[Observations on a case of transitory flutter, atrial fibrillation and atrio-ventricular dissociation after exertion].
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Arrhythmias, Cardiac↗
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Sudden unexpected death during ambulatory electrocardiographic monitoring. The Framingham Study.
This report documents the clinical and electrocardiographic events of sudden unexpected death in a 52-year-old man without known heart disease during ambulatory electrocardiographic monitoring. This death occurred two and a half hours after detailed noninvasive testing, including treadmill exercise, that was unrevealing. The sequence of S-T change suggesting epicardial injury, multiform ventricular premature depolarizations, and frequent and early cycle ventricular premature depolarizations followed by ventricular tachycardia-flutter-fibrillation precipitated by an early cycle ventricular premature depolarization were documented. The delay in cardiopulmonary resuscitation in this witnessed cardiac arrest punctuates the need for widespread dissemination of the skills of cardiopulmonary resuscitation.
Death, Sudden↗
Repaired tetralogy of Fallot in the adult.
The majority of persons living with tetralogy of Fallot are now adults and may face a number of long-term cardiac problems that necessitate reoperation. These problems include pulmonary regurgitation, tricuspid regurgitation, ventricular tachycardia, atrial flutter and/or fibrillation, pulmonary artery branch stenoses, right ventricular aneurysms, right ventricular outflow tract obstruction, residual ventricular septal defects, and coronary artery disease. Management approaches to these potential problems are discussed. Issues related to genetics, pregnancy, infective endocarditis, insurability, and employment are also reviewed with specific reference to the individual with repaired tetralogy of Fallot.
Adult↗
Ventricular beats induce variations in cycle length of rapid (type II) atrial flutter in humans. Evidence of leading circle reentry.
BACKGROUND: Slight variation in cycle lengths of common and rapid atrial flutter in humans is an established phenomenon, but its mechanisms have not been completely clarified. In a previous study, we demonstrated that in common atrial flutter the variations in atrial cycle length were due to atrial stretch affecting the revolution time of a reentrant circuit. In the present study, we investigate the nature of atrial cycle length variations in the rapid type of human atrial flutter. METHODS AND RESULTS: Atrial interval variations of 17 episodes of rapid atrial flutter in 14 patients were investigated by measuring the sequence of atrial intervals from intraesophageal or intra-atrial leads and the onset of QRS complexes from a surface lead (V1). To study whether interval variation in flutter cycle was related to ventricular activity, a phase plot was constructed in which the flutter cycle length was plotted against the time after the previous QRS complex. This showed that the interval fluctuations were strictly coupled to the moment of ventricular activation. After the onset of the QRS complex, the rapid atrial flutter interval gradually decreased by an average of 4.1% (P < .001) and reached a minimum value after 300 to 600 milliseconds. Thereafter, the intervals increased again until the next ventricular beat occurred. In 10 patients developing both common and rapid atrial flutter, two different phase relations were found. Whereas during common atrial flutter the atrial interval increased after the QRS complex, it decreased during rapid atrial flutter. In three patients, intra-atrial pressure was recorded together with the electrical activity during both common and rapid atrial flutter episodes. This showed that variations in atrial flutter cycle length were associated with the rise of atrial pressure during ventricular contraction. CONCLUSIONS: These findings indicate a role of contraction-excitation feedback caused by atrial stretch after a ventricular activation. The shortening of the atrial interval after the onset of the QRS complex as found in patients during rapid atrial flutter can be explained by stretch-induced shortening of atrial refractoriness and consequent shortening of the revolution time of a functionally determined intra-atrial circuit.
Aged↗
Trends and outcomes in the hospitalization of older Americans for cardiac conduction disorders or arrhythmias, 1991-1998.
