24-hour Ambulatory ECG Monitoring Research Articles

993-45 Atrial Fibrillation: Sotalol's Heart Rate Reductions are Selective for Circadian Hours Where Heart Rate is High

We used 24-hour ambulatory ECG monitoring (AEM) to determine sotalol's circadian heart rate (HR) effects in chronic atrial fibrillation. Sixty subjects on a stable digoxin dosage had AEM after one week of single-blind placebo (PLC) and then again after 2 weeks of double-blind sotalol (80 or 160 mg qd) or continued PLC. Circadian HR patterns (average, high and low) for AEM's with = 18 paired hours (average = 23.2 hrs) were analyzed. Baseline and endpoint HR curves (open and closed symbols) are shown for sotalol and placebo groups. Circadian HR patterns on continued placebo were stable, but sotalol produced reductions in HR which were equal for the 80 and 160 mg doses. The largest HR reductions occurred between 11 am and 7 pm, where sympathetic tone is high - consistent with sotalol's beta blocking activity. Mean reductions in 24 hour high, average and low HR were 18 BPM, 11 bpm and 7 bpm, respectively, with the high and average HR reductions being significant (p < 0.05). Sotalol's HR lowering effects in atrial fibrillation are selective for circadian hours when HR is high, having lesser effects on low HR values. The threshold for beta blocking activity is 80 mg qd, with no further lowering seen at 160 mg qd 2 .

SEX AND THE PATIENT WITH CORONARY DISEASE.

Sexual intercourse clearly requires cardiovascular work. How dangerous is it for men with coronary disease? These researchers performed 24-hour ambulatory ECG monitoring, including monitoring during exercise testing and sexual intercourse, on 88 men …

Investigation of therapeutic mechanisms of atenolol and diltiazem in patients with variable-threshold angina

The effects of β-adrenoreceptor and calcium channel-blocking agents on the balance of myocardial oxygen supply and demand were studied in 15 patients (2 women and 13 men), aged 46 to 69 (mean 62) years, with variable-threshold angina. An exercise test was performed before therapy was begun, and 24-hour ambulatory ECG monitoring was performed after 1 week of long-acting nitrate therapy, in the third week after random assignment to either atenolol or diltiazem, and in the third week after crossover. All exercise tests were positive except in one patient taking diltiazem. The exercise time to 0.1 mV ST change was 4.2 ± 1.7 minutes with no therapy, 5.1 ± 1.6 minutes with nitrates, 6.6 ± 0.8 minutes with diltiazem, and 6.5 ± 2.1 minutes with atenolol. The rate-pressure product at 0.2 mV ST change was 20.9 ± 4.6 with no therapy and 21.2 ± 5.7 and 22 ± 4.6 with nitrates and diltiazem, respectively, but fell to 15 ± 3.9 beats · min.−1 mm Hg 10−3 after atenolol (p < 0.01). There was no significant difference in the number of anginal attacks or in nitroglycerin consumption per week. The heart rate at the onset of ST-segment change during the exercise test and during ambulatory ECG monitoring was significantly lower during atenolol than during diltiazem treatment. Both atenolol and diltiazem were of similar efficacy in increasing nonischemic exercise duration in patients with variable-threshold angina and acted primarily by slowing the resting heart rate. Atenolol had a more pronounced effect on heart rate, but its effect on angina appeared to be limited by a β2-receptor blockade-induced increase in coronary vascular tone.

Antiarrhythmic effects of selective prolongation of refractoriness. Electrophysiologic actions of sematilide HCl in humans.

