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Chapter Summary

This chapter discusses the epidemiology of heart failure due to coronary atherosclerosis, as well as the pathophysiology and treatment options for promoting reverse remodeling of the left ventricle following myocardial infarction. Coronary artery disease remains the most common etiology for heart failure, regardless of whether the phenotype is heart failure with reduced ejection fraction (left ventricular ejection fraction [LVEF] up to 40%), mildly reduced ejection fraction (LVEF 41% to 49%), or preserved ejection fraction (LVEF of at least 50%) (see Fuster and Hurst's Central Illustration). The extent of coronary artery disease has a direct bearing on clinical outcome. While guideline-directed pharmacotherapy remains a cornerstone for managing heart failure with reduced ejection fraction, coronary revascularization may improve quality of life and outcome in patients with or without symptomatic angina pectoris. Surgical coronary revascularization is more effective than medical therapy alone in the setting of hemodynamically significant multivessel disease, impaired left ventricular function, ventricular enlargement, moderate or severe mitral regurgitation and relatively preserved functional capacity. Coronary bypass grafting is more beneficial than multivessel percutaneous coronary intervention among diabetic patients with ischemic cardiomyopathy. For heart failure with preserved ejection fraction, the role of microvascular dysfunction and intermittent ischemia is summarized and treatment recommendations, including revascularization, are discussed.

eFig 47-01 Chapter 47: Obstructive and Nonobstructive Coronary Disease in Heart Failure


Common risk factors for heart failure (HF) include increased age, hypertension, diabetes, obesity, valvular heart disease, metabolic syndrome, and coronary artery disease (CAD). HF prevalence is also age-dependent, increasing significantly in the Framingham Heart Study from ~1% for those aged 50 to 59 years to ~10% in those aged 80 to 89 years.1 The incidence of CAD has been found to vary globally. In the United States, 50% to 70% of all cases of HF are attributed to CAD, compared to only 10% of cases in sub-Saharan Africa and 30% to 40% of all cases in Asia and Latin America.2 The incidence of HF has also been increasing with the lifetime risk for developing HF ranging from 20% to 45% in those aged 45 to 95 years old.1 Further, data from community surveillance studies have shown that HF hospitalizations are expected to increase over time, largely driven by increases in heart failure with preserved ejection fraction (HFpEF).3

Several large community-based studies have examined the relationship between CAD and incident HF. Major advances in the treatment of acute ST-segment elevation myocardial infarction (STEMI) during the last four decades have resulted in a substantial decline in mortality rates after myocardial infarction (MI). However, HF is now an increasingly common complication among post-MI survivors. Investigators from the Framingham Heart Study evaluated the temporal trends in HF incidence after symptomatic acute MI. While the 30-day mortality ...

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