Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “arrhythmia”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 37 records · Page 2Linked to original sources
PubMed1998

Is hospital admission for initiation of antiarrhythmic therapy with sotalol for atrial arrhythmias required? Yield of in-hospital monitoring and prediction of risk for significant arrhythmia complications.

OBJECTIVES: We sought to determine the yield of in-hospital monitoring for detection of significant arrhythmia complications in patients starting sotalol therapy for atrial arrhythmias and to identify factors that might predict safe outpatient initiation. BACKGROUND: The need for hospital admission during initiation of antiarrhythmic therapy has been questioned, particularly for sotalol, with which proarrhythmia may be dose related. METHODS: The records of 120 patients admitted to the hospital for initiation of sotalol therapy were retrospectively reviewed to determine the incidence of significant arrhythmia complications, defined as new or increased ventricular arrhythmias, significant bradycardia or excessive corrected QT (QTc) interval prolongation. RESULTS: Twenty-five patients (20.8%) experienced 35 complications, triggering therapy changes during the hospital period in 21 (17.5%). New or increased ventricular arrhythmias developed in 7 patients (5.8%) (torsade de pointes in 2), significant bradycardia in 20 (16.7%) (rate <40 beats/min in 13, pause >3.0 s in 4, third-degree atrioventricular block in 1, permanent pacemaker implantation in 3) and excessively prolonged QTc intervals in 8 (6.7%) (dosage reduced or discontinued in 6). Time to the earliest detection of complications was 2.1 +/- 2.5 (mean +/- SD) days after initiation of sotalol, with 22 of 25 patients meeting criteria for complications within 3 days of monitoring. Baseline electrocardiographic intervals or absence of heart disease failed to distinguish a low risk group. Multivariate analysis identified absence of a pacemaker as the only significant predictor of arrhythmia complications (p = 0.022). CONCLUSIONS: Because clinically significant complications can be detected with in-hospital monitoring in one of five patients starting sotalol therapy, hospital admission is warranted for initiation of sotalol. Patients without pacemakers are at higher risk for these complications.

Aged↗
PubMed1991

[Methodology in clinical trials of anti-arrhythmia agents in ventricular arrhythmias. Analysis and perspective following results of the CAST study].

The results of the Cardiac Arrhythmia Suppression Trial (CAST) have not finished modifying the methodology and strategy of development of new antiarrhythmic agents for the treatment of ventricular arrhythmias. The demonstration of a dissociation between a proved antiarrhythmic effect and increased mortality in coronary patients treated with encainide or flecainide, means that, in this situation, antiarrhythmic efficacy cannot be considered to be a substitute criterion of therapeutic benefit. The consequences of these results are as follows: in phase II, the dose-effect relationships should be studied in patients with chronic ventricular extrasystole without ischemic heart disease. This model is sufficiently predictive for the selection of the dosage to be tested in phase III; in phase III, studies of benign ventricular arrhythmias, antiarrhythmic efficacy is demonstrated by ambulatory ECG recordings. If these studies include patients with ischemic heart disease, the patients must be placed on betablocker therapy and the benefits in terms of reduction of mortality have to be shown by controlled trials versus placebo. In malignant life-threatening arrhythmias, open clinical trials may be performed using provocative electrophysiological studies. The inclusion of patients with implanted automatic defibrillator devices could constitute control groups for the placebo group. The future of antiarrhythmic agents for the treatment of ventricular arrhythmias greatly depends on the search for criteria of severity of arrhythmias and the validation of intermediate criteria of efficacy.

Anti-Arrhythmia Agents↗
PubMed1992

Treatment of ventricular arrhythmias after CAST.

