[ANTI-ARRHYTHMIC SUBSTANCES IN THE TREATMENT OF THE HEART].
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Antiarrhythmic treatment was required in 35 patients aged one day to 11 8/12 years (average 5 7/12 years) for one or several of the following arrhythmias: paroxysmal supraventricular tachycardia (17), ventricular extrasystole (16), ventricular tachycardia (17), ventricular extrasystole (16), ventricular tachycardia (4), junctional tachycardia (4), and atrial flutter (3). 300 mg/m2/day oral propafenone was administered in 3 to 4 divided doses. The arrhythmia in 21 of the 35 patients had been unsuccessfully treated by digoxin (6), verapamil (5), ajmalin (4), propranolol (3), spartein (1), phenytoin (1), and lidocain (1) prior to the propafenone therapy. However, the arrhythmias could be abolished or reduced in 30 patients (85.7%) by Propafenone. In 5 patients with supraventricular tachycardia (2), junctional tachycardia (2), or ventricular extrasystole (1), propafenone therapy had no effect. In two other patients propafenone led to atrioventricular conduction disturbances and had to be discontinued. Propafenone is an effective well tolerated antiarrhythmic drug without major side effects in pediatric patients.
1. Four beta-adrenoceptor antagonists, viz. (+/-) propranolol (0.5 mg/kg), (-) alprenolol (0.25 mg/kg), practolol (5 mg/kg) and USVC 6524 (20 mug/kg), were tested for their effects on atrial flutter produced by electrical stimulation of the right atrium around the crushed inter-venae-caval bridge in anaesthetized dogs.2. All the drugs reduced atrial and ventricular rates; this was followed by the abrupt termination of flutter and restoration to normal sinus rhythm.3. Since all the drugs (including practolol, which is devoid of local anaesthetic activity) were given in doses just sufficient to block beta-adrenoceptors, it indicated that beta-adrenoceptor blockade was responsible for their antiarrhythmic property in this test procedure.4. Further evidences in support of participation of the sympathetic nervous system in poststimulatory flutter were: (i) flutter could not be produced in nine out of ten dogs whose catecholamine stores were depleted by pretreatment with reserpine; (ii) infusion of adrenaline in these animals resulted in the production of flutter; (iii) duration of flutter after termination of exposure to adrenaline was a few minutes, which is similar to the brief time previously reported to be taken for the disappearance of catecholamines from the hearts of reserpinized animals.5. The clinical significance of the above findings is discussed.
43 patients, 3 days to 12 years old, presented 68 paroxysms of supraventricular tachycardia and 2 crises of atrial flutter. 6 patients had a WPW syndrome and only 7 had an associated cardiac disease; the remaining had no other complaint but the arrhythmia. Verapamil, administered in the dose of 0.125-0.25 mg/Kg intravenously, interrupted critically the tachycardia in virtually all cases. The flutter was converted to atrial fibrillation with a slower ventricular rate. No adverse effects were observed but in two cases: one had a cardiac arrest promptly relieved and another a ventricular bradycardia corrected by atropine. Both cases had received an overdose of the drugs.
HISTORY AND CLINICAL FINDINGS: We present a 38-year-old male patient with progressive exertional dyspnoea and intermittent palpitations. The initial examination detected a regular tachycardia with a heart rate of 160 bpm. EXAMINATIONS, DIAGNOSIS: In association with intermittent palpitations the 12-lead ECG detected a typical type of atrial flutter. A transthoracic echocardiography and cardiac catheterization revealed a left ventricular dilation and marked systolic dysfunction (EF 39 %) with normal coronaries. The diagnosis of dilated cardiomyopathy was made on these findings. TREATMENT AND COURSE: On the basis of this diagnosis, we treated our patient by radiofrequency catheterablation, which successfully terminated atrial flutter. Three month after ablation the echocardiography was normal with an increase of the shortening fraction from 18 to 37 % and the patient was asymptomatic. Retrospectively the diagnosis of tachycardia-induced cardiomyopathy was made. CONCLUSION: Tachycardia-induced cardiomyopathy is a rare, but reversible form of dilated cardiomyopathy. The cornerstone in the management of these patients is to achieve a normal ventricular beating rate. Radiofrequency catheterablation is a curative therapeutic option that can terminate tachyarrhythmias and lead to significant improvement of left ventricular diameters, systolic function and symptoms in patients with tachycardia-induced cardiomyopathy.