Recent data have suggested that antiarrhythmic agents that act largely by delaying conduction may not be as effective in controlling ventricular arrhythmias as those that prolong repolarization. Recently, numerous "pure" class III agents have been developed. The antiarrhythmic and electrophysiologic profiles of sematilide, a "pure" class III agent, were determined in 27 patients with clinical ventricular arrhythmias and inducible sustained ventricular tachycardia during electrophysiologic study. After treatment with oral sematilide (mean dose, 133 +/- 29 mg every 8 hours), the patients underwent repeat 24-hour ambulatory ECG monitoring and electrophysiologic study. The baseline sinus cycle length and QT, QTc, JT, and JTc intervals were significantly increased 8 to 17% by sematilide (P = .001 to .029). There were no changes in the PR or QRS intervals. Sematilide (at a paced cycle length of 600 ms) significantly increased the atrial effective refractory period (238 +/- 32 to 264 +/- 32 ms; 11 +/- 16% increase from baseline; P = .013), atrioventricular nodal effective refractory period (296 +/- 74 to 354 +/- 71 ms; 20 +/- 19%; P = .029), and right ventricular effective refractory period (252 +/- 25 to 281 +/- 30 ms; 12 +/- 8%; P < .001) but did not significantly change the PA or HV intervals, the corrected sinus node recovery time, or the Wenckebach cycle length. Determination of the frequency-dependent effects of sematilide (n = 10) on the right ventricular monophasic action potential duration (APD90) during ventricular pacing at cycle lengths of 600 to 300 ms revealed that the APD90 was significantly prolonged by sematilide during ventricular pacing at 600 to 350 ms (APD90 increase of 40 +/- 17, 27 +/- 21, 18 +/- 18, and 14 +/- 15 ms, respectively) but not at 300 ms (APD increase of 13 +/- 19 ms). Sematilide significantly prolonged the APD90 to a greater degree at longer than at shorter cycle lengths (P = .02). The ventricular effective refractory period had a similar reverse frequency-dependent relation as the APD90. Sematilide had no effect on the ventricular effective refractory period-to-APD90 ratio or on ventricular conduction. Sematilide suppressed the induction of sustained ventricular tachycardia in 41% of all patients exposed to sematilide. Prolongation of ventricular refractoriness was correlated with ventricular tachycardia suppression. The right ventricular effective refractory period (at 600 ms) increased by 38 +/- 14 ms in patients whose sustained ventricular tachycardia was suppressed by sematilide and by 19 +/- 18 ms in patients not suppressed (P = .015). One patient developed short runs of pause-dependent nonsustained ventricular tachycardia. Eight patients were placed on long-term sematilide therapy, and during a mean follow-up period of 7.0 +/- 7.5 months, two patients developed sudden cardiac death, and one additional patient had recurrent sustained ventricular tachycardia. The electrophysiologic profile of sematilide is consistent with selective block of outward potassium currents and associated isolated lengthening of the ventricular effective refractory period and APD; sematilide demonstrates a significant degree of reverse frequency-dependence of the ventricular APD and effective refractory period; and suppression of ventricular tachycardia inducibility by sematilide appears to be correlated with increases in the right ventricular effective refractory period.

Type A behavior, social support, and coronary risk: interaction and significance for mortality in cardiac patients.

The 10-year prognostic significance of psychosocial as well as medical risk factors was examined in 150 middle-aged Swedish men. Type A behavior was assessed by means of the Structured Interview; work demand, social support, and other psychosocial factors were registered through standardized questionnaires. The clinical investigation included a standard physical examination, a frontal and sagittal chest x-ray, fasting serum lipids, glucose, and urate, and a 24-hour ambulatory ECG monitoring. Thirty-seven men died during follow-up. Mortality was similar in men with Type A (24%) and Type B (22%) behavior. In multivariate analyses, lack of social support/social isolation was an independent mortality predictor in Type A, but not in Type B men. In both groups, a high frequency of ventricular ectopic beats on 24-hour ECG monitoring and a poor self-rated general health predicted mortality over the 10-year period. The 10-year mortality experience of socially isolated Type A men was 69% and that of socially integrated Type A men was 17% (p less than 0.05). The findings offer a possible explanation for the observed inconsistencies between intervention and follow-up studies of Type A behavior and coronary heart disease. It is suggested that an important effect of Type A modification programs is to increase the availability of social support. This could be the mechanism through which Type A modification exerts its main effects on cardiovascular health.

