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Biomedical subjects

A K Bhandari

Publications and source records attributed to A K Bhandari.

At least 37 records · Page 2Linked to original sources
PubMed1989

Prognostic significance of programmed ventricular stimulation in survivors of acute myocardial infarction.

The prognostic significance of the response to programmed ventricular stimulation was studied in 75 stable survivors of acute myocardial infarction. Programmed ventricular stimulation induced sustained ventricular arrhythmias in 33 (44%) patients and did not induce these arrhythmias in 42 (56%) patients. During a mean follow up of 18 months, four patients died suddenly and three developed spontaneous sustained ventricular tachycardia. The occurrence of arrhythmic events was not significantly different in patients with inducible sustained arrhythmias and those without, but such events were predicted by the presence of mild congestive heart failure. Although the inducibility of sustained ventricular tachycardia (but not ventricular fibrillation) seemed to identify a high risk subset with an arrhythmic event rate of 21% compared with 5.5% in others, it had a low sensitivity (57%) and a low positive predictive accuracy (21%) for arrhythmic events. Programmed ventricular stimulation is not helpful in identifying a subset of patients at high risk after an uncomplicated acute myocardial infarction.

Arrhythmias, Cardiac↗
PubMed1989

Prevention of symptomatic recurrences of paroxysmal atrial fibrillation in patients initially tolerating antiarrhythmic therapy. A multicenter, double-blind, crossover study of flecainide and placebo with transtelephonic monitoring. Flecainide Supraventricular Tachycardia Study Group.

Paroxysmal atrial fibrillation (PAF) is a problematic clinical arrhythmia that is usually symptomatic. Unfortunately, few adequate trials and trial methods are available for assessment of the value of therapy, and traditional treatment has often been ineffective or associated with unacceptable side effects. Transtelephonic monitoring is a new method that allows evaluation of paroxysmal arrhythmias and arrhythmia-related symptoms in outpatients. We used a patient-initiated transtelephonic monitor system to evaluate the potential of flecainide, a class 1C antiarrhythmic, in prevention of symptomatic recurrences of PAF. Sixty-four patients qualified for the study (two or more PAF attacks documented within a 4-week baseline period) and entered a dose-finding phase to determine drug tolerance. Dose was incremented at weekly intervals from 200-300 and finally to 400 mg/day. The largest dose that was well tolerated was selected for the 4-month, double-blind, randomized, crossover comparison with placebo. Fifty-five patients entered and 53 received both treatments in the double-blind phase; 48 of these patients without protocol violations were evaluable for efficacy comparisons. Evaluable patients had undergone an average of 3.8 previous drug trials (range, 1-8); 30 were men, 18 had hypertension, and 14 had ischemic heart disease. The study demonstrated a highly significant correlation (p less than 0.0001) between perceived symptoms and documented PAF by transtelephonic monitoring. The rate of symptoms and PAF attacks was also significantly reduced by therapy (median dose, 300 mg/day). The first PAF attack occurred after a median of 3 days on placebo versus 14.5 days on flecainide (p less than 0.001) therapy. Similarly, the time interval between attacks was lengthened, from a median of 6.2 days on placebo to 27.0 days on flecainide (p less than 0.001) therapy. PAF was prevented in 15 patients (31%) during flecainide and four (9%) during placebo therapy (p = 0.013). However, during the study, 13 patients dropped out, seven because of adverse effects (five cardiac), five for other reasons, and one because of cardiac arrest/death. Adverse cardiac events occurred in a total of seven patients (11%) during flecainide therapy. Thus, transtelephonic monitoring is a useful method for documentation of the occurrence of paroxysmal arrhythmias such as PAF and its related symptoms during daily living and for assessment of new therapies in an outpatient setting.

Atrial Fibrillation↗
PubMed1988

Electrophysiologic effects of intravenous magnesium in patients with normal conduction systems and no clinical evidence of significant cardiac disease.

