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Biomedical subjects

B Olshansky

Publications and source records attributed to B Olshansky.

At least 55 records · Page 3Linked to original sources

Current-based transthoracic defibrillation.

This study examines in a prospective, multicenter trial the feasibility and advantage of current-based, transthoracic defibrillation. Current-based, damped, sinusoidal waveform shocks of 18, 25, 30, 35, or 40 amperes (A) were administered beginning with 25 A for polymorphic ventricular tachycardia (VT) and ventricular fibrillation (VF) or 18 A for monomorphic VT; success rates were compared with those of energy-based shocks beginning at 200 J for VF/polymorphic VT and 100 J for VT. The current-based shocks were delivered from custom-modified defibrillators that determined impedance in advance of any shock using a "test-pulse" technique; the capacitor then charged to the exact energy necessary to deliver the operator-selected current against the impedance determined by the defibrillator. Three hundred sixty-two patients received > 1 shock for VF, polymorphic VT, or monomorphic VT: 569 current- based shocks and 420 energy-based shocks. Current-based shocks of 35/40 A achieved success rates of up to 74% for VF/polymorphic VT; 30 A shocks terminated 88% of monomorphic VT episodes. Energy-based shocks of 300 J terminated 72% of VF/polymorphic VT; 200-J shocks terminated 89% of monomorphic VT. We could not demonstrate a significant increase in the success rate of current-based shocks over energy-based shocks for patients with high transthoracic impedance; this may be due to inadequate sample size. Thus, current-based defibrillation is clinically feasible and effective. A larger study will be needed to test whether current-based defibrillation is superior to energy-based defibrillation.

Electric Countershock↗

Management of atrial fibrillation after coronary artery bypass graft.

More than 400,000 patients undergo coronary artery bypass graft surgery (CABG) each year in the United States. At least 20-30% of these patients have atrial fibrillation (Afib), making this arrhythmia one of the most common postoperative problems. This generally benign problem can increase surgical morbidity and the cost and length of hospital stay. If not treated promptly and effectively, Afib can delay a full and rapid recovery. Afib usually occurs in paroxysms between the second and fifth postoperative day and appears directly related to effects of surgery (pericarditis, changes in autonomic tone, cardioplegia, myocardial damage, fluid shifts, etc.). Although similar to Afib in other settings, beta-adrenergic blockade is more effective in preventing and terminating Afib in the postoperative setting. The unique circumstances that precipitate postoperative Afib may explain the favorable therapeutic and prophylactic actions of beta-adrenergic blockade. Other therapies such as amiodarone, sotalol, and digoxin are surprisingly ineffective for postoperative Afib, while intravenous diltiazem is not well tested in this setting. Despite the lack of proven benefit for some of these therapies, they are still frequently used in current clinical practice. Management of postoperative Afib is initially directed at ventricular rate control, but the ultimate goal is return to sinus rhythm. The approach to therapy depends on several clinical variables, including the time course of the arrhythmia, but hemodynamic stability of the patient is the key issue. Return to sinus rhythm may be difficult to achieve early after surgery, so opting for rate control is the best initial approach. If tolerated, beta-adrenergic blockade and calcium antagonism are the best first options. Class IA and III antiarrhythmic drugs should be reserved for persistent or poorly tolerated and prolonged episodes of Afib. Elective cardioversion, either by direct current or with drugs, should be delayed for as long as possible after surgery. Anticoagulation for post-CABG Afib remains controversial. More prudent use of presently available drugs to treat Afib could reduce morbidity, cost, and duration of hospital stay after CABG. More rapid-acting and reliably effective antiarrhythmic therapies with minimal adverse effects would greatly improve management of post-CABG Afib.

Adrenergic beta-Antagonists↗

Dofetilide versus quinidine for atrial flutter: viva la difference!?

