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Biomedical subjects

A Bhandari

Publications and source records attributed to A Bhandari.

At least 37 records · Page 2Linked to original sources
PubMed1992

Combined use of beta-adrenergic blocking agents and long-term cardiac pacing for patients with the long QT syndrome.

OBJECTIVE: The objective of this study was to review our current experience using a combination of beta-adrenergic blocking agents and long-term cardiac pacing to treat patients with the idiopathic long QT syndrome. BACKGROUND: Patients with the idiopathic long QT syndrome are at high risk for sudden cardiac death. Before combination therapy, 20 of the 21 study patients experienced either cardiac arrest (n = 8) or syncope (n = 18) and 11 had documented polymorphous ventricular tachycardia. Nine of these patients had not responded to isolated beta-blocker therapy and five had not responded to isolated left cervicothoracic sympathectomy. METHOD: All patients were treated with combined beta-blocker therapy and long-term cardiac pacing at a rate designed to normalize the QT interval. RESULTS: Cardiac pacing at rates of 70 to 125 beats/min resulted in shortening of the QT and corrected QT (QTc) intervals from 517 +/- 78 and 541 +/- 62 ms to 404 +/- 37 and 479 +/- 41 ms, respectively. The mean follow-up interval after institution of pacing was 55 +/- 45 months. The only sudden death occurred in a patient who had discontinued beta-blocker therapy. Syncope occurred in four patients, two of whom had interrupted pacemaker function due to lead fracture. Pacemaker problems, partly attributable to the specific rate required for QT interval shortening and to avoidance of T wave sensing, were relatively common. No patient who continued the combination therapy died, but 10% of these patients had a recurrence of symptoms. CONCLUSIONS: Combination therapy with a beta-blocker and cardiac pacing appears to be a highly effective primary therapy for symptomatic patients with the long QT syndrome and to provide excellent adjunctive therapy for patients who require insertion of an automatic internal defibrillator.

Adrenergic beta-Antagonists↗
PubMed1991

Polymorphous ventricular tachycardia associated with acute myocardial infarction.

BACKGROUND: During a 2.9-year period, 11 patients developed polymorphous ventricular tachycardia 1-13 days after acute anterior (seven patients) or inferior (four patients) myocardial infarction. None of the 11 patients had sinus bradycardia (mean heart rate, 90 +/- 23 beats/min), but three had a sinus pause immediately before the onset of polymorphous ventricular tachycardia. In all 11 patients, the QT interval and corrected QT interval (QTc) were normal or minimally prolonged (QT, 385 +/- 34 msec; QTc, 442 +/- 40 msec). None had significant hypokalemia (mean serum potassium concentration, 4.3 +/- 0.5 meq/l) or a grossly abnormal serum magnesium or calcium concentration (2.1 +/- 0.4 and 8.9 +/- 0.7 mg/dl, respectively). METHODS AND RESULTS: Immediately before the onset of polymorphous ventricular tachycardia, symptoms and/or electrocardiographic changes consistent with recurrent myocardial ischemia occurred in nine of 11 patients. One patient died before drug therapy could be initiated. Lidocaine was used in 10 patients and proved to be effective in only one. Intravenous procainamide was used in six patients: one improved, and five had recurrence of polymorphous ventricular tachycardia. Bretylium was used in five patients and was ineffective in all cases. Overdrive pacing was used in four patients and failed to suppress recurrent arrhythmias in all cases. Four patients with persistent polymorphous ventricular tachycardia unresponsive to lidocaine, procainamide, or bretylium responded to intravenous amiodarone. One patient with polymorphous ventricular tachycardia that was consistently preceded by ST segment elevation responded to intravenous nitroglycerin. Two patients with persistent polymorphous ventricular tachycardia and obvious recurrent ischemia unresponsive to pharmacological intervention responded to emergency coronary revascularization. A third patient who experienced recurrent angina and polymorphous tachycardia was initially stabilized with pharmacological therapy but subsequently underwent elective revascularization and has remained stable without antiarrhythmic therapy. CONCLUSIONS: Post-myocardial infarction polymorphous ventricular tachycardia is not consistently related to an abnormally long QT interval, sinus bradycardia, preceding sinus pauses, or electrolyte abnormalities. This arrhythmia has a variable response to class I antiarrhythmics but may be suppressed by intravenous amiodarone therapy. It is often associated with signs or symptoms of recurrent myocardial ischemia. Furthermore, coronary revascularization appears to be effective in preventing the recurrence of polymorphous ventricular tachycardia when associated with recurrent postinfarction angina.

Aged↗
PubMed1987

Permanent cardiac pacing in patients with the long QT syndrome.