OBJECTIVE: The primary objective of this article is to review the management of ventricular arrythmias in the light of the unfavourable results reported in the Cardiac Arrhythmia Suppression Trial (CAST). STUDY SELECTION, DATA EXTRACTION AND SYNTHESIS: CAST tested the hypothesis that suppression of ventricular arrhythmias recorded on a Holter monitor in patients with myocardial infarction would lead to a decrease in subsequent mortality, presumably by preventing sudden death. In the trial, patients with a myocardial infarction which occurred six days to two years previously and with asymptomatic ventricular premature beats which could be suppressed by one of the antiarrhythmic agents flecainide, encainide or moricizine, were randomised to treatment with one of these agents or placebo. Over a mean follow-up period of 10 months, mortality was significantly higher in those patients receiving flecainide or encainide than in those receiving placebo. On the recommendation of the Data and Safety Monitoring Board the trial in these groups was terminated. More recently CAST II in which moricizine was compared to placebo was also terminated, again because of a higher mortality in the patients receiving active treatment. It is likely that much of the excess mortality can be attributed to proarrhythmic effects of the agents. CONCLUSION: Current management of ventricular arrhythmias are considered in the light of these findings. CAST suggests that specific treatment should be dictated by the presence of associated symptoms and as much by associated structural heart disease as the arrhythmia per se. In particular, specific treatment of ventricular premature beats alone should be avoided. In those with potentially lethal ventricular arrhythmias, referral for appropriate investigation and consideration of non-pharmacological measures is necessary.

Anti-Arrhythmia Agents↗
PubMed1985

Complex arrhythmias in mitral regurgitation with and without mitral valve prolapse: contrast to arrhythmias in mitral valve prolapse without mitral regurgitation.

Atrial and ventricular arrhythmias were characterized by ambulatory electrocardiography in 31 patients with nonischemic mitral regurgitation (MR), 17 of whom had echocardiographic evidence of mitral valve prolapse (MVP) and 14 of whom had other causes of MR. Frequent and complex arrhythmias were common and equally prevalent in each MR subgroup, whether or not MVP was present. Multiform ventricular ectopy was found in 77% (24 of 31), ventricular couplets in 61% (19 of 31), and ventricular salvos or ventricular tachycardia in 35% (11 of 31) of patients with MR. Arrhythmias in patients with MR were significantly more prevalent than in 63 patients with MVP who had no evidence of MR. Among patients with MVP, excess arrhythmias associated with MR were most striking with respect to frequent ventricular premature complexes (41% with MR vs 3% without MR), multiform ventricular ectopic activity (88% vs 43%), ventricular couplets (65% vs 6%), and ventricular salvos or ventricular tachycardia (35% vs 5%) (p less than 0.005 for each comparison). These data demonstrate that complex arrhythmias are common in patients with nonischemic MR irrespective of etiology, and that these arrhythmias are more strongly associated with hemodynamically important MR than with MVP alone.

Adult↗
PubMed1996

Characterization of spontaneous recurrent ventricular arrhythmias detected by electrogram-storing defibrillators in sudden cardiac death survivors with no inducible ventricular arrhythmias at baseline electrophysiologic testing.

This retrospective study characterized the recurring ventricular arrhythmias with an electrogram-storing defibrillator in survivors of sudden cardiac death who had no inducible sustained ventricular arrhythmias at baseline electrophysiologic testing (EPS). The study group was composed of 24 selected patients with documented ventricular fibrillation (VF) without need of revascularization or chronic antiarrhythmic therapy. The EPS protocol usually consisted of three extrastimuli at two drive cycles at two right ventricular sites. Nonischemic cardiomyopathy was the most frequent structural abnormality (n = 11) followed by coronary artery disease (n = 7). The mean ejection fraction was 0.37 +/- 0.13. Cardiac status did not appear to change during a mean follow-up period of 16.4 +/- 12.5 months, and eight (33%) patients received appropriate shocks in that time period. On the basis of intracardiac electrograms, 7 (88%) patients experienced VF and 1 (12%) patient had ventricular tachycardia as the first recurring arrhythmia. Four patients had additional recurrences and all were VF episodes. VF was usually present from the onset of the arrhythmia. In addition, 9 (38%) patients had nonsustained ventricular arrhythmias that were solely VF in 6 (67%). In conclusion, VF of sudden onset was the most frequent recurring sustained ventricular arrhythmia in this group.

Aged↗
PubMed1994

QT interval dispersion: a non-invasive marker of susceptibility to arrhythmia in patients with sustained ventricular arrhythmias?

