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Biomedical subjects

E Kaplinsky

Publications and source records attributed to E Kaplinsky.

At least 163 records · Page 9Linked to original sources
PubMed1982

The supernormal phase of intraventricular conduction: normalization of intraventricular conduction of premature atrial beats.

This report presents the analysis of a case in which numerous atrial extrasystoles, associated with normal intraventricular conduction, occurred during sinus rhythm conducted with right bundle branch block. The wide overlap of coupling intervals of normally conducted extrasystoles and other extrasystoles with right bundle branch block seemed prima facie to negate the possibility of supernormality. Rearrangement of these intervals, however, to allow for the timing of right bundle branch depolarization with respect to the ensuing QRS complex, resulted in a clear cut separation of all normalized complexes from those with right bundle branch block. All normalized extrasystoles were localized in a zone very early in the cycle. This finding, in the presence of atrial extrasystoles with normal P-R intervals, strongly supports the mechanism of supernormality in this case. Alternate explanations do not appear to be tenable.

Aged↗
PubMed1982

The influence of verapamil on serum digoxin concentration.

The effect of verapamil on the pharmacokinetics of digoxin was studied in 49 patients with chronic atrial fibrillation. A dose of 240 mg/day of verapamil was given to the patients who were receiving a stable dose of digoxin. Serum digoxin levels rose from 0.76 +/- 0.54 ng/ml (mean +/- SD) to 1.31 +/- 0.54 ng/ml during verapamil treatment (p less than 0.0005). This effect was dose-dependent, as shown in seven subjects who received 160 mg and then, 240 mg of verapamil: There was a stepwise rise in serum digoxin concentration from a control value of 0.60 +/- 0.11 ng/ml to 0.84 +/- 0.18 ng/ml and 1.24 +/- 0.40 ng/ml, respectively (p less than 0.01 for both steps). The effect of verapamil developed gradually within the first few days in seven subjects in whom serum digoxin concentration reached, within 7 days, 90% of the increase observed 14 days after onset of verapamil. Renal digoxin clearance decreased significantly (26.1 +/- 0.7 vs 55.1 +/- 12.3 ml/min, p less than 0.005) in six patients in whom serum digoxin concentration increased. It did not change in one patient in whom serum digoxin concentration was not influenced by verapamil. Creatine clearance did not change in any of these seven. The same effects on digoxin clearance were observed in three normal subjects. Among the 49 patients, verapamil resulted in the development of signs and symptoms that suggested digitalis toxicity in seven. Verapamil significantly increased serum digoxin concentration. The process is dose-dependent and gradual, and it is at least partially explained by reduced renal excretion without reduction in glomerular filtration. The dose of digoxin may need readjustment in patients who are concomitantly receiving verapamil.

Adult↗
PubMed1981

Reperfusion ventricular tachyarrhythmias: correlation with antecedent coronary artery occlusion tachyarrhythmias and duration of myocardial ischemia.

The incidence and severity of reperfusion ventricular tachyarrhythmias were correlated with : (1) the duration of antecedent acute coronary artery occlusion and (2) the incidence, severity, and time course of ventricular tachyarrhythmias occurring during the antecedent period of coronary occlusion in 98 dogs studied postligation for 5 to 60 minutes. The incidence of reperfusion ventricular fibrillation (VF) increased significantly as coronary artery ligation periods were lengthened from 5 minutes to either 20 minutes (2 of 19 dogs vs 12 of 18 dogs, p less than 0.001) or 30 minutes (16 of 24, p less than 0.001), but notably decreased when reperfusion was delayed further from 30 minutes to 60 minutes after coronary artery ligation (4 of 18 dogs, p less than 0.001). Seven dogs were resuscitated from VF during coronary ligation and all seven suffered VF on reperfusion, whereas 37 dogs were arrhythmia-free during ligation and only one (3%, p less than 0.001) had VF on reperfusion. In addition, reperfusion ventricular tachyarrhythmias correlated with the occurrence of both immediate ventricular tachyarrhythmias (those peaking at 5 to 6 minutes postligation) and delayed ventricular tachyarrhythmias (those peaking at 18 minutes' postligation) of the antecedent acute ligation period. These observations provide a further basis for improved clinical understanding and management of potentially malignant tachyarrhythmias consequent to early myocardial reperfusion following acute myocardial ischemia and infarction.

Animals↗
PubMed1981

The use of the balloon-tipped floating catheter in temporary transvenous cardiac pacing.