The patterns of valve motion were analyzed in 14 patients with combined aortic and mitral valve prolapse by two-dimensional echocardiography. Four patients have also tricuspid valve prolapse. In one we could find evidence of a myxomatous pulmonic valve with prolapse of the posterior cusp. By two-dimensional echocardiography all patients had redundant aortic leaflets bulging into left ventricular outflow tract during diastole. M-mode examination of the aorta was normal in five patients; eccentricity of the diastolic aortic valve echo was found in two patients; seven showed multiple echoes from the valve leaflets, with diastolic fluttering. The aortic valve was visualized in the left ventricular outflow tract during diastole in one patient. The size of the aortic root was normal in all. Six patients had transient ischemic cerebral attacks and no evidence of extracranial or intracranial vascular disease by angiography. As polyvalvular prolapse as demonstrated by echo suggest a myxomatous degeneration of the valves, we hypothesize that there may be a causal relationship between TIA and this type of pathological process.
The objective of this multicenter, randomized, double-blind, placebo-controlled study was to determine the safety and efficacy of intravenous diltiazem in the treatment of 37 patients with rapid (ventricular rate, mean +/- SD 142 +/- 17 beats/min) atrial fibrillation or flutter and moderate to severe congestive heart failure (ejection fraction, mean +/- SD 36 +/- 14%; New York Heart Association class III [23 patients], class IV [14 patients]). During the double-blind portion of the study, patients received either intravenous diltiazem, 0.25 mg/kg over 2 minutes, or placebo followed 15 minutes later by diltiazem or placebo, 0.35 mg/kg over 2 minutes, if the first dose was tolerated but ineffective. Placebo nonresponders were given open-label intravenous diltiazem in a similar fashion as in the double-blind portion of the study. In the double-blind part of the study, 21 (18 with 0.25 mg/kg, 3 with an additional 0.35 mg/kg) of the 22 patients (95%) responded to diltiazem, and 0 of 15 patients (0%) responded to placebo (p < 0.001). All 15 patients (13 with 0.25 mg/kg and 2 with an additional 0.35 mg/kg) who received placebo during the double-blind period had a therapeutic response to diltiazem during open-label therapy. Overall, 36 of 37 patients (97%) had a therapeutic response to intravenous diltiazem. Heart rate response to diltiazem after the 2-minute bolus infusions consisted of a > or = 20% decrease in heart rate from baseline in 36 patients; in addition, 17 patients also had heart rates decreased to < 100 beats/min, whereas no patient had conversion to sinus rhythm.(ABSTRACT TRUNCATED AT 250 WORDS)
The effects of intravenous verapamil on the electrocardiogram in 15 patients with heart disease in sinus rhythm and in 44 patients with supraventricular and ventricular tachyarrhythmias were evaluated. Verapamil prolonged the P-R interval without effect on the QRS duration or the Q-Tc interval. In patients with atrial flutter and fibrillation, A-V block was increased, with slowing of the ventricular rate, in almost all cases but sinus rhythm was restored in only 1 of 12 patients in atrial fibrillation and in 2 of the 11 patients with flutter. Verapamil had no effect in 3 patients with atrial fibrillation complicating WPW syndrome; in 1 of 5 patients with ventricular tachycardia it caused reversion to sinus rhythm. Sinus rhythm was restored promptly by verapamil in 13 of 17 patients with paroxysmal supraventricular tachycardias; in 2 others, sinus rhythm became established 1 to 2 hours after administration of the drug. Transient hypotension, not requiring treatment, was the only side effect noted but not in the patients with supraventricular tachycardias, in whom blood pressure generally increased after reversion to sinus rhythm by verapamil.
