DCMP
DCMP
DCMP
Cardiomyopathy
Dilated Cardiomyopathy – diagnosis and management (Nov ’11)
🠶 The ventricular walls are not thickened, although heart weight is increased.
🠶 Intracavitary thrombus formation is common in the apical portion of the ventricular cavities
and in atrial appendages and may give rise to pulmonary and systemic emboli.
– Cumulative loss of myofibrils and cardiac myocytes :(apoptosis, cellular necrosis )decrease in the wall
thickness
PHYSICAL EXAMINATION
🠶 Signs of CHF (tachycardia, pulmonary crackles, weak peripheral pulses, distended neck
veins, hepatomegaly) are present. The apical impulse usually is displaced to the left and
inferiorly.
🠶 S2 may be normal or narrowly split with accentuated P2 if pulmonary hypertension
develops.
🠶 A prominent S3 is present with or without gallop rhythm.
🠶 soft regurgitant systolic murmur (caused by MR or TR tricuspid regurgitation [TR])
may be present
CLINICAL MANIFESTATIONS
🠶 Heart failure
Syncope <1%
Clinical examination
Chest x-ray
12-lead ECG
Echocardiography
Blood tests
Endomyocardial biopsy
Cardiac CT Scan
Cardiac catheterization
DIAGNOSIS
CXR Radiography
ECG Electrocardiography
🠶 1. Sinus tachycardia, LVH, and ST-T changes are the most common findings.
On M-mode echocardiography,
🠶 End-diastolic and end-systolic dimensions of the LV are
increased
🠶 markedly reduced fractional shortening and ejection
fraction of the LV
🠶 for serial assessment of patients with DCM.
Prognosis
🠶 Approximately one third die, one third recover completely, and one third improve with
some residual cardiac dysfunction.
DIAGNOSIS
Cardiac Catheterization can be helpful to
🠶 (1) exclude anomalous coronary artery
🠶 (2) predict etiology and prognosis by obtaining endomyocardial biopsy
🠶 (3) evaluate for cardiac transplantation
🠶 (4) measurement of pulmonary vascular resistance.