Parenteral magnesium has been used for several decades in the empiric treatment of various arrhythmias, but the data on its electrophysiologic effects in man are limited. We evaluated the electrophysiologic effects of magnesium sulfate (MgSO4) administration in eight normomagnesemic patients with normal mononuclear cell magnesium content, who had no clinically significant heart disease and had normal baseline electrophysiologic properties. After administration of intravenous MgSO4, serum magnesium rose significantly from 1.9 +/- 0.1 to 4.4 +/- 1.7 mg/dl (p less than 0.02). During a maintenance magnesium infusion, we observed significant prolongation of the ECG PR interval (145 +/- 18 to 155 +/- 26 msec, p less than 0.05), AH interval (77 +/- 27 to 83 +/- 26 msec, p less than 0.002), antegrade atrioventricular (AV) nodal effective refractory period (278 +/- 67 to 293 +/- 67 msec, p less than 0.05), and sinoatrial conduction time (60 +/- 34 to 76 +/- 32 msec, p less than 0.02). No significant effect was observed on sinus cycle length, sinus node recovery time, intra-atrial or intraventricular conduction times, QRS duration (during both sinus rhythm and ventricular pacing), QT interval, HV interval, paced cycle length resulting in AV nodal Wenckebach block, AV nodal functional refractory period, retrograde ventriculoatrial (VA) effective refractory period, or atrial and ventricular refractory periods. These findings, in conjunction with the demonstrated ability of magnesium to block slow channels for sodium movement, may provide an explanation of the mechanism by which magnesium exerts its effect in the treatment of atrial and junctional arrhythmias.

Adult↗
PubMed1988

Triggered activity as a mechanism of recurrent ventricular tachycardia.

Triggered activity was shown to be the likely mechanism of recurrent tachycardia in a 28 year old Vietnamese man. During baseline electrophysiological testing the tachycardia was induced consistently by prolonged atrial or ventricular pacing but not by premature extrastimuli. Moreover, the tachycardia coupling intervals varied directly with the cycle length of the initiating drive. Procainamide and propranolol did not suppress tachycardia, but verapamil terminated it and prevented its reinitiation. The origin of the tachycardia was localised to the left ventricular inferoapical segment and four direct current countershocks of 200 J each delivered via an electrode catheter abolished the tachycardia. During 12 months of follow up the patient was not treated with antiarrhythmic agents and the tachycardia did not recur.

Adult↗
PubMed1988

Out-of-hospital cardiac arrest in patients with no overt heart disease: electrophysiologic observations and clinical outcome.

Electrophysiologic studies were performed in nine survivors of out-of-hospital cardiac arrest who had no overt heart disease on clinical, hemodynamic and angiographic evaluation. Cardiac arrest occurred during sedentary activity in seven patients and during exercise in two; no patient was on antiarrhythmic drugs at the time of cardiac arrest. Twenty-four hour ambulatory electrocardiographic monitoring demonstrated premature ventricular beats in four patients (44%). Electrophysiologic stimulation induced sustained ventricular tachycardia (VT) or fibrillation (VF) in five patients, nonsustained VT in one patient and less than five ventricular beats in the remaining three patients. Of five patients with inducible sustained VT or VF, four had complete suppression of inducible VT with antiarrhythmic therapy, and none of these four patients died suddenly or had clinical VT after an average follow-up of 27 months (range 12 to 41 months). The remaining patient with inducible sustained VT refused serial electropharmacologic testing, was treated empirically with amiodarone (400 mg/day) and died suddenly eight months later. Of the four patients with noninducible sustained VT or VF, three received no antiarrhythmic therapy and one was given a beta-blocker. None had recurrent cardiac arrest or symptomatic VT after an average follow-up of 17 months (range 13 to 20 months). Thus, inducibility of sustained VT or VF provided a reliable end point for long term antiarrhythmic therapy and noninducibility identified a subset of patients that had an excellent prognosis without specific antiarrhythmic therapy.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1987

Life-threatening ventricular tachycardia and fibrillation induced by painless myocardial ischemia during exercise testing.

