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At least 19 recordsLinked to original sources
PubMed1999

[Long-term follow up of 115 patients with ischemic heart disease and ventricular flutter induced by programmed ventricular stimulation in the absence of ventricular arrhythmia].

The clinical significance of rapid monomorphic ventricular tachycardia (VT) (> 270 beats/min), also called ventricular flutter, remains controversial in patients without documented spontaneous sustained VT. The aim of this study was to evaluate the outcome of 115 patients with ischaemic heart disease, aged 58 +/- 10 years, without spontaneous ventricular arrhythmias, but who had inducible ventricular flutter during programmed ventricular stimulation. The patients underwent stimulation to evaluate the prognosis after myocardial infarction or to investigate a malaise with or without loss of consciousness. Sustained ventricular flutter was the only inducible arrhythmia in all patients. The mean left ventricular ejection fraction (LVEF) was 42 +/- 14%. During an average follow-up period of 66 +/- 43 months, 31 deaths, including 27 of cardiac causes, were observed. The 1, 5, and 11 year survival of the whole population was 94, 79 and 64% respectively. In univariate analysis, anterior wall myocardial infarction, a low LVEF, the presence of non-sustained ventricular tachycardia (NSVT) on 24 hour Holter monitoring and Class III antiarrhythmic treatment, were poor prognostic factors (p 0.05). In multivariate analysis, the only independent predictive factors of mortality were low LVEF (p = 0.006), the presence of NSVT on Holter monitoring (p = 0.003) and the absence of betablocker therapy (p = 0.015). Medical therapy with betablockers or the implantation of an automatic defibrillator may be indicated in these patients at higher risk.

Arrhythmias, Cardiac↗
PubMed1981

[The problem of ventricular flutter and fibrillation].

Ventricular flutter evokes quick, haemodynamically little effective ventricular contractions. The still existing minimal circulation does not maintain the vital functions. Ventricular fibrillation is tantamount to the acute standstill of the cardiac circulation. If they are not treated, these malignant disturbances of the rhythm nearly always lead to death. Reentry processes or foci with rapid formation of impulses are discussed as responsible electrophysiological mechanisms. Warning arrhythmias are significant for the evocation of ventricular flutter and fibrillation. But the concept of the warning arrhythmias has no unrestricted validity. Thus also late involving ventricular extrasystoles can evoke ventricular fibrillation. Disturbances of intraventricular conduction are also significant for the development of ventricular fibrillation. In our own patients there were no disturbances of conduction only in 13.1% of the cases with ventricular fibrillation. Etiologically are of concern: acute myocardial infarction, chronic myocarditis, chronic ischaemic heart disease, current accidents, advanced stages of vitia and cardiomyopathies. Frequently ventricular fibrillation appears as paroxysmal form (paroxysmal uncoordinated ventricular tachycardia, "torsades de pointe") due to inhomogeneous repolarisation (prolongation of the QTU-time). Therapeutically only the immediate electro-shock therapy has a chance of success in ventricular flutter or fibrillation. Among our patients out of 61 patients with ventricular flutter and fibrillation 26 could be dismissed.

Aged↗
PubMed2003

Ventricular flutter induced during electrophysiologic studies in patients with old myocardial infarction: clinical and electrophysiologic predictors, and prognostic significance.