OBJECTIVE: To identify epidemiological trends and measure outcomes in elderly patients hospitalized for cardiac conduction disorders or arrhythmias. DESIGN: Review of the standard 5% samples of the Medicare Provider Analysis and Review Files to characterize 144,512 discharges from 1991 through 1998 in which the principal diagnosis was a conduction disorder or arrhythmia, using the corresponding Enrollment Databases for denominator data. SETTING: Short-stay hospitals in the United States. PARTICIPANTS: Medicare beneficiaries age 65 and older in the standard 5% sample. MEASUREMENTS: Diagnosis-specific trends and rates; discharges by year; cumulative age-, race-, and sex-specific discharge rates; mean length of stay in hospital and in intensive care; mean Medicare reimbursement to the hospital; case-fatality rate in hospital; discharge destinations of patients discharged alive. RESULTS: Annual hospitalizations for sinoatrial node dysfunction, atrial flutter, atrial fibrillation, or ventricular fibrillation increased more rapidly than did the elderly Medicare beneficiary population. Hospitalizations with a principal diagnosis of ventricular extrasystoles or asystole showed steep secular declines. Discharge rates for sinoatrial node dysfunction, a group of rhythms with a nonsinus pacemaker, atrial fibrillation, Mobitz I, or complete atrioventricular block all increased steeply and continuously with patient age. In contrast, discharge rates for atrial flutter or ventricular tachycardia or fibrillation peaked among 75- to 84-year-old patients. White men were at uniquely high risk of hospitalization for atrial flutter or ventricular tachycardia or fibrillation, and, among the white majority, men had higher discharge rates than women for nine of the 11 commonest rubrics. Whites, particularly white women, had the highest discharge rates for atrial fibrillation. Blacks, especially black women, were at disproportionate risk for hospitalization for the group of nonsinus pacemaker rhythms. Diagnosis-specific mean resource costs were strongly correlated with each other and with mean Medicare reimbursement but not with case-fatality rate. CONCLUSION: Medicare claims data demonstrated striking differences among and within diagnoses of heart blocks or arrhythmias in terms of the populations at greatest risk for hospitalization. This variation should be explored further to generate and test hypotheses about differential causation or delivery of care.
Black or African American↗
Treatment of ventricular and supraventricular tachyarrhythmias by transcutaneous cardiac pacing.
The efficacy of noninvasive transcutaneous cardiac pacing (TCP) in the treatment of tachyarrhythmic events was tested in 24 patient: 14 with ventricular tachycardia, seven with supraventricular tachycardia and three with atrial flutter. Six (42.9%) ventricular tachycardias were interrupted: in two of the ten patients on whom underdrive pacing was attempted and in all four cases in which overdrive stimulation was possible. Five of the six supraventricular tachycardias utilizing an atrioventricular bypass tract were interrupted, while the TCP was unsuccessful on the only patient with atrioventricular nodal reentrant tachycardia. TCP failed to interrupt the arrhythmia in the three cases of atrial flutter. No clinically significant untoward effects (in particular tachycardia acceleration or ventricular fibrillation) were observed, except for a tolerable thumping sensation on the chest during pacing. In four patients, TCP effects on cardiac activation was evaluated by endocavitary recording: while the mean ventricular threshold was 70 mA, atrial capture was possible on only two patients at a current intensity of 140 and 150 mA. We consider our preliminary experience with TCP in the treatment of tachycardias encouraging. The technique was easily and rapidly usable and it was immediately successful in the majority of atrioventricular reentrant tachycardias and in a relevant percentage of ventricular tachycardias. In this latter setting TCP was mostly effective in the slower tachycardias where overdrive pacing was possible. A further experience with devices provided by higher pacing rates is warranted.
Cardiac Pacing, Artificial↗
Serum potassium concentrations are inversely related to ventricular, but not to atrial, arrhythmias in acute myocardial infarction.
In a study of 1033 consecutive patients with acute myocardial infarction, serum potassium concentrations were determined on admission to hospital and studied with respect to the subsequent occurrence of atrial fibrillation and flutter and of ventricular tachycardia and fibrillation. The study cohort fulfilled the inclusion criteria for the Norwegian timolol trial in which they later took part. In multivariate analysis, with serum potassium concentrations as a continuous variable, age, the presence of ventricular tachycardia and fibrillation, and maximum level of aspartate aminotransferase greater than four times the upper limit of normal were significantly associated with the occurrence of atrial fibrillation and flutter, while serum potassium concentration was not. Serum potassium concentrations and time from onset of the infarction to hospital admission were significantly negatively associated with the occurrence of ventricular tachycardia and fibrillation; while age, cardiomegaly, transient hypotension, pathological Q-waves in the electrocardiogram, atrial fibrillation and flutter, and ventricular premature beats were positively related to these arrhythmias. Thus, there is an independent inverse relationship between serum potassium concentrations and ventricular arrhythmias in acute myocardial infarction.
