CLONIDINE TO PREVENT IMPLANTABLE CARDIOVERTER DEFIBRILLATOR FIRING

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This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Cardiac arrest or sustained ventricular tachycardia (VT) in patients with heart disease is best treated with an implantable cardioverter defibrillator (ICD). However, the ICD alone is not appropriate therapy for patients with frequent VT episodes. In fact, frequent shocks for VT may predict a poorer prognosis. Antiarrhythmic drugs are co-administered with ICDs in up to 50% of patients to prevent VT episodes, but antiarrhythmic drugs may have harmful effects. Thus, improved drugs to prevent VT without interfering with ICD function are needed. Recent data suggest that clonidine may be a new therapy to prevent ICD shocks. It may act centrally on sympathetic outflow and peripherally and selectively on cardiac Purkinje to suppress and control VT occurring in patients. The purpose of this study is to test the hypothesis that clonidine reduces frequent VT better than beta blocker in patients with ICDs. After informed consent, patients will be randomized in a single blind fashion to either clonidine or metoprolol given three times per day. Other prescribed drugs may be adjusted to promote toleration of the study drug. ICD interrogrations of episodes of VT will be the primary endpoint. Device based non-invasive programmed stimulation (NIPS) testing in a subset of these patients will allow mechanistic understanding of the clonidine effect.