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Ischemic cardiomyopathy (ICM) refers to significant systolic dysfunction with a moderate to severely impaired left ventricular ejection fraction as a consequence of myocardial ischemia and/or myocardial infarction. The condition is not listed or classified as cardiomyopathy in the position statements from the American Heart Association in 2006 or European Society of Cardiology in 2008 and no general consensus concerning the exact definition of the condition exists 1-5
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Ischemic cardiomyopathy constitutes the most common cause of heart failure in developed countries 1,2.
Risk factors for ischemic cardiomyopathy are those of myocardial ischemia and coronary artery disease.
This comprises non-modifiable and modifiable risk factors including genetic predisposition, gender and age as well as smoking, diabetes mellitus, hypertension, hyperlipidemia, sedentary lifestyle and obesity or different coronary anomalies.
Ischemic cardiomyopathy is highly associated with coronary artery disease, myocardial inflammation and coronary microvascular dysfunction 1.
Even though a general consensus with respect to the exact definition of ischemic cardiomyopathy is still lacking the following criteria have been used 1,2:
- evidence of left ventricular dysfunction with one or more of the following
- previous myocardial infarction or prior coronary revascularization
- luminal stenosis ≥75% in the left main stem or left anterior descending artery
- luminal stenosis ≥75% in two or more coronary arteries
Patients typically present with heart failure symptoms including angina, dyspnea, fatigue and syncope or nocturia and edema.
Complications of ischemic cardiomyopathy include:
- acute decompensated heart failure
- secondary mitral regurgitation
- pulmonary edema
- passive hepatic congestion
- cardiac arrest
- sudden cardiac death
The pathological correlate of ischemic cardiomyopathy consists in the impairment of left ventricular systolic function in the context of a significantly reduced myocardial blood flow and/or coronary flow reserve. This might be due to an irreversible loss of myocardium due to prior myocardial infarction and myocardial scar formation or a reversible loss of myocardial contractility due to myocardial ischemia in the setting of stunned or hibernating myocardium 1,2,5.
A cascade of metabolic, inflammatory and structural changes leads to adverse left ventricular remodeling and contractile dysfunction including 1:
- myocardial inflammation as a result of ischemia and reperfusion injury triggering adverse remodeling by inhibition of neovascularization and promotion of myocardial fibrosis
- coronary microvascular dysfunction as a result of an impaired vasomotor function, microvascular injury, obstruction and hemorrhage of the coronary microcirculation after myocardial injury and reperfusion
- functional and structural myocardial remodeling with chamber dilatation and systolic dysfunction and the following reversible and/or irreversible phenomena and alterations 1,5:
The main etiology of ischemic cardiomyopathy is coronary artery atherosclerosis. However several other less common coronary vascular conditions can impair coronary blood flow leading to myocardial ischemia and left ventricular systolic dysfunction and thus to ischemic cardiomyopathy 6:
- coronary microvascular dysfunction
- fibromuscular dysplasia
- vasospastic angina
- coronary vasculitis
- coronary artery dissection or aortic dissection with the involvement of coronaries
- coronary anomalies including anomalous course and coronary hypoplasia
Cardiac function can be assessed non-invasively with several imaging modalities in particular echocardiography and cardiac MRI. In addition, several imaging methods can assess the presence and extent of myocardial scarring and viable stunned or hibernating myocardium 1,5,7.
Chest x-ray might show an increased cardiac silhouette and signs of chronic heart failure.
Echocardiography will typically show a moderately or severely reduced left ventricular ejection (LVEF ≤35-40%) and regional wall motion abnormalities and wall thinning associated with a coronary territory.
Regional end-diastolic left ventricular wall thickness <6 mm indicates reduced contractile reserve and functional recovery 1.
Stress echocardiography might identify myocardial ischemia and suggest viable myocardium after a two-step evaluation with a low dose (5-10 µg/kg/min) and a high-dose dobutamine infusion (10-40 µg/kg/min).
A biphasic pattern with increased contractility of a myocardial segment in the low-dose regimen followed by a paradoxically reduced contractility indicates stunned or hibernating myocardium 1,5.
Cardiac CT might show a coronary luminal stenosis ≥75% or demonstrate hemodynamic relevance by CT-based fractional flow reserve (CT-FFR) in one or more of the coronary arteries. It might also provide information about the etiology (e.g. coronary artery disease, coronary dissection or coronary anomalies) Furthermore it might show perfusion defects or wall thinning in one or more coronary territories.
Invasive coronary angiography might demonstrate a luminal coronary stenosis ≥75% or proof hemodynamic relevance by the assessment of the fractional flow reserve (FFR).
Cardiac MRI will show left ventricular systolic dysfunction as well as cardiac wall motion abnormalities attributable to one or more coronary artery territories.