The effectiveness and safety of balloon-tipped, flow guided, electrodes for ventricular pacing as opposed to the fluoroscopy-guided semi-rigid bipolar electrodes have never been compared in a controlled study. A prospective study was therefore undertaken to compare both techniques in semi-elective and emergency procedures. Flow guided electrodes were inserted in 67 patients (group A) and semi-rigid electrodes in 44 patients (group B). The results of group A were judged to be superior to those of group B in four aspects: a) shorter time (6'45" vs. 13'30", p less than 0.0005); b) lower incidence of catheter displacement (13.4 vs. 32.0 percent, p less than 0.05); c) longer interval of time between implantation and catheter displacement (4.4 vs. 1.9 days, p less than 0.0005); d) lower incidence of serious ventricular arrhythmias during insertion (1.5 vs. 20.4 percent, p less than 0.005). Threshold at insertion was not significantly different (0.6 +/- 0.3 vs 0.7 +/- 0.2 milliampere). The superiority of flow-guided electrodes over fluoroscopy-guided electrodes persisted in the comparison of semielective insertions in groups A and B. We conclude that the flow-guided insertion technique is safer, more expeditious and more stable than the fluoroscopy-guided technique in semi-elective as well as in emergency insertions.

Adolescent↗
PubMed1981

Mid-systolic click and echocardiographic evidence of mitral valve prolapse during electrical pacing.

A mid-systolic click was present in a patient during three years of follow-up after implantation of a permanent transvenous pacemaker. Echocardiography revealed posterior motion of the anterior leaflet which resembled mitral valve prolapse. Both the click and echocardiographic evidence of prolapse disappeared simultaneously with resumption of sinus rhythm and during supraventricular tachyarrhythmias. Wtih spontaneous change in the position of the electrode three years after initial implantation, both the click and the posterior motion of the mitral valve disappeared. The association of mitral valve prolapse with electrical pacing is most unusual and appears to have a distinct pathophysiological mechanism.

Aged↗
PubMed1981

Failure of antiarrhythmic drugs to prevent experimental reperfusion ventricular fibrillation.

Ninety-nine adult mongrel dogs underwent acute ligation of the proximal left anterior descending coronary artery. Thirty minutes later, the occlusion was released to evaluate the effectiveness of five antiarrhythmic protocols in eliminating reperfusion ventricular fibrillation. The five protocols included: protocol 1 --i.v. lidocaine, preligation and prerelease (n = 19); protocol 2 -- i.v. lidocaine, prereperfusion only (n = 22); protocol 3 -- chronic, oral, daily amiodarone for 2 weeks preligation (n = 19); protocol 4 -- i.v. procainamide, preligation and prereperfusion (n = 21); and protocol 5 -- i.v. verapamil, prereperfusion (n = 18). Each regimen was evaluated with respect to the incidence of reperfusion ventricular fibrillation in dogs that survived to reperfusion, and the results were compared to 77 control dogs that underwent identical coronary artery occlusion and release procedures without drug therapy. The incidence of reperfusion ventricular fibrillation was as follows: protocol 1 -- seven of 15 dogs (47%); protocol 2 -- six of 18 (33%); protocol 3 -- 11 of 16 dogs (69%); protocol 4 -- eight of 17 dogs (47%); and protocol 5 -- 10 of 17 dogs (59%), compared with 36 of 60 (60%) in control dogs. Using chi-square analysis, protocol 2 was beneficial (p < 0.05). The dogs were then stratified into high- and low-risk subgroups based on the arrhythmic events of the antecedent coronary artery ligation periods, and predictive risk indexes for the occurrence of reperfusion ventricular fibrillation were developed. the Mantel-Haenszel method of statistical analysis revealed that none of these protocols resulted in a statistically significant reduction in the incidence of reperfusion ventricular fibrillation. Thus, use of these predictive indexes plus appropriate statistical methods has revealed, unexpectedly, limitations in the efficacy of a spectrum of antiarrhythmic agents in preventing reperfusion ventricular fibrillation.

Amiodarone↗
PubMed1981

Ventricular arrhythmias in acute coronary artery ligation in dogs: electrophysiological mechanism and its relation to the severity of myocardial ischemia.

Analysis of conduction characteristics within the ischemic myocardium and the incidence of ventricular arrhythmias for the first 30 minutes of coronary artery ligation identified two phases of ventricular arrhythmias with different electrophysiological mechanisms. The first phase appearing during 2-10 minutes (immediate ventricular arrhythmias: IVA) was closely related to the degree of epicardial delay and thus considered to be initiated by reentry within the ischemic epicardial zone. In contrast, the second or delayed phase (12-30 minutes, delayed ventricular arrhythmias: DVA) of ventricular arrhythmias appearing independently from epicardial delay was suggested to originate from the subendocardial Purkinje network, since endocardial activation of the ischemic zone consistently preceded the QRS complexes of ventricular arrhythmias. Measurements of myocardial adenosine triphosphate (ATP) contents demonstrated that in animals developing a profound myocardial ischemia by 3-5 minutes, epicardial delay was not observed and thereby IVA was not initiated. In contrast, epicardial delay and IVA were associated with a significant, but milder or slower ischemic process. At the time of DVA, myocardial ATP contents were at extremely low levels for both groups with and without DVA, supporting the concept that DVA is not originated from the ischemic myocardial cells, but from Purkinje fibers depressed secondarily by surrounding ischemic myocardial cells.

