itself a marker for progression. On the other hand it is possible that ICD discharge may lead to further tissue loss or the generation of new or lethal arrhythmias in a previously compromised ventricle. Evidence for these possibilities is lacking. MADIT-RIT may throw more light on the subject.

After years of effort to expand the number of patients receiving ICDs, device manufacturers are now turning their efforts to making the devices safer. Modification of triggering thresholds can go a long way to making the life of the implanted patient more comfortable. Whether these modifications will improve survival is yet to be seen.

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The confluence of atrial fibrillation and an implanted cardioverter defibrillator for primary prevention of sudden death in patients with chronic heart failure is coming under increased scrutiny as a cause for inappropriate shocks. Current guidelines advise the use of an ICD or CRT-D (cardiac resynchronization therapy–defibrillator) in chronic heart failure patients with an ejection fraction of less than 35%.

It is well known that atrial fibrillation (AF) is a common occurrence in heart failure patients. AF is the most common reason for inappropriate ICD shocks, which comprise 20%–25% of all ICD discharges (J. Am. Coll. Cardiol. 2008;51:1357-65).

Inappropriate shocks have as yet been of little concern other than a cause of transitory discomfort to the patient and its impact on the patient's quality of life. However, recent follow-up examinations of patients suggest that inappropriate shocks in heart failure are more frequent in patients who also have AF, and that such patients have an increased mortality risk.

In a study of AF in ICD patients, 85% of whom were implanted for primary prevention, 27% had either paroxysmal or chronic persistent AF at the time of implantation (J. Am. Coll. Cardiol. 2010; 55:879-85). During the 3 years of follow-up, 4% developed new AF. The incidence of inappropriate shock was twice as frequent in patients with AF, compared with those with normal sinus rhythm. Patients with persistent AF experienced a significant, twofold increase in mortality, compared with patients in sinus rhythm. In the Sudden Cardiac Death in Heart Failure Trial (SCD-HeFT) using a single-lead defibrillator, appropriate shocks occurred in 48% of patients and inappropriate shocks comprised 32% of defibrillator shocks. Patients receiving either appropriate shocks for ventricular tachyarrhythmias or inappropriate shocks had an increased risk of mortality (N. Engl. J. Med. 2008;359:1009-17).

Inexpert programming may be a major cause of inappropriate shocks, according to a retrospective analysis of 89,000 patients that focused on the physiologic causes of inappropriate shocks in patients with new-onset or chronic AF presented by Dr. Bruce Wilkoff at the annual meeting of the Heart Rhythm Society. Dr. Wilkoff, of the Cleveland Clinic Foundation, suggests that the occurrence of inappropriate shocks is largely related to a low heart rate threshold for the discharge of a shock (more than 180 bpm), a rate that often encompasses the rate of AF, making it unlikely that the ICD will discriminate that rhythm from slow ventricular tachycardia or fibrillation, thus leading to inappropriate shocks. As the device comes out of the box it is preprogrammed at 180 bpm, and according to Dr. Wilkoff the implanter rarely adjusts it. This is probably more likely to occur in patients implanted by nonelectrophysiologists, which occurs in 25% of instances. He reported that in this retrospective study, increasing the rate threshold can decrease the frequency of inappropriate shocks by 17%–28%. He further makes a plea to adjust the threshold of ICD discharge to more than 200 bpm at the time of implantation (

There is some suggestion that the single-chamber ICD, the most commonly implanted ICD for primary prevention in heart failure patients, is not as sensitive to the recognition of supraventricular tachycardia as is a dual-chamber ICD, and therefore more likely to lead to an inappropriate shock (Circulation 2007;115:9-16). The MADIT-RIT trial is currently recruiting patients in a randomized trial using a dual-chamber ICD comparing standard programming to higher rate cutoff or a longer discharge delay or both on the frequency of inappropriate shocks. An additional objective of the trial will be to examine if these changes will affect mortality and morbidity.

The cause of heart failure progression in patients is uncertain and difficult to predict. It is possible that the development of AF is itself a marker for progression. On the other hand it is possible that ICD discharge may lead to further tissue loss or the generation of new or lethal arrhythmias in a previously compromised ventricle. Evidence for these possibilities is lacking. MADIT-RIT may throw more light on the subject.

After years of effort to expand the number of patients receiving ICDs, device manufacturers are now turning their efforts to making the devices safer. Modification of triggering thresholds can go a long way to making the life of the implanted patient more comfortable. Whether these modifications will improve survival is yet to be seen.

The confluence of atrial fibrillation and an implanted cardioverter defibrillator for primary prevention of sudden death in patients with chronic heart failure is coming under increased scrutiny as a cause for inappropriate shocks. Current guidelines advise the use of an ICD or CRT-D (cardiac resynchronization therapy–defibrillator) in chronic heart failure patients with an ejection fraction of less than 35%.

It is well known that atrial fibrillation (AF) is a common occurrence in heart failure patients. AF is the most common reason for inappropriate ICD shocks, which comprise 20%–25% of all ICD discharges (J. Am. Coll. Cardiol. 2008;51:1357-65).

Inappropriate shocks have as yet been of little concern other than a cause of transitory discomfort to the patient and its impact on the patient's quality of life. However, recent follow-up examinations of patients suggest that inappropriate shocks in heart failure are more frequent in patients who also have AF, and that such patients have an increased mortality risk.

In a study of AF in ICD patients, 85% of whom were implanted for primary prevention, 27% had either paroxysmal or chronic persistent AF at the time of implantation (J. Am. Coll. Cardiol. 2010; 55:879-85). During the 3 years of follow-up, 4% developed new AF. The incidence of inappropriate shock was twice as frequent in patients with AF, compared with those with normal sinus rhythm. Patients with persistent AF experienced a significant, twofold increase in mortality, compared with patients in sinus rhythm. In the Sudden Cardiac Death in Heart Failure Trial (SCD-HeFT) using a single-lead defibrillator, appropriate shocks occurred in 48% of patients and inappropriate shocks comprised 32% of defibrillator shocks. Patients receiving either appropriate shocks for ventricular tachyarrhythmias or inappropriate shocks had an increased risk of mortality (N. Engl. J. Med. 2008;359:1009-17).

Inexpert programming may be a major cause of inappropriate shocks, according to a retrospective analysis of 89,000 patients that focused on the physiologic causes of inappropriate shocks in patients with new-onset or chronic AF presented by Dr. Bruce Wilkoff at the annual meeting of the Heart Rhythm Society. Dr. Wilkoff, of the Cleveland Clinic Foundation, suggests that the occurrence of inappropriate shocks is largely related to a low heart rate threshold for the discharge of a shock (more than 180 bpm), a rate that often encompasses the rate of AF, making it unlikely that the ICD will discriminate that rhythm from slow ventricular tachycardia or fibrillation, thus leading to inappropriate shocks. As the device comes out of the box it is preprogrammed at 180 bpm, and according to Dr. Wilkoff the implanter rarely adjusts it. This is probably more likely to occur in patients implanted by nonelectrophysiologists, which occurs in 25% of instances. He reported that in this retrospective study, increasing the rate threshold can decrease the frequency of inappropriate shocks by 17%–28%. He further makes a plea to adjust the threshold of ICD discharge to more than 200 bpm at the time of implantation (

There is some suggestion that the single-chamber ICD, the most commonly implanted ICD for primary prevention in heart failure patients, is not as sensitive to the recognition of supraventricular tachycardia as is a dual-chamber ICD, and therefore more likely to lead to an inappropriate shock (Circulation 2007;115:9-16). The MADIT-RIT trial is currently recruiting patients in a randomized trial using a dual-chamber ICD comparing standard programming to higher rate cutoff or a longer discharge delay or both on the frequency of inappropriate shocks. An additional objective of the trial will be to examine if these changes will affect mortality and morbidity.

The cause of heart failure progression in patients is uncertain and difficult to predict. It is possible that the development of AF is itself a marker for progression. On the other hand it is possible that ICD discharge may lead to further tissue loss or the generation of new or lethal arrhythmias in a previously compromised ventricle. Evidence for these possibilities is lacking. MADIT-RIT may throw more light on the subject.

After years of effort to expand the number of patients receiving ICDs, device manufacturers are now turning their efforts to making the devices safer. Modification of triggering thresholds can go a long way to making the life of the implanted patient more comfortable. Whether these modifications will improve survival is yet to be seen.

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Diabetes and CVD: To Be, Or Not to Be, Aggressive?

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Because cardiovascular deaths account for 65%–70% of deaths in patients with diabetes, the disease has been labeled by various guideline committees as a coronary heart disease risk equivalent. Although there has been some debate regarding this, the recent data from a meta-analysis of 102 prospective studies with 8.49 million person-years of follow-up – showing that diabetes confers a twofold excess risk for CHD, major strokes, and deaths attributable to other vascular diseases – leaves little room for discussion in this regard (Lancet 2010;375:2215–22).

The vast majority of national and international guidelines have recommended aggressive management strategies to reduce blood glucose, blood pressure, and lipids in patients with diabetes in the hope of reducing CV events, despite the paucity of data from well-designed, prospective, randomized, controlled trials (RCTs). However, during the past decade, several well-designed RCTs have examined and compared the role of intensive versus usual management strategies in reducing the risk of macrovascular and microvascular events in DM. These studies include the Action to Control Cardiovascular Risk in Diabetes (ACCORD), Action in Diabetes and Vascular Disease (ADVANCE), and the Veterans Affairs Diabetes Trial (VADT).

Results from all of these well-designed RCTs have been somewhat perplexing, and contrary to the prevailing concepts. First of all, the results from the intensive glucose control arm from all three trials showed that the intensive glucose control strategy was not only associated with lack of benefit in primary end point, but indeed was harmful in a certain subset of patients due to the risks associated with resultant hypoglycemia. The results of the ACCORD study are particularly important because there was increased mortality in the ACCORD intensive glycemic control arm, which persisted even 1.5 years after the therapy for intensive control of glucose was stopped. The risk of hypoglycemia is further emphasized by the recent presentation from the ADVANCE group in showing that severe symptomatic hypoglycemia was associated with nearly threefold increased risks of macrovascular events, cardiovascular mortality, and all-cause mortality (N. Engl. J. Med. 2010;363:1410–8).

The lack of benefit of an intensive glucose control strategy should not be entirely surprising, because the prevailing wisdom was based on epidemiologic data showing higher risk of CV events with higher levels of glucose. However, it is important to realize that such an association might be due to other risks and/or risk factors. For now, based on the totality of the data it seems appropriate to be not too aggressive in controlling blood glucose and to stick with the current target of HbA1C below 7% for most patients with diabetes.