INTRODUCTION: Induction of ventricular flutter during electrophysiologic (EP) studies (similar to that of ventricular fibrillation [VF]) often is viewed as a nonspecific response with limited prognostic significance. However, data supporting this dogma originate from patients without previously documented ventricular tachyarrhythmias. We examined the significance of ventricular flutter in patients with and without spontaneous ventricular arrhythmias. METHODS AND RESULTS: We conducted a cohort study of all patients with myocardial infarction (MI) undergoing EP studies at our institution. Of 344 consecutive patients, 181 had previously documented spontaneous sustained ventricular arrhythmias, 61 had suspected ventricular arrhythmias, and 102 had neither. Ventricular flutter was induced in 65 (19%) of the patients. Left ventricular ejection fraction was highest among patients with inducible VF (35 +/- 13), lowest for patients with inducible sustained monomorphic ventricular tachycardia (SMVT; 27 +/- 9), and intermediate for patients with inducible ventricular flutter (30 +/- 10). Similarly, the coupling intervals needed to induce the arrhythmia were shortest for VF (200 +/- 28 msec), intermediate for ventricular flutter (209 +/- 27 msec), and longest for SMVT (230 +/- 35 msec). During 5 +/- 8 years of follow-up, the risk for ventricular tachycardia/VF was high for patients with SMVT and ventricular flutter and low for patients with inducible VF and noninducible patients (46%, 34%, 17%, and 14%, P < 0.005). CONCLUSION: Patients with inducible ventricular flutter appear to be "intermediate" between patients with inducible VF and patients with SMVT in terms of clinical and electrophysiologic correlates. However, the prognostic value of inducible ventricular flutter is comparable to that of SMVT.

Aged↗
PubMed2002

Inducible ventricular flutter and fibrillation predict for arrhythmia occurrence in coronary artery disease patients presenting with syncope of unknown origin.

INTRODUCTION: Ventricular fibrillation and ventricular flutter (cycle length < or = 230 msec) induced at electrophysiologic studies are thought to be nonspecific findings in patients presenting with syncope of unknown origin. However, there are limited data on the prognosis of these patients in long-term follow-up. METHODS AND RESULTS: We followed 274 consecutive patients with coronary artery disease presenting with syncope or presyncope who underwent electrophysiologic studies from January 1992 to June 1999 and assessed the risk of subsequent arrhythmias stratified by the electrophysiologic result at the time of their presentation with syncope. Ventricular fibrillation was induced in 23 patients (8%); ventricular flutter in 24 (9%), sustained ventricular tachycardia in 41 (15%); and nonsustained ventricular tachycardia 42 (15%). In 37 +/- 25 months of follow-up, there have been ventricular arrhythmias in 34 patients, including 3 (13%) of 23 who had induced ventricular fibrillation, and 7 (30%) of 24 with induced ventricular flutter, compared to 13 (32%) of 41 with sustained ventricular tachycardia, 7 (17%) of 42 with nonsustained ventricular tachycardia, and only 4 (3%) of 144 noninducible patients (P < 0.001 for induced ventricular fibrillation and ventricular flutter vs noninducible patients). The inducibility of ventricular fibrillation and ventricular flutter were independent risk factors for arrhythmia occurrence in follow-up. CONCLUSION: Ventricular fibrillation and ventricular flutter induced at electrophysiologic studies have prognostic significance for arrhythmia occurrence in patients presenting with syncope. These induced arrhythmias may not be as nonspecific as previously thought and treatment should be considered for these patients.

Aged↗
PubMed1995

Does the induction of ventricular flutter or fibrillation at electrophysiologic testing after myocardial infarction have any prognostic significance?

This study examines the significance of inducing sustained ventricular fibrillation (VF) or ventricular flutter by programmed stimulation after infarction. Programmed ventricular stimulation was performed for prognostic reasons from the right ventricular apex at twice diastolic threshold using a protocol containing 4 extrastimuli. Of 502 patients tested 11 +/- 4 days after acute infarction, VF was induced in 164 (33%), ventricular flutter in 134 (27%), ventricular tachycardia (VT) in 44 (9%), and no arrhythmia in 160 (32%). All groups were similar in age, sex distribution, and sites of index infarction. Those with inducible VT had a higher incidence of multiple infarctions and a lower mean left ventricular ejection fraction at the time of testing. Without antiarrhythmic drug therapy, 8 patients (18%) with inducible VT experienced spontaneous VT or died instantaneously during the first year of follow-up. By contrast, only 1 (0.6%) patient with inducible VF, 1 (0.7%) with ventricular flutter, and 1 (0.6%) without any inducible arrhythmias experienced similar events in the same period (p < 0.001). By relating the cycle length of the induced monomorphic arrhythmia to later spontaneous electrical events, induced arrhythmias with cycle length as low as 230 ms still identified patients at high risk for spontaneous arrhythmias. Only the induction of sustained monomorphic VT with a cycle length > 230 ms indicates patients with ventricular electrical instability after infarction. The induction of VF or ventricular flutter is a negative test result with no adverse long-term prognostic significance.

