In patients with dilated cardiomyopathy, the mechanisms of life-threatening arrhythmias are likely determined by subendocardial scarring, electrolyte unbalance, stretch-induced electrophysiological changes, autonomic impairment, conduction delay, or proarrhythmic effects of drug therapy. Sudden death may occur as a consequence of ventricular fibrillation, but electromechanical dissociation or bradycardia may also be a possible underlying cause. Most of the clinical characterization of idiopathic dilated cardiomyopathy is drawn from studies also enrolling patients with cardiomyopathies secondary to recognizable underlying conditions. Secular trends have improved the ability of early diagnosis, and the therapeutic strategies used to prevent sudden death. The role of implantable cardioverter defibrillator (ICD) therapy for the primary prevention of all-cause mortality is controversial with some studies showing and others questioning the benefit of ICD in this population. revious randomized studies conducted in large heterogeneous populations showed that ICD therapy is beneficial and improves survival by about 30%. This therapy is currently recommended for all survivors of a near-fatal arrhythmia regardless of the underlying substrate.
Cellular Characterization of Autoimmune Response to Cardiac Troponin I in Idiopathic Dilated Cardiomyopathy