The Clinical Value of the 24-hour Ambulatory ECG Monitoring in Patients with Chronic Atrial Fibrillation

24-hour ambulatory ECG monitoring has been examined for the evaluation of heart rate and longest pause in 34 patients with chronic atrial fibrillation(20 patients treated with digoxin and 14 patients without treatment). Following results were obtained : 1. In 34 patients, the mean of average heart rates was /minute, fastest heart rates /minute, slowest heart rates /minute, difference between fastest and slowest heart rates in individual patients /minute and longest pauses seconds. The longest pauses of more than 4.0 seconds occurred in 4 of the 34 patients and made an exeption of comparison groups. 2. In 27 of the 34 patients, ventricular premature contractures were developed and in 11 of 27, mainly occured less than 100/24 hours and aberrant conduction occurred in all patients. 3. In 20 patients treated with digoxin(0.25mg/day), the mean of average heart rates was /minute, fastest heart rates /minute, slowest heart rates /minute, difference between fastest and slowest heart rates in individual patients /minute and longest pauses seconds. 4. In 10 patients without treatment, the mean of average heart rates was /minute, fastest heart rates /minute, slowest heart rates /minute, difference between fastest and slowest heart rates in individual patients /minute and longest pauses seconds. 5. The difference of heart rates and longest pauses between patients with treatment and without treatment were statistically not significant(P>0.05). In summary, authors seemed to consider that 24-hour ambulatory ECG was useful and safe method for clinical evaluation of patients with chronic atrial fibrillation.

The efficacy of the addition of nifedipine in patients with mixed angina compared to patients with classic exertional angina: A multicenter, randomized, double-blind, placebo-controlled clinical trial

Episodes of myocardial ischemia in patients with coronary artery disease may be due to transient increases in coronary vasomotor tone superimposed on a fixed atherosclerotic obstruction. The purpose of this study was to determine whether identification of the clinical pattern of angina could predict the therapeutic response to the addition of nifedipine to a regimen of beta blockers and/or long-acting nitrates. Seventy-two patients with stable exertional angina were divided into two groups: “classic exertional angina” (17 patients), defined as exertional angina with a stable threshold; and “mixed angina” (55 patients), defined as exertional angina provoked by a variable threshold and/or at least two episodes of rest angina within the 3 months prior to screening. Patients were studied with nifedipine and placebo in a 6-week, double-blind, crossover design that used serial anginal diaries, exercise treadmill tests, and 24-hour ambulatory ECG monitoring. In patients with mixed angina, nifedipine reduced the frequency of angina compared to that during placebo treatment (13.1 vs 9.9 episodes/3 weeks, p < 0.01) and reduced nitroglycerin consumption (11.7 vs 7.5 tablets/3 weeks, p < 0.05); while in patients with classic exertional angina, nifedipine had no symptomatic effect (7.9 vs 6.8 anginal episodes/3 weeks, NS; 6.4 vs 5.8 nitroglycerin tablets/3 weeks, NS). Patients in both groups experienced a significant decrease in the manifestations of ischemia during exercise testing. Patients with mixed angina experienced a reduction in the daily frequency of painful episodes of ST segment depression during nifedipine treatment compared to placebo (0.6 vs 0.2 episodes, p < 0.05), but there was no effect on the frequency of episodes of silent ischemia (4.2 vs 3.4 episodes, NS). In patients with classic exertional angina, the addition of nifedipine had no effect on any measure of ambulatory ischemia. We conclude that patients with mixed angina are more likely to benefit symptomatically from the addition of nifedipine therapy than patients with classic exertional angina. The lack of a consistently preferential response to nifedipine in patients with mixed angina, however, suggests that episodic coronary vasoconstriction may not be the only mechanism responsible for ischemia in these patients, and/or that nifedipine may not necessarily provide additional therapeutic benefit beyond that conferred by a regimen of beta blockers and/or nitrates.

