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At least 19 recordsLinked to original sources
PubMed1991

Relation between acute ventricular arrhythmias, ventricular late potentials and mortality in acute myocardial infarction.

The relation between ventricular late potentials and the occurrence of acute (in-hospital) and hyperacute (before hospital admission) ventricular tachycardia or fibrillation was studied in 281 consecutive patients with uninterrupted acute myocardial infarction. The prevalence of late potentials was significantly higher in patients with than without ventricular tachycardia/fibrillation (65 vs 22%; p less than 0.01). These relations persisted among patients with left bundle branch block, although a different definition was used for identifying late potentials in these patients. Multivariate analysis showed that presence of late potentials and peak creatine kinase enzyme level were the only 2 independent variables associated with early ventricular tachycardia/fibrillation. Total in-hospital mortality, as well as in-hospital cardiac mortality, was significantly higher among patients with than without acute ventricular tachycardia/fibrillation. However, at 1 year, mortality rates did not differ between the 2 groups. The following conclusions were drawn from this study: (1) Late potentials are closely related to ventricular tachycardia/fibrillation in hyperacute and acute phases of infarction. (2) Presence of left bundle branch block does not mitigate against the finding of late potentials in these patients. (3) Early ventricular tachycardia/fibrillation in acute infarction is related to large infarctions and to a high in-hospital mortality rate.

Aged↗
PubMed1987

Current approaches to drug treatment of ventricular arrhythmias.

Ventricular arrhythmias are common and cause serious problems, ranging from symptom aggravation to sudden cardiac death. New knowledge about arrhythmias and new antiarrhythmic drugs provide greater opportunities for treatment choice and evaluations. A prognostic classification of ventricular arrhythmias helps to focus management. For benign ventricular arrhythmias, the objective of drug treatment is alleviation. The best management approach to potentially malignant ventricular arrhythmias, however, is not yet known, and data from ongoing clinical studies continue to accrue, developing the knowledge base needed to devise better regimens. Symptomatic patients can be managed either by symptom alleviation, as in benign arrhythmia, or more aggressively, as in malignant ventricular arrhythmia. Treatment is not mandatory for asymptomatic patients with potentially malignant ventricular arrhythmias, because there is no evidence that reducing arrhythmia prolongs life or effectively prevents symptomatic disease. Also, antiarrhythmic drugs have the potential for causing adverse effects, even lethal ones. For malignant ventricular arrhythmia, the objective of treatment is prevention of symptomatic ventricular arrhythmia and sudden cardiac death. Effective new methods predictive of successful drug treatment in individual patients are available; these methods remove much of the empiricism from management of patients with malignant ventricular arrhythmia. Treatment deemed effective by rigorous noninvasive evaluation or by electrophysiologic studies has a high probability of success in the long term. Drug management of malignant ventricular arrhythmia should become more effective in the future as a result of newly developing approaches to drug evaluation.

Anti-Arrhythmia Agents↗
PubMed1985

Local abnormalities of right ventricular depolarization after repair of tetralogy of Fallot: a basis for ventricular arrhythmia.

Ventricular arrhythmia is common after repair of tetralogy of Fallot (TF) and may cause sudden death. To explore the mechanisms, ambulatory electrocardiographic monitoring and electrophysiologic studies were undertaken, without the use of provocative tests, in 22 patients 5 to 24 years (mean 13) after repair. His-Purkinje and right ventricular (RV) apical activation times were measured to assess conduction. Endocardial mapping of the right ventricle was performed, with additional recordings from the left ventricle in 10 patients, to detect abnormalities of local depolarization and repolarization. Local RV electrograms were fractionated or delayed in 12 patients (55%) at 1 or more RV sites (septum in 7 patients, outflow in 7, free wall in 2 and apex 1 patient), reflecting disordered depolarization, but left ventricular recordings were normal in all. Ventricular arrhythmia out of hospital was more common (p less than 0.05) and more severe (p less than 0.01) in the patients with depolarization abnormalities than in those with normal electrographic findings. In contrast, there was no association between ventricular arrhythmia and conduction disturbances. Abnormalities of RV repolarization, consisting of low-frequency signals after the T wave, were observed in 17 patients (77%), but were not associated with arrhythmia. Thus, ventricular arrhythmia during daily life was associated with fractionated depolarization at multiple sites in the right ventricle. This suggests that there are widespread areas of RV myocardial damage that provide substrates for ventricular tachycardia.

