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What is the best way to identify patients with white-coat hypertension?
Ambulatory blood pressure monitoring is currently the gold standard for detecting patients with white-coat hypertension. Women and all patients with lower office systolic blood pressures, stage I hypertension, and no target organ damage are more likely to have white-coat hypertension (strength of recommendation [SOR]: B, based on prospective cohort studies) ( TABLE ).
Self or home blood pressure monitoring has also been used to detect patients with white-coat hypertension. However, it has a low sensitivity (61%–68%) and low positive predictive value (PV+) (33%–48%) (SOR: B, short-term prospective cohort studies).
Evidence summary
White coat hypertension, also known as isolated office hypertension, refers to elevated blood pressures in a medical setting and normal blood pressures during regular daily life. Patients with white-coat hypertension are defined as patients 1) with an office blood pressure of >140 mm Hg systolic or >90 mm Hg diastolic on at least 3 separate office visits with 2 measurements each visit and 2) mean daytime blood pressure of <135 mm Hg systolic and <85 mm Hg diastolic on ambulatory blood pressure monitoring.1 Other measures of normal blood pressure on ambulatory blood pressure monitoring are <130/80 mm Hg for full 24-hour blood pressure and <120/70 mm Hg for night-time blood pressure.2 A recent Clinical Inquiry summarized 3 cohort trials—2 showed white-coat hypertension patients had lower risk of cardiovascular events and 1 showed no difference between patients with white-coat hypertension and patients with sustained hypertension.3 Identifying patients with white-coat hypertension is important to avoid overtreating individuals at lower risk of cardiovascular events.
Which patients with elevated blood pressure on repeated visits have white-coat hypertension? In studies of patients, most of whom have Stage I hypertension (140–159/90–99 mm Hg), anywhere from 10% to 50% have white-coat hypertension ( TABLE ). In a joint multivariate analysis of 2 cohort studies, which enrolled 1564 subjects with uncomplicated stage I hypertension, white-coat hypertension was associated with lower office systolic blood pressure, female gender, and nonsmoking.2 Similarly, a large international database of 2492 subjects found that women, older subjects, and those with lower and fewer office systolic blood pressure measurements were more likely to have white-coat hypertension.4 In another analysis of 1333 Italian subjects, the prevalence of white-coat hypertension was 33.3% in those with stage I hypertension, 11% with stage II, and 3 % with stage III.5 A study of more than 600 men over 20 years in Finland compared those who developed white-coat hypertension and those with sustained hypertension. The hypertensive patients had more microalbuminuria, a greater left ventricular mass on echo, increased cholesterol esters, and a greater body-mass index (all P.05) than patients with white-coat hypertension. Smoking status was similar in both groups, in contrast to other studies.6 A recent study did not find body-mass index distinguished white-coat hyperten-sion from sustained hypertension.7
TABLE
Patient attributes and white-coat hypertension
| ATTRIBUTE | SUBJECTS | COMPARISON | P VALUE |
|---|---|---|---|
| Gender, % with WCH | 5716* | 17% of females 14% of males | <.001 |
| % female WCH v SH group | 1564† | 45% v 33% | .002 |
| Ratio female: male with WCH | 2634§ | Odds ratio=1.92 (95% CI, 1.45–2.54) | <.001 |
| Mean age, WCH vs SH | 1564† | 40 vs 39 years | .52 |
| % with WCH in 4 age groups | 5716* | <35 y=12%, | <.001 |
| 35–50 y=14%, | |||
| 50–65 y=16%, | |||
| >65 y=17% | |||
| Currently smoking, % with WCH | 5716* | No=16.7%, Yes=11.3% | <.001 |
| Currently smoking % WCH v SH | 1564† | 7% v 24% | .04 |
| BMI, % WCH in 3 groups | 5716* | < 25=16% | NS |
| 25–30=15% | |||
| >30=15% | |||
| BMI, WCH group vs SH group | 1564† | 25.4 vs 25.9 | NS |
| 414‡ | 23.9 vs 24.7 | <.05 | |
| Original clinic SBP, % with WCH | 5716* | 140–159=31.2% | <.001 |
| 160–170=18.7% | |||
| 171–180=11.8% | |||
| 2492§ | 140–150=65% | .004 | |
| 151–160=53% | |||
| 161–170=33% | |||
| LV Mass (g), WCH v SH | 1564† | 160 vs 180 | .001 |
| LV Mass Index (g/m2) WCH v SH | 414‡ | 126 vs 136 | <.01 |
| WCH, white coat hypertension; SBP, systolic blood pressure; SH, sustained hypertension; CI, confidence interval; BMI, body-mass index; NS, not significant; LV, left ventricular. | |||
| *Patients referred to a blood pressure unit over 22-year period.7 | |||
| † A combination of 2 studies of clinic patients with stage I hypertension (140–159/90–99 mm Hg).2 | |||
| ‡ 50-year-old men in a community in Finland invited to a health survey with a 20-year follow-up.6 | |||
| § Data from 24 pooled studies of ambulatory blood pressure monitoring.4 | |||
Using home blood pressure as a screening tool is a problem because of the low sensitivity and poor PV+. In the THOP study (247 subjects), which used ambulatory blood pressure monitoring as the reference method, home blood pressure had a high specificity (89%) and high negative predictive value (PV–) (97%) but a lower sensitivity (68%) and low PPV (33%).8 In other words, if home blood pressure shows hypertension, there is a 97% chance the patient has sustained hypertension, but if home blood pressure returns to normal in patients with office hypertension, two thirds of patients will still have sustained hypertension. In another study that enrolled patients from a hypertension clinic, 133 untreated patients with dias-tolic blood pressure 90 to 115 mm Hg underwent ambulatory blood pressure monitoring for a reference standard. The sensitivity of home blood pressure monitoring in identifying white-coat hypertension was 61% and the PV+ was 48%.9
Recommendations from others
The European Society of Hypertension Working Group on Blood Pressure Monitoring recommends that subjects with blood pressure 140–159/90–99 mm Hg at several visits should have ambulatory blood pressure monitoring because 33% of those people will have white-coat hypertension. Women, nonsmokers, those with recent hypertension, a limited number of blood pressure determinations and small left ventricular mass on echo should also have ambulatory blood pressure monitoring. There should be a search for metabolic risk factors and target organ damage. Those patients aware that their blood pressures are lower outside the office should be considered for ambulatory blood pressure monitoring.10
The latest Joint National Committee report (JNC VII) indicates that ambulatory blood pressure monitoring may be useful to detect white-coat hypertension among patients with hypertension and no target organ damage, and those with episodic hypertension.11
Ambulatory BP monitoring better than home monitoring for ruling out white-coat hypertension
Joseph Saseen, PharmD, FCCP, BCPS
University of Colorado Health Sciences Center, Denver
Landmark placebo-controlled outcome-based trials demonstrating reduced morbidity and mortality with hypertension treatment did not differentiate essential from white-coat hypertension. Patients were included based on elevated office-based blood pressure measurements. Since we now know that the prevalence of white-coat hypertension is high, it should be ruled out before implementing antihypertensive therapy.
