Biomedical subjects

P E Karasik

Publications and source records attributed to P E Karasik.

7 recordsLinked to original sources

PubMed2000

High dispersion of ventricular repolarization after an implantable defibrillator shock predicts induction of ventricular fibrillation as well as unsuccessful defibrillation.

OBJECTIVES: To test the hypothesis that post-shock dispersion of repolarization (PSDR) is higher in T wave shocks that induce ventricular fibrillation (VF) than in those that do not, as well as in implantable cardioverter defibrillator (ICD) defibrillation shocks which fail to terminate VF when compared with those that are successful. BACKGROUND: Ventricular fibrillation has been linked to the presence of dispersion of repolarization, which facilitates reentry. Most of the studies have been done in animals, and the mechanism underlying the generation and termination of VF in humans is speculative and remains to be determined. METHODS: Monophasic action potentials (MAPs) were recorded simultaneously from the right ventricular outflow tract (RVOT) and the right ventricular apex (RVA) in 27 patients who underwent implantation and testing of an ICD. T wave shocks were used to induce VF while the termination was attempted using internal defibrillator shocks. The post-shock repolarization time (PSRT) was measured in both the RVA and RVOT MAPs, and the difference between the two recordings was defined as the PSDR. The averages of PSDR were compared between the successful and unsuccessful inductions and terminations of VF. RESULTS: T wave shocks that induced VF generated a greater PSDR (93.4 +/- 85.1 ms) than the unsuccessful ones (45.1 +/- 55.9 ms, p < 0.001). On the other hand, shocks that failed to terminate VF were associated with a greater PSDR (59.9 +/- 41.2 ms) than shocks that terminated VF (21.1 +/- 20.1 ms), p < 0.001. CONCLUSIONS: A high PSDR following a T wave shock is associated with induction of VF; while following a defibrillating shock, it is associated with its failure and the continuation of VF. Conversely, a low PSDR is associated with failure of a T wave shock to induce VF and successful termination of VF by a defibrillating shock.

Action Potentials↗

PubMed1999

An abdominal active can defibrillator may facilitate a successful generator change when a lead failure is present.

AIMS: Defibrillator generator changes are frequently performed on patients with an implantable cardioverter defibrillator in an abdominal pocket. These patients usually have epicardial patches or older endocardial lead systems. At the time of a defibrillator generator change defibrillation may be unsuccessful as a result of lead failure. We tested the hypothesis that an active can defibrillator implanted in the abdominal pocket could replace a non-functioning endocardial lead or epicardial patch. METHODS AND RESULTS: An abdominal defibrillator generator change was performed in 10 patients, (mean age = 67 +/- 13 years, nine men). Initially, a defibrillation threshold (DFT) was obtained using a passive defibrillator and the chronic endocardial or epicardial lead system. DFTs were then performed using an active can emulator and one chronic lead to simulate endocardial or epicardial lead failure. We tested 30 lead configurations (nine endocardial and 21 epicardial). Although a DFT of 7.3 +/- 4.2 joules was obtained with the intact chronic lead system, the active can emulator and one endocardial or epicardial lead still yielded an acceptable DFT of 19.9 +/- 6.1 joules. In addition, a successful implant (DFT < or = 24 joules) could have been accomplished in 28 of 30 (93%) lead configurations. CONCLUSION: An active can defibrillator in an abdominal pocket may allow for a successful generator change in patients with defibrillator lead malfunction. This would be simpler than abandoning the abdominal implant and moving to a new pectoral device and lead or tunnelling a new endocardial electrode. However, loss of defibrillation capability with a particular complex lead may be a warning of impending loss of other functions (eg. sensing and/or pacing).

Abdomen↗

PubMed1995

Relation between repolarization and refractoriness during programmed electrical stimulation in the human right ventricle. Implications for ventricular tachycardia induction.