Ventricular Ectopic Activity With Diuretic Therapy

The arrhythmogenic potential of diuretic-induced hypokalemia in patients with uncomplicated hypertension has been controversial. Thirty-two hypertensive patients with previous diuretic-induced hypokalemia, normal 24-hour ambulatory ECG monitoring, and normal exercise testing were treated with 100 mg hydrochlorothiazide (HCTZ) daily (Group 1) to induce hypokalemia or with a combination of HCTZ with amiloride (Group 2) to attempt to maintain plasma potassium levels in the normal range during diuretic therapy. Those Group 1 patients (Group 1A) with increased ventricular ectopic activity (VEA) during HCTZ therapy were subsequently potassium-repleted with amiloride and with supplemental potassium chloride to evaluate the effect of these treatments on VEA. One Group 1 patient died suddenly after 12 days of HCTZ therapy. Autopsy findings suggested an arrhythmic death. Six Group 1 patients who had increased VEA with HCTZ treatment had reductions in VEA with amiloride or supplemental potassium chloride. Group 2 patients did not have a significant increase in VEA. Thus, diuretic therapy appears to cause VEA primarily by electrolyte changes that are induced.

Long-term efficacy of oral pirmenol in suppressing ventricular premature depolarizations

Pirmenol is an investigational type 1A antiarrhythmic drug the long-term efficacy of which has not been fully determined. Therefore the long-term efficacy of oral pirmenol in supprossing ventricular premature depolarizations (VPDs) was assessed in an open-label, dose-titration study. Twelve patients (eight men and four women; mean age 57 ± 12 years) were treated for 24 to 36 months (mean 33 ± 4). Seven had structural heart disease (three valvular heart disease, two ischemic heart disease, and two hypertensive heart disease) and five did not. The mean left ventricular ejection fraction was 0.63 ± 0.13. Exclusion criteria included <30 VPDs/hr, >15 beats of ventricular tachycardia (VT), or prior failure of more than two antiarrhythmic drugs. Drug efficacy was assessed by 24-hour ambulatory ECG monitoring performed every 3 months during the first year, every 4 months during the second year, and at 6-month intervals during the third year. The mean hourly frequency of VPDs during the placebo phase was 732 ± 608. Seven patients (58%) were treated successfully with effective (>75%) long-term suppression of VPDs. Two patients (17%) had a partial response with effective suppression of VPDs for the first 16 months and 5 months of treatment, respectively. Three patients falled to show consistent suppression of VPDs while receiving pirmenol. The daily dose of pirmenol ranged from 200 to 500 mg (mean 317 ± 94 mg at the beginning of the study and 375 ± 97 mg at the end). No proarrhythmic effects were identified during long-term treatment, and none of the patients withdrew from the study prematurely. Mild side effects included dry mouth, bad taste, and urinary hesitancy. We conclude that oral pirmenol maintains effective long-term suppression of VPDs in approximately 60% of patients and is well tolerated during chronic administration. No proarrhythmic effects occurred during long-term treatment.

Social Isolation and Mortality in Ischemic Heart Disease

The effects of psychosocial and clinical factors on mortality in ischemic heart disease (IHD) were examined in a 10-year follow-up of 150 middle-aged men. Three groups of men were included: men with clinically manifest IHD, men with risk factors and healthy men. Psychosocial factors were assessed by means of standardized questionnaires. They comprised educational level, social class, marital status and a comprehensive assessment of the daily rounds of life of these men. Furthermore, a subjective rating of the own general health status was obtained. The clinical investigation included a standard physical examination, fasting serum lipids, glucose and urate, a frontal and sagittal chest X-ray and a 24-hour ambulatory ECG monitoring. During follow-up 37 men died, 20 of them from IHD. Non-survivors were discriminated from survivors by the following factors: older age, lower education, lower social class, higher systolic blood pressure, increased ventricular irritability and cardiac enlargement. Furthermore, a relative social isolation as indicated by a low social activity level and a poor self-rated general health status was characteristic of non-survivors. In multivariate analyses three factors emerged as the equally strong predictors of mortality, both from all causes and from IHD: social isolation, a poor self-rated health status and ventricular irritability. The psychosocial mortality predictors were independent of and of similar strength as the clinical predictors.