Ambulatory blood pressure monitoring is more accurate than home monitoring for ruling out white-coat hypertension. However, ease, simplicity, and availability makes home monitoring a more realistic option for routine clinical practice. When home blood pressure monitoring is used, reliable measurement devices (eg, newer automatic or manual home devices) should be used and patients should be instructed regarding proper use and documentation of blood pressure values to facilitate an appropriate clinical assessment.
1. O’Brien E, Asmar R, Beilin L, et al. on behalf of the European Society of Hypertension Working Group on Blood Pressure Monitoring. European Society of Hypertension recommendations for conventional, ambulatory and home blood pressure measurement. J Hypertens 2003;21:821-848.
2. Verdecchia P, Palatini P, Schillaci G, Mormino P, Porcellati C, Pessina AC. Independent predictors of isolated clinic (‘white-coat’) hypertension. J Hypertens 2001;19:1015-1020.
3. Rao S, Liu C-T, Wilder L. What is the best way to treat patients with white-coat hypertension?. J Fam Pract 2004;53:408-412.
4. Staessen JA, O’Brien ET, Atkins N, Anery AK. on behalf of the Ad-Hoc Working Group: Short report: Ambulatory blood pressure in normotensive compared with hypertensive subjects. J Hypertens 1993;11:1289-1297.
5. Verdecchia P, Schillaci G, Borgioni C, et al. White-coat hypertension and white-coat effect: Similarities and differences. Am J Hypertens 1995;8:790-798.
6. Bjorklund K, Lind L, Vessby B, Andren B, Lithell H. Different metabolic predictors of white-coat and sustained hypertension over a 20-year follow-up period. Circulation 2002;106:63-68.
7. Dolan E, Stanton A, Atkins N, et al. Determinants of white-coat hypertension. Blood Pressure Monit 2004;9:307-309.
8. Den Hond E, Celis H, Fagard R, et al. Self-measured versus ambulatory blood pressure in the diagnosis of hypertension. J Hypertens 2003;21:717-722.
9. Stergiou GS, Skeva II, Baibas NM, Kalkana CB, Roussias LG, Mountokalakis TD. Diagnosis of hyper-tension using home or ambulatory blood pressure monitoring: comparison with the conventional strategy based on repeated clinic blood pressure measurements. J Hypertens 2000;18:1745-1751.
10. Verdecchia P, O’Brien E, Pickering T, et al. When can the practicing physician suspect white coat hyperten-sion? Statement from the Working Group on Blood Pressure Monitoring of the European Society of Hypertension. Am J Hypertens 2003;16:87-91.
11. Chobanian AV, Bakris GL, Black HR, et al. Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. Hypertension 2003;42:1206-1252.
Ambulatory blood pressure monitoring is currently the gold standard for detecting patients with white-coat hypertension. Women and all patients with lower office systolic blood pressures, stage I hypertension, and no target organ damage are more likely to have white-coat hypertension (strength of recommendation [SOR]: B, based on prospective cohort studies) ( TABLE ).
Self or home blood pressure monitoring has also been used to detect patients with white-coat hypertension. However, it has a low sensitivity (61%–68%) and low positive predictive value (PV+) (33%–48%) (SOR: B, short-term prospective cohort studies).
Evidence summary
White coat hypertension, also known as isolated office hypertension, refers to elevated blood pressures in a medical setting and normal blood pressures during regular daily life. Patients with white-coat hypertension are defined as patients 1) with an office blood pressure of >140 mm Hg systolic or >90 mm Hg diastolic on at least 3 separate office visits with 2 measurements each visit and 2) mean daytime blood pressure of <135 mm Hg systolic and <85 mm Hg diastolic on ambulatory blood pressure monitoring.1 Other measures of normal blood pressure on ambulatory blood pressure monitoring are <130/80 mm Hg for full 24-hour blood pressure and <120/70 mm Hg for night-time blood pressure.2 A recent Clinical Inquiry summarized 3 cohort trials—2 showed white-coat hypertension patients had lower risk of cardiovascular events and 1 showed no difference between patients with white-coat hypertension and patients with sustained hypertension.3 Identifying patients with white-coat hypertension is important to avoid overtreating individuals at lower risk of cardiovascular events.
Which patients with elevated blood pressure on repeated visits have white-coat hypertension? In studies of patients, most of whom have Stage I hypertension (140–159/90–99 mm Hg), anywhere from 10% to 50% have white-coat hypertension ( TABLE ). In a joint multivariate analysis of 2 cohort studies, which enrolled 1564 subjects with uncomplicated stage I hypertension, white-coat hypertension was associated with lower office systolic blood pressure, female gender, and nonsmoking.2 Similarly, a large international database of 2492 subjects found that women, older subjects, and those with lower and fewer office systolic blood pressure measurements were more likely to have white-coat hypertension.4 In another analysis of 1333 Italian subjects, the prevalence of white-coat hypertension was 33.3% in those with stage I hypertension, 11% with stage II, and 3 % with stage III.5 A study of more than 600 men over 20 years in Finland compared those who developed white-coat hypertension and those with sustained hypertension. The hypertensive patients had more microalbuminuria, a greater left ventricular mass on echo, increased cholesterol esters, and a greater body-mass index (all P.05) than patients with white-coat hypertension. Smoking status was similar in both groups, in contrast to other studies.6 A recent study did not find body-mass index distinguished white-coat hyperten-sion from sustained hypertension.7
TABLE
Patient attributes and white-coat hypertension
| ATTRIBUTE | SUBJECTS | COMPARISON | P VALUE |
|---|---|---|---|
| Gender, % with WCH | 5716* | 17% of females 14% of males | <.001 |
| % female WCH v SH group | 1564† | 45% v 33% | .002 |
| Ratio female: male with WCH | 2634§ | Odds ratio=1.92 (95% CI, 1.45–2.54) | <.001 |
