Late ventricular potentials and spontaneous and induced ventricular arrhythmias in dilated or hypertrophic cardiomyopathies. A prospective study about 83 patients.

In a series of 83 patients with dilated (DCM) (n = 56) or hypertrophic cardiomyopathies (HCM) (n = 27), were performed 24-hour-Holter monitorings, exercise stress testings, noninvasive recordings of late ventricular potentials (LVP), and programmed ventricular stimulations (PVS) (sinus rhythm and three cycles of stimulation, two extrastimuli, two right ventricle sites) (n = 53), in order to appreciate the frequency of ventricular premature depolarisations (VPDs), to correlate these results with myocardial vulnerability to TV induction, and to compare electrophysiologic and hemodynamic results. Holter monitoring showed that 80% of group A patients had VPDs (75% Lown's grade 3 or over) and 63% in group B (37% greater than or equal to grade 3). LVP were found in 15/56 DCM, and 2/27 HCM; in comparison with a control group of 32 normal subjects, the prevalence of LVP was only significant for DCM group. LVP were more frequent in cases of VPD's greater than or equal to Lown's grade 3 at Holter monitoring in DCM group, (33% versus 7% if VPDs less than or equal to Lown's grade 3) and HCM group (20% versus 0) but the correlation was not significant. Exercise stress testing, conducted only in group B, revealed about 20% of VPDs. PVS provoked ventricular arrhythmia (greater than 5 QRS) in 13 out of 33 cases in group A and in 2 out of 20 cases in group B. There was no significant correlation between the results of these methods of study and those of hemodynamic or echocardiographic explorations except for cardiac index in group A (lower when LVP were present, and VPDs greater than or equal to grade 3 during Holter) and end diastolic diameter (larger when PVS provoked fewer ventricular arrhythmias). In group B, PVS induced monomorphic VT in 2/3 patients with syncopes. Thus: (1) ventricular arrhythmias are frequent in cardiomyopathies but LVP had a significant prevalence only in dilated forms; (2) in DCM monomorphic induced VT reproduce spontaneous crisis, whereas in HCM it is possible to provoke VT in patients with syncopes but without this clinical arrhythmia; (3) in DCM as in HCM, ventricular arrhythmia can be independent from hemodynamic disorders.