Abstract

Dynamic cardiomyoplasty and partial left ventriculectomy have shown limited and controversial results in the treatment of dilated cardiomyopathies. This study investigates causes and determinants of long-term mortality after these procedures. Forty-three patients submitted to dynamic cardiomyoplasty and 43 who underwent partial ventriculectomy were studied. Patients were in New York Heart Association (NYHA) class III or IV before the procedures. In dynamic cardiomyoplasty group, hospital mortality was 2.2% and patients were followed for 48+/-31 months. Nine hospital deaths occurred after partial ventriculectomy and the remaining patients were followed for 38+/-29 months. For patients submitted to dynamic cardiomyoplasty, 1-year event-free survival was 81.3+/-5.9%; 2-year, 65.1+/-7.2%; and 6-year, 23.1+/-6.7%. Partial left ventriculectomy patients presented event-free survival rates of 58.1+/-7.5%, 46.6+/-7.6% and 21.6+/-6.4% at the same periods, respectively. Late deaths were equally related to heart failure progression and arrhythmia events in both groups. Preoperative NYHA class IV, pulmonary hypertension and absence of left ventricular (LV) function improvement at the time of the final event were identified as independent predictors of poor long-term event-free survival and heart failure progression in cardiomyoplasty patients, while NYHA class IV, elevated serum nor-epinephrine and absence of LV function improvement were associated with these events after partial left ventriculectomy. Arrhythmia related deaths were only predicted by previous events of sustained ventricular tachycardia in partial left ventriculectomy group. Long-term results of dynamic cardiomyoplasty and partial left ventriculectomy are limited by patients' preoperative condition, by the loss of LV function benefits and by high incidence of sudden cardiac death. Palliative surgical treatment of dilated cardiomyopathies needs to be indicated earlier and may achieve better efficiency with the combination of different procedures to provide sustained improvement of LV function, to interrupt the progressive remodeling process and to prevent sudden cardiac death.

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