| Mean age, WCH vs SH | 1564† | 40 vs 39 years | .52 |
| % with WCH in 4 age groups | 5716* | <35 y=12%, | <.001 |
| 35–50 y=14%, | |||
| 50–65 y=16%, | |||
| >65 y=17% | |||
| Currently smoking, % with WCH | 5716* | No=16.7%, Yes=11.3% | <.001 |
| Currently smoking % WCH v SH | 1564† | 7% v 24% | .04 |
| BMI, % WCH in 3 groups | 5716* | < 25=16% | NS |
| 25–30=15% | |||
| >30=15% | |||
| BMI, WCH group vs SH group | 1564† | 25.4 vs 25.9 | NS |
| 414‡ | 23.9 vs 24.7 | <.05 | |
| Original clinic SBP, % with WCH | 5716* | 140–159=31.2% | <.001 |
| 160–170=18.7% | |||
| 171–180=11.8% | |||
| 2492§ | 140–150=65% | .004 | |
| 151–160=53% | |||
| 161–170=33% | |||
| LV Mass (g), WCH v SH | 1564† | 160 vs 180 | .001 |
| LV Mass Index (g/m2) WCH v SH | 414‡ | 126 vs 136 | <.01 |
| WCH, white coat hypertension; SBP, systolic blood pressure; SH, sustained hypertension; CI, confidence interval; BMI, body-mass index; NS, not significant; LV, left ventricular. | |||
| *Patients referred to a blood pressure unit over 22-year period.7 | |||
| † A combination of 2 studies of clinic patients with stage I hypertension (140–159/90–99 mm Hg).2 | |||
| ‡ 50-year-old men in a community in Finland invited to a health survey with a 20-year follow-up.6 | |||
| § Data from 24 pooled studies of ambulatory blood pressure monitoring.4 | |||
Using home blood pressure as a screening tool is a problem because of the low sensitivity and poor PV+. In the THOP study (247 subjects), which used ambulatory blood pressure monitoring as the reference method, home blood pressure had a high specificity (89%) and high negative predictive value (PV–) (97%) but a lower sensitivity (68%) and low PPV (33%).8 In other words, if home blood pressure shows hypertension, there is a 97% chance the patient has sustained hypertension, but if home blood pressure returns to normal in patients with office hypertension, two thirds of patients will still have sustained hypertension. In another study that enrolled patients from a hypertension clinic, 133 untreated patients with dias-tolic blood pressure 90 to 115 mm Hg underwent ambulatory blood pressure monitoring for a reference standard. The sensitivity of home blood pressure monitoring in identifying white-coat hypertension was 61% and the PV+ was 48%.9
Recommendations from others
The European Society of Hypertension Working Group on Blood Pressure Monitoring recommends that subjects with blood pressure 140–159/90–99 mm Hg at several visits should have ambulatory blood pressure monitoring because 33% of those people will have white-coat hypertension. Women, nonsmokers, those with recent hypertension, a limited number of blood pressure determinations and small left ventricular mass on echo should also have ambulatory blood pressure monitoring. There should be a search for metabolic risk factors and target organ damage. Those patients aware that their blood pressures are lower outside the office should be considered for ambulatory blood pressure monitoring.10
The latest Joint National Committee report (JNC VII) indicates that ambulatory blood pressure monitoring may be useful to detect white-coat hypertension among patients with hypertension and no target organ damage, and those with episodic hypertension.11
Ambulatory BP monitoring better than home monitoring for ruling out white-coat hypertension
Joseph Saseen, PharmD, FCCP, BCPS
University of Colorado Health Sciences Center, Denver
Landmark placebo-controlled outcome-based trials demonstrating reduced morbidity and mortality with hypertension treatment did not differentiate essential from white-coat hypertension. Patients were included based on elevated office-based blood pressure measurements. Since we now know that the prevalence of white-coat hypertension is high, it should be ruled out before implementing antihypertensive therapy.
Ambulatory blood pressure monitoring is more accurate than home monitoring for ruling out white-coat hypertension. However, ease, simplicity, and availability makes home monitoring a more realistic option for routine clinical practice. When home blood pressure monitoring is used, reliable measurement devices (eg, newer automatic or manual home devices) should be used and patients should be instructed regarding proper use and documentation of blood pressure values to facilitate an appropriate clinical assessment.
Ambulatory blood pressure monitoring is currently the gold standard for detecting patients with white-coat hypertension. Women and all patients with lower office systolic blood pressures, stage I hypertension, and no target organ damage are more likely to have white-coat hypertension (strength of recommendation [SOR]: B, based on prospective cohort studies) ( TABLE ).
Self or home blood pressure monitoring has also been used to detect patients with white-coat hypertension. However, it has a low sensitivity (61%–68%) and low positive predictive value (PV+) (33%–48%) (SOR: B, short-term prospective cohort studies).
Evidence summary
White coat hypertension, also known as isolated office hypertension, refers to elevated blood pressures in a medical setting and normal blood pressures during regular daily life. Patients with white-coat hypertension are defined as patients 1) with an office blood pressure of >140 mm Hg systolic or >90 mm Hg diastolic on at least 3 separate office visits with 2 measurements each visit and 2) mean daytime blood pressure of <135 mm Hg systolic and <85 mm Hg diastolic on ambulatory blood pressure monitoring.1 Other measures of normal blood pressure on ambulatory blood pressure monitoring are <130/80 mm Hg for full 24-hour blood pressure and <120/70 mm Hg for night-time blood pressure.2 A recent Clinical Inquiry summarized 3 cohort trials—2 showed white-coat hypertension patients had lower risk of cardiovascular events and 1 showed no difference between patients with white-coat hypertension and patients with sustained hypertension.3 Identifying patients with white-coat hypertension is important to avoid overtreating individuals at lower risk of cardiovascular events.