Dofetilide is more effective than quinidine to terminate atrial flutter in this animal model. It is also more capable of lengthening refractoriness more uniformly than quinidine. While the investigators describe local changes in refractoriness and dispersion of refractoriness and wavelength meticulously, it is not clear which, if any, of these properties cause flutter termination or influence reinduction. This report provides new insight into the electrophysiologic mechanisms of antiarrhythmic drugs used to treat atrial arrhythmias. Related investigations are needed to expand our knowledge of the actions of antiarrhythmic drugs, how these drugs affect critical portions of the reentrant circuit, and how to identify potential adverse effects of these agents. Application of these data may help guide the use of antiarrhythmic drugs and allow development of safer, and yet more potent, compounds. At least, it will give us pause about using more toxic and less effective drugs. While Class III drugs, specifically dofetilide, may be more potent and beneficial than quinidine in this model, it is uncertain that these results pertain to human reentrant atrial arrhythmias, particularly, atrial flutter. Perhaps dofetilide will be effective for certain types of atrial flutter requiring an anatomical center defined by an area of injury or surgical scar in the right atrium. The fact that these, and previous, data indicate a specific beneficial effect of dofetilide, particularly on atrial flutter, is interesting. Even if dofetilide proves highly effective for human atrial flutter, its safety will need to be proven in large clinical trials. The most obvious concern about dofetilide is development of serious side effects such as torsades de pointes. Clinical trials of this drug for atrial arrhythmias are presently ongoing. Ultimately, the long-term use of such a drug is dependent on the emergence of other highly effective therapies such as radiofrequency ablation.

Animals↗

Reflex vagal control of atrial repolarization.

The reflex vagal control of atrial repolarization was investigated in eight open-chest, anesthetized dogs. A monophasic action potential was recorded from the right atrium, and the action potential duration to 90% repolarization (APD90) was determined every cardiac cycle. beta-Adrenergic receptors were blocked with timolol (0.1 mg/kg). Under baseline conditions, sinus slowing during sinus arrhythmia was accompanied by a significant shortening of APD90 (24 +/- 4.0 ms). Transient occlusion (30 s) of the descending thoracic aorta increased systolic aortic pressure from 138 +/- 2.8 to 181 +/- 3.3 mmHg (P < 0.01). Heart rate decreased from 99 +/- 3.6 to 42.5 +/- 3.4 beats/min (P < 0.01), and APD90 shortened from 168 +/- 5.1 to 94 +/- 3.3 ms (P < 0.01). Release of the occlusion caused arterial hypotension (95 +/- 2.8 mmHg) and an overshoot in both rate (126 +/- 5.2 beats/min) and APD90 (189 +/- 2.3 ms). Aortic occlusion during atrial pacing (130-160 beats/min) decreased APD90 from 147 +/- 7.0 to 78 +/- 3.4 ms (P < 0.01). Cervical vagotomy or atropine eliminated changes in rate and APD90 evoked by aortic occlusion. The results indicate that there is parallel central vagal control of both sinus rate and atrial repolarization. Sinus bradycardia during reflex vagal activation does not prevent the acceleration of atrial repolarization.

Action Potentials↗

Sympathetic influences on electrical and mechanical alternans in the canine heart.

OBJECTIVE: The aim was to investigate the influence of the sympathetic nervous system on the induction of mechanical and electrical alternans in the intact canine heart. METHODS: Experiments were performed on 8 open-chest dogs anesthetized with sodium pentobarbital. A micromanometer-tipped catheter was used to measure left ventricular pressure, dp/dt and the time constant of isovolumic relaxation. Rapid atrial pacing was used to induce alternans and the left stellate ganglion was stimulated electrically to alter sympathetic tone. The longest pacing cycle length that showed a significant alternation in peak systolic pressure was defined as the alternans threshold. Electrical alternans was detected by comparing the ST-T area in the surface ECG (lead II) on alternate beats. RESULTS: The alternans threshold was 305(s.e.m. 10.4) ms under control conditions and decreased to 271(12.1), 225(33.4), and 177(6.2)ms, as the frequency of left stellate stimulation was increased to 1, 2, and 5 Hz, respectively (P < 0.001). Tau and peak -dp/dt began to alternate at the same pacing cycle length as peak +dp/dt and peak systolic pressure. Electrical alternans was only observed during mechanical alternans and the ST-T area of the strong beat was 243(143)% greater than the ST-T area of the weak beat (P < 0.001). Timolol (1 mg.kg-1) blocked the effect of left stellate stimulation (1 and 2 Hz) on mechanical and electrical alternans. CONCLUSIONS: Left sympathetic activation causes a frequency-dependent reduction in the threshold cycle length for global mechanical and electrical alternans. Alternation in relaxation occurs at the same pacing cycle length as does alternation in contraction. Repolarization alternans in the surface ECG appears to reflect underlying mechanical events.

