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PubMedDate not supplied

Ventricular tachycardia-flutter associated with disopyramide therapy: a report of three cases.

Three patients developed episodes of ventricular tachycardia and/or flutter-fibrillation while receiving disopyramide (Norpace). Syncope was the presenting complaint in all of them. The arrhythmias did not recur after disopyramide was discontinued. The Q-T interval was markedly prolonged in all three patients. One patient developed syncope associated with both quinidine and Norpace therapy. It is postulated that disopyramide, like quinidine, may provoke ventricular flutter-fibrillation in sensitive patients by similar mechanisms.

Aged↗
PubMed1992

Sudden arrhythmic death without overt heart disease.

Nine patients (eight males) are reported with one or more episodes of circulatory collapse in the absence of overt heart disease or other known causes of arrhythmias; sudden arrhythmic death occurred in one of these patients. Age at first episode ranged from 16 to 41 (mean, 28) years. In seven patients, ventricular fibrillation was documented at the time of resuscitation. One patient had ventricular flutter. In the remaining patient, documentation of the arrhythmia during the collapse was not available. Four patients had frequent early ventricular premature beats, and in three of these patients, they were accompanied by episodes of rapid nonsustained polymorphic ventricular tachycardia. Failure to suppress this ectopic activity by drug therapy seems to be of prognostic significance. Of the three patients showing persistence of frequent early ventricular premature beats, one died suddenly, and two had recurrences of symptomatic arrhythmic episodes. The value of noninvasive and invasive tests in the management of these patients is not clear, with the exception of exercise testing in patients with exercise-related arrhythmias and long-term electrocardiographic monitoring in patients with frequent spontaneous ventricular ectopic activity. Follow-up varied from 21 to 192 (mean, 84) months. One patient died suddenly 21 months after his first collapse. Selection of antiarrhythmic drug therapy was largely empirical. In view of the relative rarity of sudden arrhythmic death in the absence of heart disease and the many uncertainties about its mechanism(s) and management, a worldwide registry of these patients is suggested.

Adolescent↗
PubMed1978

[Syncopal attacks due to ventricular tachyarrhythmias ("torsade de pointe type") in a patient with a PM of hysteresis type (author's transl)].

The authors report on a patient with artificial ventricular pacemaker with hysteresis, who suffered from ventricular fibrillation known as "torsade de pointe" and ventricular flutter, often accompanied by lipothymias, with hypokalemia. The following points are considered: the pacemaker responsibility to produce arrhythmia; the pacemaker behaviour during ventricular tachyarrhythmias; the modifications of stimulation threshold and R-wave sensitivity after PM removal and the following hours.

Aged↗
PubMed2004

Significance of inducible ventricular flutter/fibrillation in risk stratification in patients with coronary artery disease.

BACKGROUND: Although inducible ventricular fibrillation (VF) has been used as an indication for prophylactic implantation of cardioverter-defibrillators (ICDs) in patients with coronary artery disease (CAD), the significance of inducible VF remains controversial. METHODS: Among 364 CAD patients who underwent electrophysiologic (EP) study for risk stratification, 23 patients, 12 without any history of VF or cardiac arrest (group A) and 11 with previously documented VF or cardiac arrest (group B), exhibited inducible ventricular flutter (VFL) or VF and subsequently underwent ICD implantation. Additionally, 11 CAD patients without previous VF or cardiac arrest, who had no inducible ventricular tachyarrhythmias but received an ICD, were included for comparison (group C). RESULTS: During 2 years of follow-up, 1 (8%), 5 (45%), and 1 (9%) patients had appropriate ICD shocks in groups A, B, and C, respectively. The survival free from appropriate ICD shocks was significantly lower in group B compared to groups A and C (p<0.05). There were no significant differences in age, sex, ejection fraction (EF), or induction protocol between groups A and B or between groups A and C. CONCLUSIONS: In CAD patients with inducible VFL/VF, patients without any history of VF or cardiac arrest had significantly lower incidence of appropriate ICD shocks when compared to those with such clinical events. Conversely, in CAD patients without any history of VF or cardiac arrest, incidence of appropriate ICD shocks was similar regardless of inducible VFL/VF. Inducible VFL/VF is therefore not useful as an indication for prophylactic ICD implantation in this patient population.