Which patients with elevated blood pressure on repeated visits have white-coat hypertension? In studies of patients, most of whom have Stage I hypertension (140–159/90–99 mm Hg), anywhere from 10% to 50% have white-coat hypertension ( TABLE ). In a joint multivariate analysis of 2 cohort studies, which enrolled 1564 subjects with uncomplicated stage I hypertension, white-coat hypertension was associated with lower office systolic blood pressure, female gender, and nonsmoking.2 Similarly, a large international database of 2492 subjects found that women, older subjects, and those with lower and fewer office systolic blood pressure measurements were more likely to have white-coat hypertension.4 In another analysis of 1333 Italian subjects, the prevalence of white-coat hypertension was 33.3% in those with stage I hypertension, 11% with stage II, and 3 % with stage III.5 A study of more than 600 men over 20 years in Finland compared those who developed white-coat hypertension and those with sustained hypertension. The hypertensive patients had more microalbuminuria, a greater left ventricular mass on echo, increased cholesterol esters, and a greater body-mass index (all P.05) than patients with white-coat hypertension. Smoking status was similar in both groups, in contrast to other studies.6 A recent study did not find body-mass index distinguished white-coat hyperten-sion from sustained hypertension.7
TABLE
Patient attributes and white-coat hypertension
| ATTRIBUTE | SUBJECTS | COMPARISON | P VALUE |
|---|---|---|---|
| Gender, % with WCH | 5716* | 17% of females 14% of males | <.001 |
| % female WCH v SH group | 1564† | 45% v 33% | .002 |
| Ratio female: male with WCH | 2634§ | Odds ratio=1.92 (95% CI, 1.45–2.54) | <.001 |
| Mean age, WCH vs SH | 1564† | 40 vs 39 years | .52 |
| % with WCH in 4 age groups | 5716* | <35 y=12%, | <.001 |
| 35–50 y=14%, | |||
| 50–65 y=16%, | |||
| >65 y=17% | |||
| Currently smoking, % with WCH | 5716* | No=16.7%, Yes=11.3% | <.001 |
| Currently smoking % WCH v SH | 1564† | 7% v 24% | .04 |
| BMI, % WCH in 3 groups | 5716* | < 25=16% | NS |
| 25–30=15% | |||
| >30=15% | |||
| BMI, WCH group vs SH group | 1564† | 25.4 vs 25.9 | NS |
| 414‡ | 23.9 vs 24.7 | <.05 | |
| Original clinic SBP, % with WCH | 5716* | 140–159=31.2% | <.001 |
| 160–170=18.7% | |||
| 171–180=11.8% | |||
| 2492§ | 140–150=65% | .004 | |
| 151–160=53% | |||
| 161–170=33% | |||
| LV Mass (g), WCH v SH | 1564† | 160 vs 180 | .001 |
| LV Mass Index (g/m2) WCH v SH | 414‡ | 126 vs 136 | <.01 |
| WCH, white coat hypertension; SBP, systolic blood pressure; SH, sustained hypertension; CI, confidence interval; BMI, body-mass index; NS, not significant; LV, left ventricular. | |||
| *Patients referred to a blood pressure unit over 22-year period.7 | |||
| † A combination of 2 studies of clinic patients with stage I hypertension (140–159/90–99 mm Hg).2 | |||
| ‡ 50-year-old men in a community in Finland invited to a health survey with a 20-year follow-up.6 | |||
| § Data from 24 pooled studies of ambulatory blood pressure monitoring.4 | |||
Using home blood pressure as a screening tool is a problem because of the low sensitivity and poor PV+. In the THOP study (247 subjects), which used ambulatory blood pressure monitoring as the reference method, home blood pressure had a high specificity (89%) and high negative predictive value (PV–) (97%) but a lower sensitivity (68%) and low PPV (33%).8 In other words, if home blood pressure shows hypertension, there is a 97% chance the patient has sustained hypertension, but if home blood pressure returns to normal in patients with office hypertension, two thirds of patients will still have sustained hypertension. In another study that enrolled patients from a hypertension clinic, 133 untreated patients with dias-tolic blood pressure 90 to 115 mm Hg underwent ambulatory blood pressure monitoring for a reference standard. The sensitivity of home blood pressure monitoring in identifying white-coat hypertension was 61% and the PV+ was 48%.9
Recommendations from others
The European Society of Hypertension Working Group on Blood Pressure Monitoring recommends that subjects with blood pressure 140–159/90–99 mm Hg at several visits should have ambulatory blood pressure monitoring because 33% of those people will have white-coat hypertension. Women, nonsmokers, those with recent hypertension, a limited number of blood pressure determinations and small left ventricular mass on echo should also have ambulatory blood pressure monitoring. There should be a search for metabolic risk factors and target organ damage. Those patients aware that their blood pressures are lower outside the office should be considered for ambulatory blood pressure monitoring.10
The latest Joint National Committee report (JNC VII) indicates that ambulatory blood pressure monitoring may be useful to detect white-coat hypertension among patients with hypertension and no target organ damage, and those with episodic hypertension.11
Ambulatory BP monitoring better than home monitoring for ruling out white-coat hypertension
Joseph Saseen, PharmD, FCCP, BCPS
University of Colorado Health Sciences Center, Denver
Landmark placebo-controlled outcome-based trials demonstrating reduced morbidity and mortality with hypertension treatment did not differentiate essential from white-coat hypertension. Patients were included based on elevated office-based blood pressure measurements. Since we now know that the prevalence of white-coat hypertension is high, it should be ruled out before implementing antihypertensive therapy.
Ambulatory blood pressure monitoring is more accurate than home monitoring for ruling out white-coat hypertension. However, ease, simplicity, and availability makes home monitoring a more realistic option for routine clinical practice. When home blood pressure monitoring is used, reliable measurement devices (eg, newer automatic or manual home devices) should be used and patients should be instructed regarding proper use and documentation of blood pressure values to facilitate an appropriate clinical assessment.
1. O’Brien E, Asmar R, Beilin L, et al. on behalf of the European Society of Hypertension Working Group on Blood Pressure Monitoring. European Society of Hypertension recommendations for conventional, ambulatory and home blood pressure measurement. J Hypertens 2003;21:821-848.
2. Verdecchia P, Palatini P, Schillaci G, Mormino P, Porcellati C, Pessina AC. Independent predictors of isolated clinic (‘white-coat’) hypertension. J Hypertens 2001;19:1015-1020.
3. Rao S, Liu C-T, Wilder L. What is the best way to treat patients with white-coat hypertension?. J Fam Pract 2004;53:408-412.
4. Staessen JA, O’Brien ET, Atkins N, Anery AK. on behalf of the Ad-Hoc Working Group: Short report: Ambulatory blood pressure in normotensive compared with hypertensive subjects. J Hypertens 1993;11:1289-1297.
5. Verdecchia P, Schillaci G, Borgioni C, et al. White-coat hypertension and white-coat effect: Similarities and differences. Am J Hypertens 1995;8:790-798.
6. Bjorklund K, Lind L, Vessby B, Andren B, Lithell H. Different metabolic predictors of white-coat and sustained hypertension over a 20-year follow-up period. Circulation 2002;106:63-68.
7. Dolan E, Stanton A, Atkins N, et al. Determinants of white-coat hypertension. Blood Pressure Monit 2004;9:307-309.
8. Den Hond E, Celis H, Fagard R, et al. Self-measured versus ambulatory blood pressure in the diagnosis of hypertension. J Hypertens 2003;21:717-722.
9. Stergiou GS, Skeva II, Baibas NM, Kalkana CB, Roussias LG, Mountokalakis TD. Diagnosis of hyper-tension using home or ambulatory blood pressure monitoring: comparison with the conventional strategy based on repeated clinic blood pressure measurements. J Hypertens 2000;18:1745-1751.
10. Verdecchia P, O’Brien E, Pickering T, et al. When can the practicing physician suspect white coat hyperten-sion? Statement from the Working Group on Blood Pressure Monitoring of the European Society of Hypertension. Am J Hypertens 2003;16:87-91.
11. Chobanian AV, Bakris GL, Black HR, et al. Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. Hypertension 2003;42:1206-1252.
1. O’Brien E, Asmar R, Beilin L, et al. on behalf of the European Society of Hypertension Working Group on Blood Pressure Monitoring. European Society of Hypertension recommendations for conventional, ambulatory and home blood pressure measurement. J Hypertens 2003;21:821-848.
2. Verdecchia P, Palatini P, Schillaci G, Mormino P, Porcellati C, Pessina AC. Independent predictors of isolated clinic (‘white-coat’) hypertension. J Hypertens 2001;19:1015-1020.