Adolescent↗
PubMed2000

[Cardiac insufficiency: prevention of ventricular arrhythmias].

Ventricular arrhythmias are particularly common in cardiac failure and their mechanisms are very complex. The prevention of these ventricular arrhythmias is only worthwhile if it results in benefits in terms of reduction of the risk of sudden death and in improvement in life expectancy. However, the relationship between complex ventricular arrhythmias and sudden death is far from established. The first problem is, therefore, to select the patients at high risk of sudden death. Unfortunately, there are no reliable markers of arrhythmic risk; only patients at low risk can be reasonably well identified on clinical and haemodynamic assessment and the results of ambulatory and signal averaged ECG. When an antiarrhythmic treatment seems to be required, the choice is very limited in practice. There is no role for Class I antiarrhythmics to play in this indication. Amiodarone, with its complex electrophysiological profile enabling an interaction with all potential mechanisms of ventricular arrhythmias, is a first-line drug in cardiac failure because of its efficacy and good myocardial tolerance. However, the benefits of amiodarone therapy in terms of reduction of global mortality have not been demonstrated, especially in view of the discordance between the results of the GESICA and CHF STAT trials. On the other hand, the value of betablockers, whether conventional molecules like bisoprolol (CIBIS II study) or metoprolol (MERIT-HF study), or molecules with a special profile such as carvedilol, has been clearly established. In association with conventional diuretics and angiotensin converting enzyme inhibitors, they reduce global mortality by about 35% and sudden death by 40%. However, the future possibly lies with non-pharmacological approaches such as the implantable defibrillator, at least in patients clearly identified as being at high risk of arrhythmic death, resuscitated from cardiorespiratory arrest due to documented ventricular fibrillation or presenting with haemodynamically poorly tolerated ventricular tachycardia. The automatic defibrillator could improve the prognosis of these patients, irrespective of their functional status (NYHA, Classes I, II or III). In practice, "rhythmological" management of cardiac failure cannot be dissociated from the haemodynamic and neuro-hormonal aspects of the affection, and only a multi-factorial approach is being realistic.

Anti-Arrhythmia Agents↗
PubMed1986

Oral antiarrhythmic agents for ventricular arrhythmias.

Ventricular tachyarrhythmia is the most common terminal event causing sudden cardiac death. Risk stratification using 24-hour Holter monitoring to identify ventricular ectopy and noninvasive techniques to detect abnormal left ventricular function is becoming routine. Many cardiologists treat patients with potentially lethal ventricular arrhythmias even though it is unknown as yet whether sudden cardiac death can be prevented. Patients with lethal ventricular arrhythmias are always treated. A number of new oral antiarrhythmic agents have become available to the clinician. The modified Vaughan-Williams classification system categorizes the drugs according to their electrophysiologic and clinical characteristics. The class IC antiarrhythmic agents are emerging as the potential drugs of first choice for patients with benign or potentially lethal ventricular arrhythmias. The betablockers (class II) are used as antiarrhythmic agents, particularly in the presence of active myocardial ischemia or high catecholamine levels and in the postmyocardial infarction patient. Amiodarone (class III) may cause serious side effects and is reserved for patients with lethal ventricular arrhythmias when all other available agents have failed.

Administration, Oral↗
PubMed1994

[Isotopic study of myocardial perfusion and innervation in 28 patients with primary hypertrophic cardiomyopathy: relation to ventricular arrhythmia].

Ventricular arrhythmias are frequent, sometimes complex and severe, in primary hypertrophic cardiomyopathy. They carry a poor prognosis. Some workers have reported that these arrhythmias are more common in patients with abnormal myocardial perfusion. Other groups have underlined the important role of the sympathetic nervous system in the development of ventricular hypertrophy and the genesis of ventricular arrhythmias. Therefore, a population of 28 patients with primary hypertrophic cardiomyopathy (PHCM) were studied by thallium 201 myocardial scintigraphy and sympathetic innervation was assessed using a structural analogue of noradrenaline, meta-iodobenzyl-guanidine (MIBG). Then, perfusion and innervation were correlated with ventricular arrhythmias observed on 24 hours holter monitoring electrocardiogram. Perfusion abnormalities were observed in 60% of patients: stable in mild left ventricular hypertrophy, labile in severe left ventricular hypertrophy. They were not related to the presence of muscular bridges and systolic compression of septal arteries demonstrated by coronary angiography. These perfusion abnormalities were closely correlated to ventricular extrasystoles observed on Holter monitoring. In this series, and compared to controls, the fixation of MIBG as determined by the Heart/Mediastinum (H/M) ratio was significantly decreased (2.27 +/- 0.31 versus 2.57 +/- 0.33 in controls). Uniform myocardial uptake of MIBG with no defect or significant global hypofixation was observed in 32% of PHCM. Regional and occasionally global hypofixation was observed in 68% of patients. In moderate hypertrophy, reduced uptake was not uniform, the lateral wall and apex being the most abnormal. Uptake of MIBG was significantly correlated to septal wall thickness and to left ventricular mass index. These defects were related to abnormal neuronal uptake of MIBG.(ABSTRACT TRUNCATED AT 250 WORDS)

