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Biomedical subjects

J J Rozanski

Publications and source records attributed to J J Rozanski.

At least 19 recordsLinked to original sources
PubMed1989

Efficacy of procainamide on ventricular tachycardia: relation to prolongation of refractoriness and slowing of conduction.

The effect of procainamide on intraventricular conduction and refractoriness, and the prevention of induction of ventricular tachycardia (VT) were studied in 29 patients who had remote myocardial infarction and inducible sustained monomorphic VT. AFter intravenous administration of 15 mg/kg procainamide, induction of VT was suppressed in seven (24%) patients (responders), while in 22 (76%) VT was still inducible (nonresponders). The percent change in paced QRS duration at a cycle length (CL) of 400 msec produced by procainamide was significantly less in responders than in nonresponders: 29.8 +/- 3.9% versus 38.9 +/- 10.8% (p = 0.0020). The percent change in the right ventricular effective refractory period (ERP) at CLs of 600 and 400 msec was significantly greater in responders than in nonresponders: 14.6 +/- 6.9% versus 7.9 +/- 7.3% (p = 0.0414) for ERP at a CL of 600 msec and 15.1 +/- 7.0% versus 8.0 +/- 7.4% (p = 0.0386) for ERP at a CL of 400 msec. Stepwise discriminant analysis showed that greater percent increase in ERP at a CL of 400 msec and lesser percent increase in paced QRS duration at a CL of 400 msec were significantly independent markers for the responders. These findings suggest that lesser slowing of conduction and greater prolongation of refractoriness by procainamide tend to abolish reentry within the reentrant circuit. Greater slowing of conduction and lesser prolongation of refractoriness tend to stabilize a reentrant circuit, and promote the continued induction of VT.

Electrocardiography↗
PubMed1989

Predictors of sustained ventricular tachycardia inducibility in patients with nonsustained ventricular tachycardia and chronic coronary artery disease.

To assess the likelihood of inducing sustained ventricular tachycardia, we analyzed a cohort of 58 retrospective and 18 prospective patients with chronic coronary artery disease who underwent electrophysiologic study because of spontaneous nonsustained ventricular tachycardia (three or more beats, lasting less than 30 seconds, at a rate greater than 100/min). In 24 of the 58 retrospective patients (41%) sustained ventricular tachycardia was inducible. Stepwise logistic regression identified two "major" variables--left ventricular aneurysm/dyskinesis/akinesis (p = 0.0001; relative risk = 11.88) and ejection fraction less than 40% (p = 0.0002; relative risk = 9.69)--and one "minor" variable--nonsustained ventricular tachycardia longer than 10 beats (p = 0.0151; relative risk = 4.21)--as significant predictors of inducibility. Nineteen patients with both major variables had a high probability of inducibility (greater than 90%). Nineteen patients with neither major variable had a low probability of inducibility (less than 5%). The remaining 20 patients with only one of the major variables had an intermediate probability of inducibility (14% to 75%). The significance of the third minor factor, nonsustained ventricular tachycardia longer than 10 beats, was confined to this intermediate group, in which it could be used to segregate relatively high (65% to 75%) and relatively low (14% to 20%) probability of inducibility. Prospective application of the predictor function stratified 18 additional patients into three groups with high (six patients), intermediate (seven patients), and low (five patients) probability of inducibility. The observed rate of inducibility in each group was 5 of 6 (83%), 2 of 7 (29%), and 0 of 5 (0%), respectively. These data suggest that patients with nonsustained ventricular tachycardia and chronic coronary artery disease can be stratified into subgroups with high, intermediate, and low probability of inducibility of sustained ventricular tachycardia on the basis of ejection fraction and regional ventricular wall motion defects alone.

Aged↗
PubMed1989

Rapid assessment of rate and antiarrhythmic drug effect on the myocardium using asymmetric biphasic pulse stimulation.

