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Biomedical subjects

A K Bhandari

Publications and source records attributed to A K Bhandari.

At least 19 recordsLinked to original sources
PubMed2000

A low amplitude His-bundle potential predicts failure of the right-sided approach for atrioventricular junction ablation.

In 30 patients with drug refractory atrial fibrillation-flutter who underwent radiofrequency (RF) ablation of the atrioventricular (AV) junction, 23 were successfully ablated using the conventional right-sided approach (group A). Seven patients required a left-sided approach (group B) after multiple applications from the conventional right-sided approach failed to produce complete AV block. The amplitude of the His-bundle potential recorded at the ablation site differed significantly between the 2 groups (0.23+/-0.11 mV in group A vs 0.12+/-0.04 mV in group B; p<0.005). Also, the amplitude of the His-bundle potential recorded in the standard position across the tricuspid annulus differed significantly between the 2 groups (0.27+/-0.35 mV in group A vs 0.11+/-0.44 mV in group B; p<0.007). There was no significant difference in the amplitude of the ventricular potential between the 2 groups. The probability of successful ablation of the AV junction with a conventional right-sided approach was 6 out of 12 patients (50%) if the His amplitude was <0.12mV, and 17 out of 18 patients (94%) if the His amplitude was >0.12mV (p<0.005). Patients in group B had a mean of 20.5+/-13.0 failed right-sided RF applications (5-33 applications), but required a mean of only 2 subsequent RF applications for success on the left side (1-6 applications). The His-amplitude recorded from the left side using the same catheter was significantly greater than that on the corresponding right-side (0.22+/-0.09 mV on the left side vs 0.12+/-0.04 mV on the right side: p<0.05). Total mean fluoroscopic time was 62+/-12min for group B and 20+/-13min for group A patients. In patients that underwent RF ablation of the AV junction, a maximum His amplitude <0.12 mV predicted a success rate of approximately 50% in the present study. An early switch to a left-sided approach may avoid multiple RF applications and prolonged fluoroscopic time in patients with a low amplitude His-bundle potential.

Adult↗
PubMed1998

Efficacy of low-energy T wave shocks for induction of ventricular fibrillation in patients with implantable cardioverter defibrillators.

The efficacy of low-energy T wave shocks for induction of ventricular fibrillation (VF) was evaluated in 33 patients undergoing implantable cardioverter defibrillator (ICD) implantation (33 sessions) or predischarge ICD testing (20 sessions). To induce VF, the ventricle was paced for eight cycles at a 400-ms cycle length (S1-S1), and the T wave was scanned with a monophasic shock (S2) delivered via the defibrillating lead system. Of 294 attempts, the T wave shocks induced VF in 65%, nonsustained ventricular tachycardia in 10%, and less than five ventricular beats in 25%. As compared with the failed T shocks, the mean energy of successful T wave shocks was higher and the S1-S2 coupling interval was shorter. When the S2 timing was examined in relation to the T wave peak, the VF induction efficacy was 37% for shocks delivered more than 70 ms before the T wave peak, 82% for shocks delivered 30-70 ms before the T wave peak, and 50% for shocks delivered less than 30 ms before or just after the T wave peak (P < .001). Thus, in patients undergoing ICD implantation or ICD conversion testing, the use of low-energy T wave shocks is an effective and safe method to provoke VF.

Adolescent↗
PubMed1993

Electrophysiological evaluation of moricizine in patients with sustained ventricular tachyarrhythmias: low efficacy and high incidence of proarrhythmia.