Animals↗

Predictors of defibrillation energy requirements with nonepicardial lead systems.

The determinants of high defibrillation energy requirements (DER) using nonepicardial lead systems (NELS) have not been well characterized. The goal of this study was to examine prospectively the influence of clinical, radiographic, echocardiographic, and procedural variables on DER during NELS placement. Data from 100 consecutive patients undergoing attempted NELS implantation were analyzed. Transvenous leads, subcutaneous patches, and monophasic shock devices from two manufacturers were used. Leads were successfully positioned for testing in 95% of patients. An adequate DER (< or = 25 J) was obtained in 73 of 95 (77%) of patients. Univariate analysis identified amiodarone therapy and left ventricular mass as predictors of high DER. With multivariate analysis, amiodarone therapy was the sole significant predictor of high DER (P = 0.002, odds ratio 5.46). The 22 patients with high NELS DER also had high epicardial DER (mean 24 +/- 9 J). The two patch epicardial DER was > 25 joules in 12 of 22 patients. Thus, adequate DER with monophasic shock waveforms can be obtained in most patients undergoing NELS testing. However, amiodarone therapy significantly increases the probability of obtaining high DER.

Amiodarone↗

Adenosine-sensitive atrial tachycardia.

Limited data suggest that adenosine termination of atrial tachycardia is uncommon. To investigate further the effect of adenosine on atrial tachycardia, adenosine (6-12 mg) was administered during sustained atrial tachycardia in 17 patients. All patients underwent electrophysiological study to exclude other mechanisms of supraventricular tachycardia. Mean patient age was 51 +/- 20 years (range 18-82 years). Seven patients had no structural heart disease. The mean atrial tachycardia cycle length was 390 +/- 80 msecs (range 260-580). Sustained atrial tachycardia was induced with atrial extrastimuli in 8 patients, and was either incessant at baseline or developed spontaneously during isoproterenol infusion in 9 patients. Adenosine terminated atrial tachycardia in 3 patients (18%), transiently suppressed atrial tachycardia in 4 patients (23%), and produced AV block without affecting tachycardia cycle length in the remaining 10 patients. Adenosine sensitivity was observed in 3 of 8 patients with tachycardias initiated and terminated by atrial extrastimuli, and in 4 of 9 patients with spontaneous, but not inducible tachycardias including 3 of 4 patients with isoproterenol facilitated tachycardias. Of multiple clinical and electrophysiological variables examined as potential predictors of adenosine sensitivity, only isoproterenol facilitation of spontaneous or inducible sustained tachycardia predicted adenosine sensitivity (P = 0.02). These observations suggest that adenosine-sensitive atrial tachycardia may be more common than previously recognized. Adenosine sensitivity does not appear to be specific for tachycardia mechanism and cannot be predicted by response to pacing. Atrial tachycardias dependent on beta-adrenergic stimulation are most likely to be terminated by adenosine.

Adenosine↗

Scatter diagram analysis: a new technique for discriminating ventricular tachyarrhythmias.

