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Dilated Cardiomyopathy Causes Diagnosis Treatment by NJE

Dilated cardiomyopathy describes a group of diseases involving the myocardium and is characterized by myocardial dysfunction that is not wholly the result of hypertension, coronary atherosclerosis, valvular dysfunction, congenital, or other structural heart disease. As a result, the heart is enlarged and the ventricles are dilated with impaired systolic function.


1. The estimated prevalence of dilated cardiomyopathy in the general adult population is approximately 1:2500. The incidence is approximately 4 to 8 per 100,000 persons per yr.

2. The incidence of dilated cardiomyopathy is greatest in middle age and among men.

3. African Americans have a three-fold increased risk for developing DCM, irrespective of comorbidities or socioeconomic factors, compared with whites.

4. It is the most common cardiomyopathy and accounts for 25% of cases of congestive heart.


The patient will present with common symptoms of congestive heart failure, which may be of insidious or sudden onset. The patient may also be asymptomatic and the diagnosis made by the unexpected finding of cardiomegaly on a chest x-ray. The history should focus also on information that could help determine the etiology. Classical signs of heart failure may be absent. When present, findings are indistinguishable from other heart failure syndromes, including:

1. Increased jugular venous pressure.

2. Narrow pulse pressure.

3. Pulmonary rales, hepatomegaly, peripheral edema.

4. S3, S4.

5. Mitral regurgitation, tricuspid regurgitation (less common).


In approximate order of occurrence:

1. Idiopathic (often a viral infection that cannot be confirmed)

2. Infections (viral [human herpesvirus 6, influenza, echovirus, cytomegalovirus, Coxsackie B, adenovirus, parvovirus, HIV], rickettsial, mycobacterial, toxoplasmosis, trichinosis, Chagas’ disease)

3. Alcoholism (15% to 40% of all cases in Western countries)

4. Uncontrolled tachyarrhythmia (“tachycardia-mediated”)

5. Sleep apnea–obstructive or nonobstructive

6. Cirrhotic–not necessarily alcohol-induced

7. End-stage renal disease-related

8. Nutritional deficiencies–selenium, L-carnitine, thiamine

9. Peripartum (greatest risk from last trimester of pregnancy to 6 months postpartum)

10. Chemotherapeutic (anthracycline, doxorubicin, daunorubicin) or pharmacologic agents (antiretrovirals, phenothiazines)

11. Substance abuse (cocaine, heroin, organic solvents “glue sniffer’s heart”)

12. Postmyocarditis

13. Toxins (cobalt, lead, phosphorus, carbon monoxide, mercury) Collagen-vascular disease (systemic lupus, rheumatoid arthritis, polyarteritis, dermatomyositis, sarcoidosis)

14. Heredofamilial neuromuscular disease (e.g., muscular dystrophy)

15. Excess hormones (acromegaly, osteogenesis imperfecta, myxedema, thyrotoxicosis, diabetes)

16. Hematologic (e.g., sickle cell anemia, hemochromatosis, hypereosinophilia)

17. Stress-induced (i.e., takotsubo or broken heart syndrome)

18. LV noncompaction

19. TTN truncating mutations (mutations in TTN, the gene encoding the sarcomere protein titin are a common cause of dilated cardiomyopathy, occurring in approximately 25% of familial cases of idiopathic dilated cardiomyopathy and in 18% of sporadic cases.


Dilated cardiomyopathy is a diagnosis of exclusion, made after ruling out other potential causes of myocardial dysfunction.


• Coronary atherosclerosis, that is, left ventricular dysfunction secondary to ischemia and/or myocardial infarction

• Valvular dysfunction (especially aortic and mitral regurgitation)

• Other cardiomyopathies (restrictive, hypertrophic)

• Pulmonary disease (embolism, obstructive, restrictive).

• Pericardial abnormalities (constrictive pericarditis, tamponade)

• Hypothyroidism/myxedema

• Athlete’s heart


• Medical history: emphasis on symptoms of dyspnea, orthopnea, paroxysmal nocturnal dyspnea, weight gain, palpitations, or signs of systemic and pulmonary embolism, substance abuse history, possible toxin exposures (especially occupational).

• Physical exam.

• Testing: laboratory, chest x-ray, ECG, echocardiogram, cardiac catheterization; myocardial biopsy is not routinely recommended unless acute myocarditis requiring immunosuppressive therapy is considered (e.g., giant cell myocarditis).


• Chemistries/metabolites (deficiencies), renal function tests (renal dysfunction).

• Cardiac biomarkers (elevation of cardiac troponin or BNP).

