[Isotope angiocardiographic study of 30 cases of ventricular tachycardia with Fourier phase analysis].

Twenty-seven patients (15 men, 12 women; mean age 48.9 years) suffering from ventricular tachycardia (VT) (n = 30) were studied by radionuclide angiocardiography with Fourier phase analysis, both in sinus rhythm and during tachycardia. VT was spontaneous, electrically inducible, sustained, haemodynamically stable and monomorphous, with a mean rate of 174 beats/min (range: 115-260 beats). Heart diseases responsible for VT were: non-obstructive cardiomyopathy (n = 7), hypertrophic cardiomyopathy (n = 1), ischaemic heart disease (n = 5), probable right ventricular arrhythmogenic dysplasia (n = 4), congenital left ventricular aneurysm (n = 2), sequela of myocarditis (n = 2) and aortic valve regurgitation (n = 1); no heart disease was detectable in 5 patients. On surface electrocardiogram there was good concordance between the initial radionuclide site of VT activation and the configuration and electrical axis of QRS. At Fourier phase analysis all 17 VT of the right lag type originated in the left ventricle, arising from the apical septum (n = 7) or lateral segment (n = 2) in case of left axis, from the basal segment (n = 6) or the lateral segment (n = 1) in case of vertical or right axis, and from the middle left septum (n = 1) in case of normal axis. Nine VT of the left lag type originated in the right ventricle, arising from the basal septum or the latero-basal region in case of vertical or right axis (n = 6), from the apical septum or the inferior-apical region in case of left axis (n = 2) and from the middle septum in case of normal axis (n = 1). Four of our patients (3 with coronary disease and 1 with congenital left ventricular aneurysm) had VT of the left lag type and an initial radionuclide site of activation in the middle part of the left septum in case of left axis (n = 2) and in the basal part of that septum in case of right axis (n = 2). Seven patients were operated upon for recurrent VT: 4 had intra-operative mapping which in every case confirmed the results of radionuclide angiocardiography, a method which in the other 3 patients was the only surgeon's guide. Correlations between the site of origin of VT at radionuclide mapping and kinetic abnormalities visualized at radiological angiography and gamma-ray angiocardiography were common in our study. In one of our patients the same lesion gave birth to 2 VT of different morphologies.(ABSTRACT TRUNCATED AT 400 WORDS)