3. Rao S, Liu C-T, Wilder L. What is the best way to treat patients with white-coat hypertension?. J Fam Pract 2004;53:408-412.
4. Staessen JA, O’Brien ET, Atkins N, Anery AK. on behalf of the Ad-Hoc Working Group: Short report: Ambulatory blood pressure in normotensive compared with hypertensive subjects. J Hypertens 1993;11:1289-1297.
5. Verdecchia P, Schillaci G, Borgioni C, et al. White-coat hypertension and white-coat effect: Similarities and differences. Am J Hypertens 1995;8:790-798.
6. Bjorklund K, Lind L, Vessby B, Andren B, Lithell H. Different metabolic predictors of white-coat and sustained hypertension over a 20-year follow-up period. Circulation 2002;106:63-68.
7. Dolan E, Stanton A, Atkins N, et al. Determinants of white-coat hypertension. Blood Pressure Monit 2004;9:307-309.
8. Den Hond E, Celis H, Fagard R, et al. Self-measured versus ambulatory blood pressure in the diagnosis of hypertension. J Hypertens 2003;21:717-722.
9. Stergiou GS, Skeva II, Baibas NM, Kalkana CB, Roussias LG, Mountokalakis TD. Diagnosis of hyper-tension using home or ambulatory blood pressure monitoring: comparison with the conventional strategy based on repeated clinic blood pressure measurements. J Hypertens 2000;18:1745-1751.
10. Verdecchia P, O’Brien E, Pickering T, et al. When can the practicing physician suspect white coat hyperten-sion? Statement from the Working Group on Blood Pressure Monitoring of the European Society of Hypertension. Am J Hypertens 2003;16:87-91.
11. Chobanian AV, Bakris GL, Black HR, et al. Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. Hypertension 2003;42:1206-1252.
Evidence-based answers from the Family Physicians Inquiries Network
Does furosemide decrease morbidity or mortality for patients with diastolic or systolic dysfunction?
No large-scale randomized, placebo-controlled trials evaluate furosemide’s effect on mortality and long-term morbidity in diastolic or systolic dysfunction. In short-term studies, furosemide reduces edema, reduces hospitalizations, and improves exercise capacity in the setting of systolic dysfunction (strength of recommendation [SOR]: B, based upon low-quality randomized controlled trials). Furosemide and other diuretics reduce symptomatic volume overload in diastolic and systolic dysfunction (SOR: C, based on expert opinion).
There is potential morbidity with the use of high-dose loop diuretics (volume contraction, electrolyte disturbances, and neuroendocrine activation).1-3 Use of high-dose loop diuretics for systolic dysfunction is associated with increased mortality, sudden death, and pump failure death (SOR: B, based on retrospective analyses of large-scale randomized controlled trials). However, diuretic resistance or disease severity may explain these latter findings.
Evidence summary
Faris et al4 conducted a meta-analysis of randomized controlled trials that used diuretics (pertanide, furosemide, furosemide-hydrochlorothiazide) in congestive heart failure (TABLE).4 Of the 18 trials, 8 were placebo-controlled and 10 used active controls (diuretics vs angiotensin-converting enzyme [ACE] inhibitors, digoxin, or ibopamine, a dopamine agonist). Three placebo-controlled trials (N=221) showed an absolute risk reduction in death of 8% in diuretic-treated patients (number needed to treat [NNT]=12.5). Four placebo-controlled trials (N=448) showed a significantly lower rate of admissions for worsening failure among diuretic-treated patients (NNT=8.5), and 4 of the active-controlled trials (N=150) showed a nonsignificant trend toward decreased admissions. Six active-controlled studies (N=174) showed significantly increased exercise capacity for patients on diuretics. One of these latter trials also assessed quality of life, edema, and New York Heart Association (NYHA) class, and demonstrated no change in these outcomes in the treatment and placebo groups.5
The studies used in this meta-analysis had numerous shortcomings: the individual trials had small numbers of patients (N=14–139), short follow-up periods (typically 4–8 weeks), and inadequate statistical power to clearly demonstrate morbidity/mortality reductions. There was significant heterogeneity between studies. Crossover studies were included, some studies did not clearly report masking and assessment of outcome measures, and assessment of study validity was not clear. Studies employed a variety of diuretic types and doses, used different controls, and did not clarify whether patients’ congestive heart failure was caused primarily by diastolic or systolic dysfunction.
It is worth noting that diuretic use also carries some risk. One large retrospective study evaluated 6796 patients using potassium-sparing diuretics vs non–potassium-sparing diuretics in the Studies of Left Ventricular Dysfunction (SOLVD) trial.6 Rates of hospitalization or death from worsening congestive heart failure were significantly higher in the non–potassium-sparing diuretic population than in the nondiuretic population (relative risk [RR]=1.31, 95% confidence interval [CI], 1.09–1.57; number needed to harm=5.78). This increased risk was not found for patients taking potassium-sparing diuretics (RR=0.99; 95% CI, 0.76–1.30).
Another retrospective study of SOLVD patients found a significant and independent association with increased risk of arrhythmic death among patients taking non–potassium-sparing diuretics (RR=1.33; 95% CI, 1.05–1.69).7
A retrospective study of 1153 patients with NYHA Class III to IV heart failure, who were enrolled in the Prospective Randomized Amlodipine Survival Evaluation (PRAISE), found high diuretic doses to be independently associated with mortality (adjusted hazard ratio [HR]=1.37; P=.004), sudden death (HR=1.39; P=.042), and pump failure death (HR=1.51; P=.034).8
The authors caution that there is no proof of causation between furosemide and death; diuretic resistance may explain the poor outcomes, or the use of loop diuretics at high doses may be proxy of more severe illness, and thus poorer outcome.
TABLE
Clinical effects of diuretics in congestive heart failure
| OUTCOME | TRIAL DESCRIPTION | N | RESULTS (REPORTED AS OR) | 95% CI | P VALUE | NNT |
|---|---|---|---|---|---|---|
| Death | 3 placebo-controlled | 221 | 0.25 | 0.07–0.84 | .03 | 12.5 |
| Admissions | 4 placebo-controlled | 448 | 0.31 | 0.15–0.62 | .001 | 8.5 |
| 4 active-controlled | 150 | 0.34 | 0.10–1.21 | .10 | 12.8 | |
| Exercise capacity | 6 active-controlled | 174 | 0.37 | 0.10–0.64 | .007 | * |
| *Unable to calculate NNT due to lack of uniform reporting of exercise times. | ||||||
| OR, odds ratio; CI, confidence interval; NNT, number needed to treat. | ||||||
| Source: Faris et al, Int J Cardiol 2002.4 | ||||||
Recommendations from others
The American College of Cardiology recommends using diuretics in the setting of left ventricular systolic dysfunction and fluid retention (level of evidence [LOE]: A), and recommends using diuretics in diastolic dysfunction to control pulmonary congestion and peripheral edema (LOE: C).9
The European Society of Cardiology notes that no randomized controlled trials have assessed survival effects of diuretics in congestive heart failure, but recommends using diuretics for symptomatic treatment of volume overload (LOE: A). This society also cites evidence that diuretic use improves exercise tolerance (LOE: B). They recommend that diuretics be used always in addition to an ACE inhibitor, that loop diuretics be used if symptoms are more than mild and if glomerular filtration rate (GFR) <30 cc/min, and that thiazide diuretics can be used with loop diuretics for synergistic effects in severe congestive heart failure. 10
Helpful in the acute setting, diuretics shouldn’t be used alone chronically
Jon Neher, MD
Valley Medical Center, Renton, Wash
Furosemide and the other loop diuretics are very satisfying to use clinically. The patient in heart failure arrives at the hospital dypsneic, cyanotic, and terrified. After a single large dose of medication, the patient diureses and begins to feel good again quite quickly.