The lack of benefits reported from the ACCORD and ADVANCE blood pressure arms of the studies also deserves mention. In ACCORD, intensive antihypertensive therapy was targeted to a systolic pressure of less than 120 mm Hg and standard therapy treated to a systolic pressure target of less than 140 mm Hg. After 1 year, the mean systolic BP was 119 mm Hg in the intensive therapy group and 134 mm Hg in the standard-therapy group. At 1 year there was no difference in the primary composite outcome (nonfatal MI, nonfatal stroke, or death from cardiovascular causes).

It should perhaps not come as a surprise that there was no improvement in the primary composite outcome, since control of BP to less than 130 mm Hg systolic has not been shown to improve coronary events in most studies. On the other hand, there has been a close correlation between systolic BP and risk of stroke rate down to a lower value of 115 mm Hg, and in the ACCORD BP study also it was shown that decreasing systolic BP to a mean value of 119 mm Hg was associated with a 41% decrease in all stroke and also a significant reduction in nonfatal strokes.

Results from the ADVANCE study are also instructive in the management of hypertension in the diabetic patient. Compared with patients assigned placebo, those who received active therapy had a mean reduction in systolic BP of 5.6 mm Hg (mean 135 mm Hg in the active group vs. 140 mg Hg with placebo) and diastolic blood pressure of 2.2 mm Hg (mean 75 mm Hg and 77 mm Hg, respectively). The relative risk of death from cardiovascular disease was reduced by 18%, and death from any cause was reduced by 14%, both significant differences. This benefit was attributed mostly to reduction in microvascular events. Thus, unlike the aggressive glucose arms of the studies it appears that the BP control strategy does work and reduces the macrovascular end points directly related to BP.

 

 

Based on these results, it is fair to conclude that the evidence supports a comprehensive risk-reduction strategy addressing most risk factors in diabetes. However, such a strategy should include consideration of possible hazards of aggressive therapy. As always, the benefit:risk ratio should be carefully evaluated for each individual patient. We should remember the old maxim and Hippocratic oath, that above all we should do no harm.

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Because cardiovascular deaths account for 65%–70% of deaths in patients with diabetes, the disease has been labeled by various guideline committees as a coronary heart disease risk equivalent. Although there has been some debate regarding this, the recent data from a meta-analysis of 102 prospective studies with 8.49 million person-years of follow-up – showing that diabetes confers a twofold excess risk for CHD, major strokes, and deaths attributable to other vascular diseases – leaves little room for discussion in this regard (Lancet 2010;375:2215–22).

The vast majority of national and international guidelines have recommended aggressive management strategies to reduce blood glucose, blood pressure, and lipids in patients with diabetes in the hope of reducing CV events, despite the paucity of data from well-designed, prospective, randomized, controlled trials (RCTs). However, during the past decade, several well-designed RCTs have examined and compared the role of intensive versus usual management strategies in reducing the risk of macrovascular and microvascular events in DM. These studies include the Action to Control Cardiovascular Risk in Diabetes (ACCORD), Action in Diabetes and Vascular Disease (ADVANCE), and the Veterans Affairs Diabetes Trial (VADT).

Results from all of these well-designed RCTs have been somewhat perplexing, and contrary to the prevailing concepts. First of all, the results from the intensive glucose control arm from all three trials showed that the intensive glucose control strategy was not only associated with lack of benefit in primary end point, but indeed was harmful in a certain subset of patients due to the risks associated with resultant hypoglycemia. The results of the ACCORD study are particularly important because there was increased mortality in the ACCORD intensive glycemic control arm, which persisted even 1.5 years after the therapy for intensive control of glucose was stopped. The risk of hypoglycemia is further emphasized by the recent presentation from the ADVANCE group in showing that severe symptomatic hypoglycemia was associated with nearly threefold increased risks of macrovascular events, cardiovascular mortality, and all-cause mortality (N. Engl. J. Med. 2010;363:1410–8).

The lack of benefit of an intensive glucose control strategy should not be entirely surprising, because the prevailing wisdom was based on epidemiologic data showing higher risk of CV events with higher levels of glucose. However, it is important to realize that such an association might be due to other risks and/or risk factors. For now, based on the totality of the data it seems appropriate to be not too aggressive in controlling blood glucose and to stick with the current target of HbA1C below 7% for most patients with diabetes.

The lack of benefits reported from the ACCORD and ADVANCE blood pressure arms of the studies also deserves mention. In ACCORD, intensive antihypertensive therapy was targeted to a systolic pressure of less than 120 mm Hg and standard therapy treated to a systolic pressure target of less than 140 mm Hg. After 1 year, the mean systolic BP was 119 mm Hg in the intensive therapy group and 134 mm Hg in the standard-therapy group. At 1 year there was no difference in the primary composite outcome (nonfatal MI, nonfatal stroke, or death from cardiovascular causes).

It should perhaps not come as a surprise that there was no improvement in the primary composite outcome, since control of BP to less than 130 mm Hg systolic has not been shown to improve coronary events in most studies. On the other hand, there has been a close correlation between systolic BP and risk of stroke rate down to a lower value of 115 mm Hg, and in the ACCORD BP study also it was shown that decreasing systolic BP to a mean value of 119 mm Hg was associated with a 41% decrease in all stroke and also a significant reduction in nonfatal strokes.

Results from the ADVANCE study are also instructive in the management of hypertension in the diabetic patient. Compared with patients assigned placebo, those who received active therapy had a mean reduction in systolic BP of 5.6 mm Hg (mean 135 mm Hg in the active group vs. 140 mg Hg with placebo) and diastolic blood pressure of 2.2 mm Hg (mean 75 mm Hg and 77 mm Hg, respectively). The relative risk of death from cardiovascular disease was reduced by 18%, and death from any cause was reduced by 14%, both significant differences. This benefit was attributed mostly to reduction in microvascular events. Thus, unlike the aggressive glucose arms of the studies it appears that the BP control strategy does work and reduces the macrovascular end points directly related to BP.

 

 

Based on these results, it is fair to conclude that the evidence supports a comprehensive risk-reduction strategy addressing most risk factors in diabetes. However, such a strategy should include consideration of possible hazards of aggressive therapy. As always, the benefit:risk ratio should be carefully evaluated for each individual patient. We should remember the old maxim and Hippocratic oath, that above all we should do no harm.

Because cardiovascular deaths account for 65%–70% of deaths in patients with diabetes, the disease has been labeled by various guideline committees as a coronary heart disease risk equivalent. Although there has been some debate regarding this, the recent data from a meta-analysis of 102 prospective studies with 8.49 million person-years of follow-up – showing that diabetes confers a twofold excess risk for CHD, major strokes, and deaths attributable to other vascular diseases – leaves little room for discussion in this regard (Lancet 2010;375:2215–22).

The vast majority of national and international guidelines have recommended aggressive management strategies to reduce blood glucose, blood pressure, and lipids in patients with diabetes in the hope of reducing CV events, despite the paucity of data from well-designed, prospective, randomized, controlled trials (RCTs). However, during the past decade, several well-designed RCTs have examined and compared the role of intensive versus usual management strategies in reducing the risk of macrovascular and microvascular events in DM. These studies include the Action to Control Cardiovascular Risk in Diabetes (ACCORD), Action in Diabetes and Vascular Disease (ADVANCE), and the Veterans Affairs Diabetes Trial (VADT).

Results from all of these well-designed RCTs have been somewhat perplexing, and contrary to the prevailing concepts. First of all, the results from the intensive glucose control arm from all three trials showed that the intensive glucose control strategy was not only associated with lack of benefit in primary end point, but indeed was harmful in a certain subset of patients due to the risks associated with resultant hypoglycemia. The results of the ACCORD study are particularly important because there was increased mortality in the ACCORD intensive glycemic control arm, which persisted even 1.5 years after the therapy for intensive control of glucose was stopped. The risk of hypoglycemia is further emphasized by the recent presentation from the ADVANCE group in showing that severe symptomatic hypoglycemia was associated with nearly threefold increased risks of macrovascular events, cardiovascular mortality, and all-cause mortality (N. Engl. J. Med. 2010;363:1410–8).

The lack of benefit of an intensive glucose control strategy should not be entirely surprising, because the prevailing wisdom was based on epidemiologic data showing higher risk of CV events with higher levels of glucose. However, it is important to realize that such an association might be due to other risks and/or risk factors. For now, based on the totality of the data it seems appropriate to be not too aggressive in controlling blood glucose and to stick with the current target of HbA1C below 7% for most patients with diabetes.

The lack of benefits reported from the ACCORD and ADVANCE blood pressure arms of the studies also deserves mention. In ACCORD, intensive antihypertensive therapy was targeted to a systolic pressure of less than 120 mm Hg and standard therapy treated to a systolic pressure target of less than 140 mm Hg. After 1 year, the mean systolic BP was 119 mm Hg in the intensive therapy group and 134 mm Hg in the standard-therapy group. At 1 year there was no difference in the primary composite outcome (nonfatal MI, nonfatal stroke, or death from cardiovascular causes).

It should perhaps not come as a surprise that there was no improvement in the primary composite outcome, since control of BP to less than 130 mm Hg systolic has not been shown to improve coronary events in most studies. On the other hand, there has been a close correlation between systolic BP and risk of stroke rate down to a lower value of 115 mm Hg, and in the ACCORD BP study also it was shown that decreasing systolic BP to a mean value of 119 mm Hg was associated with a 41% decrease in all stroke and also a significant reduction in nonfatal strokes.

Results from the ADVANCE study are also instructive in the management of hypertension in the diabetic patient. Compared with patients assigned placebo, those who received active therapy had a mean reduction in systolic BP of 5.6 mm Hg (mean 135 mm Hg in the active group vs. 140 mg Hg with placebo) and diastolic blood pressure of 2.2 mm Hg (mean 75 mm Hg and 77 mm Hg, respectively). The relative risk of death from cardiovascular disease was reduced by 18%, and death from any cause was reduced by 14%, both significant differences. This benefit was attributed mostly to reduction in microvascular events. Thus, unlike the aggressive glucose arms of the studies it appears that the BP control strategy does work and reduces the macrovascular end points directly related to BP.

 

 

Based on these results, it is fair to conclude that the evidence supports a comprehensive risk-reduction strategy addressing most risk factors in diabetes. However, such a strategy should include consideration of possible hazards of aggressive therapy. As always, the benefit:risk ratio should be carefully evaluated for each individual patient. We should remember the old maxim and Hippocratic oath, that above all we should do no harm.

