Elevated troponins are serious business, even without an MI

 

Sometimes it seems like cardiac troponin testing has become nearly as ubiquitous as the CBC and the BMP. Concern over atypical presentations of MI has contributed to widespread use in emergency departments and hospitalized patients. But once the test comes back elevated, what do you do with that information?

Typically, the next step is to consult Cardiology, which is a reasonable request with or without a suspicion of MI. Frequently, invasive management is not an option; or perhaps the diagnosis is “type 2 MI.”¹

Courtesy University of Florida

Type 2 MI is a condition in which oxygen supply/demand mismatch results in myocardial damage in the absence of a coronary plaque disruption. This can occur in severe illness of a relatively healthy patient or mild illness of a patient with multiple comorbidities. The treatment is supportive and focused on addressing the underlying acute illness. Because the options are limited, the diagnosis is often put on the back burner and may not be given much attention during an acute hospitalization.

A growing body of evidence is making it clear that any elevation in cardiac troponin is a serious predictor of risk and that the risk is highest if the patient is not having an MI.² My colleagues and I recently conducted a cohort study of more than 700 veterans at our VA Medical Center addressing this question. We evaluated long-term mortality (6 years) comparing veterans who were diagnosed with MI with those who had troponin elevation and no clinical MI. The diagnostic determination was made for all subjects prospectively as part of a quality improvement project that sought to better care for MI patients at our facility. (In some cases, only single troponin values were measured so we cannot say that all patients in our investigation had a true type 2 MI.)

We found that veterans with an elevation in troponin that was not caused by MI had higher risk of mortality risk than did MI patients.³ The risk started to diverge at 30 days and was 42.0% at 1 year, compared with 29.0% for those with MI (odds ratio, 0.56; 95% confidence interval, 0.41-0.78). This risk continued to separate and, at 6 years, was 77.7% vs. 58.7% (OR, 0.41; 95% CI 0.30-0.56). Our observations agree with other recent publications; what we tried to do in advancing the literature was to construct a robust Cox proportional hazard model to try to better understand if the risk seen in these patients is just because of their being “sicker.”

We tried to capture a number of other acute illness states with variables including TIMI score, being in hospice care, having a “do not resuscitate” order, being in the ICU, receiving CPR, and having a fever or leukocytosis, etc. Despite this modeling, elevated troponin remained a significant predictor of risk. While several variables we modeled remained significant predictors of mortality, their distribution between our two cohorts did not explain the excess mortality risk associated with non-MI troponin.

Unfortunately, there are no viable treatment options specific for patients with non-MI troponin elevation and type 2 MI. Given that the causes are multiple and heterogeneous, there may not be a common pathway to target for reducing cardiovascular risk. Regardless, the observation of non-MI troponin or type 2 MI should be taken seriously and not be ignored.

In selected patients, particularly those without known coronary artery disease, it may be appropriate to perform diagnostic testing or risk assessment with noninvasive imaging prior to discharge. Those with coronary artery disease should be treated aggressively for prevention of future cardiovascular events with both medical therapy and risk factor reduction.
 

1. Thygesen K, Alpert JS, et al. Third universal definition of myocardial infarction. J Am Coll Cardiol. 2012;60:1581-98.

2. Alcalai R, Planer D, Culhaoglu A, Osman A, Pollak A and Lotan C. Acute coronary syndrome vs nonspecific troponin elevation: clinical predictors and survival analysis. Arch Intern Med. 2007;167:276-81.

3. Winchester DE, Burke L, Agarwal N, Schmalfuss C and Pepine CJ. Predictors of short- and long-term mortality in hospitalized veterans with elevated troponin. J Hosp Med. 2016 Jun 3. doi: 10.1002/jhm.2619.

David Winchester, MD, is assistant professor in the division of cardiovascular medicine at the University of Florida (Gainesville), and practices general cardiology at the Malcom Randall VA Medical Center, Gainesville.

 

Sometimes it seems like cardiac troponin testing has become nearly as ubiquitous as the CBC and the BMP. Concern over atypical presentations of MI has contributed to widespread use in emergency departments and hospitalized patients. But once the test comes back elevated, what do you do with that information?

Typically, the next step is to consult Cardiology, which is a reasonable request with or without a suspicion of MI. Frequently, invasive management is not an option; or perhaps the diagnosis is “type 2 MI.”¹

Courtesy University of Florida

Type 2 MI is a condition in which oxygen supply/demand mismatch results in myocardial damage in the absence of a coronary plaque disruption. This can occur in severe illness of a relatively healthy patient or mild illness of a patient with multiple comorbidities. The treatment is supportive and focused on addressing the underlying acute illness. Because the options are limited, the diagnosis is often put on the back burner and may not be given much attention during an acute hospitalization.

A growing body of evidence is making it clear that any elevation in cardiac troponin is a serious predictor of risk and that the risk is highest if the patient is not having an MI.² My colleagues and I recently conducted a cohort study of more than 700 veterans at our VA Medical Center addressing this question. We evaluated long-term mortality (6 years) comparing veterans who were diagnosed with MI with those who had troponin elevation and no clinical MI. The diagnostic determination was made for all subjects prospectively as part of a quality improvement project that sought to better care for MI patients at our facility. (In some cases, only single troponin values were measured so we cannot say that all patients in our investigation had a true type 2 MI.)

We found that veterans with an elevation in troponin that was not caused by MI had higher risk of mortality risk than did MI patients.³ The risk started to diverge at 30 days and was 42.0% at 1 year, compared with 29.0% for those with MI (odds ratio, 0.56; 95% confidence interval, 0.41-0.78). This risk continued to separate and, at 6 years, was 77.7% vs. 58.7% (OR, 0.41; 95% CI 0.30-0.56). Our observations agree with other recent publications; what we tried to do in advancing the literature was to construct a robust Cox proportional hazard model to try to better understand if the risk seen in these patients is just because of their being “sicker.”