In patients with history of sustained ventricular tachycarrhythmias, the efficacy and safety of moricizine have not been systematically evaluated by electrophysiological studies. We performed electrophysiological testing in these patients in the drug-free state and then after moricizine loading, and evaluated the safety profile of moricizine during in-hospital loading and follow-up. The study population comprised of 31 patients with clinically sustained ventricular tachyarrhythmia. The underlying heart disease was coronary in 25 patients, cardiomyopathy in 5 patients, and none in 1 patient. The left ventricular (LV) ejection fraction ranged from 15%-69% (mean 39 +/- 15%). During the baseline drug-free electrophysiological testing, sustained ventricular tachycardia was inducible in 27 patients, ventricular fibrillation in 1 patient, and reproducible, nonsustained ventricular tachycardia (15-25 sec) in 3 patients. All 31 patients received moricizine to the maximum tolerated dose (851 +/- 185 mg) over a period of 2-7 days. Six patients developed ventricular proarrhythmia within the first 4 days. Proarrhythmia required multiple cardioversions in three patients, was not associated with QT prolongation, and spontaneously resolved 6-24 hours after withdrawal of moricizine. Of the remaining 25 patients, 24 underwent electrophysiological testing on moricizine and 4 patients (16%) were rendered noninducible. The VT cycle length in the other 20 patients slowed from 243 +/- 30 msec to 299 +/- 60 msec (P < 0.09). Four noninducible patients, two patients with inducible but slowed VT and one patient who had refused further testing were discharged on moricizine.(ABSTRACT TRUNCATED AT 250 WORDS)

Arrhythmias, Cardiac↗
PubMed1992

Correlation of symptoms with occurrence of paroxysmal supraventricular tachycardia or atrial fibrillation: a transtelephonic monitoring study. The Flecainide Supraventricular Tachycardia Study Group.

The purpose of this study was to determine whether symptoms recorded at the time of transtelephonic ECG monitoring (TTEM) correlate with attacks of paroxysmal supraventricular tachycardia (PSVT) or paroxysmal atrial fibrillation (PAF). We studied 113 patients with these arrhythmias who made a total of 3319 TTEM calls during their participation in double-blind, placebo-controlled, crossover, multicenter trials of flecainide therapy. Among 49 patients with PSVT, 62.7% of symptomatic calls were associated with ECG-documented PSVT as compared with 6.8% of asymptomatic calls (p less than 0.001). Similarly, among 69 patients with PAF, 69% of symptomatic calls were associated with ECG-documented PAF compared with 10.6% of asymptomatic calls (p less than 0.001). Both in patients with PSVT and PAF, an attack of PSVT or PAF could be documented by ECG in more than 70% of the calls when patients complained of tachycardia, increased sweating, or dyspnea. The sensitivity of a symptomatic call was 91% for PSVT and 89% for PAF, and it was not influenced by flecainide therapy. However, flecainide therapy was associated with a decrease in the positive predictive value of symptomatic TTEM calls and an increase in false positive TTEM transmissions. We conclude that in patients with symptomatic PSVT or PAF, there is a temporal relationship between symptoms and the occurrence of ECG-documented attacks of PSVT or PAF. However, sole reliance should not be placed on the presence or absence of symptoms as a measure of drug failure or efficacy, and it is important to document the cardiac rhythm by TTEM at the time symptoms are recorded.

Atrial Fibrillation↗
PubMed1992

Prognostic significance of programmed ventricular stimulation in patients surviving complicated acute myocardial infarction: a prospective study.