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Heart and Kidney Transplantation

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Heart and Kidney Transplantation

The comorbidity of heart failure and kidney failure poses a therapeutic dilemma for both cardiologists and nephrologists and has become a more important problem in managing an aging population. Many of the drugs used to treat heart failure have adverse effects on renal function, and chronic heart failure patients poorly tolerate chronic dialysis.

The development of left ventricular assist devices (LVADs) has expanded the therapeutic options available for the treatment of advanced heart failure, but their use has resulted in many LVAD patients experiencing progressive renal failure. As a result, more patients are going on to combined LVAD and dialysis (LVAD-D) therapy and becoming candidates for combined heart and kidney transplantation (HKT). The creation of this new chronic cardiorenal population poses important logistic and societal challenges.

There is very little information available to estimate the benefit of chronic device support or HKT, but the potential issues associated with outcome in patients with chronic left ventricular dysfunction speak to the need to consider the potential benefit of this class of therapy. Chronic renal dysfunction is a well-recognized comorbidity in heart failure patients, but until the development of LVADs, heart transplantation was an unlikely outcome. In a survey of almost 20,000 heart transplant recipients reported in the United Network for Organ Sharing database prior to December 2005, only 1.4% received both a heart and a kidney transplant (Arch. Surg. 2009;144:241-6). This was mainly because advanced renal disease has been an exclusion criteria for heart transplantation alone.

The wider application of LVADs as chronic destinations therapy and as a bridge to transplantation has made combined LVAD-D a hitherto ignored option for heart failure patients. In some cases this dual support is a planned therapeutic course. In others, it has become a matter of salvage, when renal failure occurs as a complication of LVAD implantation necessitating acute and chronic dialysis.

According to the UNOS report, prior to 2005, that is, before the wider use of LVADs, 12% of patients receiving HKT were on an LVAD at the time of HKT and 56% were on chronic dialysis. The authors developed a risk score, driven largely by the presence of peripheral vascular disease, age, the use of renal dialysis, and the need for LVAD support. The 1-year survival rate in the 274 patients receiving HKT varied from 93% in the low-risk group to 62% in the high-risk group. The 1-year risk in the high-risk group was four times that of the low-risk group.

HKT can be performed simultaneously or sequentially. Small series from simultaneous single institutions reported an operative mortality of 21% with a 5-year survival of 66% (Am. J. Transpl. 2001;1:89-92).

The benefit of this dual approach to heart failure therapy must be compared to the benefit of each organ transplantation alone. Survival benefit for heart-alone and kidney-alone transplantation now exceeds 10 years. Of concern however is the 3.8% annual mortality rate, a threefold increase since 1995, of HT patients waiting for a kidney transplant.

The relative paucity of both kidney and heart donors demands that the mortality for dual therapy must be measured against that standard. But multi-organ transplantation deprives one needy patient from a precious organ and does little to expand the availability of organ transplantation to a larger population. Nevertheless, the comorbidity of heart failure and renal failure remains a major issue in the management of the chronic heart failure patient and almost certainly will lead to a greater use of LVAD-D and HKT.

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The comorbidity of heart failure and kidney failure poses a therapeutic dilemma for both cardiologists and nephrologists and has become a more important problem in managing an aging population. Many of the drugs used to treat heart failure have adverse effects on renal function, and chronic heart failure patients poorly tolerate chronic dialysis.

The development of left ventricular assist devices (LVADs) has expanded the therapeutic options available for the treatment of advanced heart failure, but their use has resulted in many LVAD patients experiencing progressive renal failure. As a result, more patients are going on to combined LVAD and dialysis (LVAD-D) therapy and becoming candidates for combined heart and kidney transplantation (HKT). The creation of this new chronic cardiorenal population poses important logistic and societal challenges.

There is very little information available to estimate the benefit of chronic device support or HKT, but the potential issues associated with outcome in patients with chronic left ventricular dysfunction speak to the need to consider the potential benefit of this class of therapy. Chronic renal dysfunction is a well-recognized comorbidity in heart failure patients, but until the development of LVADs, heart transplantation was an unlikely outcome. In a survey of almost 20,000 heart transplant recipients reported in the United Network for Organ Sharing database prior to December 2005, only 1.4% received both a heart and a kidney transplant (Arch. Surg. 2009;144:241-6). This was mainly because advanced renal disease has been an exclusion criteria for heart transplantation alone.

The wider application of LVADs as chronic destinations therapy and as a bridge to transplantation has made combined LVAD-D a hitherto ignored option for heart failure patients. In some cases this dual support is a planned therapeutic course. In others, it has become a matter of salvage, when renal failure occurs as a complication of LVAD implantation necessitating acute and chronic dialysis.

According to the UNOS report, prior to 2005, that is, before the wider use of LVADs, 12% of patients receiving HKT were on an LVAD at the time of HKT and 56% were on chronic dialysis. The authors developed a risk score, driven largely by the presence of peripheral vascular disease, age, the use of renal dialysis, and the need for LVAD support. The 1-year survival rate in the 274 patients receiving HKT varied from 93% in the low-risk group to 62% in the high-risk group. The 1-year risk in the high-risk group was four times that of the low-risk group.

HKT can be performed simultaneously or sequentially. Small series from simultaneous single institutions reported an operative mortality of 21% with a 5-year survival of 66% (Am. J. Transpl. 2001;1:89-92).

The benefit of this dual approach to heart failure therapy must be compared to the benefit of each organ transplantation alone. Survival benefit for heart-alone and kidney-alone transplantation now exceeds 10 years. Of concern however is the 3.8% annual mortality rate, a threefold increase since 1995, of HT patients waiting for a kidney transplant.

The relative paucity of both kidney and heart donors demands that the mortality for dual therapy must be measured against that standard. But multi-organ transplantation deprives one needy patient from a precious organ and does little to expand the availability of organ transplantation to a larger population. Nevertheless, the comorbidity of heart failure and renal failure remains a major issue in the management of the chronic heart failure patient and almost certainly will lead to a greater use of LVAD-D and HKT.

The comorbidity of heart failure and kidney failure poses a therapeutic dilemma for both cardiologists and nephrologists and has become a more important problem in managing an aging population. Many of the drugs used to treat heart failure have adverse effects on renal function, and chronic heart failure patients poorly tolerate chronic dialysis.

The development of left ventricular assist devices (LVADs) has expanded the therapeutic options available for the treatment of advanced heart failure, but their use has resulted in many LVAD patients experiencing progressive renal failure. As a result, more patients are going on to combined LVAD and dialysis (LVAD-D) therapy and becoming candidates for combined heart and kidney transplantation (HKT). The creation of this new chronic cardiorenal population poses important logistic and societal challenges.

There is very little information available to estimate the benefit of chronic device support or HKT, but the potential issues associated with outcome in patients with chronic left ventricular dysfunction speak to the need to consider the potential benefit of this class of therapy. Chronic renal dysfunction is a well-recognized comorbidity in heart failure patients, but until the development of LVADs, heart transplantation was an unlikely outcome. In a survey of almost 20,000 heart transplant recipients reported in the United Network for Organ Sharing database prior to December 2005, only 1.4% received both a heart and a kidney transplant (Arch. Surg. 2009;144:241-6). This was mainly because advanced renal disease has been an exclusion criteria for heart transplantation alone.

The wider application of LVADs as chronic destinations therapy and as a bridge to transplantation has made combined LVAD-D a hitherto ignored option for heart failure patients. In some cases this dual support is a planned therapeutic course. In others, it has become a matter of salvage, when renal failure occurs as a complication of LVAD implantation necessitating acute and chronic dialysis.

According to the UNOS report, prior to 2005, that is, before the wider use of LVADs, 12% of patients receiving HKT were on an LVAD at the time of HKT and 56% were on chronic dialysis. The authors developed a risk score, driven largely by the presence of peripheral vascular disease, age, the use of renal dialysis, and the need for LVAD support. The 1-year survival rate in the 274 patients receiving HKT varied from 93% in the low-risk group to 62% in the high-risk group. The 1-year risk in the high-risk group was four times that of the low-risk group.

HKT can be performed simultaneously or sequentially. Small series from simultaneous single institutions reported an operative mortality of 21% with a 5-year survival of 66% (Am. J. Transpl. 2001;1:89-92).

The benefit of this dual approach to heart failure therapy must be compared to the benefit of each organ transplantation alone. Survival benefit for heart-alone and kidney-alone transplantation now exceeds 10 years. Of concern however is the 3.8% annual mortality rate, a threefold increase since 1995, of HT patients waiting for a kidney transplant.

The relative paucity of both kidney and heart donors demands that the mortality for dual therapy must be measured against that standard. But multi-organ transplantation deprives one needy patient from a precious organ and does little to expand the availability of organ transplantation to a larger population. Nevertheless, the comorbidity of heart failure and renal failure remains a major issue in the management of the chronic heart failure patient and almost certainly will lead to a greater use of LVAD-D and HKT.

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Changing Heart Failure Mortality

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It has become increasingly evident that there has been a significant shift in the long-term mortality of patients admitted to the hospital with heart failure. Discharge from the hospital after an acute event often leads to a revolving door, returning the patients back into the hospital with recurrent symptoms.

There is little question that the current guideline-driven therapy of beta-blockers, ACE inhibitors, and aldosterone receptor blockers have had a significant impact on chronic heart failure therapy. Yet there are almost 1 million first and readmissions annually to U.S. hospitals with the primary diagnosis of heart failure, our nation's most common admitting diagnosis. Despite increased adherence and the success of guideline therapy and inpatient educational efforts, heart failure specialists continue to be faced with an unacceptable early mortality and 60-day readmission rate of 35%.

A recent trended temporal analysis of outcomes of hospitalized patients with heart failure between 1993 and 2006 provides both good and bad news. During that period, in-hospital mortality decreased from 8.5% to 4.3%. But the 30-day postdischarge mortality rate increased from 4.3% to 6.4%. The postdischarge mortality rate during the 30 days post discharge now exceeds the in-patient mortality. During the same 30-day period, the readmission rate increased from 17.2% to 20.1%. Associated with these outcomes, the authors point out that there had been a significant shortening of the length of stay from 8.8 days in 1993 to 6.3 days in 2006 (JAMA 2010;303:2141-7). This shortened hospital stay is largely driven by Medicare reimbursement rates. Their analysis raises important question in regard to the potential effect of the shortening of hospital stay on postdischarge events.