An asymmetric biphasic pulse which stimulates the heart and neutralizes the poststimulation polarization at the electrode-myocardial interface permitting the recording of the evoked endocardial response (EER) up to approximately 1 ms poststimulation with the same electrode used for stimulation is described. Using this mode of cardiac stimulation in 20 dogs the effects on the EER of increasing heart rate and antiarrhythmic drugs, procainamide (PA) and N-acetylprocainamide (NAPA), were studied. EERs were recorded during bipolar and unipolar pacing rates of 120, 150, and 200/min before and during a five step PA or NAPA infusion which resulted in progressively increasing PA and NAPA plasma concentrations (Cps), 1.7-32.5 mg/l for PA and 8.1-116.1 mg/l for NAPA. The effects of progressively increasing heart rates were: The T wave amplitude and QS area increased with increases in rate; during pacing at 120, 150, and 200/min, the T wave amplitudes were 7.6 +/- 2.3, 8.2 +/- 2.1, and 9.8 +/- 2.5 mV and the QS areas were 905 +/- 204, 995 +/- 199, and 1101 +/- 231 mVms. The QT interval and QST area decreased with increases in rate; during pacing at 120, 150, and 200/min, the QT intervals were 265 +/- 61, 249 +/- 57, and 226 +/- 52 ms and the QST areas were 288 +/- 198, 221 +/- 154, and 154 +/- 52 mVms. The effects of the antiarrhythmic drugs, PA and NAPA, on the EER were: PA prolonged both the QS duration and QT interval at low Cp (type Ia antiarrhythmic drug property); at a therapeutic PA Cp of 15.0 +/- 0.2 mg/l and a heart rate of 120/min the percent increase of the QS duration was 12 +/- 4% (P = 0.001) and that of the QT interval was 20 +/- 6% (P less than 0.001). The prolongation of the QS duration by PA was rate dependent, the faster the rate the greater the prolongation. NAPA prolonged the QT interval at low Cp, while the QS duration was not significantly effected at low or therapeutic Cps (type III antiarrhythmic drug property); at a therapeutic NAPA Cp of 15.9 +/- 1.6 mg/l and a heart rate of 120/min the percent increase of the QS duration was 1 +/- 1% (NS) and that of the QT interval was 13 +/- 9% (P = 0.018). Our results show that the use of an asymmetric biphasic pulse allows for pacing and recording of an EER, QS and T waves, with a single electrode.(ABSTRACT TRUNCATED AT 400 WORDS)

Acecainide↗
PubMed1989

Time-dependent risk of and predictors for cardiac arrest recurrence in survivors of out-of-hospital cardiac arrest with chronic coronary artery disease.

One hundred one consecutive patients with chronic coronary artery disease who had survived out-of-hospital cardiac arrest in the absence of acute myocardial infarction underwent electrophysiologic evaluation and were followed prospectively. Ventricular tachyarrhythmias were inducible in 76 patients (75%) in the control state and were suppressed by antiarrhythmic drugs or surgery in 32 of the 76 patients (42%). During a mean follow-up of 27 months, cardiac arrest recurred in 21 patients: in two of the 25 patients in whom ventricular tachyarrhythmias were not inducible in the control state, three of the 32 in whom inducible ventricular tachyarrhythmias were suppressed after treatment, and 16 of the 44 in whom inducible ventricular tachyarrhythmias could not be suppressed after treatment. Actuarial rate of cardiac arrest recurrence was 11.2% during the first 6 months of follow-up ("high-risk early phase") and then decreased to less than 4% in each subsequent 6-month period. Multivariate Cox proportional hazards analysis identified an ejection fraction less than 35% (p = 0.0013) and persistent inducibility of ventricular tachyarrhythmias (p = 0.0025) as independent predictors of cardiac arrest recurrence for the entire follow-up period. Separate analysis of variables within and after the first 6 months showed that an ejection fraction less than 35% was the strongest predictor for early phase recurrence (p = 0.0078) but had only marginally significant predictive value for late phase recurrence (p = 0.0516). Persistent inducibility of ventricular tachyarrhythmias had no significant predictive value for early phase recurrence (p = 0.1382) but was the strongest predictor for late phase recurrence (p = 0.0061). These data suggest that, in patients with chronic coronary artery disease who survive out-of-hospital cardiac arrest, poor ejection fraction and persistent inducibility of ventricular tachyarrhythmias have a different predictive influence on early and late phase recurrence. Time-dependent risk factor analysis may have great clinical relevance in assessing an individual's changing risk over time.

