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
Dilated Cardiomyopathy	Idiopathic Myocarditis Substance abuse Connective tissue disease Nutritional deficiencies Infiltrative diseases Toxins.	Lateral displacement of the point of maximal impulse Right ventricular heave S2 at the base S3 gallops Jugular venous distension Peripheral edema	Detecting the cause (such as thyroid function tests, toxicology screening, and genetic counselling) Assessing the cardiac complications of the condition	Left ventricular hypertrophy Atrial fibrillation or premature ventricular complexes Conduction delays, AV nodal block, or left bundle branch block	Ventricular and atrial dilatation Increased left ventricular mass Global reduction in systolic function Focal wall motion abnormalities
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.	Segmental wall motion abnormalities: Location and extent of ischemia Diagnosis of mechanical complications Risk stratification
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	Pericardial effusion Cardiac tamponade
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	ST segment elevation in two or more ECG leads Cardiac arrhythmia may be present	Chamber dilation Regional wall motion abnormalities Increased left ventricular mass Increased posterior wall thickness
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.	Epsilon wave T wave inversion Prolonged S wave upstroke Localised QRS widening Paroxysmal ventricular tachycardia	Dilated, hypokinetic right ventricle Prominent apical trabeculae Dilatation of RV outflow tract
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.	In advanced beriberi, heart failure occurs. Low voltage QRS complex Prolongation of QT interval. Left bundle branch block	In advanced beriberi, heart failure occurs. Reduced ejection fraction. Reduced fractional shortening Large cardiac chamber sizes. Disturbed regional wall motion
Cardiac Tamponade	Ascending aortic dissection Collagen vascular diseases Iatrogenic - central line insertion, pacemaker insertion, and PCI Idiopathic Malignancy 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.	Low voltage QRS complex Sinus tachycardia ECG findings of pericarditis may be present	Pericardial effusion. Swinging of the heart within the effusion Reversal of right atrial and right ventricular diastolic transmural pressures. Cardiac chamber collapse
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	Sinus tachycardia Atrial fibrillation High left-ventricular voltage	The following may be present: Left ventricular enhanced systolic function Enhanced or impaired diastolic function Heart failure with preserved ejection fraction
Hypertrophic Cardiomyopathy	Familial Gene mutation Hypertension Thyroid disease Diabetes Obesity	Chest pain Congestive heart failure symptoms Dizziness Dyspnea Exercise intolerance Syncope Fatigue	Detecting the cause (Thyroid hormones, blood glucose, liver and renal function tests, blood hemoglobin) Genotyping (Genetic screening) Brain natriuretic peptide (prognosis)	ST-T wave abnormalities Axis deviation (right or left) Conduction abnormalities Sinus bradycardia with ectopic atrial rhythm Atrial enlargement	Diastolic dysfunction Septal wall thickness of >15 mm Narrowing of the LV outflow tract Abnormal systolic motion of the anterior leaflet of the mitral valve
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	Detection of Barth syndrome (Neutropenia and 3-methylgluconic aciduria) Genetic screening	Intraventricular conduction delay Voltage signs of left ventricular hypertrophy Repolarization abnormalities	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	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)	Sinus tachycardia Diffuse T wave inversions ST segment elevation Low voltage of the QRS complexes Arrhythmias such as atrial and ventricular ectopic beats	Wall motion abnormalities Systolic dysfunction Diastolic dysfunction Changes in image texture on echocardiogram Pericardial effusion Functional regurgitation
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 Sparkling myocardium.