3-Iodobenzylguanidine↗
PubMed1977

Evaluation of children with ventricular arrhythmias.

Ventricular arrhythmias are rare in childhood but may be associated with syncope and sudden death. This report describes 8 children with ventricular arrhythmias, 6 of whom suffered syncopal episodes. Ventricular tachycardia was documented in 5. One boy died suddenly. Complete cardiac investigation was carried out with exercise testing, Holter monitoring, echocardiography, cardiac catheterization, angiography, and electrophysiological studies. The spectrum of abnormalities related to the arrhythmias included prolapsing mitral valve, prolonged QT syndrome, sick sinus syndrome, congenital heart disease, cardiomyopathy, and idiopathic ventricular tachycardia. Exercise testing and Holter monitoring were particularly useful in documenting the arrhythmias and monitoring response to therapy.

Adolescent↗
PubMed1983

[Clinical and prognostic significance of hyperkinetic ventricular arrhythmias].

Ventricular arrhythmias, mainly ventricular premature beats (VPBs) are omnipresent in the general population. They may be detected or induced by means of different techniques such as routine ECG, ambulatory ECG-monitoring, exercise testing and ventricular stimulation during an intracavitary electrophysiologic study. The prevalence and clinical-prognostic significance of VPBs are highly related to the presence and severity of an underlying heart disease. Simple and complex (bigeminal, multiform, repetitive or R on T) VPBs are much more frequent in cardiac patients than in normal subjects. Acute myocardial infarction (AMI), chronic coronary heart disease (CCHD), cardiomyopathies and mitral valve prolapse are the most common clinical conditions in which VPBs occur. In apparently healthy persons, the presence of VPBs does not seem to indicate a greater risk for the future development of cardiac disease. In patients with AMI frequent, and complex VPBs often precede primary ventricular fibrillation and appear to be directly related to the size of the infarct. In the posthospital phase of AMI, as well as in CCHD, the occurrence of high-grade VPBs usually indicates more advanced degrees of both coronary and left ventricular disease as well as the possibility of cardiac and/or sudden death. In cardiomyopathies and mitral valve prolapse the VPBs do not correlate with either clinical, electrocardiographic, echocardiographic or hemodynamic parameters but their complex patterns appear to be a good indicator of patients with high sudden death risk.

Adolescent↗
PubMed1989

Clinical approach to antiarrhythmic therapy in patients with ventricular arrhythmia.

Ventricular arrhythmias can be categorized into three broad groups, namely, benign, malignant, and potentially malignant based on the presence or absence and the severity of underlying heart disease. The benign group does not require treatment, the benefits of treatment in the potentially malignant group are unproven, and the malignant group benefits the most from antiarrhythmic therapy. Because there is no ideal antiarrhythmic drug and all drugs have limitations, selection of an antiarrhythmic drug should be based on the therapeutic goal and the relative efficacies and toxicity profiles of various agents. In the absence of demonstrated beneficial effect from suppression of ventricular arrhythmia in many cardiac patients, antiarrhythmic drug therapy should be confined to patients with serious symptoms, patients with recurrent sustained ventricular tachycardia, and those resuscitated from cardiac arrest.

Anti-Arrhythmia Agents↗
PubMed1995

Autonomic, ischaemic, circadian and rhythmic factors as causes of the spontaneous variability of ventricular arrhythmias.

