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.

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  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

  
  
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  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

  
  
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  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.

  
  
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  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 and the role of viability testing with mixed results.^5-7 In patients with ischemic cardiomyopathy and significant LV dysfunction, revascularization has been shown to reverse this dysfunction, with patients with the greatest dysfunction and ischemic symptoms benefiting the most.^8,9

In a 10-year follow-up study of patients with significant ischemic dysfunction (LVEF <35%), the absolute risk reduction in all-cause mortality was 8% in coronary artery bypass grafting (CABG) + optimal medical therapy (OMT) patients compared to patients receiving OMT alone.¹⁰

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  An assessment should be made of the function of the LV. This is most practically done with echocardiography. This will provide not only an assessment of the LVEF, but it can also evaluate the status of all of the valves, any regional wall motion abnormalities, and the size and shape of the heart. In addition to assessing cardiac function, cardiac magnetic resonance (CMR) can also provide a wide range of cardiac information, including cardiac shape, size, wall thickness, volumes, mass, and global and regional wall motion abnormalities. However, CMR is much more costly, is not as readily available, is not well tolerated by patients with claustrophobia, cannot be used in patients with noncompatible implanted hardware, and its use is limited in patients with renal insufficiency because of the use of gadolinium contrast agents.

  
  
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  Patients require a recent assessment of their coronary anatomy with coronary angiography. This will determine whether they are anatomically candidates for surgical and/or percutaneous coronary interventional (PCI) revascularization.

  
  
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  Assessment of myocardial viability can be carried out using a variety of means, each having its advantages and disadvantages as determined by its sensitivity and specificity, technical limitations, expense, and availability. These modalities include single-photon emission computed tomography (SPECT), positron emission tomography (PET), late gadolinium enhancement CMR, and dobutamine echocardiography. SPECT, PET, and CMR work by assessing cellular integrity whereas dobutamine echocardiography assesses contractile reserve as a measure of viability by increasing contractility with low-dose dobutamine. Dobutamine can also be used with CMR to assess contractile reserve. Radionuclides used in SPECT imaging include thallium-201 and technetium-99m. See Table 35-1.

  
  
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  If a patient with ischemic cardiomyopathy has been determined to have viable myocardium and the coronary anatomy is amenable to surgical revascularization, then a determination should be made regarding the patient’s suitability for surgery based on the patient’s surgical risk. If the patient is deemed too high-risk, then PCI revascularization should be considered if anatomically favorable. Although controversies still remain, surgical revascularization with CABG appears to be favored over PCI in patients with severe systolic dysfunction.^11-13

  
  
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  For patients who are not candidates for coronary revascularization, OMT should be pursued. The mainstay of pharmacological management in these patients includes the use of angiotensin-converting enzyme (ACE) inhibitors, angiotensin receptor blockers (ARBs), beta blockers, aldosterone antagonists, and a combination of hydralazine and isosorbide dinitrate, as these have been shown to reduce mortality in heart failure (HF) patients.¹⁴ The selection of these medications should be individualized based on the patient’s cardiac function, clinical symptoms, and other comorbidities.

  
  
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  Cardiac resynchronization therapy (CRT) should be considered in patients with LVEF less than 35% and QRS greater than 150 ms.¹⁵

  
  
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  Those patients who fail OMT and CRT should then be considered for inotropic therapy. End-stage HF patients who have failed all other therapies may be considered for left ventricular assist device (LVAD) implantation or heart transplantation.