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PubMed1987

[Cardiac arrhythmias in active elderly persons--age dependence of heart rate and arrhythmias].

Arrhythmias and heart rate of 82 active elderly persons (mean age 79.5 yrs) were registered by 24-hour electrocardiographic recording and compared with the results of 100 asymptomatic subjects (age 34.8 yrs). In each decade 10 men and 10 women were included. Maximal heart rate was lower in old age but over 100 bpm. Minimal and nocturnal heart rates showed a steady rise with increasing age. The mean 24-hour heart rate was higher in middle-aged females than in males, whereas in the elderly no sex-related difference was observed. Sinus arrhythmia, wandering pacemaker, short lengthening of RR-intervals prevailed in younger persons. Short sinus-tachycardias in the late night were equally frequent in both groups. The frequency of supraventricular premature beats did not differ between the two groups (85.4 vs. 76%). However, high intraindividual numbers and more complex forms were more frequent in the elderly. Paroxysmal atrial fibrillation was never registered. Permanent atrial fibrillation occurred in 41% of the subjects being between 90 and 102 years of age. Ventricular arrhythmias were age-related: 87.2% of the elderly vs. 50% of the middle-age subjects had ventricular premature beats, predominantly frequent and complex forms. A significant age relation to bradycardias could not be observed: Sinus pauses over 2000 ms (11 vs. 17%), first and second degree AV-block (22 vs. 21%) occurred equally frequent in both groups. An intermittent short third degree AV-block was observed in a man 84 years old who was asymptomatic. Right bundle branch block was present only in the elderly (6.1%). No arrhythmia-related increase of mortality was observed during a seven-year follow-up.

Aged↗
PubMed1981

[Experimental arrhythmia models. Critical study of correlations with arrhythmias observed in clinical practice].

A number of different in vitro or in vivo experimental tests or models are now available for the demonstration of antiarrhythmic properties. In vitro electrophysiological studies on cells or healthy tissues usually establish the properties of antiarrhythmic agents, rather than their actual antiarrhythmic properties. New information has recently been provided by studies on abnormal tissues or tissues which have been made abnormal experimentally. The methods used to cause this dysfunction are discussed to determine their possible clinical relevance. There are over 50 in vivo arrhythmia models but only 2 or 3 are in common usage: aconitine or digitalis intoxication and experimental myocardial infarction (Harris' method and variants). The study of thresholds to ventricular fibrillation is more a study of an electrophysiological parameter than a study of an arrhythmia. Statistical studies require the uniformity of an experimental model and its stability (or relative stability) over a sufficiently long period from one animal or preparation to another. These conditions widen the gap between some experimental models and clinical reality. Present experimental models are essentially models of acute arrhythmias as experimental animals with chronic degenerative heart disease are not usually available (the problem of cardiomyopathic hamsters and Japanese woodcocks is discussed). The failure to appreciate the differences between species, the direct action of the drug under study (particularly on the autonomic nervous system), the hemodynamic changes induced by the experimental conditions, and the pharmacokinetics of the drug, often make extrapolations to clinical practice very difficult. Although the recent advances in our understanding of the mechanisms of arrhythmias derived from these models have not lead to any significant changes in the clinicians' attitude to the choice of antiarrhythmic therapy or to the introduction of new criteria of antiarrhythmic efficacity, none of the active antiarrhythmic agents used in clinical practice have been submitted to these antiarrhythmic screening tests. These models even provide an "honourable" classification of the relative efficacity of antiarrhythmic drugs.

Animals↗
PubMed1991

Ischemia-reperfusion arrhythmias and lipids: effect of human high- and low-density lipoproteins on reperfusion arrhythmias.