Several studies have examined inpatient care as it affects readmission rates. All of these studies have indicated increase compliance to guideline therapy. However, one rather striking observation has been the failure to achieve weight loss or diuresis during hospitalization. The ADHERE registry points out that 53% of patients admitted with acute congestive heart failure, presumably with volume overload, lose less than 5 pounds, and 20% actually gain weight. It is true that some heart failure may be related to causes other than fluid accumulation, but for the vast majority of patients fluid accumulation represents the primary precipitating event leading to acute heart failure. It is quite possible that the shortened hospital stay leads to premature discharge before adequate diuresis can be achieved. I have found it difficult if not impossible to obtain daily weights in the hospital, and actually urge all of my patients to buy a scale and use it to adjust their diuretic program at home. A novel idea like this would probably not be allowed in the hospital.

A subtle increase in fluid retention associated with increase in pulmonary artery pressure preceding the acute exacerbation of heart failure has been observed in a number of studies using implantable devices. These devices can continuously monitor pulmonary fluid volume and pulmonary artery pressure. Research has been carried out using pulmonary impedance measurements in an attempt to continuously measuring pulmonary fluid. Some of these devices have been incorporated into pacemaker-defibrillator devices, but as yet have not been approved for clinical use. The CHAMPION trial recently reported at the European Heart Failure Society meeting reported that using a totally implantable pulmonary artery pressure sensor in patients with NYHA Class III patients led to improvement in heart failure outcomes. In a small randomized study over a 60-day period of follow-up, symptomatic improvement and the need for rehospitalization was observed.

The issue of early readmission and mortality after acute therapy remains a dilemma facing the hospitalists, internists, and family physicians who treat most of these patients. A careful assessment of the early discharge policies is in order. The mantra of expeditious hospital discharge may be incriminated in the readmission and mortality outcomes. It is also possible that physicians are not aggressive enough with diuretic therapy, both in the hospital and after discharge. Whether an implantable pulmonary artery sensor will replace the bathroom scale remains to be seen. I have observed over time, much to my displeasure, that my bathroom scale never lies.

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It has become increasingly evident that there has been a significant shift in the long-term mortality of patients admitted to the hospital with heart failure. Discharge from the hospital after an acute event often leads to a revolving door, returning the patients back into the hospital with recurrent symptoms.

There is little question that the current guideline-driven therapy of beta-blockers, ACE inhibitors, and aldosterone receptor blockers have had a significant impact on chronic heart failure therapy. Yet there are almost 1 million first and readmissions annually to U.S. hospitals with the primary diagnosis of heart failure, our nation's most common admitting diagnosis. Despite increased adherence and the success of guideline therapy and inpatient educational efforts, heart failure specialists continue to be faced with an unacceptable early mortality and 60-day readmission rate of 35%.

A recent trended temporal analysis of outcomes of hospitalized patients with heart failure between 1993 and 2006 provides both good and bad news. During that period, in-hospital mortality decreased from 8.5% to 4.3%. But the 30-day postdischarge mortality rate increased from 4.3% to 6.4%. The postdischarge mortality rate during the 30 days post discharge now exceeds the in-patient mortality. During the same 30-day period, the readmission rate increased from 17.2% to 20.1%. Associated with these outcomes, the authors point out that there had been a significant shortening of the length of stay from 8.8 days in 1993 to 6.3 days in 2006 (JAMA 2010;303:2141-7). This shortened hospital stay is largely driven by Medicare reimbursement rates. Their analysis raises important question in regard to the potential effect of the shortening of hospital stay on postdischarge events.

Several studies have examined inpatient care as it affects readmission rates. All of these studies have indicated increase compliance to guideline therapy. However, one rather striking observation has been the failure to achieve weight loss or diuresis during hospitalization. The ADHERE registry points out that 53% of patients admitted with acute congestive heart failure, presumably with volume overload, lose less than 5 pounds, and 20% actually gain weight. It is true that some heart failure may be related to causes other than fluid accumulation, but for the vast majority of patients fluid accumulation represents the primary precipitating event leading to acute heart failure. It is quite possible that the shortened hospital stay leads to premature discharge before adequate diuresis can be achieved. I have found it difficult if not impossible to obtain daily weights in the hospital, and actually urge all of my patients to buy a scale and use it to adjust their diuretic program at home. A novel idea like this would probably not be allowed in the hospital.

A subtle increase in fluid retention associated with increase in pulmonary artery pressure preceding the acute exacerbation of heart failure has been observed in a number of studies using implantable devices. These devices can continuously monitor pulmonary fluid volume and pulmonary artery pressure. Research has been carried out using pulmonary impedance measurements in an attempt to continuously measuring pulmonary fluid. Some of these devices have been incorporated into pacemaker-defibrillator devices, but as yet have not been approved for clinical use. The CHAMPION trial recently reported at the European Heart Failure Society meeting reported that using a totally implantable pulmonary artery pressure sensor in patients with NYHA Class III patients led to improvement in heart failure outcomes. In a small randomized study over a 60-day period of follow-up, symptomatic improvement and the need for rehospitalization was observed.

The issue of early readmission and mortality after acute therapy remains a dilemma facing the hospitalists, internists, and family physicians who treat most of these patients. A careful assessment of the early discharge policies is in order. The mantra of expeditious hospital discharge may be incriminated in the readmission and mortality outcomes. It is also possible that physicians are not aggressive enough with diuretic therapy, both in the hospital and after discharge. Whether an implantable pulmonary artery sensor will replace the bathroom scale remains to be seen. I have observed over time, much to my displeasure, that my bathroom scale never lies.

It has become increasingly evident that there has been a significant shift in the long-term mortality of patients admitted to the hospital with heart failure. Discharge from the hospital after an acute event often leads to a revolving door, returning the patients back into the hospital with recurrent symptoms.

There is little question that the current guideline-driven therapy of beta-blockers, ACE inhibitors, and aldosterone receptor blockers have had a significant impact on chronic heart failure therapy. Yet there are almost 1 million first and readmissions annually to U.S. hospitals with the primary diagnosis of heart failure, our nation's most common admitting diagnosis. Despite increased adherence and the success of guideline therapy and inpatient educational efforts, heart failure specialists continue to be faced with an unacceptable early mortality and 60-day readmission rate of 35%.

A recent trended temporal analysis of outcomes of hospitalized patients with heart failure between 1993 and 2006 provides both good and bad news. During that period, in-hospital mortality decreased from 8.5% to 4.3%. But the 30-day postdischarge mortality rate increased from 4.3% to 6.4%. The postdischarge mortality rate during the 30 days post discharge now exceeds the in-patient mortality. During the same 30-day period, the readmission rate increased from 17.2% to 20.1%. Associated with these outcomes, the authors point out that there had been a significant shortening of the length of stay from 8.8 days in 1993 to 6.3 days in 2006 (JAMA 2010;303:2141-7). This shortened hospital stay is largely driven by Medicare reimbursement rates. Their analysis raises important question in regard to the potential effect of the shortening of hospital stay on postdischarge events.

Several studies have examined inpatient care as it affects readmission rates. All of these studies have indicated increase compliance to guideline therapy. However, one rather striking observation has been the failure to achieve weight loss or diuresis during hospitalization. The ADHERE registry points out that 53% of patients admitted with acute congestive heart failure, presumably with volume overload, lose less than 5 pounds, and 20% actually gain weight. It is true that some heart failure may be related to causes other than fluid accumulation, but for the vast majority of patients fluid accumulation represents the primary precipitating event leading to acute heart failure. It is quite possible that the shortened hospital stay leads to premature discharge before adequate diuresis can be achieved. I have found it difficult if not impossible to obtain daily weights in the hospital, and actually urge all of my patients to buy a scale and use it to adjust their diuretic program at home. A novel idea like this would probably not be allowed in the hospital.

A subtle increase in fluid retention associated with increase in pulmonary artery pressure preceding the acute exacerbation of heart failure has been observed in a number of studies using implantable devices. These devices can continuously monitor pulmonary fluid volume and pulmonary artery pressure. Research has been carried out using pulmonary impedance measurements in an attempt to continuously measuring pulmonary fluid. Some of these devices have been incorporated into pacemaker-defibrillator devices, but as yet have not been approved for clinical use. The CHAMPION trial recently reported at the European Heart Failure Society meeting reported that using a totally implantable pulmonary artery pressure sensor in patients with NYHA Class III patients led to improvement in heart failure outcomes. In a small randomized study over a 60-day period of follow-up, symptomatic improvement and the need for rehospitalization was observed.

The issue of early readmission and mortality after acute therapy remains a dilemma facing the hospitalists, internists, and family physicians who treat most of these patients. A careful assessment of the early discharge policies is in order. The mantra of expeditious hospital discharge may be incriminated in the readmission and mortality outcomes. It is also possible that physicians are not aggressive enough with diuretic therapy, both in the hospital and after discharge. Whether an implantable pulmonary artery sensor will replace the bathroom scale remains to be seen. I have observed over time, much to my displeasure, that my bathroom scale never lies.

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Lessons From Rosiglitazone

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As the sun sets on the most recent chapter in the rosiglitazone saga, one may search for a “teaching moment” we can all profit from. Unfortunately, the rosiglitazone experience stands out as a unique example of how not to behave in clinical trials, and how not to introduce a new drug therapy and to maintain its clinical benefit in the eyes of patients and physicians. What is of particular concern is that the story paints a dismal picture of all the players, including industry, clinical scientists, and the federal government.

In the beginning, the Food and Drug Administration did not demand rigorous assessment of cardiovascular outcomes in the studies which approved thiazolidinediones, even though the major expression of diabetes over time is heart disease. The rosiglitazone uproar that began in 2007 led the FDA to require such assessments in 2008, and that error has now been corrected. One could argue that the important changes in the agency's approval process stands as the one positive outcome of this story.

In order to understand the cardiovascular outcomes of one of the TZDs, a meta-analysis—a research tool that is messy and imprecise at best—examined rosiglitazone using the clinical data that were available at that time in regard to the cardiovascular effects of the drug (N. Engl. J. Med. 2007;356:2457-71). Although carried out in a spirit of the search for clinical truths in drug therapy, it gravitated into a confrontation between GlaxoSmithKline (GSK) and the authors of the meta-analysis when significant increases in adverse cardiovascular events were reported. This led to what appeared to many as an overt attempt by GSK to cover up any negative information about the drug. Much of the “backstory” comes from a variety of sources in the press and documents obtained as part of a Senate investigation, which described in a January 2010 report a corporate environment at GSK bent on suppressing any information that could implicate adverse cardiovascular outcomes with the drug and that could impact on its sales of more than $2 billion annually.

