The American Heart Association (AHA) defines dilated cardiomyopathy (DCM) as “a spectrum of heterogeneous myocardial disorders characterized by ventricular dilation and depressed myocardial performance in the absence of hypertension, valvular, congenital, or ischemic heart disease” (Bozkurt et al., 2016). Based on its origin, it is classified as a primary, which means confined to the myocardium, and mixed (genetic and non-genetic cause) cardiomyopathy: the list of known causes includes heart conditions (coronary heart disease, heart attack, high blood pressure), chronic metabolic diseases (diabetes, thyroid disease), infections (viral hepatitis and HIV), toxins like cobalt, alcohol, drugs (cocaine, amphetamines, doxorubicin and daunorubicin), and postpartum complications (American Heart Association
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Because of these changes, systolic dysfunction is responsible for the clinical manifestations: while some patients might never have symptoms, or only until later in disease, weakening of the heart and reduced cardiac reserve will display as dyspnea, orthopnea, and reduced ejection fractions - 25 % versus the normal 50% to 65%, fatigue, dependent edema, and jugular vein distention (AHA, 2017; Bozkurt et al., 2016; Porth, 2015). Disease progression will manifest itself in dizziness, lightheadedness and fainting spells, arrhythmias, chest pain and murmurs; mitral valve regurgitation and stasis of blood leads to thrombus formation and embolic seeding, and sudden death is possible if no heart transplant can be obtained (AHA, 2017; Porth, 2015). Treatment is directed toward symptom management and disease progression, since without transplant 5-year survival is estimated at less than 50 %; a combination of pharmacologic agents like diuretics, beta blockers, and anticoagulants, medical procedures (cardiac catheterization) and implantable devices (pacemakers or defibrillators) will be necessary, while modifiable causes (like alcohol removal) and lifestyle changes (exercise
Because of these changes, systolic dysfunction is responsible for the clinical manifestations: while some patients might never have symptoms, or only until later in disease, weakening of the heart and reduced cardiac reserve will display as dyspnea, orthopnea, and reduced ejection fractions - 25 % versus the normal 50% to 65%, fatigue, dependent edema, and jugular vein distention (AHA, 2017; Bozkurt et al., 2016; Porth, 2015). Disease progression will manifest itself in dizziness, lightheadedness and fainting spells, arrhythmias, chest pain and murmurs; mitral valve regurgitation and stasis of blood leads to thrombus formation and embolic seeding, and sudden death is possible if no heart transplant can be obtained (AHA, 2017; Porth, 2015). Treatment is directed toward symptom management and disease progression, since without transplant 5-year survival is estimated at less than 50 %; a combination of pharmacologic agents like diuretics, beta blockers, and anticoagulants, medical procedures (cardiac catheterization) and implantable devices (pacemakers or defibrillators) will be necessary, while modifiable causes (like alcohol removal) and lifestyle changes (exercise