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Biomedical subjects

R Goyal

Publications and source records attributed to R Goyal.

At least 37 records · Page 2Linked to original sources

Relationship between shock energy and postdefibrillation ventricular arrhythmias in patients with implantable defibrillators.

BACKGROUND: The relationship between postdefibrillation ventricular arrhythmias and shock strength is poorly understood in patients with implantable defibrillators. The purpose of this study was to characterize the relationship between postdefibrillation ventricular arrhythmias and shock strength. METHODS AND RESULTS: Forty-three patients with an implanted defibrillator underwent six separate inductions of ventricular fibrillation (VF) after a step-down defibrillation energy requirement (7.3 +/- 4.6 J) was determined. For each of the first three inductions of VF, the first two shocks were low energy and equal to approximately 75% of the defibrillation energy requirement (5.4 +/- 3.3 J), or to the defibrillation energy requirement plus 10 J (17.5 +/- 4.3 J). After the first two shocks, subsequent shocks were programmed to the maximum available energy (29.0 +/- 2.5 J). The alternate technique was used for the subsequent three inductions of VF. Postdefibrillation ventricular arrhythmias were noted. Postdefibrillation ventricular arrhythmias with a cycle length < or = 300 msec were more frequent after a low-energy shock (19%), than after a high-energy shock (1.5%; P = 0.005). Postdefibrillation ventricular arrhythmias with a cycle length < or = 300 msec were more frequent after a high-energy shock (32%), than after a low-energy shock (7.1%; P = 0.002). A relationship between the cycle length of the postdefibrillation ventricular arrhythmias and the absolute defibrillation energy was observed (P < 0.001; r = 0.6), and ventricular arrhythmias with a cycle length > 300 msec were uncommon after shocks < or = 10 J (P = 0.001). The characteristics of ventricular arrhythmias after maximum-energy shocks were similar to those that occurred after high-energy shocks. CONCLUSIONS: Postdefibrillation ventricular arrhythmias with a cycle length < or = 300 msec are more common after shocks of strength associated with a low probability of successful defibrillation. Postdefibrillation ventricular arrhythmias with a cycle length of > 300 msec are more common after high- and maximum-energy shocks, and are directly related to the absolute defibrillation energy.

Cardiomyopathies↗

Acute changes in spontaneous echo contrast and atrial function after cardioversion of persistent atrial flutter.

With use of transesophageal echocardiography, the short-term effects of transthoracic electrical cardioversion of atrial flutter (AFI) on atrial mechanical function and spontaneous echo contrast were determined. Thirty patients who had AFI for a mean of 6.4 +/- 12.2 months underwent transthoracic cardioversion. A transesophageal echocardiogram was recorded immediately before cardioversion, and left atrial appendage emptying velocity and spontaneous contrast were assessed serially at 1, 3, and 5 minutes after cardioversion in 28 patients, and also at 8, 10, and 15 minutes after cardioversion in a subgroup of 13 patients. Cardioversion was deferred in 2 patients (7%) because a thrombus was found in the left atrial appendage. Before cardioversion, spontaneous contrast was present in the left atrium in 7 of 28 patients (25%) who underwent cardioversion. The mean left atrial appendage emptying velocity of 54 +/- 22 cm/s before cardioversion fell by 26% to 40 +/- 25 cm/s at 1 minute after restoration of sinus rhythm (p <0.01). There were no significant changes in the mean left atrial appendage-emptying velocity between 1 and 15 minutes after cardioversion. Within 5 minutes after conversion to sinus rhythm, left atrial spontaneous echo contrast developed de novo or worsened in 12 of the 28 patients (43%). In conclusion, the results of this study demonstrate that persistent AFI may be associated with left atrial thrombi before cardioversion and that cardioversion of AFI is associated with a significant degree of atrial stunning and formation of spontaneous echo contrast.

Adult↗

Cardiac electrophysiologic effects of norepinephrine in human beings.

BACKGROUND: The electrophysiologic effects of norepinephrine (NE) in human beings have not been previously described. METHODS: The electrophysiologic effects of NE infused at a rate of 25 ng/kg/min were determined in 21 patients with a mean age of 41 +/- 11 years and without structural heart disease who underwent an electrophysiology procedure. In a subgroup of 10 patients electrophysiologic parameters were measured at baseline, after the infusion of NE, and after administration of beta-blockade while in continuous NE infusion. RESULTS: The baseline NE plasma concentration of 298 +/- 153 pg/ml increased to 708 +/- 419 pg/ml after the infusion of NE. NE significantly increased the mean blood pressure, sinus cycle length, corrected sinus node recovery time, ventriculoatrial block cycle length, and the atrial and ventricular effective refractory periods. In a subset of 10 patients 0.2 mg/kg propranolol administered during continued infusion of NE resulted in a further increase in sinus cycle length, atrial-His interval, and ventricular refractoriness. CONCLUSION: A physiologic elevation in the plasma NE concentration results in a depression of sinus node function and atrioventricular conduction and in prolongation of atrial and ventricular refractoriness. Some of NE's effects are partially offset by beta-adrenergic stimulation.

