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At least 19 recordsLinked to original sources
PubMed1982

A model of chronic ischemic arrhythmias: the relation between electrically inducible ventricular tachycardia, ventricular fibrillation threshold and myocardial infarct size.

To study the relation between inducible ventricular tachycardia and ventricular vulnerability, myocardial infarction was created in 22 closed chest mongrel dogs by inflating a balloon catheter in the left anterior descending coronary artery for 2 hours. The presence of inducible ventricular tachycardia was determined by programmed electrical stimulation of the right ventricle in each dog before and 4 days after infarction, using a transvenous electrode catheter and a "clinical" stimulation protocol. In each dog the repetitive ventricular response threshold and the ventricular fibrillation threshold were measured before and 4 days after infarction. Ventricular tachycardia was not inducible in any dog before infarction. After infarction, sustained ventricular tachycardia was inducible in 10 (45 percent) of 22 dogs and nonsustained tachycardia in an additional 4 dogs (18 percent). Ventricular fibrillation threshold was greatly reduced 4 days after infarction in dogs with inducible sustained tachycardia (mean +/- standard deviation 29 +/- 11 to 10 +/- 5 mA, p less than 0.001); the mean threshold did not change significantly in dogs without inducible sustained tachycardia. Both the ventricular fibrillation threshold and mean ventricular repetitive response threshold were reduced in the dogs with sustained ventricular tachycardia; neither was significantly altered in the dogs without sustained tachycardia. The magnitude of change in the two thresholds frequently differed; hence, a correlation was weak between the control and postinfarction repetitive response/fibrillation threshold ratio (r = 0.41). Postmortem measurement of infarct size demonstrated an association between this measurement and the presence of inducible ventricular tachycardia. Sustained ventricular tachycardia was not inducible in the presence of a small infarct. It is concluded that: (1) inducible ventricular tachycardia on the 4th day after myocardial infarction is associated with a considerable decrease in the ventricular fibrillation threshold; (2) changes in the repetitive response and fibrillation thresholds after myocardial infarction may not be parallel, complicating the use of the repetitive ventricular response threshold as a substitute for the ventricular fibrillation threshold in the postinfarction state; (3) a large infarct predisposes the heart to electrically inducible sustained ventricular tachycardia.

Animals↗
PubMed1997

Drugs versus devices in controlling ventricular tachycardia, ventricular fibrillation, and recurrent cardiac arrest.

Patients with symptomatic ventricular tachycardia, ventricular fibrillation, or aborted sudden cardiac death remain at high risk for arrhythmia recurrence. In recent years, strategies to treat these patients have changed. Concerns about the proarrhythmia risk and uncertain efficacy of class I agents have resulted in a shift in interest to non-class I antiarrhythmic drugs such as sotalol and amiodarone. Both drugs have class III antiarrhythmic properties (i.e., both lengthen repolarization and refractoriness); however, each also has its own additional electrophysiologic effects. Prospectively designed, randomized studies have shown that both sotalol and amiodarone have more potent antiarrhythmic actions than class I agents. However, even as the advantages of sotalol and amiodarone have been recognized, enthusiasm for nonpharmacologic modes of treatment, particularly the implantable cardioverter-defibrillator (ICD), has also markedly increased. The ICD has been shown to decrease dramatically the incidence of sudden death, which may lead to the reduction of total mortality. Whether patients with life-threatening ventricular tachyarrhythmias should be treated first with antiarrhythmic agents or with an ICD is an important question. The results of recent studies suggest that treatment with an ICD is more effective than electrophysiologically guided treatment with class I agents. However, results of prospectively designed randomized studies comparing the efficacy of the ICD with that of sotalol and amiodarone must become available before definitive recommendations can be made concerning the use of the ICD as first-line therapy in patients with ventricular tachycardia/ventricular fibrillation or aborted sudden cardiac death. In addition, there may be a significant role for the use of antiarrhythmic drugs in conjunction with ICDs.

Amiodarone↗
PubMed2001

Supraventricular tachycardia-ventricular tachycardia discrimination algorithms in implantable cardioverter defibrillators: state-of-the-art review.

