By Van Selby, MD
Assistant Professor of Medicine, University of California, San Francisco Cardiology Division, Advanced Heart Failure Section
Dr. Selby reports no financial relationships relevant to this field of study.
SYNOPSIS: In a large community-based cohort, the development of silent myocardial infarction on ECG was associated with increased risk of future heart failure.
SOURCE: Qureshi WT, Zhang ZM, Chang PP, et al. Silent myocardial infarction and long-term risk of heart failure: The ARIC study. J Am Coll Cardiol 2018;71:1-8.
Approximately one-half of myocardial infarctions (MI) are silent, appearing as new Q waves on the ECG of a patient with no clinical evidence of MI. Although silent MI has been associated with increased all-cause mortality and other adverse outcomes, no one has conducted a large study to determine an association between silent MI and the risk of developing heart failure (HF).
Qureshi et al analyzed data from the Atherosclerosis Risk in Communities (ARIC) study. They retrospectively evaluated 9,243 patients determined to be free of cardiovascular disease during a baseline visit between 1987 and 1989. All patients underwent three follow-up evaluations, including an ECG, approximately once every three years. Silent MI was defined as ECG evidence of MI (appearance of a major Q/QS wave or minor Q/QS wave plus major ST-T abnormalities) that was not present at baseline but was identified during any follow-up ECG in the absence of clinical evidence of MI. The primary outcome was new HF, defined as the first occurrence of HF hospitalization. During a median follow-up of 13 years, 10.6% of participants experienced a first hospitalization for HF. In a multivariate analysis adjusted for age, sex, hypertension, and other risk factors, the development of silent MI was associated with an increased risk of HF (hazard ratio [HR], 1.35; P = 0.035). The risk of HF associated with silent MI was strongest in younger patients (HR, 1.66 in patients < 53 years of age compared to HR, 1.19 in patients > 53 years of age). The risk of silent MI was similar in men and women. The development of clinical MI (with compatible symptoms and biomarkers) was an even stronger predictor of HF (HR, 2.85; P < 0.001). The authors concluded that silent MI is associated with HF and provides an opportunity to identify a new HF risk factor.
This large, well-conducted cohort study showed that > 3% of patients with no cardiovascular disease at baseline developed silent MI during the follow-up period. Given the frequency with which ECGs are obtained in routine clinical practice, it is important to understand the clinical significance of this finding. By demonstrating that silent MI is associated with increased risk of future HF, Qureshi et al built on previous work to show an association between silent MI and other adverse outcomes. These findings are not particularly surprising, as the relationship between myocardial damage and subsequent dysfunction is well known. Similarly, it is not surprising the risk of HF associated with clinical MI was stronger than that associated with silent MI. Clinically apparent MIs may represent larger infarct size, and, therefore, are more likely to cause myocardial dysfunction. But while guidelines provide clear recommendations for management following clinical MI, there are no strong data to inform the management of patients with silent MI. Although identifying silent MI as a risk factor is important, the next obvious step is to find a solution.
Based on the findings of this study, patients with silent MI but no evidence of cardiomyopathy or clinical HF could be considered American College of Cardiology/American Heart Association Stage A HF (“at risk for HF”). Management of these patients focuses on a heart-healthy lifestyle, prevention of vascular and coronary disease, and prevention of left ventricular (LV) structural abnormalities. The finding of silent MI could (and should) be used to encourage patients to increase exercise or quit smoking. In patients with silent MI and hypertension, treating with drugs that have been shown to prevent LV remodeling, such as ACE inhibitors, seems like a logical choice, although this strategy has not been evaluated in large clinical trials. ARIC is a well-organized study with much strength. However, several limitations are worth noting. Approximately 40% of patients were missing an ECG and were excluded from the analysis. The diagnosis of HF was based purely on ICD-9 codes, without validation by physician review.
Despite these limitations, based on the strength of their findings and our knowledge of cardiovascular pathophysiology, the association between silent MI and HF seems valid. Qureshi et al have identified a new HF risk factor that is cheap and easy to treat. For now, the presence of silent MI should alert the treating clinician to treat other cardiovascular risk factors aggressively. As the prevalence of HF continues to increase, future studies hopefully will provide specific interventions to decrease progression to HF in at-risk patients.