Aged↗
PubMed1975

Maximal exercise testing in patients with spontaneous angina pectoris associated with transiet ST segment elevation. Risks and electrocardiographic findings.

Six patients with spontaneous angina associated with transient ST segment elevation had a multistate maximal exercise (bicycle) test. In 5 patients, typical electrocardiographic changes were recorded during exercise, namely ST segment elevation often accompanied by an increase in the voltage of the R wave and a widening of the QRS complex. Four of these patients developed severe rhythm disturbances: ventricular tachycardia (2 cases) and ventricular flutter (1 case) were the reason for early interruption of the test in 3 patients, while 1 patient had a short run of ventricular tachycardia after exercise. These rhythm disturbances which spontaneously regressed in all cases were consistently preceded by obvious ST elevation and in 2 patients were attended by slight chest discomfort. Maximal exercise testing of patients suspected of variant angina provides important diagnostic information in many patients, but the risks of potentially lethal arrhythmias should be considered and resuscitation facilities should always be immediately available.

Adult↗
PubMed1993

[Risks and side effects in treatment of supraventricular tachycardia].

Many new antiarrhythmic drugs effective in supraventricular tachyarrhythmia are now available. Since these compounds may lead to serious side-effects, the correct indication for the antiarrhythmic treatment has to be given regarding the ratio of risk and benefit. There is no doubt that aggravation of arrhythmia i.e. acceleration of tachycardia or even degeneration into ventricular flutter (including torsades-de-pointes tachycardia) and fibrillation may be related to the cardiac diagnosis depending on the extent of disease or left ventricular dysfunction and the presenting arrhythmia and possibly the electrophysiological effects of the drug. In general, negative inotropic effects of antiarrhythmic substances are overestimated; they may even be neglected as long as the antiarrhythmic agent leads to effective suppression of the symptomatic ventricular tachyarrhythmia. The best and most important consequence of the CAST study (Cardiac Arrhythmia Suppression Trial) showing an increase in mortality with antiarrhythmic drugs compared with placebo should be that physicians handle antiarrhythmic drugs now with more care than before. The problems with risks and side-effects in antiarrhythmic drug therapy of supraventricular arrhythmias underline the requirement for careful cardiological evaluation and monitoring in all patients receiving such drugs.

Anti-Arrhythmia Agents↗
PubMed1996

Modification of ventricular tachycardia by carotid sinus massage.

A case of ventricular tachycardia (VT) was aggravated by carotid sinus massage in a woman with an old myocardial infarction. The patient presented with a wide QRS complex tachycardia with a rate of 143 beats/min, which fulfilled the classic and newer electrocardiographic criteria for the diagnosis of VT. Carotid sinus massage performed during the tachycardia resulted in its conversion to another, wide QRS complex tachycardia, with different morphology and a faster rate resembling ventricular flutter. This latter tachycardia was converted to sinus rhythm by a thump on the patient's chest. The initial tachycardia was proved to be of ventricular origin by electrophysiologic study at a later stage during a recurrence. Vagal stimulation probably resulted in inhomogeneous increase of the ventricular refractory period, creating conditions for a reentrant circuit other than the preexisting one and for the emergence of VT with a different QRS morphology and rate. Although termination and/or initiation of VT by carotid sinus massage has been reported in the past, modification of VT by carotid sinus massage has not been described previously.

Aged↗
PubMed2004

Insulin tolerance test causes hypokalaemia and can provoke cardiac arrhythmias.

We report the observation and analysis of a new adverse event during the insulin tolerance test (ITT) and propose additional safety procedures. An 8-year-old girl with growth hormone insufficiency had a cardiac arrest due to ventricular flutter when she was tested for growth hormone deficiency by the ITT. Severe hypokalaemia (K+ 2.6 mmol/l) was observed after resuscitation. Ergometry ECG revealed catecholaminergic polymorphic ventricular tachycardia, a hereditary arrhythmogenic disease. Consecutive measurements of serum potassium during ITT in 29 short children (21 boys) with growth failure revealed a mean decrease of serum potassium by 1.1 +/- 0.4 mmol/l with the nadir at 30 min after the insulin bolus. Hypokalaemia (serum potassium < 3.5 mmol/l) occurred in all but one child; severe hypokalaemia (serum potassium < 2.9 mmol/l) was measured in every third child. This observation indicates that acute hypokalaemia which is induced by insulin and catecholamine excess occurs frequently in ITT. The case shows that the combination of acute hypokalaemia and the adrenergic counterregulation in ITT is a strong trigger of cardiac arrhythmias, which can become life-threatening if the child has an arrhythmogenic disease. Therefore, we recommend ECG monitoring during ITT to enhance the detection of cardiac arrhythmias. In addition, in the case of a comatose child during ITT the determination of the glucose and potassium level as well as adequate treatment are necessary.