To reduce inappropriate therapy of supraventricular tachycardia (SVT), implantable cardioverter defibrillators (ICDs) include algorithms to discriminate ventricular tachycardia (VT) from SVT. Dual-chamber algorithms analyze atrial and ventricular rates or AV relationship. They provide advantages over single-chamber algorithms, but introduce new ways to detect SVT as VT inappropriately and to underdetect VT. Unlike pacemakers, dual-chamber ICDs require accurate atrial sensing during high ventricular rates. A postventricular atrial blanking period prevents oversensing of far-field R waves as atrial electrograms, but causes underdetection of atrial fibrillation during high ventricular rates. Tachycardias with 1:1 AV relationship and VT during atrial tachyarrhythmias present specific SVT-VT discrimination problems. The first dual-chamber algorithms performed comparably to single-chamber algorithms. Present dual-chamber algorithms correct some limitations of earlier versions.

Defibrillators, Implantable↗
PubMed1981

[Prinzmetal's variant form of angina pectoris occurring with ventricular tachycardia, ventricular flutter and fibrillation].

After a brief literature survey, the author described a patient of 42, with its first stenocardia paroxysm, accompanied by tachycardia, clonic-tonic convulsion as MAS syndrome, loss of consciousness and spontaneous restoration. After 6 hours a second stenocardia paroxysm followed, when a gigantic ST segment elevation was recorded in precordial leads, appearance of paroxysmal ventricular tachycardia, ventricular fibrillation, loss of consciousness, restored via defibrillation. ST elevation faded by the 25 the minute. The changes are stressed to be most likely due to coronary spasm of r. descendens of the left coronary artery and to changes in the small myocardial vessels. The opinion that Prinzmetal stenocardia is a variant of angina pectoris is confirmed as well as that paroxysm could be with a lethal end due to ventricular fibrillation.

Adult↗
PubMed1990

Determinants of prognosis in symptomatic ventricular tachycardia or ventricular fibrillation late after myocardial infarction. The Dutch Ventricular Tachycardia Study Group of the Interuniversity Cardiology Institute of The Netherlands.

In a multicenter study, 390 patients with sustained symptomatic ventricular tachycardia or ventricular fibrillation late after acute myocardial infarction were prospectively followed up to assess determinants of mortality and recurrence of arrhythmic events. Patients were given standard antiarrhythmic treatment, which consisted primarily of drug therapy. During a mean follow-up period of 1.9 years, 133 patients (34%) died; arrhythmic events and heart failure were the most common cause of death (41 patients [11%] died suddenly, 31 [8%] died because of recurrent ventricular tachycardia or ventricular fibrillation and 23 [6%] died of heart failure). One hundred ninety-two patients (49%) had at least one recurrent arrhythmic event; 85% of first recurrent arrhythmic events were nonfatal. Multivariate analysis of data from patients who developed the arrhythmia less than 6 weeks after infarction identified five variables as independent determinants of total mortality: 1) age greater than 70 years (risk ratio 4.5); 2) Killip class III or IV in the subacute phase of infarction (risk ratio 3.5); 3) cardiac arrest during the index arrhythmia (risk ratio 1.7); 4) anterior infarction (risk ratio 2.2); and 5) multiple previous infarctions (risk ratio 1.6). Multivariate analysis of data from patients developing the arrhythmia greater than 6 weeks after infarction identified four variables as independently predictive of total mortality: 1) Q wave infarction (risk ratio 2.1); 2) cardiac arrest during the index arrhythmia (risk ratio 1.7); 3) Killip class III or IV in the subacute phase of infarction (risk ratio 1.7); and 4) multiple previous infarctions (risk ratio 1.4). The results of the two multivariate analyses were used in a model for prediction of mortality at 1 year. The average predicted mortality rate varied considerably according to the model: for 243 patients (62%) with the lowest risk, it was 13%, corresponding to an observed mortality rate of 12%; for 92 patients (24%) with intermediate risk, it was 27%, corresponding to an observed rate of 28%; for 55 patients (14%) with the highest risk, it was 64%, corresponding to an observed rate of 54%. This study shows that patients with symptomatic ventricular tachycardia or ventricular fibrillation late after myocardial infarction who are given standard antiarrhythmic treatment have a high mortality rate. The predictive model presented identifies patients at low, intermediate and high risk of death and can be of help in designing the appropriate diagnostic and therapeutic strategy for the individual patient.