OBJECTIVE: To assess QT interval dispersion on the surface electrocardiogram in patients with sustained ventricular arrhythmias. DESIGN: A retrospective and prospective blinded controlled study of patients referred for investigation of ventricular arrhythmias at a tertiary cardiac centre. PATIENTS AND METHODS: 89 consecutive patients with sustained ventricular arrhythmias due to chronic ischaemic heart disease, cardiomyopathy, or ventricular tachycardia (VT) in a normal heart. 32 patients did not meet the inclusion criteria; therefore 57 patients were compared with a control group of 40 patients with myocardial disease but no history of arrhythmias and 12 normal controls with no myocardial disease. Standard 12 lead electrocardiograms were enlarged, the QT intervals for each lead measured, and QT dispersion calculated. RESULTS: There was a significantly greater mean QT dispersion (77 ms) in patients with sustained ventricular arrhythmias compared with the control group (38 ms, p < 0.01). This held for all groups; after myocardial infarction VT (82 (22) ms v control 38 (10) ms; p < 0.01), dilated cardiomyopathy VT (76 (18) ms v control 40 (11) ms, p < 0.01), and normal heart VT (65 (7) ms v control 32 (8), p < 0.05). There was also a greater QT dispersion in patients with impaired left ventricular function and VT, with a correlation between left ventricular function and QT dispersion in patients with VT (r = 0.56, p < 0.01). CONCLUSION: QT interval dispersion may be a further non-invasive marker of susceptibility to ventricular arrhythmias.

Arrhythmias, Cardiac↗
PubMed2006

Effects of a rate smoothing algorithm for prevention of ventricular arrhythmias: results of the Ventricular Arrhythmia Suppression Trial (VAST).

BACKGROUND: Rate smoothing, which is available in some pacemakers and implantable cardioverter defibrillators (ICDs), has been used to prevent Torsades de Pointes in patients with long QT syndrome. Its efficacy in general ventricular arrhythmia prevention has not been determined. OBJECTIVES: The purpose of the Ventricular Arrhythmia Suppression Trial (VAST) was to prospectively investigate whether rate smoothing could significantly reduce the incidence of ventricular tachyarrhythmias in a large, broad population of patients with ICDs. METHODS: Five hundred sixty-nine patients were enrolled at 57 participating centers and implanted with a commercially available Guidant ICD. A single-blinded crossover design was used in which each patient was randomized at implant to one of two treatment sequences: either rate smoothing on (RS On) followed by rate smoothing off (RS Off), or RS Off followed by RS On. This mode sequence was randomly determined and assigned in a 1:1 fashion using randomized permuted blocks by site. Each mode was followed for 6 months. Programming of rate smoothing was prescribed as 12% Down and 12% Up for the duration of the RS On period. RESULTS: Of enrolled patients, 281 were randomized to RS Off followed by RS On, and 288 to RS On followed by RS Off. With RS On, 75 (23%) patients experienced a reduction in arrhythmias, 76 (23%) saw an increase in arrhythmias, and the remaining 176 (54%) had no difference. No significant difference (P = .58) in frequency of arrhythmias with RS On vs RS Off was found. CONCLUSION: Rate smoothing does not result in a reduction in ventricular arrhythmias in a heterogeneous population of patients receiving ICDs.

Adult↗
PubMed1993

Indications for antiarrhythmic suppression of ventricular arrhythmias: a definition of life-threatening ventricular arrhythmias.

A surprising finding of the Cardiac Arrhythmia Suppression Trial (CAST), reported in 1989, is that well-tolerated and effective antiarrhythmic drugs may also be associated with an increase in mortality due to arrhythmia. Consequently, attention has been focused on the importance of the benefit-versus-risk assessment of such therapy. The benefits of antiarrhythmic therapy are reduction or elimination of arrhythmia-caused symptoms (both hemodynamic and nonhemodynamic) and of the associated risk of death. The risks of such treatment include not only noncardiac adverse effects and organ toxicity, but also early cardiac effects (proarrhythmia, heart failure, and conduction defects), as well as the newly recognized potential for late proarrhythmia or late arrhythmic death. Unfortunately, as the potential benefits of antiarrhythmic therapy increase in patients with poorer left ventricular function (owing to their being at greater risk for sudden death), the effectiveness of suppression decreases and the incidence of life-threatening complications increases. The impact of this benefit-risk profile is that the indication for most currently approved antiarrhythmic drugs needs to be limited to those patients with definite life-threatening ventricular arrhythmias that take the form of sustained ventricular tachyarrhythmias with associated hemodynamic symptoms. Broadening this indication to include patients with probable life-threatening or even possible life-threatening arrhythmias must await the availability of drugs with better benefit-risk profiles.