The clinical importance of myocardial ischemia without associated symptoms in patients with atherosclerotic coronary disease has not been clarified. We present three patients in whom painless cardiac ischemia was associated with the induction of cardiac arrest and/or ventricular tachycardia/fibrillation. In the two surviving patients, programmed ventricular stimulation did not induce ventricular arrhythmias. In one patient, successful coronary bypass surgery resulted in the elimination of exercise-induced painless myocardial ischemia and associated ventricular fibrillation; the other patient suffered a myocardial infarction after which ischemia and ventricular tachyarrhythmias could not be reproduced with exercise testing. We conclude that painless myocardial ischemia can cause life-threatening arrhythmias and is, therefore, a potentially lethal phenomenon.

Angina Pectoris↗
PubMed1987

Decline in inducibility of sustained ventricular tachycardia from two to twenty weeks after acute myocardial infarction.

To determine temporal evolution of sustained ventricular arrhythmias inducible after acute myocardial infarction (AMI), serial programmed ventricular stimulation (PVS) was performed in 27 patients 15 +/- 4 and 150 +/- 28 days after AMI. These patients did not have worsening of congestive heart failure or angina, coronary artery bypass surgery or spontaneous sustained ventricular tachycardia (VT) in the period between 2 PVS studies. During initial PVS, sustained VT or ventricular fibrillation (VF) was inducible in 17 patients (group I) and was not inducible in 10 (group II). Late PVS in group I induced sustained VT or VF in 8 patients (47%) and nonsustained VT or no VT in 9 (53%). A decrease in late inducibility of sustained VT/VF was greater for arrhythmias induced during initial PVS by triple extrastimuli and burst pacing than for those induced by double extrastimuli (88% vs 25%, p less than 0.04), but appeared to be unrelated to the morphologic characteristics or cycle length of the initially induced sustained VT or VF and to other clinical, hemodynamic or angiographic variables. During late PVS in 10 group II patients, sustained VT or VF remained noninducible in 9 (90% concordance); in 1 patient sustained VT was induced. During a mean follow-up of 14 +/- 5 months since late PVS, none of 27 patients had spontaneous sustained VT and 2 patients in group I died suddenly.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1987

Proarrhythmic effects of antiarrhythmic drugs during programmed ventricular stimulation in patients without ventricular tachycardia.

The proarrhythmic effects of class IA antiarrhythmic drugs were prospectively evaluated during programmed ventricular stimulation in 24 consecutive patients with frequent ventricular premature beats whose baseline study, performed while no antiarrhythmic drugs were being taken, showed no inducible sustained ventricular arrhythmias. No patient had nonsustained (greater than 5 beats) or sustained ventricular tachycardia by history or baseline 24 hour ambulatory electrocardiographic monitoring. Sequential stimulation studies using up to three extra-stimuli were performed after administration of procainamide, quinidine and disopyramide on different days. Proarrhythmic response was defined as induction of one or more of the following: sustained monomorphic ventricular tachycardia; sustained polymorphic ventricular tachycardia; ventricular fibrillation; reproducibly inducible nonsustained monomorphic ventricular tachycardia. During 55 antiarrhythmic drug trials (24 of procainamide, 21 of quinidine, 10 of disopyramide) in the 24 patients, 6 patients had a proarrhythmic response: sustained monomorphic ventricular tachycardia in 3, ventricular fibrillation in 2, nonsustained monomorphic ventricular tachycardia in 1. Thus, 11% of drug trials resulted in a proarrhythmic response and 25% of patients had a proarrhythmic response to one of the drugs tested. A proarrhythmic response to one drug did not predict a similar response to another drug of the same class. The 6 patients with a proarrhythmic response did not differ significantly from the other 18 patients with regard to underlying heart disease, electrocardiographic or baseline 24 hour ambulatory electrocardiographic characteristics; however, they did have a higher incidence of digoxin usage (p less than 0.02), a shorter baseline right ventricular effective refractory period (p less than 0.01) and a smaller increment in effective refractory period during antiarrhythmic drug testing (p = 0.06).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1985

Frequency and significance of induced sustained ventricular tachycardia or fibrillation two weeks after acute myocardial infarction.