In survivors of complicated myocardial infarction, the inducibility of sustained ventricular tachycardia may help identify a subset that is at increased risk for subsequent sudden cardiac death or spontaneous sustained ventricular tachycardia. We performed prehospital discharge programmed ventricular stimulation in 86 survivors of acute myocardial infarction complicated by heart failure, angina pectoris, or nonsustained ventricular tachycardia. These patients also underwent cardiac catheterization with coronary angiography and 24-hour ambulatory ECG recording. Programmed ventricular stimulation induced sustained ventricular tachycardia in 19 patients (22%) and ventricular fibrillation in six (7%) and did not induce these arrhythmias in 61 patients (71%). During an average follow-up of 18 +/- 13 months, 11 patients had arrhythmic events (seven sudden death and four nonfatal spontaneous sustained ventricular tachycardia) and 10 patients had nonsudden cardiac death. The total cardiac mortality rate was 20%. Arrhythmic events occurred in 32% of the 19 patients with inducible sustained ventricular tachycardia compared with 7% of the remaining 67 patients (p less than 0.003). By multivariate analysis the occurrence of arrhythmic events was independently predicted by both inducible sustained ventricular tachycardia and Killip class III or IV heart failure. The risk of arrhythmic events was 4.4% in the absence of both variables versus 38.4% (p less than 0.001) when both variables were present. The total cardiac mortality rate was best predicted by low left ventricular ejection fraction (less than 30%). Thus programmed ventricular stimulation is useful in risk stratification of survivors of complicated acute myocardial infarction. The prognostic utility appears to be particularly high in patients with infarction complicated by Killip class III or IV heart failure.

Arrhythmias, Cardiac↗
PubMed1991

A prospective evaluation of the immediate reproducibility of the signal-averaged ECG.

The purpose of this investigation was to prospectively evaluate the immediate reproducibility of the signal-averaged electrocardiogram (SAECG). A total of 114 patients undergoing evaluation for ventricular arrhythmias were enrolled in this protocol. Two consecutive SAECG's (40 Hz bidirectional high-pass filtering with a computer-automated system) were performed 10 minutes apart. Abnormal SAECG parameters were defined as (1) vector QRS duration more than 120 msec, (2) terminal root mean square (RMS) voltage less than 20 microV, and (3) low-amplitude signal (LAS) duration more than 40 msec. An SAECG was defined as abnormal if at least one vector parameter was abnormal. There was close correlation between vector parameters during the two SAECG observations: QRS duration had the highest reproducibility (r2 = 0.97, p less than 0.001) followed by terminal RMS voltage (r2 = 0.92, p less than 0.001), and LAS duration (r2 = 0.90, p less than 0.001). The mean (+/- SD) percentage of change between the two recordings was 2% +/- 2% of the QRS duration, 13% +/- 22% for terminal RMS voltage, and 7% +/- 11% for LAS duration. The reproducibility of an initially normal SAECG was 92% and of an initially abnormal SAECG, 96%. Seventeen patients (15%) had a change in one of the three vector parameters between the two recordings. There were no clinically significant differences between the 17 patients in whom the SAECG was nonreproducible and the 97 patients in whom the SAECG was reproducible. However, reproducibility was significantly higher in patients with an initially normal versus an initially abnormal SAECG (92% vs 76%, p = 0.03).(ABSTRACT TRUNCATED AT 250 WORDS)

Arrhythmias, Cardiac↗
PubMed1991

The role of combination therapy with mexiletine and procainamide in patients with inducible sustained ventricular tachycardia refractory to intravenous procainamide.

This study evaluated the role of serial electropharmacological testing on combination therapy with mexiletine and procainamide in 20 patients with inducible sustained ventricular tachycardia (VT) refractory to intravenous procainamide. The clinical arrhythmias were cardiac arrest in five patients, sustained VT in 11 patients, and recurrent syncope of presumably arrhythmic origin in four patients. The mean left ventricular ejection fraction (LVEF) was 0.40 +/- 0.12 (mean +/- SD). All patients had inducible sustained VT at baseline and after administration of intravenous procainamide. All 20 patients underwent electropharmacological testing on combination therapy with mexiletine and procainamide. The mean cycle length of inducible sustained VT was 251 +/- 48 ms at baseline, 324 +/- 81 ms on intravenous procainamide (P less than 0.014 vs baseline), and 365 +/- 82 ms on combination therapy (P less than 0.0001 vs baseline, P = NS vs intravenous procainamide). Combination therapy did not suppress VT inducibility, nor did it make VT more difficult to induce in 19 of 20 patients. The remaining one patient had a partial response (runs of nonsustained VT, longest 10 seconds). Furthermore, combination therapy did not significantly prolong the VT cycle length over and above that observed during testing with intravenous procainamide. Therefore, in patients with inducible sustained VT refractory to procainamide during initial electropharmacological testing, mexiletine in combination with procainamide appears to be of little or no value and serial electropharmacological testing on these drugs is of limited usefulness. Early initiation of alternative therapy may be the preferred clinical option.