Anti-Arrhythmia Agents↗
PubMed1986

Antiarrhythmic and antifibrillatory action of diltiazem on early and late phase ventricular arrhythmias following coronary artery occlusion and on reperfusion ventricular arrhythmias.

The effects of diltiazem on ventricular arrhythmias and ventricular vulnerability for fibrillation, both in the very beginning of myocardial ischemia and in the early stage of myocardial necrosis, were evaluated in 13 mongrel dogs. In part I of the study, repeated coronary occlusions were performed. Time course and extent of ventricular ectopy were continuously recorded, and changes in ventricular fibrillation threshold were assessed, both after coronary artery occlusion and release. In part II, a permanent coronary artery occlusion was performed, and the changes in frequency of ventricular arrhythmias were assessed. Diltiazem displayed strong antiarrhythmic and antifibrillatory effects on early ventricular occlusion arrhythmias. The drop in ventricular fibrillation threshold 5 min after coronary occlusion was significantly attenuated. Following the release of coronary artery obstruction, diltiazem failed to reduce the frequency of ventricular fibrillation immediately after the onset of reperfusion. However, during the early postreperfusion period, the drug was able to accelerate significantly the increase in the ventricular fibrillation threshold. Late phase ventricular arrhythmias were not influenced by the drug even when high doses were applied. The different antiarrhythmic actions of diltiazem on early and late phase ventricular arrhythmias can be assumed to be due to differences in the arrhythmogenesis at the very onset of myocardial ischemia compared to the stage of myocardial necrosis.

Animals↗
PubMed2004

Effects of class I antiarrhythmic drugs on the digitalis-induced triggered activity arrhythmia model: a rationale for the short-term use of class I drugs against triggered arrhythmias.

Delayed afterdepolarization (DAD)-induced triggered activity has been considered to be one of the generation mechanisms of ventricular arrhythmias in the presence of intracellular Ca2+ overload. In this study, we analyzed the antiarrhythmic effects of class I antiarrhythmic drugs, namely, disopyramide, procainamide, mexiletine, and flecainide, on a recently developed DAD-induced triggered arrhythmia model, which consists of a canine ventricular septum preparation cross-circulated with a blood-donor dog. After intravenous administration of ouabain to the donor dog, triggered arrhythmias were consistently induced in the cross-circulated preparation by train stimulation (cycle length: 300 ms; train number: 15). Intracoronary administration of disopyramide, procainamide, mexiletine, and flecainide as well as lidocaine suppressed the triggered arrhythmias at clinically relevant doses. Similar doses have been demonstrated to suppress intraventricular conduction in the same experimental model. These results suggest that the Na+ channel inhibition by class I drugs is an effective pharmacological intervention for suppressing Ca2+ overload, which may provide a rationale for the short-term use of class I drugs against the triggered arrhythmias in clinical practice.

Animals↗
PubMed1996

Repeated 15-minute coronary occlusions in pigs increase occlusion arrhythmias but decrease reperfusion arrhythmias that are associated with extracellular hypokalemia.

OBJECTIVES: We sought to evaluate the effects of repetitive 15-min coronary occlusions followed by 45-min reperfusions on the incidence of occlusion and reperfusion arrhythmias in pigs. BACKGROUND: Brief 2- to 5-min coronary occlusions seem to exert a protective effect on occlusion and reperfusion arrhythmias. However, because clinical ischemic episodes are often longer, it would be appropriate to assess whether such protection also occurs when longer cycles of occlusion-reperfusion are produced. METHODS: Three to four cycles of 15-min coronary occlusions with 45-min reperfusions were performed in 34 pigs, and changes in ST segment and incidence of ventricular arrhythmias were assessed. Plasma potassium ion concentrations in eight pigs and blood gas in six were measured from blood from the ischemic area during reperfusion. RESULTS: Repetitive occlusions were associated with a progressively higher ST segment elevation and a higher incidence of ST segment alternans (p < 0.001) and ventricular fibrillation (VF) (p < 0.01). However, during repetitive reperfusions, normalization of the ST segment was increasingly faster, the incidence of VF was progressively reduced (p < 0.03), and there was progressively less severe regional acidosis ([mean +/- SD] 7.06 +/- 0.12 vs. 7.26 +/- 0.06, p < 0.05) and hypokalemia (1.9 +/- 0.7 vs. 2.3 +/- 0.4 mEq/liter, p = NS). CONCLUSIONS: The progressive electrocardiographic deterioration and increasing incidence of ventricular arrhythmias during repetitive 15-min occlusions in pigs suggest increasing metabolic derangement. However, the progressively faster normalization of the ST segment and the reduced incidence of ventricular arrhythmias during reperfusion suggest an increasingly faster restoration of the metabolic and ionic balance.