BACKGROUND: Although programmed electrical stimulation is widely used for provoking sustained ventricular tachycardia (VT), the mechanism by which repetitive extrastimulation evokes VT is still little understood. Specifically, it is not clear why several closely coupled extrastimuli are frequently required to induce VT. Although regularly paced human ventricular myocardium exhibits a near constant relation between myocardial repolarization and refractoriness, the effect of repetitive extrastimulation on the relation between repolarization and excitability in the human heart and its relevance for arrhythmia induction by programmed stimulation are unknown. We hypothesized that the induction of VT by repetitive extrastimulation is facilitated by an altered relation between repolarization and refractoriness, and this leads to disturbances in ventricular impulse propagation, which trigger the onset of VT. METHODS AND RESULTS: Twenty-one patients undergoing routine electrophysiological study were paced from the right ventricular apex and outflow tract endocardium with monophasic action potential-pacing catheters placed at both sites simultaneously Monophasic action potential durations (APDs) and effective refractory periods (ERPs) were measured simultaneously at each site, during regular stimulation (S1-S1) at 400-ms cycle length and during three consecutive extrastimuli (S2 through S4) at the closest coupling intervals at which all three extrastimuli still resulted in capture. Measurements further included the repolarization level at which the earliest capture occurred, the ratio between ERP and APD, and the propagation time between the pacing and distant recording site. APD and ERP both shortened progressively with each extrastimulus. APD at 90% repolarization decreased from a baseline (S1) of 238.1 +/- 19.7 ms by 14.9% at S2, 18.9% at S3, and 22.9% at S4 (P < .0001, S1 versus S4). ERP decreased from 233.1 +/- 19.7 ms (S1) to 180.0 +/- 41.9 ms (S3) (P < .0001, S1 versus S3). While ERP shortening occurred mainly on the basis of APD shortening, there was an additional factor that contributed to ERP shortening independent of APD shortening. Each consecutive extrastimulus was able to elicit a propagated response at earlier repolarization levels than the previous one: the earliest capture for S2 occurred at 85.5 +/- 10.2% of complete repolarization, for S3 at 83.9 +/- 10.5%, and for S4 at 78.4 +/- 11.2% (P < .05 for S2 versus S3; P < .05 for S3 versus S4; P < .01 for S2 versus S4). This progressive "encroachment" of the earliest capture stimulus onto the preceding repolarization phase (at progressively less repolarized levels) correlated with a progressive delay of impulse propagation between the pacing site and the second recording site: propagation time increased from baseline (S1) by 10.5 +/- 1.3% with S2 to 19.0 +/- 1.6% with S3 and to 22.5 +/- 2.8% with S4 (P < .05, S4 versus S1). VT was induced in 11 of 21 patients. Nine of these had VT induced only when significant encroachment of extrastimuli on the preceding repolarization phase (< 81.3 +/- 7.0%) and associated conduction slowing (> 16.6 +/- 1.8%) were present. CONCLUSIONS: Repetitive extrastimulation not only shortens APD and subsequently ERP but also alters the ERP/APD relation by allowing capture to occur at progressively less complete repolarization levels. This progressive encroachment onto the preceding repolarization phase is associated with impaired impulse propagation and a high incidence of VT induction. This may help explain how repetitive, closely coupled extrastimulation induces ventricular tachycardia in the human heart.

Aged↗

PubMed1995

Prolongation of conduction time during premature stimulation in the human atrium is primarily caused by local stimulus response latency.

BACKGROUND: Conventional clinical electrophysiological techniques cannot accurately differentiate between local stimulus response latency and propagation time of the atrial response. The purpose of this study was to identify and distinguish local stimulus response latency from impulse propagation time in the human right atrium during programmed electrical stimulation. METHODS: Pacing was performed from two atrial sites (high and low right atrium) in 19 patients, using monophasic action potential recording/pacing combination catheters (interelectrode distance < 2 mm). Local stimulus response latency (interval between stimulus artifact and upstroke of the local monophasic action potential), and propagation time (interval between local and remote monophasic action potential upstroke) were evaluated at a basic cycle length (S1-S1) of 600 ms and as a function of the extrastimulus proximity (interval between extrastimulus and effective refractory period). Data are presented as means +/- SEM. RESULTS: During basic stimulation, local latency was very small (3.8 +/- 1.7 ms). During premature extrastimulation (proximity < 70 ms), local latency increased progressively with decreasing coupling intervals. Prolongation of local latency was most pronounced during stimulation close to the effective refractory period with local stimulus response latency increasing to 18.3 +/- 1.4 ms (380 +/- 7.9%) at 10 ms proximity (P < 0.002) and to 27.9 +/- 3.7 ms (630 +/- 13.2%) at 5 ms proximity, respectively (P < 0.0001). The impulse propagation time between the stimulation site and the remote recording site was on average 54.5 +/- 14.3 ms during basic stimulation, and increased up to 62.1 +/- 13.5 ms (14.0 +/- 8.4%), which was not significant. CONCLUSIONS: The intra-atrial impulse propagation remained essentially unchanged during the entire range of premature stimulation. Local stimulus response latency was negligible and constant during late coupling intervals but increased dramatically when extrastimulation approached the preceding repolarization phase. This has the following clinical impact: first, local stimulus response latency during premature extrastimulation curbs the targeted atrial response interval second, local stimulus response latency, not propagation time, seems responsible for the greater functional than effective refractory period during electrical stimulation; third, local stimulus response latency should be considered in pace mapping for accurate comparison of conduction time before pacing with that during pacing.

Aged↗

PubMed1993

Radiofrequency catheter ablation of ectopic atrial tachycardia using paced activation sequence mapping.