Adult↗
Augmented two-channel arrhythmia detection: an efficient diagnostic method for implantable devices.
ICDs are highly effective in preventing sudden cardiac death. However, inappropriate device shocks caused by false-positive diagnoses are estimated to happen in 20% of all patients. The need for implantable electrical devices to detect with precision arrhythmias requiring therapy has spawned a variety of proposals for better means of tachycardia identification. To address this problem, the augmented two-channel arrhythmia detection (A2CAD) algorithm, a real-time scheme utilizing timing and morphology from both the atrial and ventricular channels, is introduced. The algorithm uses rate detection as a first stage and augments this with morphological signal analysis in rhythms that confound the rate only diagnoses. The software executes in real-time (online), and has been tested on 60 passages of two-channel intracardiac signals. The following arrhythmias constituted the test set: 10 AF and/or atrial flutter; 15 SVT; 16 VT; 10 ventricular flutter or VF; 5 sinus tachycardia; and 4 cases of AF concurrent with VF. Results from 60 patient cases indicate 57 (95%) of 60 success rate for A2CAD, validating its potential for implementation in future implantable devices.
Algorithms↗
Modulation of atrioventricular conduction by ablation of the "slow" atrioventricular node pathway in patients with drug-refractory atrial fibrillation or flutter.
OBJECTIVES: We hypothesized that modulation of atrioventricular (AV) node conduction, allowing a reduction in ventricular rate during atrial fibrillation or flutter without affecting AV conduction during sinus rhythm, might be achieved through ablation of the "slow" AV node pathway. BACKGROUND: In patients with atrial fibrillation or flutter not amenable to a direct atrial approach, ablation of the His bundle is performed to induce complete AV block. This procedure causes pacemaker dependence. METHODS: Fourteen patients with drug-refractory paroxysmal atrial flutter or fibrillation underwent ablation of the slow AV node pathway. Radiofrequency current was delivered in six patients during sinus rhythm, in six during atrial flutter and in two during atrial fibrillation. RESULTS: The anterograde effective refractory period of the AV node was prolonged from 270 +/- 50 (mean +/- SD) to 390 +/- 87 ms (p = 0.005) and the Wenckebach cycle from 346 +/- 33 to 458 +/- 75 ms (p = 0.004) in six patients during sinus rhythm. Mean AV ratio increased from 1.6 +/- 0.5 to 3.0 +/- 0.6 (p = 0.02) in six patients with atrial flutter. Mean ventricular rate decreased from 157 +/- 38 to 67 +/- 10 beats/min in two patients with atrial fibrillation. Complete AV block was induced in two patients (transient in one, permanent in one). During a follow-up period of 5.8 +/- 3.5 months, 11 patients experienced a recurrence of atrial fibrillation at 60 to 95 beats/min. No patient had progression to any degree of AV block. CONCLUSIONS: Ablation of the slow AV node pathway allows reduction of ventricular rate during atrial fibrillation or flutter while maintaining intact AV conduction during sinus rhythm. Modulation of AV node conduction is effective in most patients as an alternative to His bundle ablation for control of ventricular rate in paroxysmal atrial fibrillation or flutter.
Adult↗
Right ventricular cardiomyopathy similar to Uhl's anomaly with atrial flutter and complete AV block.
We report an adult patient with right ventricular cardiomyopathy similar to Uhl's anomaly. In this patient an interesting manifestation is a transient atrial flutter with complete A-V block. Right ventricular cardiomyopathy (arrhythmogenic right ventricular dysplasia) is considered a cause of life-threatening arrhythmia. The right ventricular musculature is partially or totally absent and is replaced by fatty and fibrous tissue. Patients may present with ventricular arrhythmias, right heart failure or asymptomatic cardiomegaly. Only a few cases with atrioventricular conduction disturbance have been reported in the literature by now. We report such a case.
Animals↗
Safety and efficacy of flestolol, a new ultrashort-acting beta-adrenergic blocking agent, for supraventricular tachyarrhythmias.