Cardiac arrhythmias in healthy children revealed by 24-hour ambulatory ECG monitoring

Ambulatory electrocardiographic monitoring was performed on 360 healthy children, from newborn infants to junior high school students. They were divided into five groups by age: group A, 63 newborn infants on the first day of life; group B, 50 infants aged 1-11 months; group C, 53 kindergarten pupils aged 4-6 years; group D, 97 primary school pupils aged 9-12 years; and group E, 97 junior high school students aged 13-15 years. The maximal and minimal heart rates were significantly greater in infants than in older children. Sinus arrhythmia was recorded in every child. One boy in group E had an episode of sinus arrest for three seconds without any symptoms. First-degree and Wenckebach type second-degree atrioventricular blocks were not detected in group A and group B, but were most frequent in group E, especially during sleep. Supraventricular premature contractions (SVPCs) were the most common type of arrhythmia detected in this study. More than half of the children had at least one SVPC per 24-h monitoring period, and there were many children with frequent SVPCs in group E. The incidence of ventricular premature contractions (VPCs) in children of groups A and E was rather higher than in the other groups. Ventricular tachycardia was not recorded in any child except one newborn infant who had a couplet of VPCs without symptoms. Each group had different types and incidences of arrhythmias. There was a rising incidence of arrhythmias with advancing age, except in the neonatal period.

The relationship of ventricular arrhythmias to the angiographically and scintigraphically estimated extent of ventricular damage late after myocardial infarction

In order to study the quantitative relationship of ventricular arrhythmias to myocardial damage and ischemia, 61 patients with a previous myocardial infarction (at least 6 months previously) were studied by 24-hour ambulatory ECG monitoring, cardiac catheterization, and thallium-201 scintigraphy. Thirty-five patients (57%) had no ectopic beats or only infrequent, unifocal ones and 26 patients (43%) had complex ventricular arrhythmias. Left ventricular function was lower in the latter (p less than 0.05), but the number of diseased vessels did not differ in the two groups. The reduction of thallium activity in the infarct area was more marked in patients with complex arrhythmias (p less than 0.001). Multiple thallium defects were not more common in arrhythmia patients, however. These data support the view that complex ventricular arrhythmias are more closely related to the severity of ventricular damage than the presence of myocardial ischemia remote to the area of previous infarction.

Management of refractory sustained ventricular tachycardia with amiodarone: A reappraisal

We examined the value of clinical variables, chronic 24-hour ambulatory ECG monitoring, and chronic electrophysiologic (EP) testing in 49 patients with recurrent and refractory sustained ventricular tachycardia (VT) and ventricular fibrillation (VF) treated with chronic oral amiodarone in order to develop a prospective approach to the management of these patients. All patients underwent control EP studies followed by continuous telemetric cardiac monitoring during oral amiodarone administration (mean duration 29 ± 6 days, mean dose 739 ± 230 mg). Follow-up 24-hour ambulatory ECG monitoring and EP studies were performed. Thirty VT recurrences occurred in the first 4 weeks of amiodarone therapy (total incidence, 61%), with the majority (55%) in the first 3 weeks of treatment. During long-term follow-up (1 to 42, mean 15 ± 12 months), there were 12 symptomatic VT VF recurrences (incidence 24%). There was a higher incidence of VT recurrences if patients had inducible sustained or nonsustained VT at chronic EP study ( p < 0.01), or complex ventricular arrhythmias on ambulatory ECG monitoring ( p < 0.05). The sensitivity, specificity, and predictive accuracy of chronic EP testing and 24-hour ambulatory ECG monitoring were 100%, 35%, and 51%, and 58%, 84%, and 78%, respectively. Chronic EP testing correctly identified all patients who had their arrhythmia suppressed by amiodarone on long-term follow-up, while 42% of all VT recurrences occurred in patients without complex ventricular arrhythmias on 24-hour ambulatory ECG monitor. A prospective combined EP-ambulatory ECG approach to the management of patients with recurrent sustained VT VF on amiodarone is proposed, with the EP technique being used as the end point for efficacy and the ambulatory ECG technique being employed to identify early therapeutic failures. Alternative or adjunctive antiarrhythmic therapy is warranted for patients with inducible VT on chronic amiodarone therapy.