With the increasing flexibility allowed by implantable cardioverter defibrillators that use tiered therapy, it is important to match the therapy with the arrhythmia. In this article we present scatter diagram analysis, a new computationally efficient two-channel algorithm for distinguishing monomorphic ventricular tachycardia (VT) from polymorphic ventricular tachycardia and ventricular fibrillation (VF). Scatter diagram analysis plots the amplitude from one channel versus the amplitude from another channel on a graph with a 15 x 15 grid. The fraction (percentage) of the 225 grid blocks occupied by at least one sample point is then determined. We found that monomorphic VT traces nearly the same path in space and occupies a smaller percentage of the graph than a nonregular rhythm such as polymorphic VT or VF. Scatter diagram analysis was tested on 27 patients undergoing intraoperative implantable cardioverter defibrillator testing. Passages of 4.096 seconds were obtained from rate (bipolar epicardial) and morphology (patch) leads, and digitized at 125 Hz. Scatter diagram analysis distinguished 13 episodes of monomorphic VT (28.6% +/- 4.0%) from 27 episodes of polymorphic VT or VF (48.0% +/- 8.2%) with P < 0.0005. There was overlap in only one monomorphic VT episode and one polymorphic VT or VF episode.

Algorithms↗

Effectiveness of radiofrequency catheter ablation for treatment of atrial tachycardia.

Catheter ablation has been used to treat atrioventricular node reentrant and atrioventricular reentrant tachycardias with extremely high success rates. The suitability of catheter ablation for treatment of atrial tachycardia, a much less common type of supraventricular tachycardia, has not been well addressed. Fifteen patients (8 females) ranging from 10 to 83 years (mean 38 +/- 22) were referred for catheter ablation of supraventricular tachycardia. The diagnosis of atrial tachycardia was established by standard electrophysiologic techniques. A combination of activation and pace mapping was used to identify a suitable site for radiofrequency current catheter ablation. Medical therapy was unsuccessful in all but 1 patient. Two patients had surgically corrected congenital heart disease, 2 had coronary artery disease and 1 had dilated cardiomyopathy. Seven patients had depressed left ventricular function. Six patients had incessant tachycardias. Presumed tachycardia mechanism was automatic in 11 patients and reentrant in 4. Mean tachycardia cycle length was 372 +/- 74 ms. Catheter ablation was acutely successful in 12 patients (80%) with application of 11.1 +/- 6.6 lesions at a mean voltage of 60 +/- 9 V. In the other 3 patients, 16 to 38 lesions were applied. At a mean follow-up of 18.5 +/- 6.5 months, 2 patients have had recurrences with different P-wave morphologies and underwent a second successful catheter ablation procedure. An additional 2 patients had recurrences with the same P-wave morphology and 1 underwent a second successful catheter ablation procedure. Thus, radiofrequency ablation can be used in a diverse population of patients with atrial tachycardia with an acute success rate of 80% and a long-term success rate of 73%.

Adult↗

Use of multiple patches during implantation of epicardial defibrillator systems.

During implantation of epicardial automatic defibrillator systems, occasional patients have difficulty in obtaining adequate defibrillation thresholds. Of 236 consecutive patients undergoing implantation of epicardial defibrillator systems, 18 patients received a 3-patch (n = 15) or 4-patch (n = 3) defibrillator system. Twelve patients who received a multiple-patch defibrillator system had a best 2-patch defibrillation energy requirement of > or = 30 J; in the remaining 6 patients less stringent clinical criteria were used in the decision to add a third defibrillator patch (defibrillation energy requirement > 18 J in 4 patients, and > 20 J in 2 patients). Technically, multiple-patch systems were made possible with either the use of Y-connectors or defibrillators allowing output to 3 patches. In 3 patients, addition of a third epicardial patch still resulted in a defibrillation energy requirement of > or = 30 J; in these 3 patients, addition of a fourth patch resulted in a defibrillation energy requirement of < or = 20 J. All patients receiving a multiple-patch defibrillator system had a reduction in defibrillation energy requirement, and 12 patients had a reduction in defibrillation energy requirement of > or = 10 J over the best 2-patch defibrillation energy requirement. In the patients who eventually had placement of a multiple-patch system, the best 2-patch defibrillation energy requirement was > 18 J in 4 patients, > 20 J in 2 patients, > or = 30 J in 9 patients, and > 40 J in 3 patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Anti-Arrhythmia Agents↗

Autoregressive modeling of epicardial electrograms during ventricular fibrillation.