Adrenergic alpha-Agonists↗

Use of adenosine in patients hospitalized in a university medical center.

PURPOSE: Adenosine is a useful agent for the diagnosis and termination of tachycardias. The purpose of this study was to identify the rhythms for which adenosine is prescribed in hospitalized adults and to identify the reasons for its misuse. PATIENTS AND METHODS: Data were collected from the medical records of 100 patients who received intravenous adenosine while hospitalized at a university medical center. The characteristics of the patients, rhythms treated with adenosine, and dosages of adenosine were analyzed. In addition, internal medicine house officers were administered a questionnaire referring to an electrocardiogram of atrial fibrillation with a rapid ventricular response. RESULTS: The arrhythmias for which adenosine was administered consisted of regular, narrow-QRS complex tachycardias in 33% of patients; atrial fibrillation in 32% of patients; regular, wide-QRS complex tachycardias in 23% of patients; atrial flutter in 10% of patients, and multifocal atrial tachycardia in 2% of patients. The mean (+/-SD) number of doses of adenosine given to each patient was 1.6+/-0.8, and the mean dose of adenosine was 7.8+/-2.8 mg. Internal medicine house officers prescribed 70% of the doses of adenosine and were as likely to use it for patients with atrial fibrillation as were surgical house officers. There was a 2% incidence of proarrhythmia, including asystole and polymorphic ventricular tachycardia. Thirty-one percent of the 100 house officers in our survey misdiagnosed a 12-lead electrocardiogram of rapid atrial fibrillation as paroxysmal supraventricular tachycardia, suggesting that adenosine may have been misused for atrial fibrillation because of errors in rhythm diagnosis. Only 5% of those who correctly diagnosed atrial fibrillation also answered that adenosine would be likely to terminate the arrhythmia, suggesting that a misunderstanding that adenosine terminates atrial fibrillation is not a common reason for its misuse. CONCLUSIONS: Approximately 40% of hospitalized adults who are treated with adenosine receive the medication unnecessarily for atrial fibrillation or atrial flutter, and this misuse results in unnecessary expenses and risks of adverse effects. The primary reason that adenosine is misused for atrial fibrillation is the inability to recognize that rhythm on an electrocardiogram. House officers need additional education on the electrocardiographic recognition of atrial fibrillation.

Adenosine↗

Influence of right ventricular site of stimulation and infarct location on the inducibility of ventricular tachycardia in patients with coronary artery disease.

No prior studies have evaluated the relationship between the site of right ventricular stimulation, the site of prior infarction, and the inducibility of ventricular tachycardia (VT). This study was performed to determine if the location of pathologic Q waves influences the inducibility of VT at various right ventricular sites in patients with coronary artery disease (CAD) and a history of myocardial infarction (MI). In 30 patients with a history of sustained, monomorphic VT, CAD, prior MI, and pathologic Q waves, programmed ventricular stimulation was performed at the right ventricular apex, septum, and outflow tract, in random order. There was electrocardiographic evidence of an MI that was inferior in 11 patients, anterior in 10 patients, and both inferior and anterior in 9 patients. Sustained, monomorphic VT was induced in 27 of 30 patients (90%). There were no significant differences among the three sites in the rate of inducibility of VT. The rate of inducible VT at each of the three right ventricular sites was not affected by the location of prior infarction. In conclusion, among patients with sustained, monomorphic VT, CAD, and a history of MI, the incidence of inducible sustained, monomorphic VT is not influenced by the location of prior infarction, regardless of whether programmed ventricular stimulation is performed at the right ventricular apex, septum, or outflow tract.

Cardiac Pacing, Artificial↗

Effect of isoproterenol on QRS complex morphology during ventricular pacing: implications for pace mapping.

