High Troponin Levels Associated With Mental-Stress–Induced Ischemia in CAD Patients

Deborah Brauser

April 15, 2016

CHICAGO, IL — Although an association has been shown previously between elevated levels of high-sensitivity cardiac troponin I (hs-cTnI) and exercise-induced ischemia in patients with CAD, new research suggests there may also be a link with mental-stress ischemia[1].

An analysis of 587 stable CAD patients showed that those who developed ischemia after a mental stress test consisting of a public-speaking challenge had significantly higher levels of resting hs-cTnI at baseline vs those who didn't develop the condition (5.9 pg/mL vs 4.1 pg/mL, respectively, P<0.001).

Higher troponin levels were also found in those who did vs did not develop ischemia after a conventional exercise-based or pharmcological stress test (5.4 pg/mL vs 3.9 pg/mL, P<0.001).

In addition, the odds ratio (OR) for developing mental or physical stress ischemia, after adjustment for age, sex, race, and CAD risk factors, was more than double for those with hs-cTnI higher than the median level of 4.3 pg/mL vs those with lower levels (OR 2.5, P<0.001 for both comparisons).

Cardiology research fellow Dr Muhammad Hammadah (Emory Clinical Cardiovascular Research Institute, Atlanta, GA) presented the results at the American College of Cardiology (ACC) 2016 Scientific Sessions as part of the event's Young Investigator Awards competition.

"The higher levels of troponin are biological evidence of an ongoing myocardial injury in this population," Hammadah told heartwire from Medscape, noting that this was part of the largest study yet to assess mental-stress ischemia in the US.

"We are now at the phase of seeing whether these increased levels will have any prognostic information beyond the presence of ischemia and predicting adverse cardiac outcomes or not, in the future," he said.

MIPS Analysis

Hammadah noted that previous research has shown that patients with mental-stress ischemia "have double the risk of death and MI when you follow them prospectively" and that patients with CAD and higher resting troponin also have increased risk of death and MI.

So they created the Mental Stress Ischemia: Mechanisms and Prognosis Study (MIPS), with three main parts to evaluate "brain, genetic, vascular, hormonal, and behavioral correlates" of this condition and their influence on future cardiac outcomes.

The current analysis, which is part of MIPS, included 587 participants (76% men; mean age, 66 years; 32% with diabetes) who underwent 99mTc sestamibi myocardial perfusion imaging during two types of stress testing. A total of 31% had had a prior MI.

During the mental stress test, the patients were asked to give a 5-minute speech to white-coated staff on an uncomfortable topic (what they would do if a loved one were being mistreated in a nursing home). The prevalence of mental-stress–induced ischemia was 16%. Interestingly, hs-cTnI levels did not change significantly during the test.

The conventional (control) arm included either a treadmill (n=407) or pharmacologic (n=180) stress test; 34.8% developed myocardial ischemia.

Of those who developed mental-stress ischemia, 75% also developed conventional-stress ischemia. For this analysis, ischemia was defined as "new or worsening impairment in myocardial perfusion within each myocardial segment."

Biological Explanation

The unadjusted OR for mental-stress ischemia or conventional-stress ischemia for those with higher levels of resting hs-cTnI was 2.7 for both (P<0.001; 95% CI 1.7–4.2 and 1.9–3.8, respectively). And even the fully adjusted model showed a significant OR of 1.8 (95% CI 1.0–3.1, P=0.04) and 1.9 (95% CI 1.2–2.9, P=0.003), respectively.

"High troponin levels in patients with coronary artery disease may be a marker of repeated or chronic ischemic burden with both psychological and physical triggers during everyday life," summarized Hammadah.

He noted that "for many years, many people didn't believe in mental-stress ischemia." But the results showed not only a biological basis for the condition but that some patients have mental-stress ischemia (and higher resting troponin) without physical-stress ischemia, he said.

Hammadah reported that follow-up is now going on for these patients to assess hard outcomes. And a new biofeedback study has just started to evaluate stress-related myocardial blood-flow changes after psychological treatment.

The study was funded by the National Institutes of Health, and Abbott provided the troponin assays. Hammadah reports no relevant financial disclosures.

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