Aged↗
PubMedDate not supplied

[Ventricular extrasystole in comparison with manifestations of ventricular tachycardia and ventricular fibrillation in acute myocardial infarct]].

We studied 76 patients with first recent myocardial infarction being not older than 12 hours. The patients included 58 men and 18 women. Their mean age was 62 years. We recorded continuously during the first three days following infarction the heart rate, all forms of ventricular premature beats, ventricular tachycardia, ventricular fibrillation, clinical status and activity of creatinine-phosphokinase and its isoenzyme MB. The results showed that ventricular premature beats (coupled and multiform) as well as ventricular tachycardia were more frequent in the first day of illness, while ventricular premature beats (except bigeminy, for which there is no explanation) were infrequent in the second and the third day after development of an infarct. The incidence of ventricular tachycardia during the follow-up period did not differ significantly. Ventricular fibrillation developed in 7 patients (9.2%). A comparison of the relation between ventricular premature beats and malignant ventricular tachycardia, i.e. ventricular tachycardia and ventricular fibrillation, revealed that the patients with more frequent ventricular tachycardia usually had frequent ventricular premature beats, particularly more often bigeminy, trigeminy, polymorphous ventricular premature and coupled ventricular premature beats, but not ventricular premature beats with R-on-T phenomenon. Ventricular tachycardia, however, was also found in patients with an evidence of more rare ventricular premature beats. This suggests that the occurrence of aforementioned forms of ventricular premature beats denotes only a somewhat greater probability that ventricular tachycardia will occur. The fact that there is a lack of correlation between ventricular tachycardia and R-on-T phenomenon indicates that this probability is not so significant. In conclusion, the authors believe that the patients with recent myocardial infarction and ventricular premature beats should be adequately followed up, and that prophylactic antiarrhythmic therapy is not required in most cases, as it was previously widely accepted concept. It should be administered only when ventricular tachycardia develops. Patients with ventricular fibrillation had more frequent ventricular premature beats, although ventricular premature beats in these patients were not statistically more frequent from those found in the patients in whom ventricular fibrillation was not verified. The presence or absence of ventricular tachycardia and ventricular fibrillation, respectively, had no influence on the other followed up parameters.

Female↗
PubMed1988

Prospective evaluation of a discriminant function for prediction of recurrent symptomatic ventricular tachycardia or ventricular fibrillation in coronary artery disease patients receiving amiodarone and having inducible ventricular tachycardia at electrophysiologic study.

Induction of ventricular tachycardia (VT) at electrophysiologic study in patients taking amiodarone poorly predicts recurrence of VT. Consequently, a discriminant function was developed (using parameters based on retrospective data) that appeared to identify high-risk patients. These parameters included ventricular effective refractory period, corrected QT interval, initiation of a repetitive ventricular response and the mode of VT induction. In the present study these parameters were prospectively evaluated in 60 patients with coronary artery disease and sustained VT or ventricular fibrillation (VF), in whom VT was still induced at electrophysiologic study during amiodarone therapy. Thirteen patients had recurrent events (sudden death in 8 and sustained VT in 5) and 47 patients had no symptomatic arrhythmia recurrence (follow-up for 16 +/- 2 months, mean +/- standard error of the mean). The ventricular effective refractory period, corrected QT interval and presence of a repetitive ventricular response did not discriminate between patients with and without symptomatic arrhythmia recurrence. However, an easier mode of VT induction during amiodarone therapy versus control was highly predictive of arrhythmia recurrence: 9 of 13 (69%) recurrences were in this group. In contrast, only 4 of 44 (9%) patients who had either the same or harder mode of VT induction had a recurrent event. Overall, 9 of 16 (56%) patients with an easier mode of VT induction had a recurrence, including 6 of the 8 patients with subsequent sudden cardiac death. It is concluded that electrophysiologic testing during amiodarone therapy is useful to identify high-risk patients.

Administration, Oral↗
PubMed1999

Increase in heart rate precedes episodes of ventricular tachycardia and ventricular fibrillation in patients with implantable cardioverter defibrillators: analysis of spontaneous ventricular tachycardia database.

