Effect of acute hemodynamic decompensation on electrical inducibility of ventricular arrhythmias in patients with dilated cardiomyopathy and complex nonsustained ventricular arrhythmias

In patients with dilated cardiomyopathy, hemodynamic decompensation has been postulated to increase vulnerability to reentrant ventricular arrhythmias. To test this hypothesis, we performed programmed ventricular stimulation with three extrastimuli on nine patients with dilated cardiomyopathy and asymptomatic complex ventricular arrhythmias during a period of acute hemodynamic decompensation; programmed ventricular stimulation was then repeated following hemodynamic improvement with nitroprusside. These patients did not have a history of documented or suspected sustained ventricular tachycardia or fibrillation. The mean left ventricular ejection fraction was 0.21±0.04 (range 0.15 to 0.26). In the baseline state, mean right atrial pressure was 8±4 mm Hg, pulmonary artery wedge pressure was 20±3 mm Hg, and cardiac index was 3.2±0.5 L/min/m². Following acute hemodynamic decompensation, mean right atrial pressure increased to 16±5 mm Hg and pulmonary artery wedge pressure to 33±8 mm Hg; cardiac index decreased to 2.1±0.5 L/min/m². In this decompensated state, programmed ventricular stimulation failed to induce sustained or nonsustained ventricular arrhythmias in any patient. Following nitroprusside administration (mean dose 1.5±1.1 μg/kg/min), there were significant decreases in mean right atrial pressure (11±3 mm Hg) and pulmonary artery wedge pressure (16±3 mm Hg), and a significant increase in cardiac index (3.1±1.1 L/min/m² (p<0.05 for all values versus the decompensated state). In the improved hemodynamic state, programmed ventricular stimulation induced nonsustained ventricular tachycardia (six beats) in only one patient, and sustained arrhythmias in none. During a mean follow-up of 11±7 months, there were three sudden cardiac deaths and two nonsudden cardiac deaths due to refractory heart failure. Thus in patients with dilated cardiomyopathy, the presence of acute hemodynamic decompensation did not predispose to an increased inducibility of ventricular arrhythmias during programmed ventricular stimulation. Nonetheless, these patients had a high incidence of sudden death during relatively short follow-up. These findings reaffirm the limited value of programmed ventricular stimulation in patients with dilated cardiomyopathy and suggest alternate mechanisms other than reentry induced by acule hemodynamic decompensation as being responsible for increased arrhythmogenesis.