Fananapazir L, Epstein S E
Cardiovascular Diagnosis Section, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892.
Am J Cardiol. 1991 Feb 1;67(4):280-7. doi: 10.1016/0002-9149(91)90560-8.
Hemodynamic and electrophysiologic studies were performed in 30 survivors of sudden cardiac arrest with hypertrophic cardiomyopathy (HC) to determine responsible factors. Electrophysiologic abnormalities alone were present in 27 patients (90%): sinus node dysfunction in 14 (47%), delayed atrio-ventricular nodal conduction in 1 (3%), abnormal His-Purkinje conduction in 7 (23%), an inducible atrial tachycardia in 7 (23%), and inducible sustained ventricular arrhythmia in 21 (70%). Sustained ventricular arrhythmia was polymorphic ventricular tachycardia (VT) in 18 patients (86%), monomorphic VT in 2 patients (7%) and ventricular fibrillation in 1 patient (3%). In 1 patient the arrhythmia recorded during an episode of cardiac arrest and induced at electrophysiologic study was polymorphic VT. VT was induced with less than or equal to 2 extra-stimuli in only 1 patient (3%) but with less than or equal to 3 extra-stimuli in 20 patients (97%). Potential causes of sudden cardiac arrest were found in all patients and were multiple in 13 patients (43%). These were (1) ventricular electrical instability in 21 patients (70%), (2) severe left ventricular outflow tract obstruction in 8 patients (27%), (3) bradycardia in 5 patients (17%), (4) myocardial ischemia associated with hypotension in 5 patients (17%), and (5) atrial tachycardia resulting in hypotension in 4 patients (13%). Of the 21 patients with inducible sustained ventricular arrhythmia, 17 received an implantable defibrillator device and 4 were treated with antiarrhythmic drugs. Seven patients underwent left ventricular septal myectomy.(ABSTRACT TRUNCATED AT 250 WORDS)