A 34-year-old man reported heart fluttering and near syncope a few hours after marijuana smoking. In the emergency department, he was found to have a right bundle-branch-type ventricular tachycardia. The patient underwent a successful electric cardioversion. Coronary angiography showed no pericardial artery stenosis yet very slow coronary blood flow. Clinical tachycardia was also inducible in the electrophysiologic laboratory. After verapamil therapy and cessation of marijuana, his coronary flow normalized and ventricular tachycardia was no longer inducible in the electrophysiologic laboratory. Marijuana use might affect coronary microcirculation and cause ventricular tachycardia. Verapamil therapy and cessation of smoking might be curative.
BACKGROUND: Ventricular arrhythmia and sudden cardiac death late after repair of tetralogy of Fallot are devastating complications in adult survivors of early surgery, but their prediction remains difficult. METHODS: We examined surgical, electrocardiographic, and late haemodynamic data, and their relation to clinical arrhythmia and sudden death occurring over 10 years, in a multicentre cohort of patients with repaired tetralogy, who were alive in 1985. RESULTS: Of 793 patients (mean age at repair 8.2 years [SD 8], mean time from repair 21.1 years [8.7]) who entered the study, 33 patients developed sustained monomorphic ventricular tachycardia, 16 died suddenly, and 29 had new-onset sustained atrial flutter or fibrillation. Electrocardiographic markers (QRS duration, QRS rate of change between 1985 and 1995) were significantly greater in the ventricular tachycardia and sudden-death groups. Older age at repair was associated with a higher risk of sudden death and atrial tachyarrhythmia. Pulmonary regurgitation was the main underlying haemodynamic lesion for patients with ventricular tachycardia and sudden death, whereas tricuspid regurgitation was for those with atrial flutter/fibrillation. Despite adverse haemodynamics, no patient who died suddenly had undergone late reoperation. CONCLUSION: Arrhythmia and sudden death are important late sequelae for patients after repair of tetralogy of Fallot. The electrophysiological and haemodynamic substrate of sudden death resembled that of sustained ventricular tachycardia, with pulmonary regurgitation being the predominant haemodynamic lesion. Preservation or restoration of pulmonary valve function may thus reduce the risk of sudden death. Furthermore, electrocardiographic markers can help to identify patients at risk.
BACKGROUND: Automatic mode switching is defined as the ability of a pacemaker to reprogram itself from tracking to non-tracking mode in response to atrial tachyarrhythmias, and to regain tracking mode as soon as the tachyarrhythmia terminates. In contrast to upper rate behavior, mode switching does not only limit atrial tracking at a certain rate but actively drives the ventricular pacing rate back to lower rate or sensor rate as long as the atrial tachyarrhythmia persists. In contrast to DDD with mode switch, AV synchrony may be lost in DDIR mode if the sinus rate exceeds the sensor rate. DDD pacing with mode switching represents a valuable option in patients with AV block and paroxysmal atrial tachyarrhythmias. It may prevent the transition from paroxysmal to permanent atrial fibrillation after AV node ablation to a higher extent than VVI(R) pacing. On the other hand, patients with sinus node disease and normal AV conduction may benefit from DDIR mode with long AV interval. Mode switching should provide a rapid, sensitive and specific detection of atrial tachyarrhythmias, fast switch to non-tracking mode without ventricular pacing at the upper rate limit, adequate ventricular rate during the atrial tachyarrhythmia, rapid, sensitive and specific detection of conversion to sinus rhythm and fast switch back to tracking mode. In addition, oscillations between DDD and DDI mode with sudden ventricular rate changes should be avoided. MODE-SWITCHING ALGORITHMS: To achieve these aims, different mode-switching algorithms have been developed which all show specific disadvantages: reliable but slow response to atrial tachyarrhythmias, fast but unspecific switch to non-tracking mode, mode oscillations, inclination to inadequate mode-switching due to ventricular far-field sensing, failure to perform modeswitching during atrial flutter or intermittent atrial undersensing. Some of these problems can be avoided by careful atrial lead implantation providing atrial signals above 2 mV and avoiding ventricular far-field signals. Programming of mode-switching related parameters (e.g. atrial rate and number of fast beats required for mode switch), atrial blanking times, and atrial sensitivity can solve some of the problems with mode switching. Clinical results show a strong influence of device programming and atrial undersensing on mode-switching performance. Some data suggest a superiority of fast mode-switching algorithms with regard to clinical symptoms. However, loss of AV synchrony during sinus rhythm due to premature or inadequate mode switching may limit the benefit of fast mode switching. FURTHER DEVELOPMENTS: Improved performance may be achieved by a combination of different mode-switching algorithms (e.g. one algorithm for detection of atrial fibrillation, another one for detection of atrial flutter). In addition, programmability of several algorithms (e.g. mean atrial rate, beat-to-beat, x out of y) within the same device and atrial cycle-dependent sensitivity adjustment similar to automatic gain control in implantable defibrillators may further increase the clinical use of automatic mode switching.