The effect of high- and low-density lipoproteins separated from human serum on the postischemic reperfusion arrhythmias was investigated. The hearts were perfused by working heart mode with Krebs Henseleit bicarbonate buffer containing arachidonic acid (1 microgram/ml) for 5 minutes. Whole heart ischemia was induced by the use of a one-way ball valve, and hearts were perfused for 15 minutes followed by 20 minutes of reperfusion. Physiologic concentrations of high- and low-density lipoproteins were constantly infused through the atrial route during ischemic perfusion. Coronary effluent was collected via pulmonary artery cannulation for subsequent radioimmunoassay of thromboxane B2 and 6-keto-prostaglandin F1 alpha, the major stable metabolites of thromboxane A2 and prostacyclin, respectively. The incidence of ventricular arrhythmias during reperfusion was 6/6 (100%), 1/6 (17%), and 6/6 (100%) in control, high-density lipoprotein and low-density lipoprotein infusion groups, respectively. There was no significant difference in coronary flow among the three groups throughout the perfusion. Both thromboxane B2 and 6-keto-prostaglandin F1 alpha increased significantly during ischemia compared with preischemic values in all groups of hearts. However, the ratio of these two parameters varied in control and low-density lipoprotein infusion groups during ischemia, while there was no significant change in the high-density lipoprotein infusion group. These results provide the possibility that arachidonate metabolites may be involved in the regulation of ischemia-reperfusion arrhythmias and that high-density lipoprotein that was infused during ischemia markedly inhibits the incidence of ischemia-reperfusion-induced ventricular arrhythmias, due in part at least, to stabilizing the arachidonate metabolites during ischemic perfusion.

Animals↗
PubMed1988

Recruitment and baseline description of patients in the Cardiac Arrhythmia Pilot Study. The Cardiac Arrhythmia Pilot Study (CAPS) investigators.

The Cardiac Arrhythmia Pilot Study tested the feasibility of performing a large-scale study to evaluate the effect of therapy of ventricular arrhythmias after acute myocardial infarction (AMI). Ten clinical sites identified patients with greater than or equal to 10 ventricular premature complexes (VPCs)/hour, recorded 6 to 60 days after AMI in patients with an ejection fraction greater than 0.20. Patients were randomized to receive 1 of 5 agents: encainide, flecainide, imipramine, moricizine or placebo. Successful therapy was defined as greater than or equal to 70% suppression of VPCs and greater than 90% suppression of runs of ventricular tachycardia. Randomization to a second agent occurred if a patient did not achieve adequate suppression with the initial agent. Patients initially randomized to placebo continued to receive placebo. Patients were evaluated at 3-month intervals for the next year. Of 30,763 patients screened, 10,734 (35%) were younger than 70 years old and had a qualifying AMI. A Holter recording was obtained in 3,957 patients, of whom 871 (22%) had qualifying arrhythmias and 687 were eligible. Of the 687 eligible patients, 502 (73%) were randomized. Mean age of enrolled patients was 59 years. One-half of patients were randomized within 1 month after AMI. Mean ejection fraction was 0.45, with 175 (35%) patients having an ejection fraction less than 0.40. On baseline drug-free recording, 173 (35%) patients had less than 30 VPCs/hour; 149 (30%) between 30 and 100/hour and 180 (36%) greater than or equal to 100/hour. At least 1 run of ventricular tachycardia was seen in 172 (34%) patients. Drugs taken at baseline were similar in all groups with 116 (23%) patients taking digitalis, 161 (32%) taking diuretics, 203 (41%) taking beta blockers and 200 (40%) taking calcium antagonists. Slightly more patients, 53 (51%), randomized to flecainide were taking calcium antagonists. No significant relation was noted between baseline VPC frequency and ejection fraction, but baseline VPC frequency was correlated with heart rate, arrhythmia noted before AMI and right bundle branch block. As expected, a high ejection fraction correlated with lower peak creatine kinase values, an inferior location of the infarct and fewer signs of congestive heart failure. At baseline, at least 1 adverse symptom was volunteered by 192 (39%) patients. The most common symptoms were unusual tiredness or fatigue, heart beating fast or skipping beats or headache. In this study, over 20 age- and AMI-eligible patients were identified to obtain each randomized patient. The randomization process successfully distributed baseline variables across drug groups.

Anilides↗
PubMed1990

Effect of acute hemodynamic decompensation on electrical inducibility of ventricular arrhythmias in patients with dilated cardiomyopathy and complex nonsustained ventricular arrhythmias.