Aged↗
PubMed1989

Triphasic time dependence of prognostic markers in patients with sustained ventricular tachyarrhythmias and coronary artery disease.

To characterize the time dependence of prognostic markers for arrhythmia recurrence and arrhythmic death, 81 consecutive patients with documented sustained ventricular tachycardia (VT) or fibrillation (VF) and coronary artery disease (CAD) were analyzed. During follow-up, 28 patients had arrhythmia recurrence and 15 patients had sudden or arrhythmic death. Three different hazard phases were identified by fitting piece-wise exponential function curves to the distribution of both arrhythmia recurrence and sudden/arrhythmic death. An initial phase (0 to 6 months) had an arrhythmia recurrence rate of 2.1% per month; a second low-risk phase (6 to 38 months) had a rate of 0.88%; and a late high-risk phase (greater than 38 months) had a rate of 2.2%. Sudden/arrhythmic death rates in each phase were 1.1%, 0.41%, and 1.7% per month, respectively. Separate Cox regression analyses within each phase identified the following independent predictors of arrhythmia recurrence: in the early phase, ejection fraction (EF) (p = 0.033) and VT inducibility rank (p = 0.048); and in the late phase, VT inducibility rank only (p = 0.003). Likewise, independent predictors of sudden/arrhythmic death were: in the early phase, EF (p = 0.049); and in the late phase, VT inducibility rank (p = 0.008) and previous history of congestive heart failure (p = 0.032). In CAD patients with documented sustained VT/VF, the probabilities of arrhythmia recurrence and sudden/arrhythmic death each followed a similar triphasic hazard function. Highest risk occurred in the late phase and the VT inducibility rank was predictive of late phase events, while EF was a predictor of early phase events.

Adult↗
PubMed1986

Cardiac syncope: a case exhibiting dichotomy between clinical impression and electrophysiologic evaluation.

This case report illustrates the value of electrophysiologic study in patients presenting with graphically unmonitored syncope and/or sudden cardiac death, and who have clinical markers of both bradycardia and ventricular tachycardia. In our patient, a wide QRS on the electrocardiogram and Holter monitor documented high grade ventricular ectopic activity. In this case, had therapy been solely guided by the clinical impression that the patient had ventricular tachycardia, the treatment would have resulted in increasing the risk of recurrence of syncope and/or sudden cardiac death.

Cardiac Pacing, Artificial↗
PubMed1985

Externally activated antitachycardia pacemaker with noninvasive electrophysiologic re-testing capability.

An Omni Orthocor 234A special device pacemaker was implanted in nine patients for treatment of drug-resistant supraventricular tachycardia (three patients) or ventricular tachycardia (six patients). This device is activated using a special external unit, which delivers from six to 15 stimuli at preselected coupling intervals ranging from 195 to 500 ms. Serial noninvasive electrophysiology studies were performed either in the hospital or on an outpatient basis using the triggered mode, which can respond to programmed chest wall stimulation. Three patients with reciprocating supraventricular tachycardia were treated effectively by this device during an average follow-up of 2.2 years. Of the six patients with stable ventricular tachycardia amenable to pacemaker termination, only four remained successful during an average follow-up of 1.9 years. Such devices may find important use in serial noninvasive electrophysiologic testing during long-term clinical follow-up. The present form of this device is inadequate for widespread application, but may be useful for highly selected individuals.