Furthermore, it will demonstrate myocardial ischemia and/or myocardial scar tissue in a subendocardial pattern attributable to one or more coronary territories indicating an ischemic origin. Myocardial edema might be present or not depending on the chronicity.
- cine imaging: regional wall motion abnormalities in the affected vascular territory
- perfusion imaging: decreased or delayed uptake during the first-pass perfusion
- IRGE/PSIR: subendocardial or transmural late gadolinium enhancement
A scar transmurality exceeding 50% predicts a rather poor likelihood of complete functional recovery of <10% 1.
Thallium-20 and technetium-99m MIBI SPECT, technetium-99m tetrofosmin SPECT, PET-CT or PET-MRI might show decreased stress and possibly resting perfusion as well as viable or non-viable myocardium as well as decreased cardiac systolic function 1,5.
The radiology report should include the following:
- cardiac volumes and measurements including left ventricular ejection fraction
- cardiac wall motion abnormalities
- presence and extent of perfusion deficits
- presence and extent of myocardial scar or non-viable myocardium
- presence and extent of coronary artery disease
Treatment and prognosis
The management of ischemic cardiomyopathy comprises optimal medical therapy, cardiac resynchronisation therapy with or without implantable cardioverter-defibrillator for secondary prevention of sudden cardiac death as well as treatment options such as transcatheter mitral valve intervention for secondary mitral regurgitation 1 and coronary revascularization 1.
Optimal medical therapy aims at suppression of the renin-angiotensin-aldosterone system and an increased adrenergic state with angiotensin-converting enzyme inhibitors, angiotensin and mineralocorticoid receptor blockers and beta-blockers and more recently angiotensin receptor/neprilysin inhibition with the combination valsartan and sacubitril.
Coronary revascularization can be done with percutaneous coronary intervention (PCI) and coronary bypass surgery (CABG) and has been shown to improve survival in patients with ischemic heart disease and heart failure 1,7,8. However the exact strategy is still somewhat controversial and depends on symptoms, coronary anatomy myocardial viability coexisting valvular heart disease and patient comorbidities 1,7.
- 1. Cabac-Pogorevici I, Muk B, Rustamova Y, Kalogeropoulos A, Tzeis S, Vardas P. Ischaemic Cardiomyopathy. Pathophysiological Insights, Diagnostic Management and the Roles of Revascularisation and Device Treatment. Gaps and Dilemmas in the Era of Advanced Technology. Eur J Heart Fail. 2020;22(5):789-99. doi:10.1002/ejhf.1747 - Pubmed
- 2. Briceno N, Schuster A, Lumley M, Perera D. Ischaemic Cardiomyopathy: Pathophysiology, Assessment and the Role of Revascularisation. Heart. 2016;102(5):397-406. doi:10.1136/heartjnl-2015-308037 - Pubmed
- 3. Maron B, Towbin J, Thiene G et al. Contemporary Definitions and Classification of the Cardiomyopathies: An American Heart Association Scientific Statement from the Council on Clinical Cardiology, Heart Failure and Transplantation Committee; Quality of Care and Outcomes Research and Functional Genomics and Translational Biology Interdisciplinary Working Groups; and Council on Epidemiology and Prevention. Circulation. 2006;113(14):1807-16. doi:10.1161/CIRCULATIONAHA.106.174287 - Pubmed
- 4. Elliott P, Andersson B, Arbustini E et al. Classification of the Cardiomyopathies: A Position Statement from the European Society Of Cardiology Working Group on Myocardial and Pericardial Diseases. Eur Heart J. 2008;29(2):270-6. doi:10.1093/eurheartj/ehm342 - Pubmed
- 5. Schuster A, Morton G, Chiribiri A, Perera D, Vanoverschelde J, Nagel E. Imaging in the Management of Ischemic Cardiomyopathy: Special Focus on Magnetic Resonance. J Am Coll Cardiol. 2012;59(4):359-70. doi:10.1016/j.jacc.2011.08.076 - Pubmed
- 6. Sekulic M, Zacharias M, Medalion B. Ischemic Cardiomyopathy and Heart Failure. Circ Heart Fail. 2019;12(6):e006006. doi:10.1161/CIRCHEARTFAILURE.119.006006 - Pubmed
- 7. Neumann F, Sousa-Uva M, Ahlsson A et al. 2018 ESC/EACTS Guidelines on Myocardial Revascularization. Eur Heart J. 2019;40(2):87-165. doi:10.1093/eurheartj/ehy394 - Pubmed
- 8. Panza J, Ellis A, Al-Khalidi H et al. Myocardial Viability and Long-Term Outcomes in Ischemic Cardiomyopathy. N Engl J Med. 2019;381(8):739-48. doi:10.1056/NEJMoa1807365 - Pubmed