Adolescent↗
PubMed1995

Auditory stimuli as a major cause of syncope in a patient with idiopathic long QT syndrome.

A 35-year-old woman was hospitalized due to frequent attacks of syncope immediately after the ringing of a bell or alarm clock. Her standard electrocardiograms showed a long QT interval (QTc = 0.56 s) with a bizarre T-wave inversion in precordial leads. After admission, a total of 9 events of syncope were observed. Malignant ventricular tachyarrhythmia (torsade de pointes, ventricular flutter or fibrillation) was recorded during each episode, and DC shock was required to abolish such tachyarrhythmias on 3 occasions. On monitored electrocardiograms, an additional 8 events of ventricular tachycardia without syncope were also detected. Auditory stimuli appeared to be involved in the initiation of malignant ventricular arrhythmia. Immediately after auditory stimuli, changes in the QT interval and T-wave morphology resulted in ventricular premature beats, leading to ventricular tachycardia. The episodes of syncope or malignant ventricular arrhythmia were frequently observed early in the morning and near midnight. She had been treated with various types of antiarrhythmic agents, and propranolol was the most effective in preventing ventricular arrhythmia. These findings indicate that auditory stimuli may cause ventricular arrhythmia and subsequent cardiac syncope, or even sudden cardiac death, in some patients with long QT syndrome.

Acoustic Stimulation↗
PubMed1981

Efficacy of coronary bypass grafting in exercise-induced ventricular tachycardia.

The effects of coronary bypass grafting on ventricular tachycardia induced by treadmill stress testing (TST) were analyzed in nine patients by repeating the test an average of 5 months after operation. Preoperatively, eight patients experienced pain and all had ischemic ST-segment depression during exercise. Six patients had a single episode and two patients had multiple episodes of ventricular tachycardia; in one patient ventricular tachycardia degenerated into ventricular flutter necessitating direct-current cardioversion. Postoperatively, time of exercise and double product were significantly higher during TST. Electrocardiographic ischemic changes were present in only two patients and ventricular tachycardia was not observed. All patients are alive and average of 24 months after the operation, and eight of them are asymptomatic. In conclusion, among patients with coronary artery disease who have exercise-induced ventricular arrhythmias, myocardial revascularization is associated with improvement of exercise capacity and suppression of arrhythmias.

Adult↗
PubMed1999

[Suicidal Tachmalcor poisoning--a case report].

In a case report, a Tachmalcor intoxication with a dose of 18 mg/kg body weight is described. This dose caused a ventricular flutter in the patient which lasted for a total of 10 hours, despite intensive treatment. The treatment began approximately three hours after the intoxication and concentrated on therapy of the ventricular tachycardia. The use of Xylocitin 2%, defibrillation, glucagon and sodium chloride is recommended with such symptoms. Additionally, we used hemoperfusion for drug elimination. Despite the cardiac rhythm disorder of such duration, no neurological deficiencies were observed in the patient. Intoxications caused by these drugs in normal intensive therapies are extremely rare and for this reason treatment can often be very problematic. The following article reports on the successful therapy of one such patient.

Adult↗
PubMed1980

Chronic longterm electrophysiologic study of paroxysmal ventricular tachycardia.