In patients with dilated cardiomyopathy, hemodynamic decompensation has been postulated to increase vulnerability to reentrant ventricular arrhythmias. To test this hypothesis, we performed programmed ventricular stimulation with three extrastimuli on nine patients with dilated cardiomyopathy and asymptomatic complex ventricular arrhythmias during a period of acute hemodynamic decompensation; programmed ventricular stimulation was then repeated following hemodynamic improvement with nitroprusside. These patients did not have a history of documented or suspected sustained ventricular tachycardia or fibrillation. The mean left ventricular ejection fraction was 0.21 +/- 0.04 (range 0.15 to 0.26). In the baseline state, mean right atrial pressure was 8 +/- 4 mm Hg, pulmonary artery wedge pressure was 20 +/- 3 mm Hg, and cardiac index was 3.2 +/- 0.5 L/min/m2. Following acute hemodynamic decompensation, mean right atrial pressure increased to 16 +/- 5 mm Hg and pulmonary artery wedge pressure to 33 +/- 8 mm Hg; cardiac index decreased to 2.1 +/- 0.5 L/min/m2. In this decompensated state, programmed ventricular stimulation failed to induce sustained or nonsustained ventricular arrhythmias in any patient. Following nitroprusside administration (mean dose 1.5 +/- 1.1 micrograms/kg/min), there were significant decreases in mean right atrial pressure (11 +/- 3 mm Hg) and pulmonary artery wedge pressure (16 +/- 3 mm Hg), and a significant increase in cardiac index (3.1 +/- 1.1 L/min/m2) (p less than 0.05 for all values versus the decompensated state). In the improved hemodynamic state, programmed ventricular stimulation induced nonsustained ventricular tachycardia (six beats) in only one patient, and sustained arrhythmias in none.(ABSTRACT TRUNCATED AT 250 WORDS)

Arrhythmias, Cardiac↗
PubMed1987

Determinants of ventricular arrhythmias in mildly symptomatic patients with coronary artery disease and influence of inducible left ventricular dysfunction on arrhythmia frequency.

To determine the relation among ventricular arrhythmias, prognostic factors and reversible ischemia in coronary artery disease, 131 drug-free, minimally symptomatic patients were studied by radionuclide angiography and 24 hour Holter electrocardiographic monitoring. High grade ventricular arrhythmias (couplets, salvos of premature ventricular complexes and R on T phenomenon) were observed in 33 patients (25%) and were related to lower rest and exercise ejection fraction, greater number of stenotic coronary arteries and higher prevalence of regional wall motion abnormalities at rest (all p less than or equal to 0.1). Among patients with subnormal rest ejection fraction, high grade arrhythmias occurred with greater prevalence in those with reversible left ventricular dysfunction (reduction in ejection fraction) during exercise compared with those with a normal ejection fraction response (59 versus 23%, p less than 0.05), a relation observed principally in patients with multivessel disease. These data indicate that in minimally symptomatic patients with coronary artery disease, arrhythmias are related to both extent of disease and severity of regional and global ventricular dysfunction and are most prevalent in patients with ventricular dysfunction and evidence of inducible ischemia, factors indicating poor long-term prognosis during medical therapy.

Adult↗
PubMed2002

KB-R7943, a Na+/Ca2+ exchange inhibitor, does not suppress ischemia/reperfusion arrhythmias nor digitalis arrhythmias in dogs.

KB-R7943 (2-[2-[4-(4-nitrobenzyloxy)phenyl]ethyl]isothiourea methanesulfonate) has been used as a pharmacological tool to block the Ca(2+) influx-mode of the Na(+)/Ca(2+) exchanger, which is thought to contribute to ischemia/reperfusion and digitalis arrhythmias. We examined effects of KB-R7943 on ischemia/reperfusion arrhythmias in beagle dogs anesthetized with sodium pentobarbital. Lead II ECG and BP were measured. KB-R7943 or the solvent (10% DMSO) was injected i.v. as a bolus, and 5 min later, the left anterior descending coronary artery was occluded for 30 min followed by reperfusion. KB-R7943 at 5 or 10 mg/kg increased BP without changing ECG parameters including the heart rate. Although 5 mg/kg KB-R7943 deceased the number of arrhythmic beats during the ischemic period, mortality due to ischemia/reperfusion was not decreased by KB-R7943 (5 and 10 mg/kg). KB-R7943 at 5 mg/kg also did not suppress the ouabain-induced arrhythmias. These negative results suggest that Na(+)/Ca(2+) exchange inhibition may not be a useful strategy of suppressing arrhythmias.

Animals↗
PubMed1993

[Clinical analysis of cardiac arrhythmias in patients with chronic renal failure treated conservatively. I. Evaluation of cardiac arrhythmias].