The publication of the rosiglitazone meta-analysis led to the premature unblinding of the RECORD (Rosiglitazone Evaluated for Cardiac Outcomes and Regulation of Glycemia in Diabetes) study, which was at the time not quite two-thirds through its planned 6-year test of the cardiovascular effects of rosiglitazone against other non-TZD diabetes drugs. For reasons that appeared to be related more to marketing pressures than clinical knowledge, the medical leadership of the trial and the sponsor GSK agreed to publish the unplanned interim results of RECORD (N. Engl. J. Med. 2007;357:28-38). This seriously compromised the data analysis and the responsibilities of the investigators to the patients in the study. If it had been allowed to continue to conclusion without the interim analysis, it could have provided the needed clinical data to answer some of the concerns about the drug.[At the behest of the FDA, a new 16,000 patient study, Thiazolidinedione Intervention With Vitamin D Evaluation (TIDE) sponsored by GSK, to compare rosiglitazone and pioglitazone to placebo, has begun. The presumption is that patients can be recruited in this trial in the light of the publicity.[eports from the recent meeting of the FDA's Endocrinologic and Metabolic Drugs and Drug Safety and Risk Management Advisory Committees in the lay and professional press.

In that 2-day meeting, which left us exactly where we started, the lack of leadership from the FDA was astounding, with members of its staff providing contradictory information and opinions. And of the 33 member panel made up of cardiologists, endocrinologists, statisticians, and patient representatives, 12 voted to have rosiglitazone withdrawn, 17 to restrict the use of the drug with an increased patient and physician warning, 3 to leave it unchanged, and 1 abstained. It seems to this observer that at times some of the committee members were more concerned about the welfare of GSK than the safety of diabetes patients.

One could make a case for the continued use of rosiglitazone to treat diabetes if it were the only option, but with the plethora of other drugs available it does not seem to be in the patients' best interest to continue to use a drug that is potentially unsafe. Even more dubious is the argument for the continuation of the TIDE trial, which turns the drug approval process upside down and seems to be little more than a marketing effort. It is hard to imagine that patients will agree to participate in a randomized trial given the FDA advisory committee coverage and the potential risks of rosiglitazone expressed in it.

 

 

At a time when the clinical trials industry (and it has become an industry) is at the threshold of testing new complex clinical strategies for previously untreated conditions like Alzheimer's disease, we should be able to manage our research with intelligence and a sense of the primacy of our responsibility to patient care. It is critical to create an environment in which both patients and physicians believe that we are living up to those goals. The rosiglitazone saga leaves us far short of meeting that challenge.

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As the sun sets on the most recent chapter in the rosiglitazone saga, one may search for a “teaching moment” we can all profit from. Unfortunately, the rosiglitazone experience stands out as a unique example of how not to behave in clinical trials, and how not to introduce a new drug therapy and to maintain its clinical benefit in the eyes of patients and physicians. What is of particular concern is that the story paints a dismal picture of all the players, including industry, clinical scientists, and the federal government.

In the beginning, the Food and Drug Administration did not demand rigorous assessment of cardiovascular outcomes in the studies which approved thiazolidinediones, even though the major expression of diabetes over time is heart disease. The rosiglitazone uproar that began in 2007 led the FDA to require such assessments in 2008, and that error has now been corrected. One could argue that the important changes in the agency's approval process stands as the one positive outcome of this story.

In order to understand the cardiovascular outcomes of one of the TZDs, a meta-analysis—a research tool that is messy and imprecise at best—examined rosiglitazone using the clinical data that were available at that time in regard to the cardiovascular effects of the drug (N. Engl. J. Med. 2007;356:2457-71). Although carried out in a spirit of the search for clinical truths in drug therapy, it gravitated into a confrontation between GlaxoSmithKline (GSK) and the authors of the meta-analysis when significant increases in adverse cardiovascular events were reported. This led to what appeared to many as an overt attempt by GSK to cover up any negative information about the drug. Much of the “backstory” comes from a variety of sources in the press and documents obtained as part of a Senate investigation, which described in a January 2010 report a corporate environment at GSK bent on suppressing any information that could implicate adverse cardiovascular outcomes with the drug and that could impact on its sales of more than $2 billion annually.

The publication of the rosiglitazone meta-analysis led to the premature unblinding of the RECORD (Rosiglitazone Evaluated for Cardiac Outcomes and Regulation of Glycemia in Diabetes) study, which was at the time not quite two-thirds through its planned 6-year test of the cardiovascular effects of rosiglitazone against other non-TZD diabetes drugs. For reasons that appeared to be related more to marketing pressures than clinical knowledge, the medical leadership of the trial and the sponsor GSK agreed to publish the unplanned interim results of RECORD (N. Engl. J. Med. 2007;357:28-38). This seriously compromised the data analysis and the responsibilities of the investigators to the patients in the study. If it had been allowed to continue to conclusion without the interim analysis, it could have provided the needed clinical data to answer some of the concerns about the drug.[At the behest of the FDA, a new 16,000 patient study, Thiazolidinedione Intervention With Vitamin D Evaluation (TIDE) sponsored by GSK, to compare rosiglitazone and pioglitazone to placebo, has begun. The presumption is that patients can be recruited in this trial in the light of the publicity.[eports from the recent meeting of the FDA's Endocrinologic and Metabolic Drugs and Drug Safety and Risk Management Advisory Committees in the lay and professional press.

In that 2-day meeting, which left us exactly where we started, the lack of leadership from the FDA was astounding, with members of its staff providing contradictory information and opinions. And of the 33 member panel made up of cardiologists, endocrinologists, statisticians, and patient representatives, 12 voted to have rosiglitazone withdrawn, 17 to restrict the use of the drug with an increased patient and physician warning, 3 to leave it unchanged, and 1 abstained. It seems to this observer that at times some of the committee members were more concerned about the welfare of GSK than the safety of diabetes patients.

One could make a case for the continued use of rosiglitazone to treat diabetes if it were the only option, but with the plethora of other drugs available it does not seem to be in the patients' best interest to continue to use a drug that is potentially unsafe. Even more dubious is the argument for the continuation of the TIDE trial, which turns the drug approval process upside down and seems to be little more than a marketing effort. It is hard to imagine that patients will agree to participate in a randomized trial given the FDA advisory committee coverage and the potential risks of rosiglitazone expressed in it.

 

 

At a time when the clinical trials industry (and it has become an industry) is at the threshold of testing new complex clinical strategies for previously untreated conditions like Alzheimer's disease, we should be able to manage our research with intelligence and a sense of the primacy of our responsibility to patient care. It is critical to create an environment in which both patients and physicians believe that we are living up to those goals. The rosiglitazone saga leaves us far short of meeting that challenge.

As the sun sets on the most recent chapter in the rosiglitazone saga, one may search for a “teaching moment” we can all profit from. Unfortunately, the rosiglitazone experience stands out as a unique example of how not to behave in clinical trials, and how not to introduce a new drug therapy and to maintain its clinical benefit in the eyes of patients and physicians. What is of particular concern is that the story paints a dismal picture of all the players, including industry, clinical scientists, and the federal government.

In the beginning, the Food and Drug Administration did not demand rigorous assessment of cardiovascular outcomes in the studies which approved thiazolidinediones, even though the major expression of diabetes over time is heart disease. The rosiglitazone uproar that began in 2007 led the FDA to require such assessments in 2008, and that error has now been corrected. One could argue that the important changes in the agency's approval process stands as the one positive outcome of this story.

In order to understand the cardiovascular outcomes of one of the TZDs, a meta-analysis—a research tool that is messy and imprecise at best—examined rosiglitazone using the clinical data that were available at that time in regard to the cardiovascular effects of the drug (N. Engl. J. Med. 2007;356:2457-71). Although carried out in a spirit of the search for clinical truths in drug therapy, it gravitated into a confrontation between GlaxoSmithKline (GSK) and the authors of the meta-analysis when significant increases in adverse cardiovascular events were reported. This led to what appeared to many as an overt attempt by GSK to cover up any negative information about the drug. Much of the “backstory” comes from a variety of sources in the press and documents obtained as part of a Senate investigation, which described in a January 2010 report a corporate environment at GSK bent on suppressing any information that could implicate adverse cardiovascular outcomes with the drug and that could impact on its sales of more than $2 billion annually.

The publication of the rosiglitazone meta-analysis led to the premature unblinding of the RECORD (Rosiglitazone Evaluated for Cardiac Outcomes and Regulation of Glycemia in Diabetes) study, which was at the time not quite two-thirds through its planned 6-year test of the cardiovascular effects of rosiglitazone against other non-TZD diabetes drugs. For reasons that appeared to be related more to marketing pressures than clinical knowledge, the medical leadership of the trial and the sponsor GSK agreed to publish the unplanned interim results of RECORD (N. Engl. J. Med. 2007;357:28-38). This seriously compromised the data analysis and the responsibilities of the investigators to the patients in the study. If it had been allowed to continue to conclusion without the interim analysis, it could have provided the needed clinical data to answer some of the concerns about the drug.[At the behest of the FDA, a new 16,000 patient study, Thiazolidinedione Intervention With Vitamin D Evaluation (TIDE) sponsored by GSK, to compare rosiglitazone and pioglitazone to placebo, has begun. The presumption is that patients can be recruited in this trial in the light of the publicity.[eports from the recent meeting of the FDA's Endocrinologic and Metabolic Drugs and Drug Safety and Risk Management Advisory Committees in the lay and professional press.

In that 2-day meeting, which left us exactly where we started, the lack of leadership from the FDA was astounding, with members of its staff providing contradictory information and opinions. And of the 33 member panel made up of cardiologists, endocrinologists, statisticians, and patient representatives, 12 voted to have rosiglitazone withdrawn, 17 to restrict the use of the drug with an increased patient and physician warning, 3 to leave it unchanged, and 1 abstained. It seems to this observer that at times some of the committee members were more concerned about the welfare of GSK than the safety of diabetes patients.

One could make a case for the continued use of rosiglitazone to treat diabetes if it were the only option, but with the plethora of other drugs available it does not seem to be in the patients' best interest to continue to use a drug that is potentially unsafe. Even more dubious is the argument for the continuation of the TIDE trial, which turns the drug approval process upside down and seems to be little more than a marketing effort. It is hard to imagine that patients will agree to participate in a randomized trial given the FDA advisory committee coverage and the potential risks of rosiglitazone expressed in it.

 

 

At a time when the clinical trials industry (and it has become an industry) is at the threshold of testing new complex clinical strategies for previously untreated conditions like Alzheimer's disease, we should be able to manage our research with intelligence and a sense of the primacy of our responsibility to patient care. It is critical to create an environment in which both patients and physicians believe that we are living up to those goals. The rosiglitazone saga leaves us far short of meeting that challenge.