Ventricular arrhythmias present with strongly varying intensity. This spontaneous variability makes it difficult to use one of the existing arrhythmia grading systems for risk or therapy efficacy studies. We attempted to explain the variability by the changing autonomic, ischaemic, circadian, and rhythmic factors. Four (two learning, two test) 24-h Holter tapes were made within one month in 31 patients with chronic frequent ventricular ectopic beats of miscellaneous aetiology and under constant drug regimen. The data were segmented into 5-min episodes, in which ectopy (dependent variable) was measured, together with heart rate, amount of heart rate variability, fraction low-frequency heart rate variability, ST depression, and clock time (independent variables). Forty-three percent of the fluctuations in arrhythmia incidence could be explained with a multiple regression procedure, and more than 50% of the variance in arrhythmia incidence could be explained in 36% of the cases. Our study demonstrates that much of the spontaneous variability of ventricular arrhythmias can be attributed to the varying conditions. This method of dealing with arrhythmia variability might lead to an alternative to the current arrhythmia grading systems used in risk and drug efficacy studies.

Adult↗
PubMed1979

Fetal and neonatal ventricular arrhythmia.

Ventricular arrhythmia in the perinatal period is observed with greater frequency than reported in the literature. Four cases from the authors' experience and an analysis of the literature are presented. Of the total of 45 cases, nine were detected in utero, three persisted beyond the neonatal period, and two resulted in death with associated disorders. Twenty-four percent of the entire group had serious medical disorders associated with arrhythmia; however, 43% of the group with ventricular tachycardia had major associated disease.

Arrhythmias, Cardiac↗
PubMed1994

Attenuation by dexamethasone of endotoxin protection against ischaemia-induced ventricular arrhythmias.

Ventricular arrhythmias from a 30 min occlusion of the left coronary artery were assessed in Langendorff perfused isolated hearts removed from rats administered either saline, or endotoxin derived from Escherichia coli (2.5 mg kg-1 i.p.) given either 2, 4, 8, 24 or 48 h previously. Arrhythmia severity was markedly reduced in those hearts removed from rats administered endotoxin with a maximum protection at 8h; there was a marked reduction in the incidence of ventricular fibrillation (from 54% to 4%) and in the number of ventricular premature beats during the occlusion period (e.g. from 1165 +/- 144 to 37 +/- 19; P < 0.01). Dexamethasone (3 mg kg-1, given 1 h prior to endotoxin or saline) markedly attenuated the protection afforded by endotoxin.

Animals↗
PubMed1990

[Relation between cardiomyopathy and ventricular arrhythmias].

Ventricular arrhythmias (VA) with its relevant factors were studied in patients with cardiomyopathy and the relation between late potential (LP) and ventricular tachycardia (VT) was also evaluated. It is shown that the prevalence of VA was high in cardiomyopathy. However, its severity was not related to clinical symptoms, cardiac enlargement, cardiac function and level of plasma electrolytes. The relative risk and relative odds of LP positive were 7.33 and 20 times as high in patients with VT as in those without VT, respectively. The sensitivity, specificity, and accuracy of prediction to VT in LP positive patients were 66.2%, 90.9% and 80%, respectively. The patients with sustained VT and positive LP were more susceptible to sudden death. LP was useful to understand the mechanism and prognosis of VT.

Adolescent↗
PubMed1984

The relationships among ventricular arrhythmias, left ventricular dysfunction, and mortality in the 2 years after myocardial infarction.

We examined the relationships among ventricular arrhythmias, left ventricular dysfunction, and mortality after the occurrence of myocardial infarction in 766 patients who enrolled in a nine-hospital study and underwent two special tests. Frequency and repetitiveness of ventricular premature depolarizations (VPDs) were determined by computer analysis of predischarge 24 hr electrocardiographic recordings. The left ventricular ejection fraction (LVEF) was determined by radionuclide ventriculography and dichotomized at its optimal value of 30%. Frequency of VPDs was divided into three categories: (1) less than one per hour, (2) one to 2.9 per hour, and (3) three or more per hour. Repetitiveness of VPDs was also divided into three categories: (1) no repetitive VPDs, (2) paired VPDs, and (3) VPD runs. These variables were related, one at a time and jointly, to total mortality and to deaths caused by arrhythmias. The hazard ratios for dying in the higher or highest risk stratum vs the lower or lowest stratum for each variable (adjusted for the effects of the others) were: LVEF below 30%, 3.5; VPD runs, 1.9; and VPD frequency of three or more per hour, 2.0. There were no significant interactions among the three variables with respect to effects on the risk of mortality. There was a suggestion of an interaction between each risk variable and time after infarction. LVEF below 30% was a better predictor of early mortality (less than 6 months) and the presence of ventricular arrhythmias was a better predictor of late mortality (after 6 months).(ABSTRACT TRUNCATED AT 250 WORDS)

Arrhythmias, Cardiac↗
PubMed1982

Clinical management of ventricular arrhythmias.