Twenty-four hour ambulatory ECG monitoring of junior high school students in Miki City.

To evaluate incidence of serious arrhythmias among school age youths, 24-hour ambulatory ECG monitoring was performed in 100 junior high school students, including 60 subjects with some ECG abnormalities and 40 without. With this monitoring 2 cases with multifocal VPCs and 2 cases with paired VPCs or nonsustained ventricular tachycardia were found; the case with VT died suddenly after having been lost during careful follow up. It is emphasized from these results that ambulatory ECG monitoring is quite useful in selected cases in this age group and careful follow up of students with advanced grade VPCs is very important.

Asymptomatic transient ST changes during ambulatory ECG monitoring in diabetic patients

The reported higher incidence of painless myocardial infarction in diabetic patients suggests that asymptomatic transient myocardial ischemia may also be frequent in diabetes. To explore this possibility 51 subjects with type II diabetes, aged 43 to 71 years (mean ± SEM 56 ± 8), 70 nondiabetic patients with coronary artery disease (mean age 55 ± 5), and 40 nondiabetic patients without overt coronary disease (age 54 ± 9) were studied. Thirty-eight of the 51 diabetic patients (74%) had evidence of associated coronary disease and 19 (37%) had evidence of previous myocardial infarction. All subjects underwent continuous 24-hour ambulatory ECG monitoring. In 18 of 51 diabetic patients 93 episodes (73% of the total number) of asymptomatic ST segment changes were recorded; the total number of symptomatic episodes was 36, and they were observed in seven patients (27%). Forty-eight (60%) asymptomatic and 32 symptomatic episodes of significant ST changes were found in nondiabetic patients with coronary artery disease. When patients with previous myocardial infarction were examined separately, asymptomatic episodes of significant ST changes were observed in 10 of 19 diabetic patients and in 5 of 25 nondiabetic patients with coronary artery disease ( p < 0.05). In an additional 28 diabetic patients who underwent exercise stress test, 15 exhibited an abnormal ECG response; however, only five of them (33%) were symptomatic. This study suggests that the incidence of transitory myocardial ischemia, as assessed by ambulatory ECG monitoring and exercise stress test, is higher in type II diabetic patients than in nondiabetic control subjects with coronary artery disease.

Ventricular arrhythmias in severe heart failure: Incidence, significance, and effectiveness of antiarrhythmic therapy

Forty-three patients receiving maximal medical therapy for severe chronic heart failure from dilated cardiomyopathies (28 ischemic, 15 idiopathic) and ventricular premature beats (VPBs) on the 12-lead ECG had baseline 24-hour ambulatory ECG monitoring. Complex VPBs (multiform, repetitive—couplets, R on T phenomenon) and asymptomatic, nonsustained ventricular tachycardia were present in 38 patients (88%) and 22 patients (51%), respectively. Twenty-three patients (group I) were placed on long-term antiarrhythmic therapy (20 patients received procainamide and the remaining quinidine). Twenty patients (group II) did not receive antiarrhythmic therapy. At baseline, no significant differences between the two groups were noted for age, functional class, type of cardiomyopathy, medical therapy for heart failure, cardiothoracic ratio, radionuclide ejection fraction, or rate and complexity of the ventricular arrhythmias on the 24-hour ambulatory ECG tracings. At a mean follow-up period of 16 months (range 1 to 37), there were 16 deaths, 10 (62%) of which were sudden and unexpected. No significant differences in the incidence of sudden death and overall mortality were noted between the two groups. Among patients with nonsustained ventricular tachycardia, those who died suddenly had a lower mean left ventricular ejection fraction (0.15 ± 0.01) when compared to the survivors (0.23 ± 0.02; p < 0.01). It is concluded that (1) patients with severe heart failure have a high mortality from both sudden and nonsudden cardiac death, (2) incidence of complex VPBs is very high, (3) sudden death is more common when the left ventricular function is severely compromised, and (4) apparently, therapeutic plasma levels of conventional antiarrhythmic drugs do not protect this group of patients from dying.