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Caring for Adults With Congenital Heart Disease

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As the cardiology community has become aware of the steadily growing number of adults with complex congenital heart disease over the past 2 decades, we've embarked on a multipronged effort to address the organization of care, the workforce needs, and the funding to increase the knowledge base in this area.

Now is a good time to look at how the landscape has changed since the 32nd Bethesda Conference in 2000 on “Care of the Adult With Congenital Heart Disease,” to give ourselves a grade on our accomplishment, and to examine the factors that will facilitate future progress. It is particularly prescient to examine the needs of this population as a distinct chronic care model as we go stumbling forward in our efforts for health care reform.

The 32nd Bethesda Conference convened a panel of cardiologists, surgeons, health policy experts, and government (health care) administrators to define the broad outlines of health care delivery to the ACHD population. It proposed the organization of care into regional ACHD centers that could serve as home base for complex patients, support other providers throughout the region through consultation, train ACHD cardiologists, and advance the field through research. The conference also proposed specific training and funding requirements to meet workforce needs. So, what have we accomplished in the decade since that report? We have taken significant steps to carry out the vision of that conference, but we have not overcome one pervasive element that is continuing to hold back our progress. Accomplishments first, then challenges:

In regard to regionalization, the Adult Congenital Heart Association (ACHA), an organization of patients and health professionals, has developed a roster of self-designated ACHD centers and has an ongoing consensus project, Vision 2020, to define regional centers of care.

Preparation of the workforce has been advanced through several different actions. The new Adult Congenital and Pediatric Cardiology (ACPC) section of the American College of Cardiology provides a forum for pediatric and adult cardiologists and a catalyst for developing research teams, advocating criteria for third-tier subspecialty certification, and defining educational needs.

The development and publication of the ACC/American Heart Association Guidelines for the Management of Adults With Congenital Heart Disease in 2008, an ambitious project, provides guidance for the general cardiologist managing ACHD patients and indicates the best process for integration with ACHD regional centers (J. Am. Coll. Cardiol. 2008;52:143–263).

So, where do we stand?

We have seen an encouraging collaboration between pediatric and adult cardiologists with career interests in ACHD, but although there is increasing interest in this career track, the numbers of trainees entering this pathway is still small and some who have taken the additional years of training complain of the paucity of job opportunities. Why? Because disease burden and clinical need do not translate into full-time equivalents at medical centers. Most centers must focus increasingly on the bottom line. The ACHD population, on average, represents the younger end of the adult age spectrum and therefore, a higher proportion of the underinsured, making a poor business case for a center to support the appropriate infrastructure for individuals with so many special needs.

It should surprise no one that the major obstacle to the development of an appropriate system of care for ACHD patients comes down to money. This population is more complex, and needs highly specialized care. This is not a recipe for a profit center. It is, rather, a cost center. Yet I believe that our present system of non-care is ultimately more costly than an appropriate level of care. Patients with ACHD are more likely to be admitted for inpatient care through the emergency department. For the lack of proactive management, a patient with single ventricle may slip into unremitting failure and require heart transplantation decades before it's necessary.

We must look at the costs of the present system and propose a system of care for ACHD patients that will produce better results at no increase or even lower costs over the intermediate and long term. This is a unique population, with a complex profile, that has never before existed. ACHD patients are also, in general, at the beginning of their productive lives, so the differences in outcomes with proactive care will have a sustained impact on society.

If a case can be made for a sustainable business model, it will unleash all the great ideas that we have developed over the past decade. It is an interesting and compelling challenge to which I invite others to join in what should be a creative and meaningful effort.

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As the cardiology community has become aware of the steadily growing number of adults with complex congenital heart disease over the past 2 decades, we've embarked on a multipronged effort to address the organization of care, the workforce needs, and the funding to increase the knowledge base in this area.

Now is a good time to look at how the landscape has changed since the 32nd Bethesda Conference in 2000 on “Care of the Adult With Congenital Heart Disease,” to give ourselves a grade on our accomplishment, and to examine the factors that will facilitate future progress. It is particularly prescient to examine the needs of this population as a distinct chronic care model as we go stumbling forward in our efforts for health care reform.

The 32nd Bethesda Conference convened a panel of cardiologists, surgeons, health policy experts, and government (health care) administrators to define the broad outlines of health care delivery to the ACHD population. It proposed the organization of care into regional ACHD centers that could serve as home base for complex patients, support other providers throughout the region through consultation, train ACHD cardiologists, and advance the field through research. The conference also proposed specific training and funding requirements to meet workforce needs. So, what have we accomplished in the decade since that report? We have taken significant steps to carry out the vision of that conference, but we have not overcome one pervasive element that is continuing to hold back our progress. Accomplishments first, then challenges:

In regard to regionalization, the Adult Congenital Heart Association (ACHA), an organization of patients and health professionals, has developed a roster of self-designated ACHD centers and has an ongoing consensus project, Vision 2020, to define regional centers of care.

Preparation of the workforce has been advanced through several different actions. The new Adult Congenital and Pediatric Cardiology (ACPC) section of the American College of Cardiology provides a forum for pediatric and adult cardiologists and a catalyst for developing research teams, advocating criteria for third-tier subspecialty certification, and defining educational needs.

The development and publication of the ACC/American Heart Association Guidelines for the Management of Adults With Congenital Heart Disease in 2008, an ambitious project, provides guidance for the general cardiologist managing ACHD patients and indicates the best process for integration with ACHD regional centers (J. Am. Coll. Cardiol. 2008;52:143–263).

So, where do we stand?

We have seen an encouraging collaboration between pediatric and adult cardiologists with career interests in ACHD, but although there is increasing interest in this career track, the numbers of trainees entering this pathway is still small and some who have taken the additional years of training complain of the paucity of job opportunities. Why? Because disease burden and clinical need do not translate into full-time equivalents at medical centers. Most centers must focus increasingly on the bottom line. The ACHD population, on average, represents the younger end of the adult age spectrum and therefore, a higher proportion of the underinsured, making a poor business case for a center to support the appropriate infrastructure for individuals with so many special needs.

It should surprise no one that the major obstacle to the development of an appropriate system of care for ACHD patients comes down to money. This population is more complex, and needs highly specialized care. This is not a recipe for a profit center. It is, rather, a cost center. Yet I believe that our present system of non-care is ultimately more costly than an appropriate level of care. Patients with ACHD are more likely to be admitted for inpatient care through the emergency department. For the lack of proactive management, a patient with single ventricle may slip into unremitting failure and require heart transplantation decades before it's necessary.

We must look at the costs of the present system and propose a system of care for ACHD patients that will produce better results at no increase or even lower costs over the intermediate and long term. This is a unique population, with a complex profile, that has never before existed. ACHD patients are also, in general, at the beginning of their productive lives, so the differences in outcomes with proactive care will have a sustained impact on society.

If a case can be made for a sustainable business model, it will unleash all the great ideas that we have developed over the past decade. It is an interesting and compelling challenge to which I invite others to join in what should be a creative and meaningful effort.

As the cardiology community has become aware of the steadily growing number of adults with complex congenital heart disease over the past 2 decades, we've embarked on a multipronged effort to address the organization of care, the workforce needs, and the funding to increase the knowledge base in this area.

Now is a good time to look at how the landscape has changed since the 32nd Bethesda Conference in 2000 on “Care of the Adult With Congenital Heart Disease,” to give ourselves a grade on our accomplishment, and to examine the factors that will facilitate future progress. It is particularly prescient to examine the needs of this population as a distinct chronic care model as we go stumbling forward in our efforts for health care reform.

The 32nd Bethesda Conference convened a panel of cardiologists, surgeons, health policy experts, and government (health care) administrators to define the broad outlines of health care delivery to the ACHD population. It proposed the organization of care into regional ACHD centers that could serve as home base for complex patients, support other providers throughout the region through consultation, train ACHD cardiologists, and advance the field through research. The conference also proposed specific training and funding requirements to meet workforce needs. So, what have we accomplished in the decade since that report? We have taken significant steps to carry out the vision of that conference, but we have not overcome one pervasive element that is continuing to hold back our progress. Accomplishments first, then challenges:

In regard to regionalization, the Adult Congenital Heart Association (ACHA), an organization of patients and health professionals, has developed a roster of self-designated ACHD centers and has an ongoing consensus project, Vision 2020, to define regional centers of care.

Preparation of the workforce has been advanced through several different actions. The new Adult Congenital and Pediatric Cardiology (ACPC) section of the American College of Cardiology provides a forum for pediatric and adult cardiologists and a catalyst for developing research teams, advocating criteria for third-tier subspecialty certification, and defining educational needs.

The development and publication of the ACC/American Heart Association Guidelines for the Management of Adults With Congenital Heart Disease in 2008, an ambitious project, provides guidance for the general cardiologist managing ACHD patients and indicates the best process for integration with ACHD regional centers (J. Am. Coll. Cardiol. 2008;52:143–263).

So, where do we stand?

We have seen an encouraging collaboration between pediatric and adult cardiologists with career interests in ACHD, but although there is increasing interest in this career track, the numbers of trainees entering this pathway is still small and some who have taken the additional years of training complain of the paucity of job opportunities. Why? Because disease burden and clinical need do not translate into full-time equivalents at medical centers. Most centers must focus increasingly on the bottom line. The ACHD population, on average, represents the younger end of the adult age spectrum and therefore, a higher proportion of the underinsured, making a poor business case for a center to support the appropriate infrastructure for individuals with so many special needs.

It should surprise no one that the major obstacle to the development of an appropriate system of care for ACHD patients comes down to money. This population is more complex, and needs highly specialized care. This is not a recipe for a profit center. It is, rather, a cost center. Yet I believe that our present system of non-care is ultimately more costly than an appropriate level of care. Patients with ACHD are more likely to be admitted for inpatient care through the emergency department. For the lack of proactive management, a patient with single ventricle may slip into unremitting failure and require heart transplantation decades before it's necessary.

We must look at the costs of the present system and propose a system of care for ACHD patients that will produce better results at no increase or even lower costs over the intermediate and long term. This is a unique population, with a complex profile, that has never before existed. ACHD patients are also, in general, at the beginning of their productive lives, so the differences in outcomes with proactive care will have a sustained impact on society.

If a case can be made for a sustainable business model, it will unleash all the great ideas that we have developed over the past decade. It is an interesting and compelling challenge to which I invite others to join in what should be a creative and meaningful effort.