Patients with heart disease and decreased heart rate variability (HRV) have an increased risk of all-cause mortality as well as arrhythmic death. The question of acute changes in HRV immediately preceding arrhythmic events remains unanswered. We analyzed data from patients with implantable cardioverter defibrillators who had ventricular tachycardia (VT) or ventricular fibrillation (VF) detected by the device. The device stores 1,000 consecutive RR intervals preceding the arrhythmic event detection and before device interrogation. Compared to this control segment, the mean heart rate (HR) increased prior to the arrhythmic event for both VT (88.5 vs 72.7 beats/min, P < 0.0005) and VF (85.4 vs 73.3 beats/min, P < 0.05) patients. No difference in HRV (as analyzed by a time-domain, frequency-domain [fast Fourier transform], and a nonlinear technique) has been detected. We estimated the amount of ectopic beats from the number of RR intervals that differed from the preceding RR interval by > 10%. The frequency of such beats was significantly higher in the prearrhythmic data segments than in the control segments for VT (10.7 vs 6.6/50 beats, P < 0.05) although not for VF (9.8 vs 6.1/50 beats, NS). We conclude that the HR and frequency of ectopic beats are higher prior to onset of the arrhythmic events, although HRV does not change markedly. These results are consistent with sympathetic activation being the predominant autonomic change prior to VT/VF onset in this patient population.

Adult↗
PubMed1983

Comparative effectiveness of pacing techniques for termination of well-tolerated sustained ventricular tachycardia.

Ventricular tachycardias can be terminated by a variety of pacemaker techniques, including rapid and slow stimulation. Fast tachycardias are typically poorly tolerated, and require prompt intervention, usually with rapid pacing. Termination of ventricular tachycardia by slow or single capture pacemaker stimulation techniques is attractive, because of its presumed safety and the possibility of using simple implantable pacers. To identify factors favoring termination, single capture stimulation was used in 390 episodes of ventricular tachycardia in 21 patients, 16 with coronary artery disease, able to tolerate ventricular tachycardia for several minutes. Single capture stimulation terminated 223 episodes (57%) in 18 patients, and two were accelerated. Of 157 episodes exposed to 2-3 programmed extrastimuli or rapid pacing 149 (94%) were terminated and 7 were accelerated. Direct current cardioversion was needed in 12 episodes. Without medications, only two patients tolerated VT. Only one patient had reliable termination with single capture stimulation over several days. Systolic blood pressure was similar in episodes terminated and not terminated by single capture stimulation, but the ventricular rate was significantly lower in episodes terminated, 116 +/- 19 vs. 1.33 +/- 24 (p less than 0.001). Termination of ventricular tachycardia was not affected by QRS morphology. Single capture termination of ventricular tachycardia is largely unpredictable, with limited reproducibility over a period of time. Although comparatively safe, single capture techniques are not likely to prove useful in the long-term treatment of many patients with recurrent ventricular tachycardia.

Adolescent↗
PubMed1997

Heart rate variability and dispersion of QT interval in patients with vulnerability to ventricular tachycardia and ventricular fibrillation after previous myocardial infarction.

OBJECTIVES: This study was designed to compare QT dispersion measured from the standard 12-lead electrocardiogram and 24-h heart rate variability in patients with vulnerability to either ventricular tachycardia or ventricular fibrillation after a previous myocardial infarction. BACKGROUND: Increased QT interval dispersion and reduced heart rate variability have been shown to be associated with vulnerability to ventricular tachyarrhythmias, but the data have mainly been pooled from patients with presentation of stable ventricular tachycardia and ventricular fibrillation. METHODS: QT dispersion and time domain and two-dimensional vector analysis of heart rate variability were studied in 30 survivors of ventricular fibrillation with a previous myocardial infarction and with inducible unstable ventricular tachyarrhythmia by programmed electrical stimulation and in 30 postinfarction patients with clinical and inducible stable monomorphic sustained ventricular tachycardia. Both of these patient groups were matched, with respect to age, gender and left ventricular ejection fraction, with an equal number of postinfarction control patients without a history of arrhythmic events or inducible ventricular tachyarrhythmia and arrhythmia-free survival during a follow-up period of 2 years. Forty-five age-matched healthy subjects served as normal control subjects. RESULTS: Standard deviation of all sinus intervals and long-term continuous RR interval variability analyzed from Poincaré plots were reduced in patients with vulnerability to ventricular fibrillation (p < 0.001 for both), but not in patients with ventricular tachycardia (p = NS for both), compared with postinfarction control subjects. Corrected QT (QTc) dispersion was significantly broader both in patients with ventricular fibrillation (p < 0.001) and in those with ventricular tachycardia (p < 0.05) than in matched postinfarction control subjects. Heart rate variability performed better than QTc dispersion in predicting vulnerability to ventricular fibrillation. CONCLUSIONS: Increased QT dispersion is associated with vulnerability to both ventricular tachycardia and ventricular fibrillation. Low heart rate variability is specifically related to susceptibility to ventricular fibrillation but not to stable monomorphic ventricular tachycardia, suggesting that the autonomic nervous system modifies the presentation of life-threatening ventricular arrhythmias.