A permanent pacemaker was inserted in eight patients with the long QT syndrome. All had recurrent syncope or seizures, six had documented torsade de pointes and four had aborted sudden death. Among the eight patients, permanent pacing was instituted in three who were unsuccessfully treated with both a beta-adrenergic blocking agent and left cardiothoracic sympathectomy, and in two who proved refractory or intolerant to beta-blockers. Another three patients had pacemaker implantation and long-term beta-blocker therapy because of spontaneous atrioventricular (AV) block in one, aborted sudden death in one and patient preference in one. After pacing (70 to 85 beats/min), there was no significant change in the mean corrected QT interval, but the mean QT interval decreased significantly (534.4 +/- 51.4 to 425.6 +/- 18.9 ms, p less than 0.0001). Over a mean follow-up period of 35.1 +/- 18.9 months, all patients are alive and currently free of syncope. One patient without a history of stress-induced syncope had two syncopal episodes (believed to be due to hyperventilation) while under severe emotional stress, but has been symptom free for the past 5 years. One patient with an atrial demand (AAI) pacemaker developed dizziness due to documented episodes of AV block, but remains asymptomatic after conversion to atrial rate-responsive dual chamber (DDD) pacing. Either atrial or ventricular pacing combined with beta-blocker therapy appears to be effective treatment for a subset of patients with the long QT syndrome, by either preventing episodes of torsade de pointes or alleviating symptoms due to bradycardia from beta-blocker therapy.

Adolescent↗
PubMed1987

Hemodynamic and electrophysiologic effects of encainide in patients with bundle branch block.

Electrophysiologic studies were performed in 6 consecutive patients with bundle branch block and organic heart disease. All were studied after intravenous (0.9 mg/kg) encainide and 3 of the 6 after 36-72 hours of oral encainide (50 mg every 6 hours). After intravenous encainide, mean H-Q increased from 51 +/- 20 msec to 58 +/- 25 msec (14% p less than or equal to .05). After oral encainide (3 patients) H-Q increased to 90 +/- 39 msec (56% p less than or equal to .05, compared to baseline). Programmed ventricular stimulation was performed in 5. In 1 patient without spontaneous ventricular tachycardia, tachycardia was non-inducible before and after encainide. Of 5 patients with spontaneous arrhythmia, 3 had ventricular tachycardia induced before and after intravenous encainide at mean cycle lengths of 287 +/- 130 msec and 407 +/- 261 msec, (not significant) respectively, while 1 had ventricular tachycardia induced only after encainide. Four patients began chronic treatment with oral encainide (2 patients with inducible rapid ventricular tachycardia after encainide were excluded). All suffered major adverse outcomes. One died suddenly after an electrophysiology study demonstrated inducible ventricular tachycardia, which occurred only after encainide. One experienced new syncope after baseline H-Q increased 75% after encainide. Two patients developed new sustained atrial tachycardias and 1 patient developed persistent ventricular tachycardia on encainide.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1986

Effective termination of reentrant supraventricular tachycardia by single dose oral combination therapy with pindolol and verapamil.

We evaluated the efficacy of single oral dose combining 20 mg pindolol and 120 mg verapamil in termination of paroxysmal supraventricular tachycardia (SVT) in 12 patients with recurrent symptomatic tachycardia. All had electrically inducible SVT lasting longer than 30 minutes. Patients were administered placebo or crushed pindolol and verapamil on 2 consecutive days after tachycardia was electrically induced and allowed to sustain for 30 minutes. With placebo, SVT lasted 186 +/- 18 minutes (mean +/- SEM); five patients converted spontaneously within 121 to 180 minutes. With pindolol and verapamil, 9 of 12 patients (responders) converted to sinus rhythm within 8 to 74 minutes. The mean duration of SVT in the nine responders was 28 +/- 8 minutes compared with 168 +/- 20 minutes on placebo (p less than 0.001). Before termination, tachycardia rate on pindolol and verapamil slowed significantly from 182 +/- 5 to 164 +/- 7/min (p less than 0.05) compared with no significant change in the rate of SVT on placebo. The mean systolic blood pressure during tachycardia was 97 +/- 5 mm Hg with placebo and 101 +/- 7 mm Hg with pindolol and verapamil. Serum levels of pindolol and verapamil obtained in seven patients at time of spontaneous termination of tachycardia were 66 +/- 13 and 56 +/- 14 ng/ml, respectively. The side effects with pindolol and verapamil included lightheadedness in one patient and symptoms of rapid palpitations in three. A single oral dose of pindolol and verapamil is safe and effective in termination of acute paroxysmal SVT and may be the initial therapy of choice in selected patients.

Adult↗
PubMed1985

Clinical symptoms in patients with sustained ventricular tachycardia.