Electrophysiologic study, 24-hour ambulatory electrocardiographic monitoring, treadmill exercise test and angiographic evaluations were performed in 45 patients 14 +/- 3 days (mean +/- standard deviation) after acute myocardial infarction. Electrophysiologic study protocol included burst ventricular pacing and 1 to 3 ventricular extrastimuli at 2 cycle lengths from right ventricular apex, right ventricular outflow and left ventricle. Sustained monomorphic ventricular tachycardia (VT) (13 patients) or ventricular fibrillation (VF) (7 patients) was induced in 20 patients (44%) (group I). In these 20 patients, VT/VF was inducible with 2 extrastimuli in 10 patients, 3 extrastimuli in 9 patients and burst pacing in 1 patient. In the remaining 25 patients (56%), induction of no fewer than 7 ventricular beats were noted (group II). Severe left ventricular (LV) wall motion abnormalities occurred in 70% of group I patients and 22% of group II patients (p less than 0.005). There was no difference in the site of infarction, frequency and grade of ventricular ectopic rhythm on ambulatory electrocardiographic monitoring, double product on submaximal exercise, LV ejection fraction, and number of obstructed coronary arteries (70% or greater) (p greater than 0.1) between group I and group II patients. During a mean follow-up of 10 +/- 3 months, 1 patient in each group died suddenly, and in 1 group I patient spontaneous sustained VT developed which was identical in morphologic configuration to that induced during electrophysiologic study. In conclusion, electrical induction of sustained VT or VF during electrophysiologic study is common in patients 2 weeks after acute myocardial infarction.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1985

Electrophysiologic testing in patients with the long QT syndrome.

Electrophysiologic studies were performed in 15 patients with syncope and/or cardiac arrest who had the long QT syndrome and 11 control subjects who had normal QT intervals. The syndrome was familial in five patients and idiopathic in 10. All patients had a prolonged QT (546 +/- 68 msec, mean +/- SD) and corrected QT (550 +/- 51 msec). Incremental atrial pacing at cycle lengths of 600 to 400 msec resulted in shortening of the QT interval, but there was no significant difference in the magnitude or percent of shortening of the QT interval between patients with the long QT syndrome and control subjects. Intravenous propranolol did not influence the QT interval measured at fixed atrial-paced cycle lengths in patients with either the familial or idiopathic form of the syndrome. Programmed right and left ventricular stimulation with up to three extrastimuli before and during isoproterenol infusion did not induce sustained ventricular tachycardia or ventricular fibrillation in any of the patients. However, rapid polymorphic nonsustained ventricular tachycardia was induced in six of the 15 patients (40%). Neither the inducibility of nonsustained ventricular tachycardia nor the results of electropharmacologic testing with beta-blockers proved to be of any prognostic value during the mean follow-up period of 28 +/- 17 months. Electrophysiologic studies are of limited value in the diagnosis and treatment of patients with the long QT syndrome.

Adolescent↗
PubMed1984

Pulmonary artery aneurysms: echocardiographic features in 5 patients.

Two-dimensional (2-D) echocardiographic studies were performed in 5 patients (2 adults, 3 pediatric cases) with proved aneurysm of the main pulmonary artery (PA). Two-dimensional echocardiography correctly localized the site of the aneurysm in all 5 patients and accurately categorized the type of aneurysm as saccular in 2 patients and fusiform in 3 patients. Fusiform aneurysms were characterized by their huge size, which made it impossible to image them completely in any single 2-D sector plane in 2 patients and by their tendency to cause displacement of the left atrium in 1 patient. Two-dimensional echocardiographic diagnosis of PA aneurysm was suggested prospectively without knowledge of angiographic findings in 3 of 5 patients. Two-dimensional echocardiography appears to be a useful noninvasive technique in the recognition of PA aneurysms.