Aged↗
PubMed1993

Electrophysiologic variables characterizing the induction of ventricular tachycardia versus ventricular fibrillation after myocardial infarction: relation between ventricular late potentials and coupling intervals for the induction of sustained ventricular tachyarrhythmias.

OBJECTIVES: The aim of this study was to analyze the relations between the presence of ventricular conduction delay and the necessary coupling intervals for the induction of sustained ventricular tachyarrhythmias. METHODS: The electrophysiologic and signal-averaged electrocardiographic (ECG) data from 83 patients with previous myocardial infarction and inducible sustained monomorphic ventricular tachycardia (n = 71) and ventricular fibrillation (n = 12) were analyzed. RESULTS: The sum of the coupling intervals needed for inducing ventricular tachycardia and ventricular fibrillation was 485 +/- 59 ms and 387 +/- 36 ms, respectively (p < 0.001). The mean difference between the effective refractory period and the second coupling interval for the induction of ventricular tachycardia and ventricular fibrillation was -3 +/- 40 ms and 24 +/- 29 ms, respectively (p < 0.02). QRS duration and duration of terminal low amplitude signals of the QRS complex (p < 0.004) were longer in patients with inducible ventricular tachycardia than in patients with inducible ventricular fibrillation. The root mean square of the voltage during the last 40 ms of QRS complex was lower in patients with inducible ventricular tachycardia than in patients with inducible ventricular fibrillation (p < 0.007). Patients with inducible ventricular tachycardia presented with a greater prevalence of ventricular late potentials than that of patients with inducible ventricular fibrillation (p < 0.007). For arrhythmia induction, significantly shorter coupling intervals were necessary in patients without than in patients with ventricular late potentials. A positive correlation was found between the cycle length of the induced ventricular tachycardia and the filtered QRS duration as well as with the sum of the coupling intervals. CONCLUSIONS: Induction of ventricular fibrillation requires shorter coupling intervals than does induction of ventricular tachycardia. The presence of ventricular conduction delay seems to be a marker of facilitated induction of sustained monomorphic ventricular tachycardia rather than of ventricular fibrillation. The coupling intervals required to induce ventricular tachycardia or fibrillation are longer in patients with than in those without an abnormal signal-averaged ECG.

Adult↗
PubMed2003

Electrocardiographic manifestations: ventricular tachycardia.

Ventricular tachycardia is a serious rhythm disturbance that originates from any part of the myocardium or conduction system below the atrioventricular node. Ventricular tachycardia (VT) presents with a wide QRS complex and a rate greater than 120 beats/min. Ventricular tachycardia is frequently encountered as a complication of coronary artery disease or cardiomyopathy; furthermore, VT is also seen in patients with medication adverse effect or electrolyte disturbance. Ventricular tachycardia presents electrocardiographically in several forms, including monomorphic and polymorphic VT. As is true in most Emergency Department presentations, the Emergency Physician must approach the dysrhythmic patient from an undifferentiated perspective, in this instance, the wide complex tachycardia (WCT) scenario. The electrocardiographic differential diagnosis of WCT classically includes VT and supraventricular tachycardia with aberrant intra-ventricular conduction. This article will review the electrocardiographic presentations encountered in patients with ventricular tachycardia.