Aged↗
PubMed1979

Right ventricular apical activation times in patients with conduction disturbances occurring during acute transmural myocardial infarction.

His bundle and right ventricular apical electrograms were recorded in 18 patients with acute transmural myocardial infarction in whom catheter insertion was considered necessary for clinical reasons. The V-RVA and H-V intervals were of normal duration (5 to 30 and 35 to 55 msec, respectively) in five patients (Group 1) with persistently narrow (less than 100 msec) QRS complexes. In contrast, 13 patients (Group 2) who manifested a "complete" right bundle branch block pattern within 96 hours after admission had prolonged V-RVA intervals (range 50 to 80 msec, mean 59.2 msec) and H-V intervals that were at the upper limits of normal or prolonged (range 55 to 90 msec, mean 63 msec). In 6 of these 13 patients, the duration of the V-RVA interval became normal when the "complete" right bundle branch block pattern disappeared and was replaced by a "complete" left bundle branch block pattern in three patients and by narrow QRS complexes in the three other patients. This study showed that transmural myocardial infarction in itself did not increase the duration of the V-RVA interval even when "complete" left bundle branch block was present. Moreover, a prolonged V-RVA interval coexsting with a "complete" right bundle branch block pattern was not due to distal right bundle branch block but resulted from a conduction disturbance located in the proximal portions of the right bundle, or perhaps, even within the His bundle itself.

Adult↗
PubMed1979

Mode of operation induced by rapid external chest wall stimulation in patients with normally functioning QRS-inhibited (VVI) pacemakers.

The effects of rapid external chest wall stimulation were evaluated in 10 patients with normally-operating unipolar, lithium-powered, QRS-inhibited pacemakers functioning in their control VVI (QRS-inhibited) mode. Stimuli delivered at slow rates resulted in the expected pacemaker inhibition. On the other hand, during rapid (greater than 900/min) external chest wall stimulation, 8 pacemakers reverted to a VOO mode, 1 to a VVI mode and 1 to either a VVI or VOO mode. No pacemaker was totally inhibited by rapid chest wall stimulation. In accordance with the manufacturer's specifications, the rate to which the implanted pacemakers reverted during the VOO modes produced by the fast external stimuli were the same as those of the VOO modes induced by proper application of an external magnet. Although rapid external chest wall stimulation proved to be a safe procedure, more studies are necessary to determine its usefulness in the follow-up of patients with implanted QRS-inhibited (VVI) pacemakers. At present, conclusions cannot be drawn regarding whether these pacemakers will revert to a mode of operation similar to that induced by rapid external chest wall stimulation when subjected to extrinsic sources of strong electromagnetic interference.

Cardiac Pacing, Artificial↗
PubMed1977

Alternans of the ST segment in Prinzmetal's angina.

Alternans of the elevated ST segment (STEA) was found in 8 of 21 patients (38%) with Prinzmetal's variant angina. In addition to STEA, all eight patients had varying cardiac arrhythmias: multiple premature ventricular depolarizations in eight, ventricular tachycardia in five, and ventricular fibrillation in three. There was no consistent temporal relationship between the occurrence of STEA and the cardiac arrhythmias. Alternans occurred during periods when no arrhythmias were present. All eight patients underwent coronary angiography. Spontaneous coronary artery spasm was documented angiographically in three patients including two who had minimal or no coronary atherosclerotic disease. Six patients had severe, fixed, occlusive coronary artery disease. Possible mechanisms for STEA include: 1) failure of regions of myocardium to depolarize on alternate beats due to variation in conduction and refractoriness between ischemic and nonischemic zones of myocardium, and 2) electrical alternans of the transmembrane action potential during phase 2 and 3 (repolarization) caused by changes in the rate and extent of electrolyte transfer across cell membranes during ischemia. It is postulated that STEA is an electrocardiographic sign in the surface ECG of a dysequilibrium of refractory periods during ischemia and reflects an unstable electrical state of the myocardium.

Adult↗