Comparison of Lorcainide and Quinidine in the Treatment of Ventricular Ectopy

Lorcainide, a new type I antiarrhythmic agent, was compared to quinidine in respect to antiarrhythmic efficacy and clinical safety. Thirteen subjects completed an open, randomized, crossover study with analysis of 24-hour ambulatory ECG monitoring and drug blood levels. The QRS and Q-T intervals increased with both lorcainide and quinidine. The mean reduction in total ventricular premature beats (VPBs) with quinidine was 16 percent compared to 68 percent with lorcainide (p less than .05). With lorcainide eight of 13 subjects had a significant (greater than 82 percent) reduction in VPBs compared to only three of 13 subjects taking quinidine (p less than .05). This same relationship was observed when mean VPB/1,000 heartbeats was analyzed. Ventricular tachycardia was no longer present in five of nine subjects taking lorcainide and in two of nine taking quinidine. No relationship could be established between drug level and arrhythmia suppression in this small population. Some CNS effects were reported in both groups, but no significant hematologic, chemical, or urinary adverse effects were seen with either drug. Thus, lorcainide compares favorably to quinidine in regard to arrhythmia suppression, but was limited in its clinical utility by CNS side effects.

Arrhythmia in young patients with mitral valve prolapse.

Twenty four-hour ambulatory ECG monitoring were examined in 68 patients (33 patients in a young group and 35 patients in an adult group) with mitral valve prolapse (MVP) in order to characterize the features of arrhythmias in young patients with MVP in comparison with those in adult patients. Diagnosis of MVP was made by two-dimensional echocardiography. On 24-hour ambulatory ECG monitoring 29 patients (88%) in a young group had arrhythmias which was as frequent as those in adult group, but serious ventricular arrhythmias were more often detected in the young group (7 patients) than in the adult group (2 patients). It was considered that arrhythmias in young patients with MVP were frequently serious but accompanied without any symptoms and cardiac dysfunction.

A longitudinal study of the prognostic significance of ventricular ectopic beats in the elderly.

The prognostic significance of ventricular ectopic beats occurring in healthy, elderly individuals has only been assessed previously in short-term, longitudinal studies. 30 healthy, elderly people underwent 24-hour ambulatory electrocardiographic monitoring and approximately 2.5 years later subsequent morbidity and mortality was assessed. 1 individual could not be traced and 4 had died. Details of the cardiovascular health status of the remaining 25 were assessed by a questionnaire. There was no correlation between the numbers of ventricular ectopic beats and subsequent cardiovascular morbidity. Similarly, the results show no differences between ventricular ectopic beat activity and mortality 2.5 years later. On the basis of this study it is concluded that routine 24-hour ambulatory ECG monitoring does not provide clinically relevant predictive information in regard to cardiovascular morbidity or mortality.

Phenytoin therapy for ventricular arrhythmias occurring late after surgery for congenital heart disease

Sudden death late after surgery for congenital heart disease is usually attributed to ventricular dysrhythmias, which may be difficult to suppress. In this study 19 consecutive patients with ventricular premature complexes (VPCs) documented by 24-hour ambulatory ECG monitoring were treated with phenytoin orally. Sixteen patients had undergone previous repair of the tetralogy of Fallot; three had undergone aortic valve surgery. Nine of these children had been unresponsive to previous antiarrhythmic therapy. Before treatment, four patients had ventricular tachycardia, three had couplets, six had frequent multiform VPCs, four had infrequent multiform VPCs, and two had frequent uniform VPCs. During treatment with phenytoin, the arrhythmia was decreased in all 19 patients and was completely suppressed in 15; the four remaining patients had only uniform VPCs on repeat ambulatory ECG. The mean serum level was 16.8 μg/ml (range 12 to 25 μg/ml) with a mean dose of 3.4 mg/kg (range 2 to 4 mg/kg). In one patient a skin rash led to discontinuation of phenytoin; no other side effects occurred. In summary, phenytoin was used to successfully suppress ventricular dysrhythmias in 19 consecutive patients with VPCs late after surgery for congenital heart disease. Phenytoin would appear to be the drug of choice for this patient group.