The practitioner, however, needs to be wary of the resulting impression that diuretics are “good” for heart failure. ACE inhibitors, beta blockers, and (in severe cases) spironolactone are “good” for heart failure because they prolong lives. One must not allow diuretic therapy—started for acute decompensation— to prevent use of more important long-term medications by causing dehydration, hypotension, or electrolyte disturbances.
1. Reyes AJ. Diuretics in the treatment of patients who present congestive heart failure and hypertension. J Hum Hypertens 2002;16 Suppl 1:S104-S113.
2. van Kraaij DJ, Jansen RW, Gribnau FW, Hoefnagels WH. Diuretic therapy in elderly heart failure patients with and without left ventricular systolic dysfunction. Drugs Aging 2000;16:289-300.
3. Kramer BK, Schweda F, Riegger GAJ. Diuretic treatment and diuretic resistance in heart failure. Am J Med 1999;106:90-96.
4. Faris R, Flather M, Purcell H, Henein M, Poole-Wilson P, Coats A. Current evidence supporting the role of diuretics in heart failure: a meta analysis of randomised controlled trials. Int J Cardiol 2002;82:149-158.
5. Parker JO. The effects of oral ibopamine in patients with mild heart failure—a double blind placebo controlled comparison to furosemide. The Ibopamine Study Group. Int J Cardiol 1993;40:221-227.
6. Domanski M, Norman J, Pitt B, et al. Diuretic use, progressive heart failure, and death in patients in the Studies of Left Ventricular Dysfunction (SOLVD). J Am Coll Cardiol 2003;42:705-708.
7. Cooper HA, Dries DL, Davis CE, Shen YL, Domanski MJ. Diuretics and risk of arrhythmic death in patients with left ventricular dysfunction. Circulation 1999;100:1311-1315.
8. Neuberg GW, Miller AB, O’Connor CM, et al. Diuretic resistance predicts mortality in patients with advanced heart failure. Am Heart J 2002;144:31-38.
9. Hunt SA, Baker DW, Chin MH, et al. ACC/AHA guidelines for the evaluation and management of chronic heart failure in the adult: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee to Revise the 1995 Guidelines for the Evaluation and Management of Heart Failure). 2001. American College of Cardiology. Last updated March 12, 2002. Available at: www.acc.org/clinical/ guidelines/failure/hf_index.htm. Accessed on March 4, 2005.
10. Remme WJ, Swedberg K. Task Force for the Diagnosis and Treatment of Chronic Heart Failure, European Society of Cardiology. Guidelines for the diagnosis and treatment of chronic heart failure. Eur Heart J 2001;22:1527-1560.
No large-scale randomized, placebo-controlled trials evaluate furosemide’s effect on mortality and long-term morbidity in diastolic or systolic dysfunction. In short-term studies, furosemide reduces edema, reduces hospitalizations, and improves exercise capacity in the setting of systolic dysfunction (strength of recommendation [SOR]: B, based upon low-quality randomized controlled trials). Furosemide and other diuretics reduce symptomatic volume overload in diastolic and systolic dysfunction (SOR: C, based on expert opinion).
There is potential morbidity with the use of high-dose loop diuretics (volume contraction, electrolyte disturbances, and neuroendocrine activation).1-3 Use of high-dose loop diuretics for systolic dysfunction is associated with increased mortality, sudden death, and pump failure death (SOR: B, based on retrospective analyses of large-scale randomized controlled trials). However, diuretic resistance or disease severity may explain these latter findings.
Evidence summary
Faris et al4 conducted a meta-analysis of randomized controlled trials that used diuretics (pertanide, furosemide, furosemide-hydrochlorothiazide) in congestive heart failure (TABLE).4 Of the 18 trials, 8 were placebo-controlled and 10 used active controls (diuretics vs angiotensin-converting enzyme [ACE] inhibitors, digoxin, or ibopamine, a dopamine agonist). Three placebo-controlled trials (N=221) showed an absolute risk reduction in death of 8% in diuretic-treated patients (number needed to treat [NNT]=12.5). Four placebo-controlled trials (N=448) showed a significantly lower rate of admissions for worsening failure among diuretic-treated patients (NNT=8.5), and 4 of the active-controlled trials (N=150) showed a nonsignificant trend toward decreased admissions. Six active-controlled studies (N=174) showed significantly increased exercise capacity for patients on diuretics. One of these latter trials also assessed quality of life, edema, and New York Heart Association (NYHA) class, and demonstrated no change in these outcomes in the treatment and placebo groups.5
The studies used in this meta-analysis had numerous shortcomings: the individual trials had small numbers of patients (N=14–139), short follow-up periods (typically 4–8 weeks), and inadequate statistical power to clearly demonstrate morbidity/mortality reductions. There was significant heterogeneity between studies. Crossover studies were included, some studies did not clearly report masking and assessment of outcome measures, and assessment of study validity was not clear. Studies employed a variety of diuretic types and doses, used different controls, and did not clarify whether patients’ congestive heart failure was caused primarily by diastolic or systolic dysfunction.
It is worth noting that diuretic use also carries some risk. One large retrospective study evaluated 6796 patients using potassium-sparing diuretics vs non–potassium-sparing diuretics in the Studies of Left Ventricular Dysfunction (SOLVD) trial.6 Rates of hospitalization or death from worsening congestive heart failure were significantly higher in the non–potassium-sparing diuretic population than in the nondiuretic population (relative risk [RR]=1.31, 95% confidence interval [CI], 1.09–1.57; number needed to harm=5.78). This increased risk was not found for patients taking potassium-sparing diuretics (RR=0.99; 95% CI, 0.76–1.30).