Ventricular pace mapping may be used to identify the site of origin of idiopathic ventricular tachycardia. Isoproterenol is often required to induce this type of ventricular tachycardia, but its effect on QRS morphology during pace mapping is unknown. Therefore, this study was performed to evaluate the effect of isoproterenol on QRS morphology during ventricular pacing. The study population consisted of 20 patients (mean age 38 +/- 14 years) undergoing a clinically indicated electrophysiology procedure. Ventricular overdrive pacing was performed in trains of 12 stimuli at cycle lengths of 400, 350, 300, and 250 ms, first in the baseline state during an infusion of isoproterenol, and again after isoproterenol washout. Pacing was performed at the right ventricular apex in 10 patients, in the right ventricular outflow tract in 6 patients, and in the left ventricle in 4 patients. Visual evaluation revealed no apparent effects of isoproterenol on QRS morphology at any of the three pacing sites or at any of the pacing cycle lengths. It was concluded that QRS morphology during ventricular pacing is not affected by isoproterenol infusion. Therefore, in patients with idiopathic ventricular tachycardia, even if the induction of tachycardia requires infusion of isoproterenol, successful pace mapping may be performed in its absence.

Aged↗

Trisomy 12 in chronic lymphocytic leukemia--geographical variation.

Incidence of trisomy 12 was studied in 60 cases of chronic lymphocytic leukemia (CLL) with chromosome 12 specific alpha-satellite DNA probe by fluorescence in situ hybridization (FISH). Trisomy 12 was observed in 37 (61.8%) patients. Cells with trisomy 12 were detected in a varying proportion, ranging from > 2% to 86%. Patients with trisomy 12 were predominantly observed with total white blood cell (WBC) count > 80 x 10(9) l(-1) (P < 0.001). In addition, the percentage of trisomy 12 positive lymphocytes correlated with the high WBC counts. Trisomy 12 was observed equally in typical and atypical CLL. 90% of our patients were in the intermediate and high risk groups. It was seen that there was significantly higher percentage of trisomy 12 positive lymphocytes ( > 10%) in the high risk groups (P < 0.05). A higher incidence of FMC7 positivity in atypical CLL was seen in our study. However, there was no significant relationship found between trisomy 12 positivity and expression of either FMC7 or CD23 in our cases. It appears that the CLL that we see at our centre is at a different phase of evolution and perhaps biologically different compared to the CLL seen in the West.

Adult↗

Randomized comparison of a 90 uF capacitor three-electrode defibrillation system with a 125 uF two-electrode defibrillation system.

INTRODUCTION: A variety of factors, including the number of defibrillation electrodes and shocking capacitance, may influence the defibrillation efficacy of an implantable defibrillator system. Therefore, the purpose of this study was to compare the defibrillation energy requirement using a 125 uF two-electrode defibrillation system and a 90 uF three-electrode defibrillation system. METHODS AND RESULTS: The defibrillation energy requirements measured with both systems were compared in 26 consecutive patients. The two-electrode system used a single transvenous lead with two defibrillation coils in conjunction with a biphasic waveform from a 125 uF capacitor. The three-electrode system used the same transvenous lead, utilized a pectoral implantable defibrillator generator shell as a third electrode, and delivered the identical biphasic waveform from a 90 uF capacitor. The two-electrode system was associated with a higher defibrillation energy requirement (10.8 +/- 5.5 J) than was the three-electrode system (8.9 +/- 6.7 J, p < 0.05), however, the leading edge voltage was not significantly different between systems (361 +/- 103 V vs. 397 +/- 123 V, P = 0.07). The two-electrode system also had a higher shocking resistance (49.0 +/- 9.0 ohms vs. 41.4 +/- 7.3 ohms, p < 0.001) and a lower peak current (7.7 +/- 2.6 A vs. 10.1 +/- 3.7 A, p < 0.001) than the three-electrode system. CONCLUSIONS: A three-electrode defibrillation system that utilizes a dual coil transvenous lead and a subcutaneous pectoral electrode with lower capacitance is associated with a lower defibrillation energy requirement than is a dual coil defibrillation system with higher capacitance. This finding suggests that the utilization of a pectoral generator as a defibrillation electrode in conjunction with smaller capacitors is a more effective defibrillation system and may allow for additional miniaturization of implantable defibrillators.

Aged↗

Effect of ventricular shock strength on cardiac hemodynamics.