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Inappropriate therapy of supraventricular tachyarrhythmias by an ICD is still a common problem. Dual chamber (DDD) ICDs provide additional atrial sensing and should result in higher specificity for detection of supraventricular tachyarrhythmias. However, a direct comparison of different dual chamber algorithms has not been reported. The detection algorithms of four different DDD ICDs were tested: Phylax AV, Defender IV, Ventak AV III DR, and Gem DR 7271. Based on arrhythmias recorded from patients undergoing invasive electrophysiological studies and in many cases of catheter ablation at our institution, a library consisting of 71 supraventricular and 15 ventricular tachyarrhythmias was created. The library consists of episodes of atrial fibrillation, atrial flutter with different AV conduction, typical and atypical AV nodal reentrant tachycardia, AV reentrant tachycardia, sinus tachycardia, and ventricular tachycardia with and without ventriculoatrial conduction. Atrial fibrillation was appropriately classified by all four algorithms. However, the specificity for detection of other supraventricular tachyarrhythmias achieved by the Biotronik (12%) and the Guidant (11%) devices was significantly lower compared to the specificity of the ELA (28%) and the Medtronic DDD ICD (20%). This is due to the fact that the Biotronik and the Guidant algorithm classified all supraventricular tachyarrhythmias resulting in a stable ventricular rate as ventricular tachycardia, whereas the ELA and Medtronic algorithms performed a more detailed analysis by assessment of PR association, atrial onset, or timing of the atrial event relative to the ventricular event, respectively. Atrial fibrillation, the most common supraventricular tachyarrhythmia in patients with ICD, was detected by all devices.
Thirty nine cases, in which sudden cardiac death (SCD) was suspected, were studied to evaluate the mechanism and the prediction of SCD in arrhythmia-patients using electrophysiological studies (EPS). The 39 cases (28 male and 11 female) were located by surveying 2098 patients who underwent EPS for the evaluation of arrhythmias. Age at time of EPS ranged from 4 to 86 years, average 50.5 years. Time from EPS to death was 2 to 163 months, average 27.9 months. Underlying heart disease was: dilated cardiomyopathy in 11, old myocardial infarction in 5, ischemic heart disease in 5, hypertensive heart disease in 5, valvular heart disease in 3, hypertrophic cardiomyopathy in 2, arrhythmogenic right ventricular dysplasia in 1, myocarditis in 1, sarcoidosis in 1, cor pulmonale in 1, and no obvious heart disease in 4. Fifteen had a permanent pacemaker implanted. SCD in cases without a permanent pacemaker (24 cases): 2 had chronic complete A-V block (one BH block, one HV block), 1 had advanced A-V block (HV block), 3 had bundle branch block with first degree HV block, 9 had ventricular tachycardia (VT), 3 had sick sinus syndrome (SSS), 3 had paroxysmal atrial flutter, 1 had WPW syndrome and paroxysmal atrial fibrillation, 1 had paroxysmal atrial tachycardia, and 3 had premature ventricular beats and first degree HV block. SCD in cases with permanent pacemaker (15 cases): 5 had SSS, and 10 had A-V block. In 3 of the 5 with SSS and 7 of the 10 with A-V block, VT was found before pacemaker implantation. In our study, brady and tachyarrhythmias coexisted in 25 cases (64%).(ABSTRACT TRUNCATED AT 250 WORDS)
Plasma atrial natriuretic peptide (ANP) concentrations were measured before and 1 hour after cardioversion in 40 patients (27 with atrial flutter and 13 with atrial fibrillation) admitted for elective cardioversion. Fourteen (11 with atrial flutter and 3 with atrial fibrillation) had clinical evidence of congestive heart failure (CHF). Conversion to sinus rhythm was successful in 39 patients. The mean ANP concentration in the entire group decreased after cardioversion from 38 +/- 4 to 17 +/- 2 pmol/liter (p less than 0.001). In the subgroup with CHF, the ANP level, which was not significantly higher than that in the group without CHF, decreased from 47 +/- 8 to 19 +/- 3 pmol/liter (p less than 0.01). Neither mode of cardioversion (spontaneous 1, pharmacologic 2 and direct-current countershock 36) nor