During ventricular fibrillation (VF), electrograms from bipolar epicardial electrodes generally appear to have little organization or structure. We sought to identify any well defined organization or structure in these signals by determining if they could be modeled as an autoregressive stochastic process with a white noise excitation during the short time period (6.5-8 s) typically used by automatic implantable defibrillators. The autoregressive model is then used to synthesize VF signals using a white noise excitation with the same probability distribution function as the estimated excitation determined from the autoregressive model for that particular true VF episode. Both the original and ten synthesized VF signals for each patient are then compared using root mean square (rms) amplitude, the number of zero crossings per second, the amplitude distribution of the signals, the rate, and percent variation of rate. The results of examining the synthesized VF waveforms indicate that the rms amplitudes are similar to the true VF waveforms. While the synthesized VF signals had higher rate, more regular RR intervals, more zero crossings per second, and spent less time at baseline than the VF signal from which they were generated, these differences are generally not significant (p > or = 0.05). The use of such synthesized VF signals may allow more thorough testing of VF detection algorithms than is possible with the present limited libraries of human VF recordings.

Defibrillators, Implantable↗

Coronary artery bypass in patients with previously placed implantable defibrillators.

Four patients with previously placed implantable defibrillators required coronary revascularization several years after the original device was inserted. Three patients had a conventional system of epicardial patches and leads, and one patient had a nonthoracotomy system placed. All four patients were successfully revascularized without evidence of perioperative infarction or significant morbidity. The patient with the nonthoracotomy device did require manipulation of the endocardial lead at a separate setting. This limited experience suggests that patients needing revascularization after placement of an implantable defibrillator can be successfully bypassed.

Aged↗

Adenosine-sensitive ventricular tachycardia. Clinical characteristics and response to catheter ablation.

BACKGROUND: Sustained ventricular tachycardia in the absence of structural heart disease may have diverse mechanisms. Termination of the tachycardia by adenosine suggests triggered automaticity as the etiology in many of these patients. We examined the clinical characteristics, electrophysiological responses, and results of catheter ablation in this patient subgroup. METHODS AND RESULTS: Intravenous adenosine terminated sustained ventricular tachycardia in seven of 14 consecutive patients without evidence of structural heart disease. In each of these patients, the tachycardia had a left bundle branch block, inferior-axis QRS configuration and occurred predominantly during stress or exertion. A morphologically similar sustained tachycardia was induced in six of seven patients during programmed ventricular stimulation, although day-to-day reproducibility was poor. Signal-averaged ECGs were normal in all patients. Imaging with 123I-metaiodobenzylguanidine did not reveal focal abnormalities in any of five patients. A discrete site of origin was identified in the free wall of the pulmonary infundibulum in all patients. Limited application of direct current shocks (two patients) or radiofrequency energy (five patients) resulted in long-term abolition of spontaneous and inducible ventricular tachycardia in all patients. CONCLUSIONS: Adenosine-sensitive ventricular tachycardia appears to arise from relatively discrete sites predominantly located in the free wall of the pulmonary infundibulum. The localized nature of this tachycardia renders it amenable to long-term cure by catheter ablation techniques.

Adenosine↗

Characterization of double potentials during ventricular tachycardia. Studies during transient entrainment.