INTRODUCTION: The effect of implantable defibrillator shocks on cardiac hemodynamics is poorly understood. The purpose of this study was to test the hypothesis that ventricular defibrillator shocks adversely effect cardiac hemodynamics. METHODS AND RESULTS: The cardiac index was determined by calculating the mitral valve inflow with transesophogeal Doppler during nonthoracotomy defibrillator implantation in 17 patients. The cardiac index was determined before, and immediately, 1 minute, 2 minutes, and 4 minutes after shocks were delivered during defibrillation energy requirement testing with 27- to 34-, 15-, 10-, 5-, 3-, or 1-J shocks. The cardiac index was also measured at the same time points after 27- to 34-, and 1-J shocks delivered during the baseline rhythm. The cardiac index decreased from 2.30 +/- 0.40 L/min per m2 before a 27- to 34-J shock during defibrillation energy requirement testing to 2.14 +/- 0.45 L/min per m2 immediately afterwards (P = 0.001). This effect persisted for > 4 minutes. An adverse hemodynamic effect of similar magnitude occurred after 15 J (P = 0.003) and 10-J shocks (P = 0.01), but dissipated after 4 minutes and within 2 minutes, respectively. There was a significant correlation between shock strength and the percent change in cardiac index (r = 0.3, P = 0.03). The cardiac index decreased 14% after a 27- to 34-J shock during the baseline rhythm (P < 0.0001). This effect persisted for < 4 minutes. A 1-J shock during the baseline rhythm did not effect the cardiac index. CONCLUSION: Defibrillator shocks > 9 J delivered during the baseline rhythm or during defibrillation energy requirement testing result in a 10% to 15% reduction in cardiac index, whereas smaller energy shocks do not affect cardiac hemodynamics. The duration and extent of the adverse effect are proportional to the shock strength. Shock strength, and not ventricular fibrillation, appears to be most responsible for this effect. Therefore, the detrimental hemodynamic effects of high-energy shocks may be avoided when low-energy defibrillation is used.

Adult↗

Differential effect of adenosine on anterograde and retrograde fast pathway conduction in patients with atrioventricular nodal reentrant tachycardia.

INTRODUCTION: Several studies have shown that the fast pathway is more responsive to adenosine than the slow pathway in patients with AV nodal reentrant tachycardia. Little information is available regarding the effect of adenosine on anterograde and retrograde fast pathway conduction. METHODS AND RESULTS: The effects of adenosine on anterograde and retrograde fast pathway conduction were evaluated in 116 patients (mean age 47 +/- 16 years) with typical AV nodal reentrant tachycardia. Each patient received 12 mg of adenosine during ventricular pacing at a cycle length 20 msec longer than the fast pathway VA block cycle length and during sinus rhythm or atrial pacing at 20 msec longer than the fast pathway AV block cycle length. Anterograde block occurred in 98% of patients compared with retrograde fast pathway block in 62% of patients (P < 0.001). Unresponsiveness of the retrograde fast pathway to adenosine was associated with a shorter AV block cycle length (374 +/- 78 vs 333 +/- 74 msec, P < 0.01), a shorter VA block cycle length (383 +/- 121 vs 307 +/- 49 msec, P < 0.001), and a shorter VA interval during tachycardia (53 +/- 23 vs 41 +/- 17 msec, P < 0.01). CONCLUSION: Although anterograde fast pathway conduction is almost always blocked by 12 mg of adenosine, retrograde fast pathway conduction is not blocked by adenosine in 38% of patients with typical AV nodal reentrant tachycardia. This indicates that the anterograde and retrograde fast pathways may be anatomically and/or functionally distinct. Unresponsiveness of VA conduction to adenosine is not a reliable indicator of an accessory pathway.

Adenosine↗

Long-term evaluation of the ventricular defibrillation energy requirement.

INTRODUCTION: Defibrillation energy requirements in patients with nonthoracotomy defibrillators may increase within several months after implantation. However, the stability of the defibrillation energy requirement beyond 1 year has not been reported. The purpose of this study was to characterize the defibrillation energy requirement during 2 years of clinical follow-up. METHODS AND RESULTS: Thirty-one consecutive patients with a biphasic nonthoracotomy defibrillation system underwent defibrillation energy requirement testing using a step-down technique (20, 15, 12, 10, 8, 6, 5, 4, 3, 2, and 1 J) during defibrillator implantation, and then 24 hours, 2 months, 1 year, and 2 years after implantation. The mean defibrillation energy requirement during these evaluations was 10.9+/-5.5 J, 12.3+/-7.3 J, 11.7+/-5.6 J, 10.2+/-4.0 J, and 11.7+/-7.4 J, respectively (P = 0.4). The defibrillation energy requirement was noted to have increased by 10 J or more after 2 years of follow-up in five patients. In one of these patients, the defibrillation energy requirement was no longer associated with an adequate safety margin, necessitating revision of the defibrillation system. There were no identifiable clinical characteristics that distinguished patients who did and did not develop a 10-J or more increase in the defibrillation energy requirement. CONCLUSION: The mean defibrillation energy requirement does not change significantly after 2 years of biphasic nonthoracotomy defibrillator system implantation. However, approximately 15% of patients develop a 10-J or greater elevation in the defibrillation energy requirement, and 3% may require a defibrillation system revision. Therefore, a yearly evaluation of the defibrillation energy requirement may be appropriate.