Adult↗
PubMed1991

Flecainide acetate prevents recurrence of symptomatic paroxysmal supraventricular tachycardia. The Flecainide Supraventricular Tachycardia Study Group.

Oral flecainide acetate was administered to 34 patients with documented symptomatic paroxysmal supraventricular tachycardia (PSVT) with a double-blind, placebo-controlled, 8-week crossover trial design. PSVT was defined as a regular tachycardia of at least 120 beats/min without evidence of atrioventricular dissociation. The study required considerable patient cooperation. Patients first entered a 4-week qualifying phase followed by a 3-week, open label, flecainide dose-ranging phase. They were then randomized in a blind fashion to receive either placebo or tolerated flecainide dose for an 8-week treatment period and then crossed over after four symptomatic documented episodes of PSVT or at the end of the treatment period. By all efficacy parameters analyzed, flecainide was superior to placebo. Flecainide was associated with an actuarial 79% freedom from symptomatic PSVT events compared with only 15% on placebo at 60 days (p less than 0.001). Of the 34 patients, 29 had recurrence of symptomatic PSVT at least once during the placebo phase; only eight patients had a recurrence during the flecainide phase (p less than 0.001). The median time to the first symptomatic PSVT event was 11 days in the placebo group and greater than 55 days in the flecainide group (p less than 0.001). Likewise, the interval between attacks was a median of 12 days on placebo compared with more than 55 days on flecainide (p less than 0.001). Finally, the flecainide slowed symptomatic PSVT heart rates to 143 +/- 12 beats/min from 178 +/- 12 on placebo (p less than 0.02) in the seven patients who had events in the placebo and flecainide treatment phases.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1991

Wide complex tachycardias. Differential diagnosis and management.

The majority of wide complex tachycardias are secondary to VT. The differential diagnosis of wide complex tachycardia also includes SVT with aberrancy or underlying bundle branch block and antegrade SVT conduction over an accessory pathway (antidromic SVT). VT is usually the result of reentry and most commonly arises in an area of diseased myocardium in the setting of previous myocardial infarction or cardiomyopathy. VT, however, can also occur in patients with structurally normal hearts. Criteria useful in diagnosis of wide complex tachycardia include clinical criteria (presence of structural heart disease or a history of previous myocardial infarction) and electrocardiographic criteria (the presence of capture or fusion beats, relation of atrial or ventricular activity, QRS duration and axis, and morphology). The acute management of wide complex tachycardia includes cardioversion and intravenous pharmacologic therapy. Almost all patients with VT require chronic therapy, although in rare patients treatment of acute precipitating factors may be sufficient. While pharmacologic therapy has been the mainstay of treatment for these patients, there have been many exciting advances using surgical, device, and ablative therapies.

Anti-Arrhythmia Agents↗
PubMed1991

Narrow complex tachycardias. Differential diagnosis and management.

Narrow complex tachycardias are a common clinical problem and can be divided into those in which the arrhythmic circuit is located exclusively in the atrium (pharmacologic treatment is oriented toward altering atrial electrophysiologic properties) and those that involve the AV node or an accessory pathway (pharmacologic therapy is directed toward slowing conduction or increasing refractoriness in these structures). The electrocardiographic diagnosis of the mechanism responsible for SVT includes the regularity of the RR interval; the AV conduction ratio; the presence of P waves, P wave morphology, and the relationship of the P waves to the QRS complexes; and the response of the arrhythmia and atrial activity to vagal maneuvers. Acute therapy includes cardioversion in hemodynamically unstable patients and vagal maneuvers and specific pharmacologic therapy for SVT based on the electrocardiographic diagnosis. There have been recent exciting advances in the nonpharmacologic treatments of SVT, most notably surgery and radiofrequency percutaneous catheter ablation for AV nodal reentry, AV reciprocating tachycardia, atrial flutter, and atrial tachycardias.