associated CHF influenced ANP response to cardioversion. One patient with atrial flutter and "failed cardioversion" had unchanged ANP level. The decrease after cardioversion in ANP concentration correlated with its control level (r = 0.88, p less than 0.001) but not with the decrease in heart rate. The ANP level in patients with atrial fibrillation was 45 +/- 9 vs 38 +/- 5 pmol/liter in those with atrial flutter (difference not significant). Arrhythmia duration, left atrial size, and ventricular rate or arterial blood pressure did not correlate with ANP concentration in any subgroup. It is concluded that (1) the ANP level is elevated comparably in patients with both atrial flutter and fibrillation regardless of the presence or absence of CHF; and (2) the level decreases, independent of the mode of cardioversion or presence of CHF, promptly after successful cardioversion.
Certain general conclusions suggest themselves on the basis of our extensive experience with treating arrhythmias in patients following open heart surgery, our specific results with verapamil therapy in the treatment of atrial fibrillation and atrial flutter in patients following open heart surgery, and the results of verapamil therapy administered in other groups of patients. First, verapamil can provide highly effective, rapid, and safe control of the ventricular response in the treatment of atrial fibrillation and atrial flutter in patients following open heart surgery. Usually, it should be used in concert with digitalis therapy. Second, extrapolation from the data of others suggests that verapamil has an important role to play in the treatment of most other supraventricular arrhythmias in patients following open heart surgery, particularly if temporary wire electrodes are not available.
Supraventricular tachycardia constitutes a significant clinical problem, frequently requiring medical intervention. We analyzed data in 413 consecutive patients with supraventricular tachycardia treated at our center with the catheter ablative technique and found the following outcome. Among 272 patients who had regular narrow QRS tachycardia without ventricular pre-excitation during sinus rhythm (Group I), control was achieved in all but one case (success rate 99.6%). Patients in Group II had ventricular pre-excitation during sinus rhythm and narrow or wide QRS tachycardia. Elimination of ventricular pre-excitation and control of the tachycardia was achieved in 104 of the 106 cases in this group (a success rate of 98%). Group III patients had atrial flutter-fibrillation as the predominate arrhythmia and control of rapid ventricular response was successfully achieved with atrioventricular junctional ablation in all 35 cases. Serious complications were related to anticoagulation and were seen in less than 2% of the cases. There were no instances of thromboembolic phenomena or death related to these procedures. It is concluded that the catheter ablative technique with radio frequency as the energy source is a highly effective means for control of supraventricular tachycardia with minimal associated risk of serious complications.
The Authors tested the effectiveness of amiodarone hydrochloride i.v. in 50 cases of supraventricular hyperkinetic arrhythmias recently aroused. 50 patients, aged 41 to 85 years, with paroxysmal supraventricular tachycardia (PSVT, 21 cases), atrial flutter (7 cases) or fibrillation (22 cases) were treated with 4 mg/Kg of body weight of amiodarone i.v. over 2 min., followed by other 1500 mg/24 hours over 48 hours while amiodarone per os was started for antiarrhythmic prophylaxis; a 12 leads surface ECG and blood pressure were periodically recorded. The sinus rhythm was restored within 3 hours in every case of PSVT (100% of success), within 30 hours in 19 cases of atrial fibrillation (86% of success) and in 5 cases of atrial flutter (71% of success). A slowing down of ventricular frequency ranging from 15 to 40% occurred within 10 min. in case of failure of restoration of sinus rhythm; a slight and transient lengthening of P-R occurred in 1 case; no particular side effects nor noteworthy changes of blood pressure were observed. Amiodarone i.v. proved to be a very effective remedy, handy and well tolerated for the arrhythmias considered above.