Dilated cardiomyopathy differential diagnosis

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Abdelrahman Ibrahim Abushouk, MD[2]

Overview

Dilated cardiomyopathy should be differentiated from other causes of cardiac dysfunction, in particular acute coronary syndrome, other cardiomyopathies (hypertrophic, restrictive, and ARVC/D), myocarditis, pericarditis, and cardiac toxicities.

Differentiating Dilated Cardiomyopathy from other Diseases

Dilated cardiomyopathy should be differentiated from other causes of cardiac dysfunction, in particular acute coronary syndrome, other cardiomyopathies (hypertrophic, restrictive, and ARVC/D), myocarditis, pericarditis, and cardiac toxicities.

Disorders	Etiology	Clinical Presentation	Laboratory Findings	Electrocardiogram	Echocardiography
Acute Coronary Syndrome	Atherosclerosis Coronary thrombosis Plaque rupture	Chest Pain Dyspnea Palpitations Nausea, vomiting, and sweating	Elevated blood troponin levels (after 6 hours of attack onset) Elevated blood CK-MB levels	ST segment changes T wave changes Pathological Q waves.
Acute Pericarditis	Idiopathic Viral infection Connective tissue diseases (e.g. SLE) Dressler's Syndrome (after MI) Familial Mediterranean fever	Sharp chest pain (that increases with breathing/cough, reduced with leaning forward) Pericardial friction rub Fever (for inflammatory causes)	CBC: Increased WBCs count Modest increase in CK-MB Elevated CRP levels.	Slight ST segment elevation in several leads Diffuse T wave inversion
Amphetamine/Cocaine Cardiomyopathy	Illicit drug use	History of drug use Chest pain Palpitation Other symptoms of amphetamine/cocaine intoxication	Drug and toxicology screen Elevated serum CK (rhabdomyolysis) Impaired electrolytes levels
Arrhythmogenic right ventricular cardiomyopathy (ARVC/D)	Idiopathic (but may be due to resolving myocarditis or genetic alterations in desmosomal proteins as plakoglobin and desmoplakin	Frequently symptomless until sudden cardiac death. Palpitations (Ventricular arrhythmia and conduction abnormalities) Exertional dyspnea Syncope	Diagnostic criteria are based on: Electrocardiogram Imaging modalities as 2D echocardiography and MRI.
Wet Beriberi	Inadequate thiamine intake (rice-based foods, alcoholism, and malnutrition) Increased thiamine loss (protracted vomiting) Inadequate absorption (after bariatric surgery or genetic mutation)	Palpitations Respiratory distress Edema of the legs Severe lactic acidosis.	Thiamine replacement test Reduced urinary thiamine Reduced erythrocyte transketolase and thiamine pyrophosphate activities.
Cardiac Tamponade	Ascending aortic dissection Collagen vascular diseases Iatrogenic - central line insertion, pacemaker insertion, and PCI Idiopathic Malignancy - breast cancer, Kaposi's sarcoma, lung cancer, lymphomas Penetrating trauma Pericarditis MI treatment (heparin & thrombolytics)	Acute tamponade: Cardiogenic shock, hypotension, cold extremities, peripheral cyanosis, and decreased urine output. Subacute tamponade: Peripheral edema with gradual progression to the aforementioned clinical picture.	Increased serum CK-MB and troponin Cause-related investigations as serum inflammatory markers, diagnostic pericardiocentesis, and Gallium 67 imaging.		Echocardiography to score the European Society of Cardiology (ESC) Working Group on Myocardial and Pericardial Diseases
Hyperthyroidism	Primary: Grave's disease, toxic thyroid nodules and adenoma Secondary: Pituitary adenomas and intracranial tumors Tertiary:Intracranial tumors involving the hypothalamus	Goiter Palpitations Anxiety Heat intolerance Weight loss Diarrhea Exophthalmus	Elevated T3 and T4 hormones TSH: Reduced in 1ry and Elevated in 2ry hyperthyroidism. Thyroid stimulating antibodies: Elevated only in Grave's disease
Hypertrophic Cardiomyopathy	Familial Gene mutation Hypertension Thyroid disease Diabetes Obesity	Chest pain Congestive heart failure symptoms Dizziness Dyspnea Exercise intolerance Syncope Fatigue	The diagnosis is based on Electrocardiogram		Echocardiography according to ACCF/AHA Guideline for the Diagnosis and Treatment of Hypertrophic Cardiomyopathy
Left ventricular noncompaction	Genetic mutations (sporadic or familial) Autosomal-dominant inheritance	Dyspnea on exertion Fatigue Pedal edema Exercise intolerance In infants, cyanosis, dysmorphic features, and failure to thrive	Diagnosis can be based on: Echocardiography Steady-state free precession MRI, showing prominent trabeculations and a non-compacted to compacted (NC/C) myocardium ratio > 2.3
Myocarditis	Bacterial infections Lyme disease Medications Viral infections	Sharp chest pain Leg edema Dyspnea on exertion Orthopnea Palpitations Syncope Systemic symptoms as fever and joint pain	Diagnostic Imaging (Echocardiography and MRI). Creatine kinase (CK-MB) Cardiac troponin I (cTnI) or T (cTnT) Increased CRP and ESR Serological markers such as Fas, Fas ligand, interleukin-10 or antimyosin autoantibodies Viral antibody titres or autoantibodies (to reach the cause)
Restrictive Cardiomyopathy	Systemic diseases, such as Sarcoidosis Hemochromatosis	Dyspnea on exertion Orthopnea Syncope Kussmaul sign S3 and S4 gallops	To verify the cause: measuring iron overload and myocardial biopsy	Low QRS voltages Conduction abnormalities.	Wall and valvular thickening and sparkling myocardium.