Methods: The study population consisted of 70 severe heart failure pts with CRTD, (13 ? and 57?), mean age 61±15 years, with underlying disease ischemic cardiomyopathy in 36 and dilated cardiomyopathy in 34. Forty-six pts received CRTD as primary prevention (group A) and 20 pts as secondary prevention (group B). We analyzed the occurrence of ventricular tachycardia including appropriate VT therapies.Fifty-one pts underwent 24h Holter monitoring HRT analysis with calculation of 2 parameters, TO and TS. Abnormal values: TO>0, TS<2.5msec/RR. Pts were defined as HRT (+) when TO or/and TS were abnormal and as HRT (-) when both TO and TS were normal or when HRT could not be calculated because of none or too few suitablePVCs.
Results: Fifty-two pts were found as clinical responders, 8 super responders and 11 pts poor responders. Seven pts died of pump failure. After 10 years follow-up including at least one device replacement, we found almost similar incidence of sustained ventricular tachycardia (VT) (15%) in both groups, irrelevant to clinical improvement and underlying substrate. Pts who received CRTD as secondary prevention, although good responders, continued to experience VT and appropriate therapies. HRT was found abnormal in 51% of all pts, responders or not.
Conclusion: Due to electrical and mechanical heterogeneity among severe heart failure pts the antiarrhythmic effect of CRTD is unpredictable. The ventricular arrhythmia risk in CRT pts is independent to CRT-induced improvement of the failing heart and the cardiac autonomic status.