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From Cottage Industry to Corporate Medicine

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American Medicine has been in transition since the mid-20th century and is about to change yet again into a new model.

It has shifted from a cottage industry comprised of myriad private offices to a corporate model dominated by hospitals and the insurance industry and funded in large part by the federal government.

The cottage industry model had as its philosophic foundation the importance and preservation of the physician's financial and medical independence in dealing with patients. Over time, the transition from physician-owned private practice to multispecialty physician–owned clinics became a natural outgrowth of the complexity of modern medical care. The technological developments in cardiology made a close relationship between hospitals and cardiologists a clinical if not economic necessity.

Beginning in the mid-20th century, the American hospital changed from a place where the private physicians could treat pneumonia and remove gallbladders to the current destination of critically ill patients cared for by salaried hospital physicians. The growth of the American hospital can be traced to the huge expenditures by the federal government in the post–World War II years. Since then, hospitals have continued to grow and have become the dominant player in the medical structure of the community.

As health economics changed, however, the need and desire to control the community medical practice patterns led to a variety of financial arrangements between hospitals and physicians, most of which linked the practitioners closer to the hospitals. The shift has occurred as more young physicians—facing major training debt and a reluctance to take on the paperwork required of health insurance compliance—see health care organizations managed by hospitals as a means to a better lifestyle and financial approach to practicing medicine.

The insurance industry's involvement with health care started in 1933, when insurance companies began selling prepaid hospital plans. They were soon consolidated into Blue Cross, which provided depression-era hospitals with needed income and stability. Physicians later reluctantly signed on to Blue Shield in 1944 with the proviso that they would control the plan. The next step was Medicare and Medicaid created in the environment of angry protests from both the American Hospital Association and the American Medical Association during the Johnson administration in 1965 (“The Social Transformation of American Medicine” by Paul Starr [Basic Books, 1982]).

And now we have president Obama's health care legislation, which portends a further evolution of the relationship between hospitals and practicing physicians, particularly cardiologists.

Even before the new health care legislation was passed, the balance between physician-owned and hospital-based practices had undergone major changes. Between 2005 and 2008, the number of physician-owned practices decreased from 70% to less than 50%. The American College of Cardiology estimates that there has been a 50% decrease in private practice in the last year as cardiologists migrated to hospital practices.

For the private cardiologists who own their own clinics, the recent decrease in Medicare reimbursement rates for imaging tests has been the death knell and has forced many to merge their practices with hospitals. The charges for cardiac imaging, which provided much of the financial support for the private physician–owned offices, was the first target of health care planners aimed at decreasing costs by limiting the presumed overuse of outpatient testing. As a result, it decreased testing reimbursement by 27%–40% and accelerated the migration of cardiologists to hospitals.

Paradoxically, if there is no change in utilization, Medicare will end up paying twice as much for a nuclear or echo study as a result of the cost shift from doctor's office fee to hospital reimbursement, according the ACC.

The new model of health care, provided by hospitals and supported by the insurance industry, has now become dominant in many communities. Because of their size and ability to control local practice standards, these collaboratives tend to overwhelm their competition. In Massachusetts, where the new model of health care is playing out, major conflicts have already occurred between hospital-based insurance plans such as Partners HeathCare System, perceived as high-cost providers, and low-cost plans. The Department of Justice is investigating Partners for possible anticompetitive behavior. Although this is not on the scale of Goldman Sachs' misadventures, it is worth noting as we move through the new health care paradigm.

Slowly but surely the American doctor is being incorporated into hospital-insurance alliances supported in a large part by the federal government and private insurers. This may not be all bad, and probably not news to most of you, but it is worth considering how we arrived at this moment in history.

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American Medicine has been in transition since the mid-20th century and is about to change yet again into a new model.

It has shifted from a cottage industry comprised of myriad private offices to a corporate model dominated by hospitals and the insurance industry and funded in large part by the federal government.

The cottage industry model had as its philosophic foundation the importance and preservation of the physician's financial and medical independence in dealing with patients. Over time, the transition from physician-owned private practice to multispecialty physician–owned clinics became a natural outgrowth of the complexity of modern medical care. The technological developments in cardiology made a close relationship between hospitals and cardiologists a clinical if not economic necessity.

Beginning in the mid-20th century, the American hospital changed from a place where the private physicians could treat pneumonia and remove gallbladders to the current destination of critically ill patients cared for by salaried hospital physicians. The growth of the American hospital can be traced to the huge expenditures by the federal government in the post–World War II years. Since then, hospitals have continued to grow and have become the dominant player in the medical structure of the community.

As health economics changed, however, the need and desire to control the community medical practice patterns led to a variety of financial arrangements between hospitals and physicians, most of which linked the practitioners closer to the hospitals. The shift has occurred as more young physicians—facing major training debt and a reluctance to take on the paperwork required of health insurance compliance—see health care organizations managed by hospitals as a means to a better lifestyle and financial approach to practicing medicine.

The insurance industry's involvement with health care started in 1933, when insurance companies began selling prepaid hospital plans. They were soon consolidated into Blue Cross, which provided depression-era hospitals with needed income and stability. Physicians later reluctantly signed on to Blue Shield in 1944 with the proviso that they would control the plan. The next step was Medicare and Medicaid created in the environment of angry protests from both the American Hospital Association and the American Medical Association during the Johnson administration in 1965 (“The Social Transformation of American Medicine” by Paul Starr [Basic Books, 1982]).

And now we have president Obama's health care legislation, which portends a further evolution of the relationship between hospitals and practicing physicians, particularly cardiologists.

Even before the new health care legislation was passed, the balance between physician-owned and hospital-based practices had undergone major changes. Between 2005 and 2008, the number of physician-owned practices decreased from 70% to less than 50%. The American College of Cardiology estimates that there has been a 50% decrease in private practice in the last year as cardiologists migrated to hospital practices.

For the private cardiologists who own their own clinics, the recent decrease in Medicare reimbursement rates for imaging tests has been the death knell and has forced many to merge their practices with hospitals. The charges for cardiac imaging, which provided much of the financial support for the private physician–owned offices, was the first target of health care planners aimed at decreasing costs by limiting the presumed overuse of outpatient testing. As a result, it decreased testing reimbursement by 27%–40% and accelerated the migration of cardiologists to hospitals.

Paradoxically, if there is no change in utilization, Medicare will end up paying twice as much for a nuclear or echo study as a result of the cost shift from doctor's office fee to hospital reimbursement, according the ACC.

The new model of health care, provided by hospitals and supported by the insurance industry, has now become dominant in many communities. Because of their size and ability to control local practice standards, these collaboratives tend to overwhelm their competition. In Massachusetts, where the new model of health care is playing out, major conflicts have already occurred between hospital-based insurance plans such as Partners HeathCare System, perceived as high-cost providers, and low-cost plans. The Department of Justice is investigating Partners for possible anticompetitive behavior. Although this is not on the scale of Goldman Sachs' misadventures, it is worth noting as we move through the new health care paradigm.

Slowly but surely the American doctor is being incorporated into hospital-insurance alliances supported in a large part by the federal government and private insurers. This may not be all bad, and probably not news to most of you, but it is worth considering how we arrived at this moment in history.

American Medicine has been in transition since the mid-20th century and is about to change yet again into a new model.

It has shifted from a cottage industry comprised of myriad private offices to a corporate model dominated by hospitals and the insurance industry and funded in large part by the federal government.

The cottage industry model had as its philosophic foundation the importance and preservation of the physician's financial and medical independence in dealing with patients. Over time, the transition from physician-owned private practice to multispecialty physician–owned clinics became a natural outgrowth of the complexity of modern medical care. The technological developments in cardiology made a close relationship between hospitals and cardiologists a clinical if not economic necessity.

Beginning in the mid-20th century, the American hospital changed from a place where the private physicians could treat pneumonia and remove gallbladders to the current destination of critically ill patients cared for by salaried hospital physicians. The growth of the American hospital can be traced to the huge expenditures by the federal government in the post–World War II years. Since then, hospitals have continued to grow and have become the dominant player in the medical structure of the community.

As health economics changed, however, the need and desire to control the community medical practice patterns led to a variety of financial arrangements between hospitals and physicians, most of which linked the practitioners closer to the hospitals. The shift has occurred as more young physicians—facing major training debt and a reluctance to take on the paperwork required of health insurance compliance—see health care organizations managed by hospitals as a means to a better lifestyle and financial approach to practicing medicine.

The insurance industry's involvement with health care started in 1933, when insurance companies began selling prepaid hospital plans. They were soon consolidated into Blue Cross, which provided depression-era hospitals with needed income and stability. Physicians later reluctantly signed on to Blue Shield in 1944 with the proviso that they would control the plan. The next step was Medicare and Medicaid created in the environment of angry protests from both the American Hospital Association and the American Medical Association during the Johnson administration in 1965 (“The Social Transformation of American Medicine” by Paul Starr [Basic Books, 1982]).

And now we have president Obama's health care legislation, which portends a further evolution of the relationship between hospitals and practicing physicians, particularly cardiologists.

Even before the new health care legislation was passed, the balance between physician-owned and hospital-based practices had undergone major changes. Between 2005 and 2008, the number of physician-owned practices decreased from 70% to less than 50%. The American College of Cardiology estimates that there has been a 50% decrease in private practice in the last year as cardiologists migrated to hospital practices.

For the private cardiologists who own their own clinics, the recent decrease in Medicare reimbursement rates for imaging tests has been the death knell and has forced many to merge their practices with hospitals. The charges for cardiac imaging, which provided much of the financial support for the private physician–owned offices, was the first target of health care planners aimed at decreasing costs by limiting the presumed overuse of outpatient testing. As a result, it decreased testing reimbursement by 27%–40% and accelerated the migration of cardiologists to hospitals.

Paradoxically, if there is no change in utilization, Medicare will end up paying twice as much for a nuclear or echo study as a result of the cost shift from doctor's office fee to hospital reimbursement, according the ACC.

The new model of health care, provided by hospitals and supported by the insurance industry, has now become dominant in many communities. Because of their size and ability to control local practice standards, these collaboratives tend to overwhelm their competition. In Massachusetts, where the new model of health care is playing out, major conflicts have already occurred between hospital-based insurance plans such as Partners HeathCare System, perceived as high-cost providers, and low-cost plans. The Department of Justice is investigating Partners for possible anticompetitive behavior. Although this is not on the scale of Goldman Sachs' misadventures, it is worth noting as we move through the new health care paradigm.