On in-patient basis 24-hr electrocardiographic Holter monitoring was performed in 20 patients with chronic renal failure (c.r.f.) on conservative treatment (10 women and 10 men, aged 43.6 +/- 9.8 years), in 10 patients with chronic primary glomerulonephritis without arterial hypertension and renal failure (2 women and 8 men, aged 34.2 +/- 10.5 years), and in 10 patients with primary arterial hypertension without clinical symptoms of renal disease (1 woman and 9 men, aged 36.6 +/- 9.5 years). No atrio-ventricular conduction disturbances were found in patients with c.r.f. Supraventricular and ventricular arrhythmias occurred in 90% of the patients. Ventricular arrhythmias were observed in 8% of c.r.f. patients. Among them simple ventricular extrasystoles (Lown 0-3) predominated and they were found in 65% of the patient. Numbers of ventricular extrasystoles were small and amounted to 44.7 per 24 hrs. Cardiac arrhythmias registered in both comparative groups were not different from those found in c.r.f. patients. The results suggest that chronic renal failure in patients on conservative treatment does not peculiarly predispose to the occurrence of cardiac arrhythmias.

Adult↗
PubMed1995

[Radiofrequency ablation of heart arrhythmias. Results in the first 150 patients treated at the Arrhythmia center in Oslo].

The authors review the first 150 patients with cardiac arrhythmias who were treated with radio-frequency ablation at a Norwegian arrhythmia centre. The clinical success rate (either electrophysiological cure or a dramatic reduction in the severity and frequency of the attacks) was 97%. 11 patients were treated for two or more arrhythmias. In 27 patients two, occasionally three, sessions were required to obtain a satisfactory clinical result. Repeat ablation is scheduled for three cases where the treatment was unsuccessful. Among 190 ablations, 13 complications occurred, none of which resulted in permanent sequelae. The time spent on each procedure, and particularly the long time spent on fluoroscopy during the earlier procedures, demonstrates the existence of a learning curve for ablation. This lends support to the authorities' restriction of treatment of arrhythmias by ablation to only two laboratories in a population of four million.

Adolescent↗
PubMed2006

Recommendations for participation in leisure-time physical activity and competitive sports in patients with arrhythmias and potentially arrhythmogenic conditions Part I: Supraventricular arrhythmias and pacemakers.

This document by the Study Group on Sports Cardiology of the European Society of Cardiology extends on previous recommendations for sports participation for competitive athletes by also incorporating guidelines for those who want to perform recreational physical activity. For different supraventricular arrhythmias and arrhythmogenic conditions, a description of the relationship between the condition and physical activity is given, stressing how arrhythmias can be influenced by exertion or can be a reflection of the (patho)physiological cardiac adaptation to sports participation itself. The following topics are covered in this text: sinus bradycardia; atrioventricular nodal conduction disturbances; pacemakers; atrial premature beats; paroxysmal supraventricular tachycardia without pre-excitation; pre-excitation, asymptomatic or with associated arrhythmias (i.e. Wolff-Parkinson-White syndrome); atrial fibrillation; and atrial flutter. A related document discusses ventricular arrhythmias, channelopathies and implantable cardioverter defibrillators.

Cardiac Pacing, Artificial↗
PubMed2002

[Therapy of cardiac arrhythmias. Clinical significance of potassium- and magnesium aspartate in arrhythmias].

UNLABELLED: Potassium and magnesium deficiencies usually coexist and represent a risk factor for cardiac arrhythmias. Serum levels--in particular of magnesium--are inconclusive for establishing a possible electrolyte deficiency. Basic treatment of arrhythmia should therefore include the administration of potassium and magnesium, since the benefit is great, and the possible side effects is negligible. A placebo-controlled study involving patients with cardiac arrhythmias revealed that appreciably fewer ventricular asystoles occurred after three weeks of treatment with potassium and magnesium aspartate, even when serum levels were within the normal range prior to initiating treatment. Patients older than 50, and those with previous coronary heart disease and/or myocardial infarction derived particular benefit from this form of treatment. CONCLUSION: These results underscore the key role played by potassium and magnesium in the treatment of cardiac arrhythmias.