Adult↗
PubMed1984

Polymorphous ventricular tachycardia associated with a marked prolongation of the Q-T interval induced by amiodarone.

We report the case of a patient who developed a life-threatening polymorphous ventricular tachycardia ( PVT ) after six weeks of treatment with amiodarone. The Q-T interval was markedly prolonged at 0.86 second. The drug induction of PVT was strongly suggested by the fact that PVT resolved four days after withdrawal of amiodarone when the Q-T interval had shortened to 0.60 second; the arrhythmia has not recurred in the nine months of follow-up since then. Amiodarone, though a very effective antiarrhythmic agent, may induce serious PVT .

Aged↗
PubMed1984

Efficacy of left cardiac sympathectomy in the treatment of patients with the long QT syndrome.

Ten patients with the long QT syndrome and recurrent syncope and/or cardiac arrest caused by ventricular arrhythmias underwent left stellate (one patient) or left cervicothoracic sympathectomy (nine patients) after failing to respond to high-dose beta-blocker therapy. The syndrome was familial in four and idiopathic in six. All patients had a prolonged resting QT interval (548 +/- 51 msec, mean +/- SD) and corrected QT interval (QTc) (556 +/- 43 msec). After sympathectomy the mean QTc shortened significantly from 556 +/- 43 to 508 +/- 65 msec (p less than .05) but the QTc remained abnormal in all but one patient. Over a mean follow-up period of 38.6 +/- 19 months, eight patients developed recurrent symptoms that included cardiac arrest in three (one fatal, two nonfatal), syncope in four, and presyncope in six. The addition of beta-blockers was ineffective in suppressing the recurrent symptoms. The control of symptoms required more extensive sympathectomy (three patients), chronic atrial pacing (three patients), and implantation of an automatic internal defibrillator (one patient). Only one patient has remained asymptomatic without drug or pacemaker therapy. In conclusion, left cervicothoracic sympathectomy proved inadequate for long-term control of symptoms in most patients with the long QT syndrome. These patients usually required concomitant drugs, more extensive surgery, or long-term cardiac pacing for symptomatic relief.

Adolescent↗
PubMed1983

Myocardial texture characterization by two-dimensional echocardiography.

Twenty-four normal subjects and 181 patients with various cardiac disorders (36 autopsies) were studied by 2-dimensional echocardiography. In vitro echocardiographic studies were performed on 26 of 36 autopsied hearts utilizing an ultrasonically visible metallic probe to correlate myocardial echo patterns with histopathologic features. All normal subjects and the majority of patients with ventricular hypertrophy due to valvular or hypertensive lesions showed a uniformly speckled or an echolucent appearance of the myocardium (type I texture). No autopsied heart with this texture had gross fibrosis (visible to the naked eye) or infiltrative disease. All patients with infiltrative disorders (amyloidosis, 7 of 7; Pompe's disease, 4 of 4) had multiple, discrete, and small (3 to 5 mm) highly refractile echoes (HREs) in the myocardium involving the ventricle or ventricles completely (type IIA texture) or partly (type IIB texture). However, this finding was non-specific and was observed in many other conditions such as left heart hypoplastic syndrome (10 of 10), hypertrophic cardiomyopathy (19 of 26), and chronic renal failure (4 of 9). In the noninfiltrative group, HREs in the autopsied cases were shown to result from gross fibrosis or endocardiofibroelastosis utilizing in vitro echocardiographic studies and metallic probe-guided biopsies, while HREs in the autopsied cases with cardiac amyloidosis could be correlated only with amyloid deposits since fibrosis was absent. Larger HREs (greater than 5 mm) presenting as broad patches or long linear echoes in the myocardium (type IIC texture) was seen in old myocardial infarctions (9 of 21) and congestive cardiomyopathy (4 of 26) and were correlated with large areas of myocardial fibrosis. Two-dimensional echocardiographic studies of myocardial texture help identify various infiltrative and degenerative processes in the heart.

Adult↗