Slowly but surely the American doctor is being incorporated into hospital-insurance alliances supported in a large part by the federal government and private insurers. This may not be all bad, and probably not news to most of you, but it is worth considering how we arrived at this moment in history.

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Ever since Dr. Joseph L. Goldstein and Dr. Michael S. Brown established the foundation of the cholesterol hypothesis, the medical community has taken aim at lowering serum cholesterol in men and women throughout the world. The initial attempts to lower cholesterol with diet, exercise, and occasionally surgery met with only marginal success.

Not until the introduction of statin therapy to our therapeutic armamentarium did we achieve measurable success in both lowering cholesterol and an associated decrease in atherosclerotic cardiovascular disease mortality and morbidity.

Our success in lowering cholesterol has been measured by a number of international epidemiology studies, the first of which was performed in 1996-1997, the Lipid Treatment Assessment Project (L-TAP) (Arch. Intern. Med. 2000;160:459-67).

The most recent study, L-TAP 2, was an international survey carried out in more than 10,000 patients in nine countries between 2006 and 2007 (Circulation 2009;120:28-34) and catalogues the profound decrease in cholesterol lowering that has been achieved during the last 10 years.

The result of L-TAP 2 points out the significant success that has been achieved during that period in lowering serum LDL cholesterol and raising HDL cholesterol. Successful cholesterol-lowering to the country-specific levels was achieved in 73% of all patients and 67% of high-risk patients. Most of the success was achieved in patients with low to moderate risk.

Comparable data in the earlier L-TAP study reported successful lowering in only 38% and 18% respectively. Dr. Antonio Gotto, in an accompanying editorial, suggests this success was likely due to “the introduction of more effective lipid-lowering therapies” rather than improved patient compliance or physician awareness.

Unfortunately, the very-high-risk patients, those with coronary artery disease and at least two major risk factors, remain a serious problem. Successful lowering of serum cholesterol to the target of below 70 mg/dL was reached in only 30% of the very-high-risk patients. Because of the delayed introduction of the higher potency drugs atorvastatin and rosuvastatin, their use was limited to approximately one-half of the patients in L-TAP 2.

It is possible that the more widespread introduction of these drugs or even more potent drugs in the future will result in further cholesterol lowering in the very-high-risk patients who are still undertreated yet have reached therapeutic goal. The strong association of hypertension, obesity, and diabetes in the high-risk group emphasizes the importance of a multidimensional therapeutic approach to the high-risk population.

The minimal target for cholesterol treatment is yet to be determined, but the Treating to New Targets (TNT) study comparing high- and low-dose atorvastatin, indicated that treatment to an LDL cholesterol level of 77 mg/dL, compared with 101 mg/dL, was associated with a 22% in the reduction of the risk of a first major cardiovascular event (J. Am. Coll. Cardiol. 2006;48:1793-9).

The authors noted that their study was limited by the uncertainty about the nature of the patients and participating physicians. This uncertainty provides an important message in light of our current health care debate. It can be presumed that patients in L-TAP 2 are unique and hardly representative of this country's population as whole. This is important to keep in mind as we search for better prevention of cardiovascular disease in America. It is fair to assume that the nearly 50 million Americans without health insurance would not have been among the patients included in L-TAP 2 and are probably outside of the cholesterol prevention programs. Their cholesterol levels do not appear on the radar screen.

A recent study suggests that adherence to current cholesterol guidelines could prevent 20,000 myocardial infarctions and 10,000 deaths annually (Ann. Intern. Med. 2009;150:243-54).

Our ability to provide quality cardiovascular care is seriously limited by the economic barriers to access to care both acute and preventative. To successfully deal with our national epidemic of cardiovascular disease we need to mitigate those economic barriers and improve the accessibility to health care to all Americans.

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Ever since Dr. Joseph L. Goldstein and Dr. Michael S. Brown established the foundation of the cholesterol hypothesis, the medical community has taken aim at lowering serum cholesterol in men and women throughout the world. The initial attempts to lower cholesterol with diet, exercise, and occasionally surgery met with only marginal success.

Not until the introduction of statin therapy to our therapeutic armamentarium did we achieve measurable success in both lowering cholesterol and an associated decrease in atherosclerotic cardiovascular disease mortality and morbidity.

Our success in lowering cholesterol has been measured by a number of international epidemiology studies, the first of which was performed in 1996-1997, the Lipid Treatment Assessment Project (L-TAP) (Arch. Intern. Med. 2000;160:459-67).

The most recent study, L-TAP 2, was an international survey carried out in more than 10,000 patients in nine countries between 2006 and 2007 (Circulation 2009;120:28-34) and catalogues the profound decrease in cholesterol lowering that has been achieved during the last 10 years.

The result of L-TAP 2 points out the significant success that has been achieved during that period in lowering serum LDL cholesterol and raising HDL cholesterol. Successful cholesterol-lowering to the country-specific levels was achieved in 73% of all patients and 67% of high-risk patients. Most of the success was achieved in patients with low to moderate risk.

Comparable data in the earlier L-TAP study reported successful lowering in only 38% and 18% respectively. Dr. Antonio Gotto, in an accompanying editorial, suggests this success was likely due to “the introduction of more effective lipid-lowering therapies” rather than improved patient compliance or physician awareness.

Unfortunately, the very-high-risk patients, those with coronary artery disease and at least two major risk factors, remain a serious problem. Successful lowering of serum cholesterol to the target of below 70 mg/dL was reached in only 30% of the very-high-risk patients. Because of the delayed introduction of the higher potency drugs atorvastatin and rosuvastatin, their use was limited to approximately one-half of the patients in L-TAP 2.

It is possible that the more widespread introduction of these drugs or even more potent drugs in the future will result in further cholesterol lowering in the very-high-risk patients who are still undertreated yet have reached therapeutic goal. The strong association of hypertension, obesity, and diabetes in the high-risk group emphasizes the importance of a multidimensional therapeutic approach to the high-risk population.

The minimal target for cholesterol treatment is yet to be determined, but the Treating to New Targets (TNT) study comparing high- and low-dose atorvastatin, indicated that treatment to an LDL cholesterol level of 77 mg/dL, compared with 101 mg/dL, was associated with a 22% in the reduction of the risk of a first major cardiovascular event (J. Am. Coll. Cardiol. 2006;48:1793-9).

The authors noted that their study was limited by the uncertainty about the nature of the patients and participating physicians. This uncertainty provides an important message in light of our current health care debate. It can be presumed that patients in L-TAP 2 are unique and hardly representative of this country's population as whole. This is important to keep in mind as we search for better prevention of cardiovascular disease in America. It is fair to assume that the nearly 50 million Americans without health insurance would not have been among the patients included in L-TAP 2 and are probably outside of the cholesterol prevention programs. Their cholesterol levels do not appear on the radar screen.

A recent study suggests that adherence to current cholesterol guidelines could prevent 20,000 myocardial infarctions and 10,000 deaths annually (Ann. Intern. Med. 2009;150:243-54).

Our ability to provide quality cardiovascular care is seriously limited by the economic barriers to access to care both acute and preventative. To successfully deal with our national epidemic of cardiovascular disease we need to mitigate those economic barriers and improve the accessibility to health care to all Americans.

Ever since Dr. Joseph L. Goldstein and Dr. Michael S. Brown established the foundation of the cholesterol hypothesis, the medical community has taken aim at lowering serum cholesterol in men and women throughout the world. The initial attempts to lower cholesterol with diet, exercise, and occasionally surgery met with only marginal success.

Not until the introduction of statin therapy to our therapeutic armamentarium did we achieve measurable success in both lowering cholesterol and an associated decrease in atherosclerotic cardiovascular disease mortality and morbidity.

Our success in lowering cholesterol has been measured by a number of international epidemiology studies, the first of which was performed in 1996-1997, the Lipid Treatment Assessment Project (L-TAP) (Arch. Intern. Med. 2000;160:459-67).

The most recent study, L-TAP 2, was an international survey carried out in more than 10,000 patients in nine countries between 2006 and 2007 (Circulation 2009;120:28-34) and catalogues the profound decrease in cholesterol lowering that has been achieved during the last 10 years.

The result of L-TAP 2 points out the significant success that has been achieved during that period in lowering serum LDL cholesterol and raising HDL cholesterol. Successful cholesterol-lowering to the country-specific levels was achieved in 73% of all patients and 67% of high-risk patients. Most of the success was achieved in patients with low to moderate risk.

Comparable data in the earlier L-TAP study reported successful lowering in only 38% and 18% respectively. Dr. Antonio Gotto, in an accompanying editorial, suggests this success was likely due to “the introduction of more effective lipid-lowering therapies” rather than improved patient compliance or physician awareness.

Unfortunately, the very-high-risk patients, those with coronary artery disease and at least two major risk factors, remain a serious problem. Successful lowering of serum cholesterol to the target of below 70 mg/dL was reached in only 30% of the very-high-risk patients. Because of the delayed introduction of the higher potency drugs atorvastatin and rosuvastatin, their use was limited to approximately one-half of the patients in L-TAP 2.

It is possible that the more widespread introduction of these drugs or even more potent drugs in the future will result in further cholesterol lowering in the very-high-risk patients who are still undertreated yet have reached therapeutic goal. The strong association of hypertension, obesity, and diabetes in the high-risk group emphasizes the importance of a multidimensional therapeutic approach to the high-risk population.

The minimal target for cholesterol treatment is yet to be determined, but the Treating to New Targets (TNT) study comparing high- and low-dose atorvastatin, indicated that treatment to an LDL cholesterol level of 77 mg/dL, compared with 101 mg/dL, was associated with a 22% in the reduction of the risk of a first major cardiovascular event (J. Am. Coll. Cardiol. 2006;48:1793-9).

The authors noted that their study was limited by the uncertainty about the nature of the patients and participating physicians. This uncertainty provides an important message in light of our current health care debate. It can be presumed that patients in L-TAP 2 are unique and hardly representative of this country's population as whole. This is important to keep in mind as we search for better prevention of cardiovascular disease in America. It is fair to assume that the nearly 50 million Americans without health insurance would not have been among the patients included in L-TAP 2 and are probably outside of the cholesterol prevention programs. Their cholesterol levels do not appear on the radar screen.

A recent study suggests that adherence to current cholesterol guidelines could prevent 20,000 myocardial infarctions and 10,000 deaths annually (Ann. Intern. Med. 2009;150:243-54).

Our ability to provide quality cardiovascular care is seriously limited by the economic barriers to access to care both acute and preventative. To successfully deal with our national epidemic of cardiovascular disease we need to mitigate those economic barriers and improve the accessibility to health care to all Americans.

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