We tried to capture a number of other acute illness states with variables including TIMI score, being in hospice care, having a “do not resuscitate” order, being in the ICU, receiving CPR, and having a fever or leukocytosis, etc. Despite this modeling, elevated troponin remained a significant predictor of risk. While several variables we modeled remained significant predictors of mortality, their distribution between our two cohorts did not explain the excess mortality risk associated with non-MI troponin.

Unfortunately, there are no viable treatment options specific for patients with non-MI troponin elevation and type 2 MI. Given that the causes are multiple and heterogeneous, there may not be a common pathway to target for reducing cardiovascular risk. Regardless, the observation of non-MI troponin or type 2 MI should be taken seriously and not be ignored.

In selected patients, particularly those without known coronary artery disease, it may be appropriate to perform diagnostic testing or risk assessment with noninvasive imaging prior to discharge. Those with coronary artery disease should be treated aggressively for prevention of future cardiovascular events with both medical therapy and risk factor reduction.
 

1. Thygesen K, Alpert JS, et al. Third universal definition of myocardial infarction. J Am Coll Cardiol. 2012;60:1581-98.

2. Alcalai R, Planer D, Culhaoglu A, Osman A, Pollak A and Lotan C. Acute coronary syndrome vs nonspecific troponin elevation: clinical predictors and survival analysis. Arch Intern Med. 2007;167:276-81.

3. Winchester DE, Burke L, Agarwal N, Schmalfuss C and Pepine CJ. Predictors of short- and long-term mortality in hospitalized veterans with elevated troponin. J Hosp Med. 2016 Jun 3. doi: 10.1002/jhm.2619.

David Winchester, MD, is assistant professor in the division of cardiovascular medicine at the University of Florida (Gainesville), and practices general cardiology at the Malcom Randall VA Medical Center, Gainesville.

 

Sometimes it seems like cardiac troponin testing has become nearly as ubiquitous as the CBC and the BMP. Concern over atypical presentations of MI has contributed to widespread use in emergency departments and hospitalized patients. But once the test comes back elevated, what do you do with that information?

Typically, the next step is to consult Cardiology, which is a reasonable request with or without a suspicion of MI. Frequently, invasive management is not an option; or perhaps the diagnosis is “type 2 MI.”¹

Courtesy University of Florida

Type 2 MI is a condition in which oxygen supply/demand mismatch results in myocardial damage in the absence of a coronary plaque disruption. This can occur in severe illness of a relatively healthy patient or mild illness of a patient with multiple comorbidities. The treatment is supportive and focused on addressing the underlying acute illness. Because the options are limited, the diagnosis is often put on the back burner and may not be given much attention during an acute hospitalization.

A growing body of evidence is making it clear that any elevation in cardiac troponin is a serious predictor of risk and that the risk is highest if the patient is not having an MI.² My colleagues and I recently conducted a cohort study of more than 700 veterans at our VA Medical Center addressing this question. We evaluated long-term mortality (6 years) comparing veterans who were diagnosed with MI with those who had troponin elevation and no clinical MI. The diagnostic determination was made for all subjects prospectively as part of a quality improvement project that sought to better care for MI patients at our facility. (In some cases, only single troponin values were measured so we cannot say that all patients in our investigation had a true type 2 MI.)

We found that veterans with an elevation in troponin that was not caused by MI had higher risk of mortality risk than did MI patients.³ The risk started to diverge at 30 days and was 42.0% at 1 year, compared with 29.0% for those with MI (odds ratio, 0.56; 95% confidence interval, 0.41-0.78). This risk continued to separate and, at 6 years, was 77.7% vs. 58.7% (OR, 0.41; 95% CI 0.30-0.56). Our observations agree with other recent publications; what we tried to do in advancing the literature was to construct a robust Cox proportional hazard model to try to better understand if the risk seen in these patients is just because of their being “sicker.”

We tried to capture a number of other acute illness states with variables including TIMI score, being in hospice care, having a “do not resuscitate” order, being in the ICU, receiving CPR, and having a fever or leukocytosis, etc. Despite this modeling, elevated troponin remained a significant predictor of risk. While several variables we modeled remained significant predictors of mortality, their distribution between our two cohorts did not explain the excess mortality risk associated with non-MI troponin.

Unfortunately, there are no viable treatment options specific for patients with non-MI troponin elevation and type 2 MI. Given that the causes are multiple and heterogeneous, there may not be a common pathway to target for reducing cardiovascular risk. Regardless, the observation of non-MI troponin or type 2 MI should be taken seriously and not be ignored.

In selected patients, particularly those without known coronary artery disease, it may be appropriate to perform diagnostic testing or risk assessment with noninvasive imaging prior to discharge. Those with coronary artery disease should be treated aggressively for prevention of future cardiovascular events with both medical therapy and risk factor reduction.
 

1. Thygesen K, Alpert JS, et al. Third universal definition of myocardial infarction. J Am Coll Cardiol. 2012;60:1581-98.

2. Alcalai R, Planer D, Culhaoglu A, Osman A, Pollak A and Lotan C. Acute coronary syndrome vs nonspecific troponin elevation: clinical predictors and survival analysis. Arch Intern Med. 2007;167:276-81.

3. Winchester DE, Burke L, Agarwal N, Schmalfuss C and Pepine CJ. Predictors of short- and long-term mortality in hospitalized veterans with elevated troponin. J Hosp Med. 2016 Jun 3. doi: 10.1002/jhm.2619.

David Winchester, MD, is assistant professor in the division of cardiovascular medicine at the University of Florida (Gainesville), and practices general cardiology at the Malcom Randall VA Medical Center, Gainesville.