Acid-Base Equilibrium↗
PubMed2000

Antiarrhythmic efficacy of dipyridamole in treatment of reperfusion arrhythmias : evidence for cAMP-mediated triggered activity as a mechanism responsible for reperfusion arrhythmias.

BACKGROUND: Intracellular calcium overload is believed to play an important role in development of reperfusion arrhythmias. Dipyridamole, an inhibitor of cellular uptake of adenosine, may prevent or terminate reperfusion arrhythmias by reducing intracellular calcium overload. METHODS AND RESULTS: First, we tested for a preventive effect of dipyridamole. Sixty-one patients who underwent primary PTCA for treatment of acute anterior wall myocardial infarction were enrolled in this prospective study. Patients were divided into dipyridamole (DP) and nondipyridamole (non-DP) groups. The 2 groups had similar baseline characteristics. In the DP group, dipyridamole 0.5 mg/kg was infused intravenously for 3 minutes immediately before reperfusion during primary PTCA. Arrhythmias after reperfusion were analyzed from continuous ECG recordings. None of the patients in the DP group (n=23) had accelerated idioventricular rhythms (AIVR) or ventricular tachycardia (VT). In contrast, 7 (18.4%) had AIVR and 3 (7.9%) had VT in the non-DP group (n=38; P<0.01). Second, we tested for a termination effect of dipyridamole. Dipyridamole 0.5 mg/kg was infused intravenously while continuous ECG recordings were obtained in 9 patients who had either sustained AIVR (n=7) or sustained VT (n=2) after reperfusion of occluded coronary artery. Arrhythmias were terminated in all patients. CONCLUSIONS: These results indicate that administration of dipyridamole can prevent and terminate reperfusion arrhythmias such as AIVR and VT. cAMP-mediated triggered activity may, at least in part, be responsible for reperfusion-induced AIVR and VT.

Adenosine↗
PubMed1990

[Spontaneous variability of ventricular arrhythmias in follow-up of anti-arrhythmia therapy].

The question of the reliability of ambulatory Holter monitoring for assessment of antiarrhythmic treatment has not been adequately resolved. Even though treatment efficacy had been individually assessed with Holter monitoring in the CAST study, during long-term treatment with class IC antiarrhythmic drugs, there were more deaths among patients receiving active drug than in those in the placebo group. Basic biostatistical considerations: Due to the spontaneous variability of frequency and complexity of ventricular arrhythmias, parametric models were developed with the aid of which normal ranges for spontaneous variability of singular ventricular premature complexes (VPC), couplets and salvos can be calculated. We designed a model which enables rapid visual analysis of the results: spontaneous variability = log (EE Day 2 + 0.01/EE Day 1 + 0.01) where EE is the number of ectopic events. For both days, the mean values per hour are applied. The use of parametric models prerequisites normal distribution of the data which can be achieved with logarithmic transformation. A constant is added to all mean values to preclude the mathematically-inadmissible form of log 0. The magnitude of the constant results in some degree of underestimation of the spontaneous variability. We chose the smallest constant, c = 0.01, consistent with a normal distribution of data. Figure 1 shows the normal range of the variability quotients for VPC in patients with cardiac disease and complex ventricular arrhythmias. The contiguous regions above and below the normal range designate active areas indicative of reduction or aggravation. Determinants of spontaneous variability: Frequency of arrhythmias: The number of VPC per unit of time exerts considerable influence on the spontaneous variability. The more infrequent an arrhythmia, the greater is the fluctuation to be anticipated. The differences in the variability of VPC, couplets and salvos are almost exclusively due to their differing frequencies since, in the presence of comparable frequency, they cannot be distinguished statistically from each other (Figure 2). Type and extent of underlying cardiac disease: In our patient population, there were no differences in spontaneous variability of arrhythmias between patients with coronary artery disease and those with dilated cardiomyopathy (Figure 3). Although in patients with coronary artery disease, as compared to those with noncoronary disease, a higher degree of spontaneous variability has been reported for VPC but, due to the inhomogeneity of the latter group, valid comparison is encumbered. The ejection fraction, the left ventricular filling pressure and the end-diastolic volume do not exert meaningful influence on the spontaneous variability (Figures 4 to 6).(ABSTRACT TRUNCATED AT 400 WORDS)

Anti-Arrhythmia Agents↗
PubMed1998

[Cardiac arrhythmias in sleep apnea. Increased cardiovascular risk caused by nocturnal arrhythmia?].