Another retrospective study of SOLVD patients found a significant and independent association with increased risk of arrhythmic death among patients taking non–potassium-sparing diuretics (RR=1.33; 95% CI, 1.05–1.69).7
A retrospective study of 1153 patients with NYHA Class III to IV heart failure, who were enrolled in the Prospective Randomized Amlodipine Survival Evaluation (PRAISE), found high diuretic doses to be independently associated with mortality (adjusted hazard ratio [HR]=1.37; P=.004), sudden death (HR=1.39; P=.042), and pump failure death (HR=1.51; P=.034).8
The authors caution that there is no proof of causation between furosemide and death; diuretic resistance may explain the poor outcomes, or the use of loop diuretics at high doses may be proxy of more severe illness, and thus poorer outcome.
TABLE
Clinical effects of diuretics in congestive heart failure
| OUTCOME | TRIAL DESCRIPTION | N | RESULTS (REPORTED AS OR) | 95% CI | P VALUE | NNT |
|---|---|---|---|---|---|---|
| Death | 3 placebo-controlled | 221 | 0.25 | 0.07–0.84 | .03 | 12.5 |
| Admissions | 4 placebo-controlled | 448 | 0.31 | 0.15–0.62 | .001 | 8.5 |
| 4 active-controlled | 150 | 0.34 | 0.10–1.21 | .10 | 12.8 | |
| Exercise capacity | 6 active-controlled | 174 | 0.37 | 0.10–0.64 | .007 | * |
| *Unable to calculate NNT due to lack of uniform reporting of exercise times. | ||||||
| OR, odds ratio; CI, confidence interval; NNT, number needed to treat. | ||||||
| Source: Faris et al, Int J Cardiol 2002.4 | ||||||
Recommendations from others
The American College of Cardiology recommends using diuretics in the setting of left ventricular systolic dysfunction and fluid retention (level of evidence [LOE]: A), and recommends using diuretics in diastolic dysfunction to control pulmonary congestion and peripheral edema (LOE: C).9
The European Society of Cardiology notes that no randomized controlled trials have assessed survival effects of diuretics in congestive heart failure, but recommends using diuretics for symptomatic treatment of volume overload (LOE: A). This society also cites evidence that diuretic use improves exercise tolerance (LOE: B). They recommend that diuretics be used always in addition to an ACE inhibitor, that loop diuretics be used if symptoms are more than mild and if glomerular filtration rate (GFR) <30 cc/min, and that thiazide diuretics can be used with loop diuretics for synergistic effects in severe congestive heart failure. 10
Helpful in the acute setting, diuretics shouldn’t be used alone chronically
Jon Neher, MD
Valley Medical Center, Renton, Wash
Furosemide and the other loop diuretics are very satisfying to use clinically. The patient in heart failure arrives at the hospital dypsneic, cyanotic, and terrified. After a single large dose of medication, the patient diureses and begins to feel good again quite quickly.
The practitioner, however, needs to be wary of the resulting impression that diuretics are “good” for heart failure. ACE inhibitors, beta blockers, and (in severe cases) spironolactone are “good” for heart failure because they prolong lives. One must not allow diuretic therapy—started for acute decompensation— to prevent use of more important long-term medications by causing dehydration, hypotension, or electrolyte disturbances.
No large-scale randomized, placebo-controlled trials evaluate furosemide’s effect on mortality and long-term morbidity in diastolic or systolic dysfunction. In short-term studies, furosemide reduces edema, reduces hospitalizations, and improves exercise capacity in the setting of systolic dysfunction (strength of recommendation [SOR]: B, based upon low-quality randomized controlled trials). Furosemide and other diuretics reduce symptomatic volume overload in diastolic and systolic dysfunction (SOR: C, based on expert opinion).
There is potential morbidity with the use of high-dose loop diuretics (volume contraction, electrolyte disturbances, and neuroendocrine activation).1-3 Use of high-dose loop diuretics for systolic dysfunction is associated with increased mortality, sudden death, and pump failure death (SOR: B, based on retrospective analyses of large-scale randomized controlled trials). However, diuretic resistance or disease severity may explain these latter findings.
Evidence summary
Faris et al4 conducted a meta-analysis of randomized controlled trials that used diuretics (pertanide, furosemide, furosemide-hydrochlorothiazide) in congestive heart failure (TABLE).4 Of the 18 trials, 8 were placebo-controlled and 10 used active controls (diuretics vs angiotensin-converting enzyme [ACE] inhibitors, digoxin, or ibopamine, a dopamine agonist). Three placebo-controlled trials (N=221) showed an absolute risk reduction in death of 8% in diuretic-treated patients (number needed to treat [NNT]=12.5). Four placebo-controlled trials (N=448) showed a significantly lower rate of admissions for worsening failure among diuretic-treated patients (NNT=8.5), and 4 of the active-controlled trials (N=150) showed a nonsignificant trend toward decreased admissions. Six active-controlled studies (N=174) showed significantly increased exercise capacity for patients on diuretics. One of these latter trials also assessed quality of life, edema, and New York Heart Association (NYHA) class, and demonstrated no change in these outcomes in the treatment and placebo groups.5
The studies used in this meta-analysis had numerous shortcomings: the individual trials had small numbers of patients (N=14–139), short follow-up periods (typically 4–8 weeks), and inadequate statistical power to clearly demonstrate morbidity/mortality reductions. There was significant heterogeneity between studies. Crossover studies were included, some studies did not clearly report masking and assessment of outcome measures, and assessment of study validity was not clear. Studies employed a variety of diuretic types and doses, used different controls, and did not clarify whether patients’ congestive heart failure was caused primarily by diastolic or systolic dysfunction.
It is worth noting that diuretic use also carries some risk. One large retrospective study evaluated 6796 patients using potassium-sparing diuretics vs non–potassium-sparing diuretics in the Studies of Left Ventricular Dysfunction (SOLVD) trial.6 Rates of hospitalization or death from worsening congestive heart failure were significantly higher in the non–potassium-sparing diuretic population than in the nondiuretic population (relative risk [RR]=1.31, 95% confidence interval [CI], 1.09–1.57; number needed to harm=5.78). This increased risk was not found for patients taking potassium-sparing diuretics (RR=0.99; 95% CI, 0.76–1.30).
Another retrospective study of SOLVD patients found a significant and independent association with increased risk of arrhythmic death among patients taking non–potassium-sparing diuretics (RR=1.33; 95% CI, 1.05–1.69).7
A retrospective study of 1153 patients with NYHA Class III to IV heart failure, who were enrolled in the Prospective Randomized Amlodipine Survival Evaluation (PRAISE), found high diuretic doses to be independently associated with mortality (adjusted hazard ratio [HR]=1.37; P=.004), sudden death (HR=1.39; P=.042), and pump failure death (HR=1.51; P=.034).8
The authors caution that there is no proof of causation between furosemide and death; diuretic resistance may explain the poor outcomes, or the use of loop diuretics at high doses may be proxy of more severe illness, and thus poorer outcome.