Aged↗
PubMed2001

Use of high-frame rate imaging and doppler tissue echocardiography in the diagnosis of fetal ventricular tachycardia.

Ventricular tachycardia has rarely been diagnosed in the fetus. We describe a 31-week-old fetus with ventricular tachycardia and severely depressed ventricular function. M-mode and 2-dimensional Doppler tissue echocardiography were used in this study to assess the nature of the arrhythmia. The complete atrioventricular dissociation inherent to the diagnosis of ventricular tachycardia was particularly easy to detect with M-mode Doppler tissue echocardiography. Moreover, the onset and the pattern of propagation of the ventricular arrhythmia could be easily identified with 2-dimensional Doppler tissue echocardiography. Doppler tissue echocardiography facilitates the diagnosis of ventricular tachycardia and adds new information that is not available by other techniques.

Adult↗
PubMed1986

The incidence and morphology of ischaemic ventricular tachycardia.

Ventricular arrhythmias are a frequent cause of sudden death in patients with coronary artery disease. The incidence and relationship of ventricular tachycardia to periods of myocardial ischaemia in these patients has not been fully investigated. Ambulatory ST-segment monitoring was performed in 100 consecutive patients with chest pain, of whom 74 had significant coronary artery disease. Recordings were analysed for ST-segment changes and episodes of ventricular tachycardia (greater than 3 beats, rate greater than 100 beats min-1). None of the 26 patients with normal coronary arteries, one of the 22 patients (4.5%) with single vessel disease, one of the 22 patients (4.5%) with double vessel disease and four of the 30 patients (13%) with triple vessel disease, had episodes of non-sustained ventricular tachycardia. Four of these six patients had episodes of reversible ST-segment change but ventricular tachycardia was related to these episodes in only two patients. These two patients had multiple episodes of tachycardia which occurred after the onset of ST-segment change and terminated before the ST-segment returned to baseline; they occurred in clusters with a mean of 12 episodes in each cluster. ST-segment change did not follow episodes of ventricular tachycardia in any patient. The number of ventricular complexes in each episode varied between three and 24 beats and were uniform in three of the six patients. The mean heart rate before the onset of tachycardia was 79 +/- 8 beats per minute and the rate of tachycardia had a mean of 170 +/- 34 beats a minute. Less than 10% of the episodes had a prematurity index of less than 1.(ABSTRACT TRUNCATED AT 250 WORDS)

Angina Pectoris↗
PubMed1985

Histopathologic factors conducive to experimental ventricular tachycardia.

Ventricular tachyarrhythmia is the leading cause of sudden cardiac death. Determination of the substrates conducive to the initiation of this arrhythmia remains an important clinical goal. The purpose of this study was to correlate histopathologic findings, specifically: pattern (heterogeneous versus homogeneous infarct morphology), distribution (viable epicardial and/or endocardial rim), and infarct size, with susceptibility to the initiation of sustained ventricular tachycardia employing programmed electrical stimulation in two canine models of experimental myocardial infarction. Twenty-one adult dogs were randomly divided into two groups: 12 dogs underwent two-stage, 2-hour occlusion of the proximal left anterior descending coronary artery and nine animals underwent permanent, complete occlusion of the left anterior descending coronary artery with latex embolization. With programmed ventricular pacing with two premature ventricular extrastimuli, initiation of ventricular tachycardia was attempted, open chest, two weeks after infarction. Electrophysiologic evaluation of the infarct type correlated significantly with the histologic morphology of the infarction (p less than 0.001). The presence of a viable epicardial rim was an extremely important variable for ability to induce sustained ventricular tachycardia (p = 0.04). The presence of an endocardial rim was not significant (p = 1.0). Infarct size alone was only marginally related to ventricular tachycardia inducibility (p = 0.08). Nonuniform infarcts were more conducive to the initiation of sustained ventricular tachycardia than were homogeneous infarcts (p = 0.025). The presence of a large, nonuniform infarct correlated best with inducibility (p = 0.0002). Thus in these experimental models, specific infarct morphologies correlate significantly with susceptibility to inducible sustained ventricular tachyarrhythmias.

Animals↗