Ventricular arrhythmias are associated with a high risk of sudden cardiac death. Thus, a sense of urgency attends the issue of identifying and treating susceptible patients in advance of the catastrophic event. Expeditious selection of the most appropriate and least toxic drugs for each patient at risk can be accomplished in more than 80% of cases with an inexpensive noninvasive approach.

Arrhythmias, Cardiac↗
PubMed1995

Coronary angioplasty for the control of intractable ventricular arrhythmia.

Ventricular arrhythmias (VAs) that occur following an acute extensive anterior myocardial infarction (MI) usually respond to conventional antiarrhythmic regimes of treatment. Rarely, the VA may prove intractable to therapy. This report is of three patients who presented at varying time frames (3 h to 10 weeks) following an anterior MI. They exhibited sustained monomorphic ventricular tachycardia and hemodynamic instability despite multiple antiarrhythmic drug therapy, intravenous magnesium, direct-current cardioversion (DCCV), overdrive pacing (in one case), and intra-aortic balloon counterpulsation (IABP). Although there was no clinical evidence of continuing ischemia and although coronary angiography that was done in each case showed the infarct-related artery (IRA) to subtend akinetic areas on left ventricular (LV) angiogram, percutaneous transluminal coronary angioplasty (PTCA) of the IRA was done in all three cases. Reestablishing patency of the IRA helped in controlling the VA dramatically with average therapeutic doses of antiarrhythmic drugs. All three patients showed this control to have been maintained over a follow-up period of more than 1 year, with partial improvement in LV function and signal-averaged electrocardiogram negative for late potentials. Thus, in patients with extensive infarction and intractable VA, PTCA of the IRA may provide control of VA even in the absence of clinical signs of active ischemia or viable muscle mass.

Angioplasty, Balloon, Coronary↗
PubMed1991

Combination antiarrhythmic treatment among class Ia, Ib, and II agents for ventricular arrhythmias.

Ventricular arrhythmia suppression trials were performed to compare the efficacies and side effects of disopyramide and mexiletine used alone and in combination, and to compare the efficacies and side effects of mexiletine and propranolol used alone and in combination, in patients with chronic ventricular premature contractions (VPCs, greater than or equal to 3000 beats/day). The study on the combination of disopyramide and mexiletine included 26 patients (19 men and 7 women). Disopyramide 100 mg tid or mexiletine 150 mg tid was administered as single-drug therapy, and disopyramide 50 mg plus mexiletine 100 mg tid was administered as combination therapy. Each patient underwent Holter monitoring during four different periods: baseline, disopyramide alone, mexiletine alone, and combination therapy. The mean number of VPCs/hr at baseline was 796 +/- 522 (mean +/- SD), which was significantly decreased with all three therapies (p less than 0.01 in each) to a) 415 +/- 480 with disopyramide alone, b) 341 +/- 368 with mexiletine alone, and c) 345 +/- 408 with the combination therapy. The number of patients demonstrating a significant reduction in VPCs (greater than or equal to 75%) and the elimination of ventricular tachycardia (VT; three or more consecutive VPCs) did not differ significantly among the three therapies. The prematurity index (PI), vulnerability index (VI), and QTc tended to be aggravated by disopyramide therapy alone, but these values were corrected by combination therapy. No patients withdrew from the study due to side effects during combination therapy, although three patients withdrew from the study due to severe side effects during single-drug therapy.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1987

Conduction of the impulse in the ischemic myocardium--implications for malignant ventricular arrhythmias.

Ventricular arrhythmias occurring consequent to regional disturbances of myocardial perfusion are the most frequent cause of sudden cardiac death. They are related to marked changes of impulse propagation in the ischemic region, which consist of circulating excitation with re-entry. Mapping of the impulse during ventricular tachycardias and ventricular fibrillation shows that the circus movements change their shape and localization from beat to beat. Zones of tissue which block the impulse during one beat may conduct the impulse at a fast rate during the next beat. The main cause underlying this behavior is the depression of the ischemic action potential. This depression is caused by the partial inactivation and the prolonged recovery of the rapid sodium inward current. In addition to the decrease in resting potential, other factors, such as acidosis, contribute to the inactivation of the inward currents generating the upstroke of the action potential. An increase of coupling resistance between myocardial cells and/or an increase of extracellular resistance appear to be less important for explaining conduction disturbances in acute ischemia.

Action Potentials↗