Anti-Arrhythmia Agents↗
PubMed1990

The long-term prognosis of patients with out-of-hospital cardiac arrest but no inducible ventricular tachycardia.

The long-term prognosis of patients successfully resuscitated from cardiac arrest who do not have acute precipitating factors and in whom ventricular arrhythmias cannot be induced during baseline electrophysiologic testing is controversial. The purpose of this investigation was to evaluate the long-term risk of recurrent sudden death and determine the clinical, angiographic, hemodynamic, and electrophysiologic predictors of recurrent cardiac arrest in such patients. Twenty-six (37%) of 71 consecutive patients with a single episode of aborted sudden death did not have inducible ventricular arrhythmias (less than 7 intraventricular responses) during baseline drug-free electrophysiologic study and they form the basis of this report. Their mean age was 54 +/- 13 (mean +/- SD) years and the left ventricular ejection fraction (LVEF) was 0.47 +/- 0.17. After a mean follow-up period of 16 months, 11 patients (42%) had a recurrent cardiac arrest (fatal in 10 patients). The actuarial incidence of recurrent cardiac arrest was 30 +/- 10% at 1 year and 55 +/- 13% at 3 years. Patients with LVEF less than or equal to 0.40 had a significantly higher occurrence of recurrent cardiac arrest than those with LVEF greater than 0.40 (p = 0.02; 1-year actuarial incidence of 57 +/- 17% versus 13 +/- 19%). Patients with recurrent sudden death had a significantly greater incidence of dilated cardiomyopathy (55% versus 7%; p = 0.02) and baseline frequent premature ventricular contractions (PVCs greater than 10/hr; 64% versus 17%, p = 0.036) or nonsustained ventricular tachycardia (36% versus 0%; p = 0.37) than patients without these characteristics.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

Day to day reproducibility of electrically inducible ventricular arrhythmias in survivors of acute myocardial infarction.

Day to day reproducibility of the response to programmed ventricular stimulation has not been evaluated in survivors of acute myocardial infarction. Programmed ventricular stimulation was performed prospectively on 2 consecutive days in 56 patients on an average of 12 +/- 5 days (range 7 to 29) after an acute myocardial infarction. No patient had a history of documented or suspected sustained ventricular tachycardia or fibrillation occurring greater than 48 h after infarction. During initial programmed ventricular stimulation, 21 patients had induction of sustained ventricular tachycardia or fibrillation (Group I), and 35 patients had induction of either nonsustained ventricular tachycardia or no ventricular tachycardia (Group II). Repeat programmed ventricular stimulation in Group I patients induced sustained ventricular tachycardia or fibrillation in 16 of 21 patients (reproducibility 76%); the maximal induced response in the other 5 patients was nonsustained ventricular tachycardia in 2 patients and fewer than six repetitive ventricular responses in 3 patients. The day to day reproducibility was significantly higher for inducible sustained ventricular tachycardia of cycle length greater than or equal to 240 ms compared with rapid sustained ventricular tachycardia of cycle length less than 240 ms (100% versus 44%, p less than 0.009) or ventricular fibrillation (100% versus 43%, p less than 0.009). Repeat programmed ventricular stimulation in Group II patients did not induce sustained ventricular arrhythmias in 31 of 35 patients (reproducibility 89%). Thus, in survivors of acute myocardial infarction, inducible slow sustained ventricular tachycardia was a highly reproducible finding, whereas inducibility of rapid sustained ventricular tachycardia and ventricular fibrillation showed a significant day to day variability.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

Prospective evaluation of parenteral magnesium sulfate in the treatment of patients with reentrant AV supraventricular tachycardia.