Adult↗
PubMed1998

Safety of oral propafenone in the treatment of arrhythmias in infants and children (European retrospective multicenter study). Working Group on Pediatric Arrhythmias and Electrophysiology of the Association of European Pediatric Cardiologists.

This study was designed to assess adverse effects of oral propafenone in a large number of pediatric patients. Retrospective data from 27 European centers covering 772 patients treated with oral propafenone were analyzed. The following arrhythmias were treated: reentrant supraventricular tachycardia in 388 patients, atrial ectopic tachycardia in 66, junctional ectopic tachycardia in 39, atrial flutter in 21, ventricular premature complexes in 140, ventricular tachycardia in 78, and other arrhythmias in 39 patients. Two hundred forty-nine patients (32.3%) had structural heart disease. Significant electrophysiologic side effects and proarrhythmia were found in 15 of 772 patients (1.9%): sinus node dysfunction in 4, complete atrioventricular block in 2, aggravation of supraventricular tachycardia in 2, acceleration of ventricular rate during atrial flutter in 1, ventricular proarrhythmia in 5, and unexplained syncope in 1 patient. Cardiac arrest or sudden death occurred in 5 of 772 patients (0.6%): 2 patients had supraventricular tachycardia due to the Wolff-Parkinson-White syndrome and a normal heart; the remaining 3 patients had structural heart disease. Overall, adverse cardiac events were more common in the presence (12 of 249 patients, 4.8%) than in the absence (8 of 523 patients, 1.5%) of structural heart disease (p <0.01). There was no difference between patients treated for supraventricular and ventricular arrhythmias. Thus, propafenone is a relatively safe drug for the treatment of several pediatric tachyarrhythmias. Proarrhythmic effects seem to be less frequent than those reported for encainide or flecainide and occur predominantly in patients with structural heart disease.

Administration, Oral↗
PubMed1995

Fetal arrhythmias, pediatric arrhythmias, and pediatric electrophysiology.

The practice of pediatric electrophysiology has been altered drastically and irrevocably over the past 5 years. With the advent of widespread application of transcatheter radiofrequency ablative techniques in young patients, decision-making in the management of childhood arrhythmias has focused less on palliative medical therapies and more on the potential for curative, nonsurgical interventions. This review examines the published contributions in the area of pediatric catheter ablation, antiarrhythmic drug therapy, postoperative arrhythmias, fetal arrhythmias, and electrocardiographic phenomena after cardiac transplantation.

Adolescent↗
PubMedDate not supplied

[The anti-arrhythmia activity of amino acid-containing trimecaine derivatives on models of early occlusive and reperfusion arrhythmias in cats].

Experiments were conducted on models of early occlusion and reperfusion arrhythmias in cats to study the antiarrhythmic activity of trimecain, its morpholine analogue (MPT), and MPT derivatives containing glycine, magnesium salt of aspartic acid, and N-acetylglutaminic acid. All the compounds were injected in doses of 5% of LD50. A 22.5 mg/kg dose of trimecain prevented cardiac rhythm disorders after occlusion of the coronary arteries as well as after restoration of the coronary blood flow. Replacement of the diethyl group in the structure of trimecain by the morpholine ring led to diminution of antiarrhythmic activity, and MPT in a dose of 28.0 mg/kg, in distinction from the former, had no effect on the frequency of the occurrence of early occlusion arrhythmias and the duration of reperfusion arrhythmias. Introduction of amino acids as an anion into the MPT structure raised the antiarrhythmic activity of the last named.

Amino Acids↗
PubMedDate not supplied

[The anti-arrhythmia and pro-arrhythmia properties of sigma-receptor ligands].

It has been found that the sigma 1- and sigma 3-receptor antagonists, DuP 734 intraperitoneally and XJ 448 intravenously, had antiarrhythmic effects against epinephrine-induced arrhythmias in rats. The ED50 for antiarrhythmic effect of DuP 734 was 0.157 mg/kg after intraperitoneal administration. Other sigma-receptor antagonists (rimcazole, BMY 14802, haloperidol) did not affect the incidence of epinephrine-induced arrhythmias. sigma 1-Receptor agonists (DTG, N-allyl-normetazocine, (+)-3-PPP, (-)-3-PPP) had proarrhythmic effect after systemic administration. The sigma-agonist N-allyl-normetazocine and sigma-antagonist XJ 488 had no effect on the incidence of epinephrine-induced arrhythmias after intracerebroventricular administration. Therefore, it appears that the central nervous system does not play a significant role in the antiarrhythmic or proarrhythmic effects of sigma ligands. We hypothesize that these effects of sigma ligands might be dependent on their action on cardiac sigma receptors.