Nine patients with recurrent paroxysmal ventricular tachycardia underwent chronic electrophysiologic studies to delineate effective drug therapy for prevention of recurrence of this arrhythmia. The frequency of attacks of ventricular tachycardia necessitating hospitalization ranged from 2 to 12 (mean 5 +/- 4) attacks per year. Pacing induction of ventricular tachycardia was performed prior to and following intravenous or oral administration of procainamide (eight patients), disopyramide phosphate (nine patients), aprindine (five patients) and propranolol (four patients). Successful drug response (prevention of ventricular tachycardia induction or induction of nonsustained episodes of tachycardia) was noted in six of nine patients (66 percent). Lack of drug effect on the ability to sustain ventricular tachycardia was noted in three patients (34 percent). In addition, a deleterious drug response, manifested by potentiation of ventricular flutter or fibrillation, was observed in two of the three patients who failed to respond to drugs. Chronic drug therapy based on successful response in six patients resulted in cure of ventricular tachycardia in five of six patients (83 percent), one patient having one attack necessitating hospitalization. Of the three patients who demonstrated lack of drug effect during chronic electrophysiologic studies, one died suddenly and two had recurrent episodes of ventricular tachycardia while receiving a drug that did not prevent induction of ventricular tachycardia.

Adult↗
PubMed1988

[Hemodynamics in ventricular arrhythmias and in their treatment].

The hemodynamic consequences of ventricular tachyarrhythmias are influenced by age, underlying cardiac disease, left ventricular ejection fraction, and possibly by atrial natriuretic peptide. Severity and frequency of the rhythm disorder play, of course, a major role, e.g., monomorphic or polymorphic ventricular premature complexes (VPC), rare or frequent VPC, ventricular tachycardia, ventricular flutter or fibrillation, torsade de pointes, and tachycardia, etc. The therapeutic approach with antiarrhythmic drugs or cardiac pacemakers in cases of conduction disturbances have an additional impact on cardiac performance. Compared to ventricular pacing, a significant higher cardiac output was observed during AV sequential (so called "physiological") pacing evaluated by radionuclide ventriculography. Especially in patients with a reduced left ventricular ejection fraction, the negative inotropic effects of antiarrhythmic drugs are of major importance. A decrease of cardiac output may occur under beta-blocking agents, propafenone, flecainide and particularly disopyramide. On the other hand, amiodarone does not impair cardiac output significantly during acute high dose loading and longterm therapy. In general, negative inotropic effects of antiarrhythmic substances are overestimated; they may even be neglected as long as the antiarrhythmic agent leads to effective suppression of the symptomatic ventricular tachyarrhythmia.

Amiodarone↗
PubMed2006

Antitachycardia pacing for spontaneous rapid ventricular tachycardia in patients with prophylactic cardioverter-defibrillator therapy.

AIMS: Antitachycardia pacing (ATP) has not routinely been used in patients who received implantable cardioverter defibrillators (ICDs) for primary prevention of sudden death. This study investigated the efficacy of empirical ATP to terminate rapid ventricular tachycardia (VT) in heart failure patients with prophylactic ICD therapy. METHODS AND RESULTS: Ninety-three patients with a mean left ventricular ejection fraction of 22 +/- 7% (range: 9-35%) due to nonischemic or ischemic cardiomyopathy received prophylactic ICDs with empiric ATP. At least 2 ATP sequences with 6-pulse burst pacing trains at 81% of VT cycle length (CL) were programmed in one or two VT zones for CL below 335 +/- 23 ms and above 253 +/- 18 ms. Ventricular flutter and fibrillation (VF) with CL below 253 +/- 18 ms were treated in a separate VF zone with ICD shocks without preceding ATP attempts. During 38 +/- 27 months follow-up, 339 spontaneous ventricular tachyarrhythmias occurred in 36 of 93 study patients (39%). A total of 232 VT episodes, mean CL 293 +/- 22 ms, triggered ATP in 25 of 36 patients with ICD interventions (69%). ATP terminated 199 of 232 VT episodes (86%) with a mean CL of 294 +/- 23 ms in 23 of 25 patients (88%) who received ATP therapy. ATP failed to terminate or accelerated 33 of 232 VT episodes (14%) with a mean CL of 287 +/- 19 ms in 12 of 25 patients (48%) who received ATP therapy. CONCLUSIONS: Painfree termination of rapid VT with empirical ATP is common in heart failure patients with prophylactic ICD therapy. The occasional inability of empiric ATP to terminate rapid VT in almost 50% of patients who receive ATP for rapid VT warrants restrictive ICD programming with regard to the number of ATP attempts in order to avoid syncope before VT termination occurs.

Cardiac Pacing, Artificial↗
PubMed1992

Electropharmacology of dofetilide, a new class III agent, in anaesthetised dogs.