In sleep-disordered breathing (SDB), the greatest clinical relevance attaches to obstructive sleep apnea on account of its high prevalence and its concomitance with diseases of the cardiovascular system. The high mortality rate of untreated patients is believed to be due to the consequences of these latter diseases. Thus, for example, in addition to systemic arterial hypertension, elevated rates of such disorders as pulmonary hypertension, right heart insufficiency, coronary heart disease, myocardial infarction and stroke are also found. Up until quite recently bradycardic and tachycardic arrhythmias occurring during sleep have been held responsible of the increased mortality rate of these patients. Till the mid-eighties the prevalence of bradycardic arrhythmias was reported to be more than 30%. However, the importance of cardiac arrhythmias has been overestimated, as is supported in particular by current studies on large non-selected samples showing a much lower prevalence of apnea-related arrhythmias. In the differential diagnosis, however, consideration must be given to SDB in patients with nocturnal arrhythmias and heart rate variations.

Adult↗
PubMed1987

Effects of nicainoprol on reperfusion arrhythmia in the isolated working rat heart and on ischemia and reperfusion arrhythmia and myocardial infarct size in the anesthetized rat.

The effect of the novel antiarrhythmic agent nicainoprol on coronary occlusion and reperfusion arrhythmia was investigated in isolated working rat hearts and in anesthetized rats. In isolated working rat hearts nicainoprol (10(-6) M, 5 X 10(-6) M and 10(-5) M) induced concentration-related protection against reperfusion arrhythmia without changing the cardiodynamics, with the exception of a decrease in heart rate at the highest concentration. Enzyme levels (lactate dehydrogenase and creatine kinase) in the coronary venous effluent, and cardiac tissue concentrations of glycogen, lactate, ATP and creatine phosphate were not affected by nicainoprol. Given to anesthetized rats, nicainoprol (5 and 10 mg/kg i.v.) reduced dose dependently in the early post occlusion (0-30 min) period, the percentage of animals with premature ventricular complexes (PVCs) and ventricular tachycardia while completely preventing the occurrence of ventricular fibrillation. In the reperfusion period no animal treated with 5 mg/kg and 12% of the rats treated with 10 mg/kg showed PVCs (the only form of arrhythmia observed in this period) versus 60% of the control rats. Both doses of nicainoprol induced a decrease in heart rate, blood pressure and myocardial oxygen consumption. The ratio of infarct mass to ventricular mass was significantly reduced by 20% at a dose of 5 mg/kg and by 28% at the dose of 10 mg/kg. Nicainoprol could be useful in the prevention and treatment of arrhythmias associated with acute myocardial infarction.

Anesthesia↗
PubMed1997

Antiarrhythmic effects of increasing the daily intake of magnesium and potassium in patients with frequent ventricular arrhythmias. Magnesium in Cardiac Arrhythmias (MAGICA) Investigators.

OBJECTIVES: This study sought to assess potential antiarrhythmic effects of an increase in the daily oral intake of magnesium and potassium in patients with frequent ventricular arrhythmias. BACKGROUND: Magnesium and potassium contribute essentially to the electrical stability of the heart. Despite experimental and clinical evidence for the antiarrhythmic properties of the two minerals, controlled data in patients with stable ventricular arrhythmias are lacking. METHODS: In a randomized, double-blind study, 232 patients with frequent ventricular arrhythmias (> 720 ventricular premature beats [VPBs]/24 h) confirmed at baseline and after 1 week of placebo therapy were subsequently treated over 3 weeks with either 6 mmol of magnesium/12 mmol of potassium-DL-hydrogenaspartate daily or placebo. RESULTS: Compared with placebo pretreatment, active therapy resulted in a median reduction of VPBs by -17.4% (p = 0.001); the suppression rate was 2.4 times greater than that in patients randomized to 3 weeks of placebo therapy (-7.4%, p = 0.038). The likelihood of a > or = 60% (predefined criterion) or > or = 70% suppression rate (calculated from the placebo-controlled run-in period) was 1.7 (25% vs. 15%, p = 0.044) and 1.5 times greater in the active than in the placebo group (20% vs. 13%, p = 0.085), respectively. No effect of magnesium and potassium administration was observed on the incidence of repetitive and supraventricular arrhythmias and clinical symptoms of the patients. CONCLUSIONS: To our knowledge, this study is the first to provide controlled data on the antiarrhythmic effect of oral administration of magnesium and potassium salts when directed to patients with frequent and stable ventricular tachyarrhythmias. A 50% increase in the recommended minimum daily dietary intake of the two minerals for 3 weeks results in a moderate but significant antiarrhythmic effect. However, with the given therapeutic regimen, repetitive tachyarrhythmias and patient symptoms remain unchanged.