Animals↗
PubMedDate not supplied

[The effect of anti-arrhythmia agents on ventricular arrhythmias arising as a consequence of disorders in the myocardial blood supply].

The protective and therapeutic effects of some antiarrhythmic drugs of classes I-IV were studied in the experiments on 103 cats and 75 dogs. The antiarrhythmic drugs of classes 1a (N-propylaimaline bromide, aimaline, ethacizine), 1b (trimecaine) and IV (finoptine) were shown to prevent with various effectiveness the occurrence of early occlusion and reperfusion ventricular arrhythmias. The antiarrhythmic drugs of classes II (anapriline) and III (cordaron) proved to be ineffective in these cases. Ventricular arrhythmia in dogs occurring at the late stage of experimental infarction is reliably relieved in all cases with the antiarrhythmic drugs of class 1a, in most cases--those of classes 1b and III. The antiarrhythmic drugs of classes II and III are ineffective on this model. The experimental results analysed with regard to modern concepts of the genesis of modelled arrhythmias may be used as the experimental basis for a rational choice of antiarrhythmic drugs.

Animals↗
PubMed1991

Avoiding interpretive pitfalls when assessing arrhythmia suppression after myocardial infarction: insights from the long-term observations of the placebo-treated patients in the Cardiac Arrhythmia Pilot Study (CAPS)

The Cardiac Arrhythmia Pilot Study (CAPS) was a 1 year trial that analyzed the safety and effectiveness of arrhythmia suppression in 502 patients surviving acute myocardial infarction who had greater than or equal to 10 ventricular premature depolarizations/h or greater than or equal to 5 runs of ventricular tachycardia on a Holter recording obtained 6 to 60 days after the acute infarction. Because 100 of these patients received placebo in a double-blind fashion for 1 year, a comprehensive objective analysis was performed of spontaneous arrhythmia changes based on real data rather than statistical estimates. In the CAPS placebo group, 19% developed some serious clinical event in 1 year (death, heart failure, proarrhythmia) that could likely be attributable to antiarrhythmic drug toxicity. A significant reduction in the frequency of ventricular premature depolarizations (p = 0.004) occurred in the first few weeks of "therapy" with a further significant (p less than 0.04) decrease between 3 to 12 months. After initiation of placebo antiarrhythmic therapy, 27% had "apparent ventricular premature depolarization suppression" (greater than or equal to 70% reduction) after one Holter recording evaluation and nearly half (48%) after six Holter recordings to assess suppression were performed.(ABSTRACT TRUNCATED AT 250 WORDS)

Anti-Arrhythmia Agents↗
PubMed2001

Is arrhythmia detection by automatic external defibrillator accurate for children?: sensitivity and specificity of an automatic external defibrillator algorithm in 696 pediatric arrhythmias.

BACKGROUND: Use of automatic external defibrillators (AEDs) in children aged <8 years is not recommended. The purpose of this study was to develop an ECG database of shockable and nonshockable rhythms from a broad age range of pediatric patients and to test the accuracy of the Agilent Heartstream FR2 Patient Analysis System for sensitivity and specificity. METHODS AND RESULTS: Children aged </=12 years who either developed arrhythmias or were at risk for developing arrhythmias were studied. Two sources were used for the database: children whose rhythms were recorded prospectively via a modified AED and children who had arrhythmias captured on paper and digitized for subsequent analysis. The rhythms were divided into 5-second strips, classified by 3 reviewers, and then assessed by the AED analysis algorithm. A total of 696 five-second rhythm strips from 191 children (81 female and 110 male) aged 1 day to 12 years (median 3.0 years) were analyzed. There was 100% specificity for nonshockable rhythms. Sensitivity for ventricular fibrillation was 96%. CONCLUSIONS: There was excellent AED rhythm analysis sensitivity and specificity in all age groups for ventricular fibrillation and nonshockable rhythms. The high specificity and sensitivity indicate that there is a very low risk of an inappropriate shock and that the AED correctly identifies shockable rhythms, making the algorithm both safe and effective for children.

Adult↗