“Ischemic cardiomyopathy” denotes the presence of obstructive epicardial coronary atherosclerosis with decreased left ventricular systolic dysfunction. An obsolete use of the term “ischemic cardiomyopathy” was “a dilated cardiomyopathy with impaired contractile performance not explained by the extent of coronary artery disease or ischemic damage.”¹ Although the commonly used term ischemic cardiomyopathy is not supported by the American Heart Association² or by the European Society of Cardiology,³ it is still in widespread use to distinguish clinically dilated cardiomyopathy from ischemic heart disease with heart failure.^{4,5,6,7,8,9,10,11,12,13,14}

Clinically, ischemic cardiomyopathy is defined as left ventricular ejection fraction <35% to 40%, increased left end-diastolic diameter (6.5 cm), and evidence of coronary occlusive disease. The latter is generally defined as >70% stenosis (diameter narrowing) in ≥1 epicardial coronary vessel on angiography, history of myocardial infarction or revascularization, or demonstrable ischemia.^8,12 “Demonstrable ischemia” generally indicates evidence of segmental wall motion abnormalities or documented myocardial infarction.

Chronic ischemic heart disease affects an estimated 3 million people in the United States and is the most common cause of heart failure worldwide.^15,16 Overall, there are more than 5 million Americans with heart failure, most caused by the sequelae of coronary ischemia, with over 80,000 new cases annually.¹⁶

Although coronary artery frequently disease presents as stable angina or acute coronary syndromes (ST elevation and non-ST elevation infarcts and sudden death), a substantial proportion of patients present with signs and symptoms of heart failure. The clinical findings are similar to those in heart failure of any cause, but angiography will demonstrate coronary artery stenoses, with irreversible wall motion abnormalities in areas of occlusion. In many cases of “ischemic cardiomyopathy,” the clinical course is initially that of acute infarction, treated by percutaneous interventions or open surgery, and then progresses to end-stage heart failure.

Between 75% and 90% of patients with ischemic cardiomyopathy are men, with a mean age of about 60 at the time of surgery.^8,12 Risk factors are frequently present, including hypertension (50% to 70%) and diabetes mellitus (30% to 45% of patients). Hyperlipidemia and smoking are also common, with a minority of patients with concomitant cerebrovascular or peripheral vascular disease. Between 20% and 50% of patients have no prior history of acute coronary syndrome.^8,12

Patients with ischemic cardiomyopathy are at increased risk for ventricular tachycardia, ventricular fibrillation, and sudden cardiac death.¹⁷ Up to one-third of patients require implantable defibrillators.^8,17 Various findings on electrocardiograms are associated with increased risk for ventricular fibrillation, including voltage criteria for left ventricular hypertrophy.¹⁷

The size of the infarct, as characterized by late gadolinium enhancement cardiac magnetic resonance, correlates with the risk of sustained monomorphic ventricular tachycardia, which may progress to ventricular fibrillation.⁵ Because monomorphic tachycardias may be mapped to specific sites by electrophysiologic studies, hearts from patients with ischemic cardiomyopathy frequently show patches of endocardial scarring indicative of prior ablation sites.

At explant or autopsy, approximately one-third of hearts will demonstrate implantable cardioverter defibrillators. These may be either single lead (tip of right ventricular apex) or dual (atrioventricular), with a second lead in the right atrium. Atrioventricular defibrillators are indicated in those at risk for bradycardia from intrinsic sinus node dysfunction or conduction system disease, or use of medications with negative chronotropic properties.

In heart failure of any cause, including that caused by ischemic heart disease, intraventricular dyssynchrony may necessitate biventricular pacing. In order to access the left ventricle, a lead is placed in the coronary sinus coursing to an anterior cardiac vein, in addition to the right atrial and ventricular pacemaker leads. These three pacing wires are often found at autopsy in patients with chronic ischemic heart disease and will have been removed in explanted hearts. Indications for resynchronization therapy include a QRS duration of ≥120 ms with moderate or severe heart failure and a QRS duration of ≥150 ms for patients with mild symptoms.¹¹

There are several surgical approaches to the treatment of chronic ischemic heart disease: coronary bypass grafting, mitral valve repair or replacement, and, in the case of aneurysm, surgical ventricular reconstruction.

The rationale behind coronary bypass surgery in patients with stable, healed infarcts is based on the presence of myocardial tissue that is not irreversibly damaged by ischemia, but is not contracting. The pathologic features of these areas have not been characterized, although the extent of transmural extent of scar has been negatively correlated with functional recovery after revascularization. Survival after coronary artery bypass surgery is better in patients with lower scar burden and lesser degrees of cardiac dilatation (as assessed by endsystolic volume).⁸

There is some evidence that bypass surgery may be superior to medical treatment in selected patients.¹³ Patients who are candidates for surgery include those with <50% stenosis of the left main coronary artery by angiography, no recent myocardial infarction (7 days or earlier), and no evidence of unstable angina.¹³

Postoperative complications include arrhythmias (33%), renal failure, infection, multiorgan failure, stroke, and respiratory failure (all <5%).¹²

In ischemic heart disease (and also idiopathic dilated cardiomyopathy), left ventricular systolic dysfunction is frequently complicated by functional mitral regurgitation, which is a relatively common cause of mitral valve repair and replacement. Mitral insufficiency is the result of posteromedial papillary muscle scarring or, more commonly, remodeling of the ventricle without necessarily dilatation of the annulus. Morbidity and mortality are directly related to the severity of mitral regurgitation, leading to mitral valve surgery in about 25% of patients with chronic ischemic heart disease.⁷

The surgical options include mitral annuloplasty using an undersized ring as well as valve replacement, which are frequently performed concomitantly with coronary artery bypass surgery. In contrast to mitral valve prolapse, a portion of the valve is typically not removed during the repair. If the valve is replaced, the valve appears essentially unremarkable. Long-term complications of annuloplasty rings include recurrent regurgitation, which eventually results in reoperation with removal of the ring and valve replacement. In such cases, the pathologist will receive as a surgical specimen both the explanted ring and the valve itself, which may show nonspecific fibrosis.

Hospital mortality is as high as 2.3% for mitral repair and 12.5% for mitral replacement in the setting of ischemic cardiomyopathy with concomitant bypass grafting.⁴ Medium-term survival at 2.5 years was reported as 92% for mitral repair and 73% for valve replacement in the same study.⁴

With idiopathic dilated cardiomyopathy, there is an increased risk of thrombi developing in the left side of the heart, especially in areas of healed infarct. Left ventricular thrombi are detected in up to 20% of patients and left atrial thrombin up to 40%.¹⁸