We questioned 113 patients with subsequently diagnosed sustained ventricular tachycardia (VT) regarding the symptoms that prompted their seeking hospital treatment, eliciting the following: 15% of patients had lost consciousness, 15% had near syncope, 35% had mild lightheadedness and 35% had no cerebral symptoms. Patients with preexisting congestive heart failure or a VT rate of 200 beats per minute or greater more often lost consciousness. Other symptoms included palpitations in 57% of patients, chest pain in 27%, dyspnea in 25%, weakness in 6%, nausea or diaphoresis in 3% each and flushing in 2%. In approximately 50% of patients who had mild lightheadedness or no cerebral symptoms, their condition was incorrectly diagnosed as supraventricular tachycardia based on the absence of severe symptoms during the tachycardia. In some patients, VT may be associated with mild or atypical symptoms. The differentiation of supraventricular from ventricular tachycardia should be based on electrocardiographic criteria and should not be influenced by the nature or severity of a patient's symptoms. The severity of cerebral symptoms is at least partially related to the VT rate and a patient's underlying heart disease.

Adult↗
PubMed1984

Electrophysiologic testing in bundle branch block and unexplained syncope.

Thirty-two patients with bundle branch block and unexplained syncope underwent electrophysiologic testing, including programmed ventricular stimulation with up to triple extrastimuli. The infranodal conduction time (HV) was 70 ms or greater in 12 patients. Pathologic infranodal block during atrial pacing occurred in 2 patients. Unimorphic ventricular tachycardia (VT) was induced in 9 patients (28%) and polymorphic VT in 5 (16%). A permanent pacemaker was implanted in patients with infranodal block during atrial pacing and, generally, in patients with an HV of 70 ms or more. Patients with inducible unimorphic or sustained polymorphic VT were treated with an antiarrhythmic drug. The mean follow-up period was 19 +/- 14 months (+/- standard deviation). Three patients died suddenly: a noncompliant patient with inducible sustained VT; a patient with a normal electrophysiologic study treated empirically with quinidine for premature ventricular complexes; and a patient with an HV of 70 ms and no inducible VT treated with a permanent pacemaker. The actuarial incidence of sudden death was 10% at 45 months of follow-up. Only 2 patients had recurrent syncope; both had a normal electrophysiologic study. Approximately 50% of patients with bundle branch block and unexplained syncope who undergo electrophysiologic testing are found to have a clinically significant abnormality (HV of 70 ms or more, infranodal block during atrial pacing and inducible unimorphic VT), and some patients have more than 1 abnormality. Long-term management guided by the results of electrophysiologic testing generally is successful in preventing recurrent syncope.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1984

Programmed ventricular stimulation in mitral valve prolapse: analysis of 36 patients.

Programmed ventricular stimulation with 3 extrastimuli was performed in 36 patients with mitral valve prolapse (MVP). Among 11 patients without transient cerebral symptoms, none had inducible ventricular tachycardia (VT) or ventricular fibrillation (VF), whether or not nonsustained VT or ventricular premature complexes (VPC) were present during ambulatory electrocardiographic recordings. These patients remained well without antiarrhythmic drug therapy for 6 to 57 months (mean 23) of follow-up. Two patients with recurrent unexplained syncope and no documented ventricular arrhythmia during electrocardiographic monitoring also had no inducible VT or VF. Among 20 patients with syncope or presyncope and documented nonsustained VT or VPCs during electrocardiographic monitoring, polymorphic nonsustained VT was induced in 8, sustained unimorphic VT in 2, and VF in 3. In 1 patient who had inducible polymorphic nonsustained VT, electrocardiographic monitoring during syncope showed sinus rhythm. Among 3 patients with a history of sustained VT or VF, unimorphic VT was induced in each. Patients with MVP who have asymptomatic ventricular ectopic activity and no inducible VT may have a benign prognosis without treatment. In patients who have transient cerebral symptoms and documented nonsustained VT or VPCs, VT or VF is inducible in 65%, most often polymorphic VT. It is unclear in which patients this finding is clinically significant and in which it is a nonspecific response to programmed stimulation.

Adult↗
PubMed1984

Catheter-induced His bundle ablation in a patient with reentrant tachycardia associated with a nodoventricular tract.

A patient with refractory tachycardia associated with a nodoventricular tract in whom tachycardia was successfully controlled with catheter-induced ablation of the His bundle is reported. Tachycardia was always initiated by ventricular impulses that blocked retrogradely in the nodoventricular tract and conducted by way of the His-Purkinje system. The His bundle ablation was successfully accomplished by delivering two direct current countershocks of 400 J each in the region of the His bundle. Postablation, the patient manifested stable 1:1 anterograde conduction via the atrioventricular (AV) node-nodoventricular fiber over a wide range of heart rates (50 to 180 beats/min). A permanent pacemaker was not implanted at the patient's request. During 16 months of follow-up, the patient has had stable sinus rhythm with no sustained tachycardia. Brief asymptomatic episodes of ectopic atrial tachycardia have been recorded on ambulatory electrocardiographic monitoring. This case 1) demonstrates the potential role of ablation of the His bundle in patients with refractory tachycardia associated with a nodoventricular tract provided that the His bundle is a critical component in the initiation of the tachycardia or a part of the tachycardia circuit; 2) reveals stable 1:1 AV conduction over a nodoventricular tract; and 3) emphasizes the utility of the phase image technique for diagnosis of a Mahaim tract.