OBJECTIVES: Although ectopic atrial tachycardia is infrequent, it can be an important clinical challenge. We sought to define an alternative therapeutic approach to this refractory problem. BACKGROUND: Radiofrequency energy catheter ablation has been used to treat a variety of ventricular and supraventricular arrhythmias but has not been proved efficacious in the management of ectopic atrial tachycardia. METHODS: Ten patients (14 to 47 years of age) referred with refractory ectopic atrial tachycardia were studied. Mapping techniques included identification of earliest atrial activation, confirmation of concordance of P wave configuration during spontaneous tachycardia and pacing from the ablation catheter, and paced activation sequence mapping. The paced activation sequence mapping compared the activation sequence at multiple atrial sites during spontaneous tachycardia with that recorded during pacing from the ablation catheter. The catheter was steered to a point where pacing reproduced the spontaneous activation sequence. RESULTS: Foci were right atrial in eight patients and left atrial in two. In 8 of 10 patients, 514 +/- 97 (SE) J and 5.7 +/- 2.3 (SD) J radiofrequency energy applications ablated the ectopic focus. Seven of these eight patients presented with one focus and one had two discrete and stable foci. Ablation was unsuccessful in two patients with multiple foci. No complications occurred. An arrhythmia focus recurred in two patients and one patient underwent successful repeat ablation. The other patient was managed medically. All seven patients with successful ablation are symptom free after 6.5 +/- 3.8 months. CONCLUSIONS: Our preliminary experience suggests that with the use of both paced activation sequence mapping and standard techniques, radiofrequency ablation of ectopic atrial tachycardia may be a safe and effective form of therapy.

Adolescent↗

PubMed1993

Effect on coronary artery anatomy of radiofrequency catheter ablation of atrial insertion sites of accessory pathways.

OBJECTIVES: The purpose of this study was to analyze the effects of radiofrequency catheter ablation of the atrial insertion site of accessory pathways on the angiographic appearance of coronary arteries. BACKGROUND: Radiofrequency catheter ablation of accessory pathways requires the application of energy to the endocardial surface of the atrioventricular groove adjacent to the major epicardial coronary arteries. A systematic analysis of the effect of radiofrequency ablation on coronary arteries has not previously been demonstrated. METHODS: Seventy consecutive patients with 76 accessory pathways (7 right free wall, 44 left free wall, 12 posteroseptal, 8 anteroseptal and 5 midseptal) were studied. Quantitative coronary angiography was performed before, immediately after and a mean of 69 +/- 42 days after radiofrequency catheter ablation. RESULTS: Coronary artery diameter adjacent to the ablating electrode was 2.6 +/- 0.9 mm before ablation, 2.7 +/- 0.9 mm immediately after ablation and 2.7 +/- 1.0 mm at the time of follow-up study. Angiographic findings were unchanged from baseline in 69 of 70 patients immediately after ablation and in all 70 patients at the time of follow-up study. CONCLUSIONS: Radiofrequency catheter ablation of the atrial insertion site of accessory pathways does not result in short-term angiographic changes in coronary artery anatomy.

Adolescent↗

PubMed1993

Optimization of biphasic waveforms for human nonthoracotomy defibrillation.

BACKGROUND: Biphasic waveforms reduce defibrillation threshold (DFT) in a wide variety of models. Although there are several human studies of long-duration, high-tilt biphasic waveform defibrillation, the specific biphasic waveform shape required to achieve optimal DFT reduction is unknown. METHODS AND RESULTS: This study tested the effect of single capacitor biphasic waveform tilt modification on DFT using a paired study design in 18 patients undergoing nonthoracotomy defibrillator implantation. Baseline DFT was obtained using a 65% tilt, simultaneous pulse, bidirectional monophasic shock from a right ventricular cathode to a coronary sinus or superior vena cava lead and a subscapular patch. The single-capacitor biphasic waveform shocks, delivered over the same pathways, consisted of either both phases at 65% tilt (65/65 biphasic waveform) to produce an overall tilt of 88% and a delivered energy 11% greater than monophasic shock or both phases at 42% tilt (42/42 biphasic waveform) to produce an overall tilt of 66% and delivered energy equal to monophasic shock. The 65/65 biphasic waveform reduced stored energy DFT 25%, from 16.2 +/- 4.4 J with monophasic shock to 12.1 +/- 5.3 J (P < .02); however, it did not significantly reduce the delivered energy DFT. In contrast, the 42/42 biphasic waveform required 49% less stored energy (16.2 +/- 4.4 J, monophasic shock, vs 8.3 +/- 3.3 J, biphasic waveform; P < .001) and 49% less delivered energy (14.2 +/- 3.8 J, monophasic shock, vs 7.3 +/- 2.9 J, biphasic waveform; P < .001) than monophasic shock for successful defibrillation. The 42/42 biphasic waveform delivered energy DFT was 4.6 +/- 5.2 J (39%) less than 65/65 biphasic waveform DFT (P < .002). CONCLUSIONS: DFT reduction is an inherent electrophysiological property of biphasic waveforms that is independent of delivered energy. Overall biphasic waveform tilt and the relative amplitudes of the waveform phases are important factors in defibrillation efficacy. Defibrillation with a 42/42 biphasic waveform is more efficacious than 65/65 biphasic waveform defibrillation; however, the optimal biphasic waveform remains unknown.

Adult↗