Arrhythmias, Cardiac↗
PubMed1976

Quinidine-induced ventricular flutter and fibrillation without digitalis therapy.

Three cases are described with documented ventricular flutter and fibrillation during quinidine medication without concomitant digitalis therapy. In all three patients the arrhythmia developed while they were receiving moderate doses of quinidine. Although no changes in QRS width were observed after administration of quinidine, there was marked prolongation of the Q-T interval. The mechanism of development of ventricular flutter and fibrillation in patients taking quinidine may be similar to that in patients with the Q-T prolongation syndrome.

Adult↗
PubMed1985

Sudden nocturnal death in young males from ventricular flutter.

Two young males who had no organic heart disease died unexpectedly during the night. In one patient, the monitor ECG showed a sinoatrial block and the electrophysiologic study revealed a sinoatrial conduction time at the upper limit of normal and a prolonged PA interval. The surface ECG showed left axis deviation. Ventricular ectopic beats were confined to the night when he died from ventricular flutter. The ECG of the other patient was normal except for the change in QRS configuration found when the preceding RR interval was prolonged, suggesting a phase 4 block in intraventricular conduction. He was completely free from arrhythmia except for the ventricular ectopic beats which developed around 9:00 p.m. and the ventricular flutter following an R-on-T type ventricular ectopic beat which resulted in death during the night. The autopsy showed no organic heart disease. ST elevation suggestive of acute ischemia was not found and the QT intervals were normal in both cases. No electrolyte imbalances were found. These 2 cases can be diagnosed as pokkuri disease which is well known in Japan. The victims are exclusively young males who have no apparent diseases to which death can be attributed.

Adult↗
PubMed1993

[Reproducible ventricular flutter during programming of a DDD pacemaker].

A bipolar DDD pacemaker system was implanted in a 51-year-old woman with a 2 degrees (Mobitz type) atrioventricular block. The first postimplantation control was unremarkable, but she collapsed 9 weeks later with dyspnoea, tachycardia and profound perspiration. Ventricular flutter occurred twice during routine ambulatory pacemaker function tests one week later. The first episode was terminated by a precordial blow with a fist, but the second required electrical defibrillation. During the subsequent hospitalization abnormal electrolyte balance and digitalis intoxication were excluded. Left-heart catheterization with coronary angiography showed normal left-ventricular function at rest and normal coronary arteries. There was no evidence for an arrhythmogenic right ventricle. Electrophysiological testing with programmed ventricular stimulation provoked ventricular tachycardia with torsade de pointes and transition to ventricular fibrillation. Antiarrhythmic treatment with sotalol, 160 mg twice daily by mouth, failed to suppress the episodes of torsade de pointes. But further programmed ventricular stimulation was uneventful after the sotalol dosage had been increased to 160 mg three times daily.

Female↗
PubMed2000

Ventricular flutter in a neonate--severe electrolyte imbalance caused by urinary tract infection in the presence of urinary tract malformation.

Male infants under the age of 3 months presenting with pyelonephritis in the presence of urinary tract malformation (UTM) are prone to transient pseudohypoaldosteronism. This may resemble congenital adrenal hyperplasia (CAH). Hyponatremia, hyperkalemia, dehydration, and metabolic acidosis are the primary findings that permit the diagnosis of CAH. We report a case of transient pseudohypoaldosteronism resulting from pyelonephritis and vesicouretric reflux. The 17-day-old boy presented with a salt-losing episode simulating adrenal insufficiency. An initial diagnosis of CAH was made. The severe metabolic imbalance resulted in ventricular flutter that resolved after correction of the metabolic acidosis and the electrolyte and volume depletion. Early diagnosis is essential because both conditions are potentially fatal and treatment differs significantly. Differential diagnosis may be achieved by urinalysis and abdominal ultrasound scan.

Acidosis↗