Adult↗
PubMed1983

Long-term efficacy and toxicity of high-dose amiodarone therapy for ventricular tachycardia or ventricular fibrillation.

Amiodarone was administered to 154 patients who had sustained, symptomatic ventricular tachycardia (VT) (n = 118) or a cardiac arrest (n = 36) and who were refractory to conventional antiarrhythmic drugs. The loading dose was 800 mg/day for 6 weeks and the maintenance dose was 600 mg/day. Sixty-nine percent of patients continued treatment with amiodarone and had no recurrence of symptomatic VT or ventricular fibrillation (VF) over a follow-up of 6 to 52 months (mean +/- standard deviation 14.2 +/- 8.2). Six percent of the patients had a nonfatal recurrence of VT and were successfully managed by continuing amiodarone at a higher dose or by the addition of a conventional antiarrhythmic drug. One or more adverse drug reactions occurred in 51% of patients. Adverse effects forced a reduction in the dose of amiodarone in 41% and discontinuation of amiodarone in 10% of patients. The most common symptomatic adverse reactions were tremor or ataxia (35%), nausea and anorexia (8%), visual halos or blurring (6%), thyroid function abnormalities (6%) and pulmonary interstitial infiltrates (5%). Although large-dose amiodarone is highly effective in the long-term treatment of VT or VF refractory to conventional antiarrhythmic drugs, it causes significant toxicity in approximately 50% of patients. However, when the dose is adjusted based on clinical response or the development of adverse effects, 75% of patients with VT or VF can be successfully managed with amiodarone.

Aged↗
PubMed1983

Long-term follow-up of patients with recurrent unexplained syncope evaluated by electrophysiologic testing.

Electrophysiologic testing was performed in 53 patients with recurrent syncope that remained unexplained despite a thorough neurologic and noninvasive cardiac evaluation. Fifteen patients had no structural heart disease, 9 had mitral valve prolapse and 29 had structural heart disease other than mitral valve prolapse. Nonsustained ventricular tachycardia was induced in 15 patients (28%), sustained ventricular tachycardia was induced in 9 (17%), ventricular fibrillation was induced in 4 (8%) and sinus node function was abnormal in 2 (4%). Female sex and lack of structural heart disease were independently associated with a negative electrophysiologic study (p less than 0.001). Patients with inducible ventricular tachycardia or ventricular fibrillation were treated with drugs selected on the basis of the results of electropharmacologic testing. The recurrence rate of syncope was 43% over a 31 +/- 10 month period (mean +/- standard deviation) of follow-up in patients with a negative electrophysiologic study, 40% over a 22 +/- 6 month period in patients with inducible nonsustained ventricular tachycardia, 0% over a 30 +/- 12 month period in patients with inducible sustained ventricular tachycardia and 25% over a 21 +/- 10 month period in patients with inducible ventricular fibrillation. In patients with recurrent unexplained syncope undergoing electrophysiologic testing, a potential cause of syncope is least likely to be found in women without structural heart disease. The results of programmed ventricular stimulation must be interpreted with regard to the method of induction of ventricular tachycardia and the type of ventricular tachycardia induced. The excellent response rate in patients with inducible sustained ventricular tachycardia whose therapy is guided by the results of electropharmacologic testing suggests that sustained ventricular tachycardia is a clinically significant response.(ABSTRACT TRUNCATED AT 250 WORDS)

Amiodarone↗
PubMed1983

Doppler echocardiographic studies in sequential atrioventricular pacing.

Six patients with sequential atrioventricular pacemakers were studied by Doppler echocardiography. A commercially available continuous wave system (transcutaneous aortovelography) was used and the transducer was placed in the suprasternal notch and angled to obtain peak aortic arch blood flow velocity. Changes in Doppler peak velocity have been previously shown to correlate closely and reliably with changes in hemodynamically measured stroke volume/cardiac output in the same patients following interventions. In all patients, the pacemaker was programmed from DVI mode to VVI (heart rate was kept constant) and then back to DVI, with the Doppler transducer held in a fixed position all the time, and peak velocities measured after the patient had been in any particular mode for at least 1 minute. Five of 6 patients showed reduction in peak velocities ranging from 13-25% (mean 18.4%) when the pacing mode was switched from DVI to VVI. Doppler peak velocity remained unchanged in 1 patient. Doppler echocardiography represents a simple, noninvasive method for estimating increments in stroke volume/cardiac output obtained with sequential AV pacing.

Atrioventricular Node↗