Defibrillators, Implantable↗

A prospective evaluation of two defibrillation safety margin techniques in patients with low defibrillation energy requirements.

INTRODUCTION: In patients undergoing defibrillator implantation, an appropriate defibrillation safety margin has been considered to be either 10 J or an energy equal to the defibrillation energy requirement. However, a previous clinical report suggested that a larger safety margin may be required in patients with a low defibrillation energy requirement. Therefore, the purpose of this prospective study was to compare the defibrillation efficacy of the two safety margin techniques in patients with a low defibrillation energy requirement. METHODS AND RESULTS: Sixty patients who underwent implantation of a defibrillator and who had a low defibrillation energy requirement (< or = 6 J) underwent six separate inductions of ventricular fibrillation, at least 5 minutes apart. For each of the first three inductions of ventricular fibrillation, the first two shocks were equal to either the defibrillation energy requirement plus 10 J (14.6+/-1.0 J), or to twice the defibrillation energy requirement (9.9+/-2.3 J). The alternate technique was used for the subsequent three inductions of ventricular fibrillation. For each induction of ventricular fibrillation, the first shock success rate was 99.5%+/-4.3% for shocks using the defibrillation energy requirement plus 10 J, compared to 95.0%+/-17.2% for shocks at twice the defibrillation energy requirement (P = 0.02). The charge time (P < 0.0001) and the total duration of ventricular fibrillation (P < 0.0001) were each approximately 1 second longer with the defibrillation energy requirement plus 10 J technique. CONCLUSION: This study is the first to compare prospectively the defibrillation efficacy of two defibrillation safety margins. In patients with a defibrillation energy requirement < or = 6 J, a higher rate of successful defibrillation is achieved with a safety margin of 10 J than with a safety margin equal to the defibrillation energy requirement.

Aged↗

Changes in cardiac repolarization following short periods of ventricular pacing.

INTRODUCTION: "Cardiac memory" (primary T wave change) is thought to occur after 15 minutes to several hours of right ventricular (RV) pacing. The two components of the temporal change in repolarization are memory and accumulation. The purpose of this study was to examine quantitatively the effect of short periods of ventricular pacing on the human cardiac action potential, using monophasic action potential (MAP) recordings. METHODS AND RESULTS: Thirty-one patients (ages 43+/-14 years) with structurally normal hearts undergoing a clinically indicated electrophysiologic procedure were enrolled. Catheters were placed in the right atrium (RA) and RV, and a MAP catheter was positioned at the RV septum. APD90 was calculated from digitized MAP recordings. MAP morphology comparisons were performed using the root mean square (RMS) of the difference between complexes. All pacing was at 500-msec cycle length. There were four pacing protocols: (1) RA pacing was performed for approximately 15 minutes to evaluate temporal stability of the MAP recordings (5 pts); (2) to evaluate the memory phenomenon, four successive 1-minute episodes of RV pacing were interspersed with 2 minutes of RA pacing (5 pts); (3) the accumulation phenomenon was evaluated by assessing the effects of 1, 5, 10, and 15 minutes of RV pacing on the MAP during RA pacing (16 pts); and (4) 20 minutes of RV pacing was followed by 10 minutes of RA pacing to correlate visually apparent T wave changes with changes in MAP recordings (5 pts). In the control patients, no changes in APD90 or RMS analysis were noted during 14.9+/-1.4 minutes of RA pacing. In the second protocol, RMS of the difference between the baseline MAP complexes and the signal average of the first 50 beats following each of four 1-minute RV pacing trains demonstrated progressively greater differences in morphology after successive episodes of RV pacing. In protocol 3, RMS analysis identified a progressively greater difference between the baseline MAP recording and the average of the first 50 beats after 1, 5, 10, and 15 minutes of RV pacing. In protocol 4, visually apparent changes in T waves occurred in parallel with the RMS of the difference between the baseline MAP recordings and the average of the first 50 beats after 20 minutes of RV pacing. Similar changes also were demonstrated by APD90 analysis. CONCLUSION: This study is the first to demonstrate that episodes of abnormal ventricular activation as short as 1 minute in duration may exert lingering effects on the repolarization process once normal ventricular activation resumes.

Action Potentials↗