This study prospectively assessed the electrophysiologic effects of parenteral magnesium sulfate administration on paroxysmal atrioventricular (AV) reentrant supraventricular tachycardia and the efficacy of magnesium to terminate these arrhythmias. Eleven normomagnesemic patients, seven with orthodromic reentrant supraventricular tachycardia that used an accessory AV pathway, and four with typical AV nodal reentry were examined. All patients had a history of sustained supraventricular tachycardia requiring pharmacologic therapy or electrical cardioversion for termination of tachycardia. After baseline electrophysiologic study, including documentation of sustained supraventricular tachycardia that was reproducibly induced, parenteral magnesium sulfate (a bolus of 0.3 mEq/kg of elemental magnesium infused over a 10-minute period followed by a maintenance infusion of 0.2 mEq/kg/hr) was administered during sustained supraventricular tachycardia. The serum magnesium concentration increased from (mean +/- standard deviation) 1.9 +/- 0.2 mg/dl to 4.0 +/- 0.6 mg/dl (p = 0.0001). Except for flushing and mild diaphoresis during infusion of the magnesium sulfate bolus, and dry heaves in one patient, there were no untoward effects or significant changes in systolic blood pressure. During administration of magnesium, the tachycardia cycle length increased from 319 +/- 39 msec to 348 +/- 43 msec (p = 0.0001). Slowing of the tachycardia occurred predominantly in the antegrade limb of the circuit at the level of the AV node with the AH interval increasing from 171 +/- 66 msec to 197 +/- 68 msec (p = 0.0001), whereas there was no significant change in the HV interval (43 +/- 3 msec to 43 +/- 4 msec, p = NS) or the VA interval (106 +/- 43 msec to 110 +/- 47 msec, p = NS) during tachycardia.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

Effect of acute hemodynamic decompensation on electrical inducibility of ventricular arrhythmias in patients with dilated cardiomyopathy and complex nonsustained ventricular arrhythmias.

In patients with dilated cardiomyopathy, hemodynamic decompensation has been postulated to increase vulnerability to reentrant ventricular arrhythmias. To test this hypothesis, we performed programmed ventricular stimulation with three extrastimuli on nine patients with dilated cardiomyopathy and asymptomatic complex ventricular arrhythmias during a period of acute hemodynamic decompensation; programmed ventricular stimulation was then repeated following hemodynamic improvement with nitroprusside. These patients did not have a history of documented or suspected sustained ventricular tachycardia or fibrillation. The mean left ventricular ejection fraction was 0.21 +/- 0.04 (range 0.15 to 0.26). In the baseline state, mean right atrial pressure was 8 +/- 4 mm Hg, pulmonary artery wedge pressure was 20 +/- 3 mm Hg, and cardiac index was 3.2 +/- 0.5 L/min/m2. Following acute hemodynamic decompensation, mean right atrial pressure increased to 16 +/- 5 mm Hg and pulmonary artery wedge pressure to 33 +/- 8 mm Hg; cardiac index decreased to 2.1 +/- 0.5 L/min/m2. In this decompensated state, programmed ventricular stimulation failed to induce sustained or nonsustained ventricular arrhythmias in any patient. Following nitroprusside administration (mean dose 1.5 +/- 1.1 micrograms/kg/min), there were significant decreases in mean right atrial pressure (11 +/- 3 mm Hg) and pulmonary artery wedge pressure (16 +/- 3 mm Hg), and a significant increase in cardiac index (3.1 +/- 1.1 L/min/m2) (p less than 0.05 for all values versus the decompensated state). In the improved hemodynamic state, programmed ventricular stimulation induced nonsustained ventricular tachycardia (six beats) in only one patient, and sustained arrhythmias in none.(ABSTRACT TRUNCATED AT 250 WORDS)

Arrhythmias, Cardiac↗