BACKGROUND: Double potentials have been recorded during reentrant tachycardias in animal models. Although they have also been recorded during ventricular tachycardia in humans, their meaning is uncertain. METHODS AND RESULTS: We used transient entrainment as a method to help further understand the meaning of double potentials recorded during ventricular tachycardia in humans. Three patients with ventricular tachycardia (cycle lengths, 500, 450, and 290 msec) were studied. During transient entrainment of ventricular tachycardia (pacing cycle length, 470-260 msec), both double potential deflections were captured at the pacing cycle length. One deflection was captured with a short activation time, and the other deflection was captured with a long activation time. During ventricular pacing, the deflections were associated by the long rather than the short interdeflection interval. At termination of pacing, each double potential deflection was associated with separate but sequential QRS complexes, and each deflection maintained the same electrogram morphology at relatively "slow" overdrive pacing rates. The short interdeflection interval shortened further with faster pacing rates (to less than the ventricular refractory period), making it unlikely that both deflections of the double potential represent active depolarization of the same tissue. In two patients, at a critically rapid pacing rate, one of the double potential deflections changed morphology abruptly, associated with a shortened stimulus-to-double potential time interval (from 520 to 110 msec and from 530 to 240 msec, respectively), indicating a change in the direction of activation that caused that deflection. Interruption of ventricular tachycardia was associated with disappearance of the double potentials at the same recording site. The double potentials did not immediately bracket an area of slow conduction. CONCLUSIONS: These data suggest that double potentials recorded only during ventricular tachycardia represent activation wave fronts on either side of an area of block within a reentrant circuit. Thus, double potentials recorded during ventricular tachycardia in these patients do not appear to represent slow conduction per se but rather appear to represent an area of block at the center of a reentrant circuit around which the reentrant wave front circulates.

Aged↗

Nonthoracotomy lead system for implantable defibrillator.

Over a 2-year period, 110 patients underwent attempted implantation of an automatic cardioverter-defibrillator using the nonthoracotomy lead system. Indications included sustained monomorphic ventricular (n = 62), nonsustained with poor ventricular function (n = 7), ventricular fibrillation (n = 21), ventricular tachycardia/fibrillation (n = 18), and familial long QT syndrome (n = 2). There were 90 male and 20 female patients. Mean age was 57 +/- 15 years. Sixty percent had previous coronary bypass or valve operations, or both. Mean left ventricular ejection fraction was 30% +/- 14%, cardiac index was 2.4 +/- 0.9 L/m2, and systolic pulmonary artery pressure was 41 +/- 14 mm Hg. Under general anesthesia, the nonthoracotomy lead was introduced through the left subclavian vein. The subcutaneous patch and generator were placed posteriorly on the serratus muscle and left upper quadrant, respectively. The length of the procedure was 116 +/- 44 minutes and the mean number of defibrillation shocks for a successful implant was 8 +/- 4. Eighty-five patients (77%) had successful implantations. Failures were due to high defibrillation threshold (n = 23) and inability to place a right ventricular lead (n = 2). Predictors of failure included preoperative antiarrhythmic drugs and cardiac index of 1.8 +/- 4 L/m2 or less (p = 0.004). Three patients (2.7%) died after the operation of heart failure (n = 2) and chronic heart transplant rejection (n = 1). Complications included lead migration or dislodgment (n = 8), infection (n = 1), and hematoma (n = 3). In summary, the nonthoracotomy lead system may provide an alternative in patients undergoing cardioverter-defibrillator implantation.

Aged↗

Atrial flutter--update on the mechanism and treatment.

Atrial flutter is a common and usually benign but symptomatic supraventricular tachycardia. There is a striking similarity between patients with atrial flutter suggesting a common substrate despite the presence or absence of underlying heart disease. In man, the mechanism is a single reentrant circuit originating in the right atrium whose center appears to be functional within the anatomical constraints of the right atrium. The reentrant circuit of atrial flutter contains an area of slow conduction in the inferior right atrium but the size and exact location is uncertain. Drug therapy directed at terminating and preventing atrial flutter has been available for many years. The efficacy and safety of this therapy is not as well tested as is the same therapy for atrial fibrillation. The most effective way to terminate atrial flutter is a nonpharmacological approach. Several nonpharmacological methods provide new treatment options in the management of patients with drug resistant or hemodynamically unstable atrial flutter. The use of anticoagulation for this disorder is still evolving. There is a risk of clinically apparent thromboemboli in some patients with atrial flutter although the risk appears less than that for atrial fibrillation. In the future, refinements and improvements in therapy for atrial flutter will likely be derived from a better understanding of its mechanism.

Animals↗