Adult↗
PubMed1999

Antiarrhythmic effect of magnesium sulfate against occlusion-induced arrhythmias and reperfusion-induced arrhythmias in anesthetized rats.

The antiarrhythmic effect of magnesium sulfate (Mg) as well as the hemodynamics were studied using the coronary ligation and reperfusion models in rats. In the study on coronary ligation arrhythmia, i.v. administration of Mg (0.6, 2, 6, 20 and 60 micromol) was conducted at 5 min after coronary ligation. Mg had an action to decrease the total number of premature ventricular contraction (PVC), the duration of ventricular tachycardia (VT), the frequency of VT and ventricular fibrillation (Vf) and the mortality ratio for 30 min after coronary ligation. In the 6-60 micromol groups, significant antiarrhythmic action (p < 0.01 vs. control) was attained. In the study on reperfusion arrhythmia, i.v. administration of Mg (20, 60 and 200 micromol) was conducted at 4 min after coronary ligation, and at 1 min after ligation, the coronary artery was reperfused. Mg had an action to decrease the frequency of Vf, the mortality ratio and the duration of VT and Vf and to extend the interval between the initiation of reperfusion and the occurrence of VT and Vf for 10 min after reperfusion. In the 200 micromol group, significant antiarrhythmic action (p < 0.05 vs. control) was attained. Administration of Mg decreased the heart rate and blood pressure. We concluded that Mg can control myocardial ischemia-induced and reperfusion-induced arrhythmia and that sudden cardiac death which occurs as a result of arrhythmia can be prevented.

Anesthesia↗
PubMed1992

[The pro-arrhythmia effects of anti-arrhythmia agents--theoretical and clinical aspects].

Proarrhythmic action of an antiarrhythmic drug is defined as 1) Worsening of preexisting arrhythmia (for example, increase of number of premature beats; frequency, rate, and duration of tachycardias at supraventricular or ventricular level); 2) induction of arrhythmias (supraventricular: for example, atrial tachycardia with block; ventricular: monomorphic or polymorphic ventricular tachycardia, torsade de pointes, ventricular fibrillation); 3) occurrence of bradycardia (sick sinus syndrome; atrioventricular and intraventricular conduction disturbances). The pathophysiology of proarrhythmic action is either facilitation of conduction block and reentry, or abnormal impulse formation. Induction of incessant monomorphic ventricular tachycardia or torsade de pointes is of special clinical relevance. Incessant ventricular tachycardia can be experimentally explained by an increase of functional conduction block and decrease of the wavelength of excitation (conduction velocity x refractory period) as actions favoring reentry; this is clinically most frequently seen with the application of class IC (and A)-drugs. Abnormal QT prolongation and torsade de pointes are most likely due to early afterdepolarizations of the cell membrane, and development of triggered activity; these arrhythmias are seen following the application of substances prolonging repolarization (class III and class IA-antiarrhythmic drugs). Independent of the precise electrophysiologic mechanism, arrhythmias may, under clinical conditions, also be provoked secondary to the negative inotropic action of these drugs. Proarrhythmic actions most frequently are concentration-dependent; rarely are they idiosyncratic. Usually, these side-effects are seen during the first days after initiation or increase of the antiarrhythmic drug dose; they may, however, manifest themselves only after a couple of months.(ABSTRACT TRUNCATED AT 250 WORDS)

Anti-Arrhythmia Agents↗