CAD Extent May Foreshadow Risk of Heart Failure After First MI
The number of occluded coronary arteries at the time of first MI may predict whether patients will subsequently develop heart failure (HF), a large population-based study suggests. The findings underscore the importance of understanding how HF emerges over time once an MI has occurred, the researchers say.
“Diffuse atherosclerosis may directly or indirectly exert an adverse effect on long-term prognosis of MI, either because of the extent of ischemic damage or by causing subsequent events (eg, recurrent MI) that increase the risk of HF,” write Yariv Gerber, PhD (Mayo Clinic, Rochester, MN), and colleagues in a study published online March 30, 2016, in JAMA Cardiology.
The study involved 1,922 residents of Olmsted County, MN, who had a first MI diagnosed between 1990 and 2010, and who had no prior HF.
Over approximately 7-year follow-up, 31% of the cohort developed HF. Of these people, 50.2% had HF with reduced ejection fraction, 31.6% had HF with preserved ejection fraction, and the remainder had no ejection fraction assessment available.
The likelihood of subsequent HF increased with increasing number of occluded coronary arteries at time of MI. This observation was consistent at both short- and long-term follow-up.
Furthermore, when the two HF groups—with reduced and preserved ejection fraction—were analyzed separately, the results remained consistent for the adverse impact of CAD extent. The findings also held true after adjustment for baseline characteristics of the compared groups and accounting for competing risks during follow-up.
Recurrent MI was associated with increased risk for HF over follow-up (HR 4.01; 95% CI 3.03-5.30), but did not confound the association between CAD and HF, nor did infarct size.
Path Leading to HF Unclear
Gerber and colleagues say while the mechanisms through which concomitant atherosclerosis in coronary vessels other than the culprit artery adversely affect HF risk after MI require further study, it appears that factors different from infarct size and culprit-vessel patency are involved in the process.
“Patients with both epicardial and endocardial CAD may have chronic hypoperfusion that leads to increased myocardial stiffness secondary to chronic inflammation and fibrosis,” the researchers write. “The increased myocardial stiffness, in turn, may impair systolic and diastolic function.”
Due to the
observational nature of the study, Gerber and colleagues say they cannot rule
out the effect of residual confounding from unmeasured variables. Additionally,
all patients were from a single community consisting of persons of mostly white
race/ethnicity, which they note, may limit the generalizability of the results
to other patient groups.
- Gerber Y, Weston SA, Enriquez-Sarano M, et al. Atherosclerotic burden and heart failure
- after myocardial infarction. JAMA Cardiol. 2016;Epub ahead of print.
- The study was supported by grants from the National Institutes of Health, the Rochester Epidemiology Project, and the National Institute on Aging.
- Gerber reports no relevant conflicts of interest.
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