[Pharmacokinetics and efficacy of delayed-action hydroquinidine in patients with ventricular extrasystole].
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Calculations about the variability of PVCs are usually based upon the results of two Holter ECGs, either successive ones or separated by a short interval. No studies are available indicating whether the criteria calculated for short control intervals also holds true when evaluating chronic antiarrhythmic treatment over longer control periods. This study was performed to investigate the influence of the length of the control interval on the spontaneous variability and thus on the reduction of PVCs required to secure an antiarrhythmic effect. In a prospective study, 444 ambulatory ECGs were obtained in 90 patients with CAD or IDC and untreated ventricular arrhythmia of Lown grade IV. Patient follow-up was carried out over an average of 181 +/- 297 days. The degree of arrhythmia was expressed as the mean hourly PVC rate. The variability of PVC counts between two Holter ECGs was defined as the logarithm of the quotient PVCday 2(n + 1)/PVCday 1(n + 1). The spontaneous distribution of variability quotients was defined separately (mean +/- 2 SD) for each of four ranges of control intervals (0-6 days, 7-89 days, 90-364 days, greater than or equal to 365 days). The per cent reduction (R) in PVC frequency necessary to establish drug efficacy, was calculated according to the formula R (%) = 10(0)-10(-2SD) X 100, whereas the percentage change necessary to prove aggravation of arrhythmia (A) was assessed by the formula A (%) = 10(0)+10(+2SD X 100. R increased from 63% (0-6 days), 81% (7-89 days), 93% (90-364 days) to 98% (greater than or equal to 365 days).(ABSTRACT TRUNCATED AT 250 WORDS)
In 34 patients with ventricular tachyarrhythmias the effect of the antiarrhythmic therapy of sotalol (160-320 mg p.o.) in combination with the type-I-B-agent mexiletine (600-800 mg p.o.) or tocainide (800-1200 mg p.o.) was studied by Holter monitoring. In all patients 2.2 +/- 1.1 drugs trials had failed, including amiodarone in 8 patients and beta blocking substances in 15 patients. The combination of sotalol with mexiletine or tocainide reduced ventricular ectopic beats by 79% and complex ventricular arrhythmias (pairs and salvoes) by 85%. A significant reduction of ventricular ectopic beats (greater than 80%) was reached in 74% of the patients, of pairs and salvoes (greater than 90%) in 79%. There was no difference in the antiarrhythmic efficacy between the combination of sotalol/mexiletine and sotalol/tocainide. Intervals of the resting ECG or laboratory values did not change significantly. In 5 patients with sotalol/tocainide and 1 patient with sotalol/mexiletine, side effects were observed which necessitated discontinuation of the treatment. The results show that sotalol, in combination with mexiletine or tocainide, has a potent antiarrhythmic effect in patients with otherwise drug-refractory ventricular arrhythmias.
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Repeated annual 24-hour Holter's ECG monitoring sessions were used as a basis for 4-year follow-up of 108 male coronary patients with episodes of painless myocardial ischemia in the course of their everyday routines, and 144 control patients showing no signs of transient asymptomatic ischemia at 24-hour Holter's ECG monitoring. Four years of follow-up demonstrated no differences between the two groups, compared with respect to the incidence of myocardial infarction and associated mortality as well as aggravations of coronary heart disease, in terms of clinical pattern of the disease, the incidence of acute coronary episodes and survival rates. There were no sudden deaths in either of the groups. Transient painless myocardial ischemic episodes are shown to carry no additional risk of myocardial infarction and sudden death in elderly coronary patients with occasional anginal attacks.
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In a prospective study, the influence of the length of the time interval on spontaneous variability was investigated in 100 patients with CAD or IDC and untreated ventricular arrhythmia of Lown grade IV. Patient follow-up was carried out over 260 +/- 387 days. In each of the 498 ambulatory Holter tapes, the mean hourly arrhythmia count (AC) of couplets and salvos was verified. The variability of ACs between two Holter ECGs was defined as the logarithm of the quotient AC day 2(n + 0.01)/AC day 1(n + 0.01). The spontaneous distribution of variability quotients (means +/- 2 SD) was defined separately for couplets and salvos and for each of four ranges of control intervals (0-6 days, 7-89 days, 90-364 days, greater than or equal to 365 days). The percentage change in arrhythmia count necessary to establish drug efficacy (R), was calculated according to the formula R(%) = (10(0) - 10(-2SD].100, whereas the percentage change necessary to prove aggravation of arrhythmia (A) was assessed by the formula A(%) = (10(0) + 10(+2SD].100. For couplets, R extended from 90%, 94%, 98% to 99%; A increased from 1114%, 1895%, 6153% to 14032%, respectively. For salvos, R remained almost unchanged at a high level with 95%, 98%, 98%, 99%. The figures of A were 2189%, 4650%, 5698% and 9650%, respectively. It is concluded that the spontaneous variability of complex ventricular arrhythmias is remarkably high with short control intervals and increases further with longer ones.(ABSTRACT TRUNCATED AT 250 WORDS)
The incidence and significance of ventricular arrhythmia induced by programmed electrical stimulation in subjects with complex ventricular ectopy were studied in 46 consecutive subjects: 34 with heart disease, 12 with an apparently normal heart. The procedure consisted of delivering on one spontaneous and 2 imposed rhythms one, two, then three extrastimuli. Significant arrhythmia with more than 6 ventricular complexes was induced in 17 patients (37%), including 6 (13%) with sustained ventricular tachycardia and 11 with unsustained ventricular tachycardia. Induction of ventricular arrhythmia was observed in 12 of the 14 patients with a history of myocardial infarction. At the end of a mean follow-up period of 12 +/- 4 months, there were 2 sudden deaths, and 3 patients had clinically sustained ventricular tachycardia. Clinical ventricular tachycardia occurred in the group of 17 patients inducible during programmed electrical stimulation. The patients who died suddenly belonged to the group of 29 patients without induced ventricular arrhythmia. This study shows a high proportion of significant stimulation-induced arrhythmia in patients who had suffered from myocardial infarction more than 3 months previously and who had complex ventricular ectopy. Owing to the good condition of this group of patients after a mean follow-up of 12 months, we were unable to determine the influence of stimulation-induced arrhythmia on mortality. However, it must be noted that spontaneous sustained tachycardia occurred in the group of patients with significant induced ventricular arrhythmia.
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