TABLE
Clinical effects of diuretics in congestive heart failure
| OUTCOME | TRIAL DESCRIPTION | N | RESULTS (REPORTED AS OR) | 95% CI | P VALUE | NNT |
|---|---|---|---|---|---|---|
| Death | 3 placebo-controlled | 221 | 0.25 | 0.07–0.84 | .03 | 12.5 |
| Admissions | 4 placebo-controlled | 448 | 0.31 | 0.15–0.62 | .001 | 8.5 |
| 4 active-controlled | 150 | 0.34 | 0.10–1.21 | .10 | 12.8 | |
| Exercise capacity | 6 active-controlled | 174 | 0.37 | 0.10–0.64 | .007 | * |
| *Unable to calculate NNT due to lack of uniform reporting of exercise times. | ||||||
| OR, odds ratio; CI, confidence interval; NNT, number needed to treat. | ||||||
| Source: Faris et al, Int J Cardiol 2002.4 | ||||||
Recommendations from others
The American College of Cardiology recommends using diuretics in the setting of left ventricular systolic dysfunction and fluid retention (level of evidence [LOE]: A), and recommends using diuretics in diastolic dysfunction to control pulmonary congestion and peripheral edema (LOE: C).9
The European Society of Cardiology notes that no randomized controlled trials have assessed survival effects of diuretics in congestive heart failure, but recommends using diuretics for symptomatic treatment of volume overload (LOE: A). This society also cites evidence that diuretic use improves exercise tolerance (LOE: B). They recommend that diuretics be used always in addition to an ACE inhibitor, that loop diuretics be used if symptoms are more than mild and if glomerular filtration rate (GFR) <30 cc/min, and that thiazide diuretics can be used with loop diuretics for synergistic effects in severe congestive heart failure. 10
Helpful in the acute setting, diuretics shouldn’t be used alone chronically
Jon Neher, MD
Valley Medical Center, Renton, Wash
Furosemide and the other loop diuretics are very satisfying to use clinically. The patient in heart failure arrives at the hospital dypsneic, cyanotic, and terrified. After a single large dose of medication, the patient diureses and begins to feel good again quite quickly.
The practitioner, however, needs to be wary of the resulting impression that diuretics are “good” for heart failure. ACE inhibitors, beta blockers, and (in severe cases) spironolactone are “good” for heart failure because they prolong lives. One must not allow diuretic therapy—started for acute decompensation— to prevent use of more important long-term medications by causing dehydration, hypotension, or electrolyte disturbances.
1. Reyes AJ. Diuretics in the treatment of patients who present congestive heart failure and hypertension. J Hum Hypertens 2002;16 Suppl 1:S104-S113.
2. van Kraaij DJ, Jansen RW, Gribnau FW, Hoefnagels WH. Diuretic therapy in elderly heart failure patients with and without left ventricular systolic dysfunction. Drugs Aging 2000;16:289-300.
3. Kramer BK, Schweda F, Riegger GAJ. Diuretic treatment and diuretic resistance in heart failure. Am J Med 1999;106:90-96.
4. Faris R, Flather M, Purcell H, Henein M, Poole-Wilson P, Coats A. Current evidence supporting the role of diuretics in heart failure: a meta analysis of randomised controlled trials. Int J Cardiol 2002;82:149-158.
5. Parker JO. The effects of oral ibopamine in patients with mild heart failure—a double blind placebo controlled comparison to furosemide. The Ibopamine Study Group. Int J Cardiol 1993;40:221-227.
6. Domanski M, Norman J, Pitt B, et al. Diuretic use, progressive heart failure, and death in patients in the Studies of Left Ventricular Dysfunction (SOLVD). J Am Coll Cardiol 2003;42:705-708.
7. Cooper HA, Dries DL, Davis CE, Shen YL, Domanski MJ. Diuretics and risk of arrhythmic death in patients with left ventricular dysfunction. Circulation 1999;100:1311-1315.
8. Neuberg GW, Miller AB, O’Connor CM, et al. Diuretic resistance predicts mortality in patients with advanced heart failure. Am Heart J 2002;144:31-38.
9. Hunt SA, Baker DW, Chin MH, et al. ACC/AHA guidelines for the evaluation and management of chronic heart failure in the adult: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee to Revise the 1995 Guidelines for the Evaluation and Management of Heart Failure). 2001. American College of Cardiology. Last updated March 12, 2002. Available at: www.acc.org/clinical/ guidelines/failure/hf_index.htm. Accessed on March 4, 2005.
10. Remme WJ, Swedberg K. Task Force for the Diagnosis and Treatment of Chronic Heart Failure, European Society of Cardiology. Guidelines for the diagnosis and treatment of chronic heart failure. Eur Heart J 2001;22:1527-1560.
1. Reyes AJ. Diuretics in the treatment of patients who present congestive heart failure and hypertension. J Hum Hypertens 2002;16 Suppl 1:S104-S113.
2. van Kraaij DJ, Jansen RW, Gribnau FW, Hoefnagels WH. Diuretic therapy in elderly heart failure patients with and without left ventricular systolic dysfunction. Drugs Aging 2000;16:289-300.
3. Kramer BK, Schweda F, Riegger GAJ. Diuretic treatment and diuretic resistance in heart failure. Am J Med 1999;106:90-96.
4. Faris R, Flather M, Purcell H, Henein M, Poole-Wilson P, Coats A. Current evidence supporting the role of diuretics in heart failure: a meta analysis of randomised controlled trials. Int J Cardiol 2002;82:149-158.
5. Parker JO. The effects of oral ibopamine in patients with mild heart failure—a double blind placebo controlled comparison to furosemide. The Ibopamine Study Group. Int J Cardiol 1993;40:221-227.
6. Domanski M, Norman J, Pitt B, et al. Diuretic use, progressive heart failure, and death in patients in the Studies of Left Ventricular Dysfunction (SOLVD). J Am Coll Cardiol 2003;42:705-708.
7. Cooper HA, Dries DL, Davis CE, Shen YL, Domanski MJ. Diuretics and risk of arrhythmic death in patients with left ventricular dysfunction. Circulation 1999;100:1311-1315.
8. Neuberg GW, Miller AB, O’Connor CM, et al. Diuretic resistance predicts mortality in patients with advanced heart failure. Am Heart J 2002;144:31-38.
9. Hunt SA, Baker DW, Chin MH, et al. ACC/AHA guidelines for the evaluation and management of chronic heart failure in the adult: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee to Revise the 1995 Guidelines for the Evaluation and Management of Heart Failure). 2001. American College of Cardiology. Last updated March 12, 2002. Available at: www.acc.org/clinical/ guidelines/failure/hf_index.htm. Accessed on March 4, 2005.
10. Remme WJ, Swedberg K. Task Force for the Diagnosis and Treatment of Chronic Heart Failure, European Society of Cardiology. Guidelines for the diagnosis and treatment of chronic heart failure. Eur Heart J 2001;22:1527-1560.
Evidence-based answers from the Family Physicians Inquiries Network