Flestolol, a new ultrashort-acting (half-life 6.9 minutes) beta-blocking drug, was administered by intravenous infusion to 18 patients with new-onset atrial fibrillation or flutter and rapid ventricular response (120 beats/min or more for at least 30 minutes). Drug dose of flestolol was progressively increased until at least 1 of 3 endpoints was achieved: at least a 20% reduction in heart rate from baseline, heart rate 100 beats/min or less, or conversion to normal sinus rhythm. Flestolol was then administered as a maintenance infusion up to 24 hours. When flestolol was discontinued, patients were monitored for 1 additional hour. The mean ventricular response at baseline of 133 +/- 12 beats/min decreased to 103 +/- 20 beats/min at the end of flestolol titration (p less than 0.0001). Fourteen patients (78%) achieved defined endpoints. All 14 patients who continued to receive maintenance infusion had a sustained response. When flestolol was discontinued, ventricular response increased 33 +/- 23% within 60 minutes. The only adverse effect seen was hypotension in 2 patients. Flestolol is effective in slowing ventricular response in new-onset atrial fibrillation and flutter, maintains a therapeutic effect during continuous infusion and rapidly loses therapeutic effect when discontinued.
Adrenergic beta-Antagonists↗
[Ventricular fibrillation induced by transesophageal stimulation performed for the treatment of atrial flutter].
The authors describe a case of ventricular fibrillation occasionally induced by high rate transesophageal pacing, performed to treat an atrial flutter. They conclude that, although this technique is generally safe and well tolerated, it must be performed exclusively where an intensive care can be provided.
Aged↗
Verapamil for control of ventricular rate in paroxysmal supraventricular tachycardia and atrial fibrillation or flutter: a double-blind randomized cross-over study.
The effectiveness of verapamil in controlling ventricular rate was evaluated in 20 patients with atrial fibrillation or flutter with a rapid ventricular response (Group 1) and 30 patients with paroxysmal supraventricular tachycardia (Group 2). In Group 1 low-dose verapamil (0.075 mg/kg body weight) decreased the mean ventricular rate from 146 to 114 beats/min (p < 0.01) compared to a decrease of 145 to 132 beats/min (p < 0.01) after placebo. In Group 2, 14 of 29 patients converted to sinus rhythm after low-dose verapamil, nine of 15 after high-dose verapamil (0.15 mg/kg body weight), and one of 24 after placebo (p < 0.01). We conclude that verapamil results in a clinically significant slowing of the ventricular response in atrial fibrillation or atrial flutter and is superior to placebo for conversion of paroxysmal supraventricular tachycardia to sinus rhythm.
Adult↗
Acute ventricular rate control in atrial fibrillation and atrial flutter.
Atrioventricular node blocking agents including beta-adrenergic blockers, non-dihydropyridine calcium channel blockers and digoxin are usually effective in controlling ventricular rate in atrial fibrillation and flutter. Intravenous beta-blockers and non-dihydropyridine calcium channel blockers are equally effective in rapidly controlling the ventricular rate. The addition of digoxin to the regimen causes a favorable outcome but digoxin as a single agent is generally less effective in slowing the ventricular rate in acute setting. Clonidine, magnesium, and amiodarone have also been used for acute ventricular rate control in atrial fibrillation. Limited data suggest that combination regimens provide better ventricular rate control than any agent alone. The agent of first choice is usually individualized depending upon the clinical situation. Beta-blockers are preferable in patients with myocardial ischemia, myocardial infarction and hyperthyroidism and in post-operative state, but should be avoided in patients with bronchial asthma and chronic obstructive pulmonary disease where non-dihydropyridine calcium channel blockers are preferred. Beta-blockers are preferred drugs used for acute ventricular rate control in atrial fibrillation during pregnancy. In atrial fibrillation with Wolff-Parkinson-White syndrome, beta-blockers, calcium channel blockers and digoxin should be avoided, as these drugs are selective atrioventricular node blockers without slowing conduction through the accessory pathway, which can lead to increased transmission of impulses preferentially through the accessory pathway and precipitate ventricular fibrillation. The drug of choice for atrial fibrillation in pre-excitation syndrome is procainamide but propafenone, flecainide and disopyramide have also been used. When clinical condition is unstable or patient is hemodynamically compromised, immediate electrical cardioversion is the treatment of choice, as the best measure to control ventricular rate is by conversion to sinus rhythm. Factors precipitating rapid ventricular rate should be treated as well.
Atrial Fibrillation↗
[Should protocol of programmed ventricular stimulation be adapted to each patient? ].
