A 65-year-old man with a past medical history of coronary artery disease (CAD), diabetes mellitus, hypercholesterolemia, and hypertension (HTN) presents with a 1-month history of intermittent chest pain and shortness of breath that was associated with exertion. He underwent an exercise stress test that was positive. This was followed by a coronary angiography that demonstrated significant 3-vessel CAD. A transthoracic echocardiogram demonstrated a left ventricular ejection fraction (LVEF) of 30%.
It would be reasonable in a patient with multivessel CAD and a significant reduction in left ventricular (LV) function to presume that his/her cardiac dysfunction is directly related to myocardial ischemia resulting from a decrease in coronary blood flow and coronary flow reserve (CFR). Although all of the following are associated with LV dysfunction, whether the myocardium is stunned, hibernating, or infarcted depends on the duration, chronicity, severity, and repetitiveness of the myocardial ischemia (Figure 35-1). These different states of the myocardium can also coexist in different parts of the heart.
Ischemia-associated left ventricular dysfunction. Schematic illustration of ischemia-induced myocardial injury. Abbreviations: CAD, coronary artery disease; CFR, coronary flow reserve.
Stunned myocardium—Acute myocardial ischemia can lead to subsequent contractile dysfunction. However, if the myocardium is just stunned and the ischemia is promptly relieved, the contractile function of the myocardium is eventually restored, usually over a period of hours to days.1 The aberration in a stunned myocardium appears to be predominantly metabolic in nature, not structural.2,3
Hibernating myocardium—In contradistinction to stunned myocardium, when myocardial ischemia persists and becomes chronic, it can lead to an adaptive response of decreasing basal metabolic demand by reducing contractility and cellular activity. This is associated with changes to both cellular and extracellular structures.4
Myocardial infarction—Acute myocardial ischemia that is significant enough to cause myocyte necrosis can lead to myocardial infarction (MI) and subsequent myocardial dysfunction. This can also be a result of extracellular fibrotic changes due to chronic ischemia or repetitive myocardial stunning. Infarcted myocardial tissue does not regain contractile function with revascularization.
Nonischemic cardiomyopathy—In the setting of proven severe CAD, absent any other obvious diagnoses, a patient’s myocardial dysfunction is likely due to ischemic cardiomyopathy. However, this does not preclude the possibility that 1 or more of the many nonischemic cardiomyopathy diagnoses is partially or solely responsible for his/her myocardial dysfunction.
In patients with significant CAD and impaired LV function, considerations should be made as to whether they would benefit from coronary revascularization (Figure 35-2). The role of coronary revascularization to improve LV function and ultimately improve mortality has been extensively studied. Although the overall body of evidence appears to support its role and benefits, the topic remains controversial. Three major randomized controlled trials (RCTs) have looked into this ...