In open chest anaesthetised dogs, dofetilide increased the ventricular effective refractory period over the dose range 1-100 micrograms/kg i.v. and the ventricular fibrillation threshold at doses between 3-100 micrograms/kg and was 80-1000 times more potent than sematilide, racemic sotalol, d-sotalol or quinidine. The maximal increases in ventricular fibrillation threshold induced by sematilide and quinidine were less than that induced by the other drugs. A change in the character of the induced arrhythmia from true ventricular fibrillation to a rapid ventricular flutter, with frequent spontaneous conversion, was observed following all drugs. No adverse haemodynamic effects of dofetilide, sematilide or d-sotalol were observed, but quinidine induced marked cardiac depression and racemic sotalol also impaired left ventricular contractility. All drugs reduced heart rate, though the effect of racemic sotalol was clearly greater than that of the other agents. Dofetilide is a potent class III antiarrhythmic agent with antifibrillatory properties and a favourable haemodynamic profile.

Action Potentials↗
PubMedDate not supplied

[Atypical form of long-QT syndrome--a case report].

An unusual case of familial Long QT syndrome is reported. After a longstanding symptom free interval this eight year old girl experienced multiple episodes of malignant ventricular arrhythmias including ventricular tachycardias of the torsades-de-pointes type and ventricular flutter. The treatment with beta- and alpha-blocking agents, phenytoin, calcium antagonists, clonidine and magnesium in increasing doses and varying combinations was unsuccessful. A left sided cardiac sympathectomy failed also to control the life threatening ventricular arrhythmias and to decrease the relative high mean heart rate. Finally a consecutive right cardiac sympathetic denervation in combination with an experimental class I antiarrhythmic agent led to a subjective and objective improvement in the patient's condition which allowed discharge from hospital. Despite a symptom free interval of four months and nearly normalized Holter ECG results the longterm prognosis remains unclear. This unusual case discloses interesting features, because 1) it supports the theory of an intracardiac cellular anomaly rather than the imbalance hypothesis, 2. chronic beta-blocker treatment possibly resulted in an up-regulation of beta-adrenergic receptors which made beta-blocking agents ineffective despite high doses, and 3. an consecutive right sided cardiac sympathectomy resulting in bilateral cardiac sympathetic denervation had to be done-an intervention which is seldom performed in the Long QT syndrome.

Anti-Arrhythmia Agents↗
PubMed1992

Polymorphous ventricular tachycardia in a newborn with the long QT interval.

We have reported a case of long QT syndrome in a neonate who had ventricular tachycardia 30 minutes after birth. On the third day, while being weaned from lidocaine, the patient had ventricular flutter and required cardioversion. Treatment with propranolol (5 mg/kg/day) maintained normal sinus rhythm. We believe this may be the first reported case of long QT syndrome and normal AV conduction in a neonate who had multiple episodes of ventricular tachycardia despite medical treatment.

Female↗
PubMed1993

[Drug-induced ventricular tachycardia].

Certain drugs can induce ventricular tachycardia (VT) by creating reentry, ventricular after potentials or exaggerating the slope of phase 4. These may or may not be symptomatic, sustained or non-sustained and have variable ECG appearances: monomorphic or polymorphic, bidirectional, torsades de pointes. They risk degenerating into ventricular flutter of fibrillation and have been held responsible for the increased mortality observed unexpectedly in some long-term treatments. The drugs responsible are mainly those used in cardiology, probably due to predisposing circumstances (cardiomegaly, cardiac failure, previous severe ventricular arrhythmias, therapeutic associations, metabolic abnormalities). These include primarily the antiarrhythmic drugs (IA, IC, sotalol and bepridil), digitalis, sympathomimetics and phosphodiesterase inhibitors. These complications may be toxic or idiosyncratic, in patients with or without cardiac disease, and may also occur with other drugs: vasodilators and anti-anginal drugs (lidoflazine, vincamine, fenoxedil), psychotropic agents (phenothiazine and imipramine), antimitotics, antimalarials (chloroquine) or antibiotics (erythromycin, pentamidine). The prognosis is severe and the treatment is often difficult which makes prevention, helped by repeated surface ECG (or Holter monitoring), very important with careful assessment of patients at risk.

Anti-Arrhythmia Agents↗