          1. Persistently increased cardiac troponin T levels are a marker of poor outcome in cardiomyopathy patients.

• Endocrine (particularly thyroid).

• Iron studies (hemochromatosis, deficiency).

• Rheumatologic and inflammatory (ANA, ESR, CRP).

• Others as indicated (HIV, Lyme, neurohormonal).


Chest x-ray:

 • Cardiac silhouette enlargement (particularly 

left ventricle)

 • Pulmonary vascular redistribution and congestion (Kerley B lines, cephalization of vasculature), pleural effusion (may appear as unilateral, most often on the right side)


• ECG findings are typically nonspecific, and sinus tachycardia is usually a reflection of underlying heart failure. Large voltage in precordial leads and low voltage in limb leads may be seen in advanced disease.

• Intraventricular conduction defects and left bundle branch block

• Arrhythmias (atrial fibrillation, premature ventricular or atrial contractions, ventricular tachycardia)


• Low ejection fraction with global hypokinesis

• Four-chamber enlargement (LV enlargement usually predominates)

• Mitral or tricuspid regurgitation (tethering due to incomplete leaflet closure caused by ventricular dilation)

Cardiac catheterization:

• On initial presentation to exclude obstructive epicardial coronary artery disease Cardiac magnetic resonance imaging (CMRI):

• Particularly if infiltrative or inflammatory etiology suspected.



• Treatment of underlying disease (systemic lupus, alcoholism)

• Dietary sodium restriction (<2 g/day)

• Exercise training has been shown to be associated with reduced risk for hospitalization and death in patients with history of heart failure in limited trials; enrollment in a formal cardiac rehabilitation program may be beneficial in improving patient’s functional status.


• Identify and treat the etiology of the acute exacerbation, when able. A helpful mnemonic is a FAILURE: failure to take medications, anemia/ arrhythmia, ischemia/infection/infarction, lifestyle (dietary indiscretion), upregulation of cardiac output (hyperthyroidism or pregnancy), renal failure, embolus (pulmonary).

• Diuretics are indicated for all patients with current symptoms or history of heart failure and reduced left ventricular ejection fraction (LVEF) with evidence of volume overload to improve symptoms. It is important to note that diuretics have not been shown to improve mortality rates.

• Patients with associated coronary atherosclerosis (angina, ECG changes, reversible defects on myocardial perfusion imaging) may benefit from percutaneous or surgical revascularization.


• Diuretics and digoxin as noted in “Acute General Rx.”

• ACE inhibitors (and angiotensin receptor blockers) have been shown to have favorable effects on ventricular remodeling in patients with cardiomyopathy and a demonstrable mortality benefit in these patients. They also reduce afterload and improve cardiac output. Therefore, they are recommended in all patients with reduced LV systolic function (EF ≤40%), regardless of symptoms unless specific contraindications exist.

• Beta-blockers work by inhibiting the adverse effects of the sympathetic nervous system in patients with ventricular systolic dysfunction (EF ≤40%). Only carvedilol, long-acting metoprolol succinate, and bisoprolol have shown a mortality benefit in patients with LV systolic dysfunction. Unless specifically contraindicated, they should be started after the acute exacerbation has resolved and titrated to the maximum tolerated dose.

• Aldosterone antagonists (spironolactone and eplerenone) have shown mortality benefit along with a decreased rate of hospitalization for heart failure in patients with symptomatic heart failure and reduced LV systolic function (EF ≤35%). They should be used following label guidelines and with close monitoring of renal function and potassium.

• Additional medical therapies (hydralazine/ nitrates, digitalis) can be considered in certain patient subpopulations with persistent symptoms on otherwise optimal medical management.

• Digoxin has no mortality benefit but has been shown to improve patients’ quality of life in appropriately selected patients.

• The angiotensin receptor-neprilysin inhibitor sacubitril/valsartan in place of an ACE inhibitor or angiotensin receptor blocker and on top of optimal medical therapy in patients with class II-IV heart failure and an EF of 40% or less was found to significantly reduce multiple heart failure endpoints, including death, hospitalizations, and CV death in comparison to enalapril. This medication was approved in the U.S. in 2015.

• Ivabradine was FDA approved in 2015 for patients with stable, symptomatic chronic heart failure with left ventricular ejection fraction ≤35% who are in sinus rhythm with resting heart rates ≥70 beats/min and either of the following:

 (1) are on maximally tolerated doses of beta-blockers or (2) have a contraindication to beta-blocker use. It acts by blocking the hyperpolarization-activated cyclic nucleotide-gated (HCN) channel responsible for the cardiac pacemaker current, which regulates heart rate.



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