The authors report the case of a 56 year old patient in whom the mechanisms of a wide QRS complex tachycardia recorded on an intensive care monitor could not be determined. The patient also had episodes of atrial flutter with left bundle branch block. Programmed ventricular stimulation with 3 extrastimuli triggered a non-specific ventricular flutter. One week later, the patient was resuscitated from a cardiac arrest which was undocumented. It was therefore important to elucidate the mechanism of the initial tachycardia. A second session of programmed ventricular stimulation was undertaken. As the use of 2 extrastimuli triggered runs of unsustained polymorphic ventricular tachycardia, the classical protocol was stopped. An infusion of low-dose isoproterenol was used to repeat programmed stimulation with a single extrastimulus. This protocol triggered sustained monomorphic ventricular tachycardia at 240/min. The diagnosis of ventricular tachycardia could therefore be continued.
Cardiac Pacing, Artificial↗
Intravenous amiodarone for therapy of atrial fibrillation and flutter in critically ill patients with severely depressed left ventricular function.
A retrospective review was done to determine the efficacy and hemodynamic effects of slow intravenous amiodarone administration on invasively monitored patients with acute onset of atrial fibrillation or atrial flutter and left ventricular ejection fractions < 15%. Eight patients met predefined inclusion criteria. All received 300 mg amiodarone intravenously over 1 hour. Seven reverted to sinus rhythm within 1 hour, with return of most hemodynamic variables to baseline. Before reversion, each patient experienced a beneficial slowing of heart rate (mean, 28%) resulting in significant improvement of stroke volume index (mean, 49%) and left ventricular stroke work index (mean, 61%). No patient had hemodynamic deterioration attributable to amiodarone infusion. Slow intravenous infusion of amiodarone appears to be an effective and hemodynamically well-tolerated therapy for atrial fibrillation and atrial flutter in critically ill patients with marked depression of left ventricular systolic function.
Acute Disease↗
The clinical characteristics of acute myocardial infarction in aged patients.
Age is one of the important prognostic factors for acute myocardial infarction. This study was performed to clarify the clinical characteristics and outcome of acute myocardial infarction in Chinese geriatric patients. The study subjects included 742 patients, divided by age into 2 groups: Group A greater than or equal to 65 years, 321 cases; and Group B less than 65 years, 421 cases. The following characteristics were compared between these 2 groups: sex composition; presence of chest pain, heart failure or shock at presentation; cardiac functional status; occurrence of various complications, and follow-up data. Males were less prominent in the older group: 229 patients (71.3%) in Group A, and 371 patients (88.1%) in Group B. At onset, the older patients presented with less chest pain (72% vs 86.5%) and more heart failure (35.2% vs 20.2%), but the occurrence of shock was similar (5.9% vs 4.5%, for Groups A and B, respectively). During hospitalization, more patients in Group A showed impaired cardiac function, as evidenced by a higher percentage of patients identified as in Killip class III or IV (35.4% vs 21.1%). Concerning complications, the older group showed a higher incidence of hypotension, low cardiac output, lung edema, frequent premature ventricular beats, atrial flutter and/or fibrillation, complete heart block and intraventricular conduction defects, but ventricular septal defects, ventricular tachycardia and ventricular fibrillation did not show any difference in occurrence. Life table analysis showed that the survival rate was significantly lower for Group A during the follow-up period of 5 years.(ABSTRACT TRUNCATED AT 250 WORDS)
Age Factors↗
[The use of Cordanum in combination with Corinfar-Retard for the treatment of ectopic arrhythmias in the sick sinus syndrome in patients with ischemic heart disease].
38 patients with ischemic heart disease (IHD) and sick sinus syndrome (SSS) received combined therapy with nifedipine (Corinfar-Retard) and talinolol (Cordanum). The former drug had a positive chronotropic effect on the heart, the latter's chronotropic effect was slightly negative. All the patients had sinus bradycardia and ectopic arrhythmia which needed therapeutic correction: supraventricular and ventricular extrasystoles, fibrillation paroxysms or/and atrial flutter, paroxysmal supraventricular tachycardia, ventricular tachycardia. Cordanum was given in a dose 50 mg twice a day, Corinfar-Retard 20 mg twice a day for 16 days. 30 patients responded to the treatment. In addition to good subjective response, episodes of extrasystoles, paroxysms, flutter and fibrillation occurred much less frequently. Side effects resulted in the treatment discontinuation in 3 patients.
Adult↗