Hemodynamically, DCM is characterized by depressed myocardial systolic function and systolic pump failure. Left ventricular (LV), and often right ventricular (RV), contractile force is diminished, resulting in a low cardiac output and increased end-systolic and end-diastolic ventricular volumes and intracavitary pressures. LV, and often RV, dilatation accompanied by compensatory hypertrophy are the hallmarks of DCM. Histologic findings are nonspecific.
Approximately 80 percent of cases of DCM are of unknown etiology; that is, they are not associated with specific cardiac or systemic disorders (.T.a.ble...,5!...-!,) and are considered idiopathic.3 The idiopathic form of DCM is the cause in approximately 25 percent of all cases of congestive heart failure (CHF) and the primary indication for cardiac transplantation in the United States. The prevalence of idiopathic DCM is estimated to be approximately 36 cases per 100,000 population. Blacks and males have a 2.5-fold increase in risk compared to whites and females. Most patients are diagnosed between the ages of 20 and 50 years, and the majority have advanced symptoms of CHF at the time of initial presentation.3
CLINICAL FEATURES AND DIAGNOSIS As a result of systolic pump failure, the patient presents with signs and symptoms of CHF: dyspnea on exertion, orthopnea, and paroxysmal nocturnal dyspnea. Depressed ventricular contractile function and dilatation may result in the formation of mural thrombi, and the patient may present with manifestations of peripheral embolization (e.g., an acute neurologic deficit, flank pain, and hematuria or a pulseless, cyanotic extremity). Chest pain with features of typical angina pectoris occurs in approximately one-third of patients. Chest pain in these patients is felt to be due to limited coronary vascular reserve rather than atherosclerotic coronary artery disease.
Murmurs are frequently heard during cardiac auscultation and are not necessarily indicative of primary valvular disease. Ventricular dilatation and the resultant annular dilatation and displacement of the papillary muscles of the atrioventricular valves inhibit leaflet coaptation and complete valve closure. Holosystolic regurgitant murmurs of mitral and tricuspid valve origin are frequently heard at the apex or lower left sternal border in the patient with biventricular failure. On occasion an apical diastolic rumble may be heard and is due either to accentuated, early-diastolic atrial-to-ventricular flow (the result of mitral regurgitation and left atrial overload) or to a loud summation gallop. An enlarged, pulsatile liver may be found if tricuspid insufficiency is significant. Bibasilar rales and dependent edema are common additional findings.
The chest x-ray invariably shows an enlarged cardiac silhouette and increased cardiothoracic ratio; biventricular enlargement is common. Evidence of pulmonary venous hypertension ("cephalization" of flow and enlarged hila) is also frequent and may serve to differentiate cardiac enlargement due to myocardial failure from that due to a large pericardial effusion.
The electrocardiogram (ECG) is almost always abnormal. Left ventricular hypertrophy and left atrial enlargement are the most common findings. Q or QS waves and poor R-wave progression across the anterior precordium may produce a pseudoinfarction pattern. Atrial fibrillation and ventricular ectopy are frequently encountered rhythm disturbances.
Echocardiographic studies in a symptomatic patient demonstrate a decreased ejection fraction, increased systolic and diastolic volumes, and ventricular and atrial enlargement.
TREATMENT AND DISPOSITION A timely workup is indicated in patients who present with newly diagnosed symptomatic CHF, and evaluation typically requires hospitalization. Echocardiography is indicated to exclude known causes of heart failure that may be correctable (e.g., precordial effusion or valvular disease), to estimate ejection fraction, and to rule out other potential complications (e.g., mural thrombi) that may be amenable to therapy. Symptom-directed therapy is best initiated in the in-patient setting in order to minimize adverse drug effects. Almost all patients will benefit symptomatically from digitalis glycoside therapy and diuretics, but these drugs have not been shown to improve survival rates. The use of angiotensin-converting enzyme inhibitors and b blockers, specifically carvedilol, have been shown to improve survival rates in patients with DCM and CHF.45 Patients with complex ventricular ectopy may benefit from amiodarone therapy.6
Patients with a known DCM and chronic CHF may present to the emergency department with a mild-to-moderate worsening of symptoms. In most instances, the cause is noncompliance with medical therapy or dietary indiscretion. Such patients can often be managed in the emergency department with intravenous diuretics, reinstitution of prescribed medications, counseling of the patient, and timely referral to the primary care physician. 7 However, other causes of an acute exacerbation of symptoms in a disease characterized by a slow and progressive history must be considered ( I,aMe §.l-2.) and, if present or suspected, require hospitalization for definitive management.
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