Adenosine Triphosphate↗
PubMed1981

Failure of antiarrhythmic drugs to affect epicardial delay during acute experimental coronary artery occlusion and reperfusion: correlation with lack of antiarrhythmic efficacy.

Five antiarrhythmic drug protocols were studied to evaluate their efficacy in reducing the incidence of coronary artery ligation and/or reperfusion ventricular arrhythmias and to determine whether their antiarrhythmic activity correlated with their effect on epicardial delay. Protocols were as follows: I) preligation lidocaine (N = 19); II) preligation amiodarone (N = 18); III) preligation procainamide (N = 19); IV) prereperfusion lidocaine (N = 19); V) prereperfusion verapamil (N = 18); and control (no drug, N = 61). A total of 50 (82%) of the 61 control animals developed ventricular arrhythmias during coronary artery ligation and 29 (68%) of the 53 control dogs that survived until reperfusion developed ventricular arrhythmias upon reperfusion. None of these treatment protocols had a significant effect in reducing the incidence of either ventricular arrhythmias or ventricular fibrillation during coronary artery ligation or reperfusion compared with the control animals (P greater than .05). Correspondingly, the mean maximal epicardial delay during coronary artery ligation was also unchanged by each of these drug treatment protocols compared with the control group. Similarly, none of these treatment protocols demonstrated significant effect in preventing reperfusion ventricular arrhythmias or a consistent effect on the degree of mean maximal epicardial delay during reperfusion. Although the lack of antiarrhythmic efficacy of these agents precludes further speculation, further study is warranted to determine whether changes in epicardial delay can be used as markers for antiarrhythmic activity.

Animals↗
PubMed1980

Intramyocardial activation in early ventricular arrhythmias following coronary artery ligation.

Subendocardial, subepicardial and intramyocardial activation in the ischemic zone was investigated in 20 anesthetized open chest dogs 0-30 minutes after the ligation of the left anterior descending coronary artery. Single and composite electrograms and lead 2 of the ECG were recorded. Coronary artery ligation produced marked delay, fragmentation, and reduction in amplitude in the electrical activity of the subepicardial and intramyocardial muscle layers. The activation remained synchronous in the subendocardial muscle layers. Extension of electrical activity in the ischemic subepicardium and intramyocardium beyond the T wave of the surface ECG preceded the onset of immediate ventricular arrhythmias (IVA) during the initial ten minute period after coronary artery ligation. However, a second surge of delayed ventricular arrhythmias (DVA), 10-30 minutes after ligation, was not associated with the appearance of diastolic electrical activity in any of the subepicardial or myocardial layers. It appears that subepicardial as well as intramyocardial reentry could play an important role in the genesis of the immediate ventricular arrhythmias (1-10 minutes after ligation). In contrast, no obvious reentrant activity as evidenced by delayed and fragmented electrical activity could be observed in the electrogram from any of the myocardial electrical activity could be observed in the electrogram from any of the myocardial layers with the appearance of delayed ventricular ectopic activity 10-30 minutes after ligation.

Animals↗
PubMed1980

Permanent overdrive pacing for the suppression of recurrent ventricular tachycardia in a newborn with long QT syndrome.

A newborn with long QT interval and repetitive ventricular tachycardia of the "torsade de pointes" type was seen at the age of one day. The arrhythmia was resistant to lidocaine, propranolol and atropine, but was controlled by isoproterenol infusion. A transvenous pacemaker, inserted at three days of age, suppressed the ventricular tachycardia at stimulation rates above 100/minute. At 19 days of age a permanent pacemaker at pulse rate of 119 beats/minute was implanted. At one year of age the infant was thriving and was completely free of ventricular arrhythmia.

Cardiac Pacing, Artificial↗
PubMed1980

The beneficial effect of the beta blocker timolol in stable agina pectoris.

Timolol is a new beta blocker with cardioselective properties. A single blind controlled study was performed to assess the efficacy of timolol maleate in doses of 10 to 30 mg per day in 20 patients affected by stable angina pectoris. The patients received a placebo for a baseline period of 2 weeks, followed by 12 weeks of timolol. The number of anginal attacks dropped from 14.9 attacks per week in the baseline period to a minimum of 4.6 attacks per week in the sixth week of treatment (P less than 0.01). The number of tablets of nitroglycerin taken per week was reduced from 6.5 during the baseline period to 2.3 in the sixth week of treatment. Resting heart rate decreased from a baseline mean value of 72 beats per minute to 51.7 and 53.7 per minute at weeks 6 and 12 respectively (P less than 0.01). Blood pressure both at rest and during exercise was significantly reduced. The mean work index measured during bicycle ergometry was 127 units before treatment; it increased by 29.4 units and 36.1 units during week 6 and week 12 respectively (P less than 0.05). There was a marked symptomatic improvement in 50% of the patients. Mild fatigue was a common side effect but it disappeared following reduction of dose. We concluded that timolol maleate significantly reduces the number of anginal attacks and increases the work capacity of patients affected by stable angina pectoris

Adrenergic beta-Antagonists↗
PubMed1980

A preclinical study of EO-122, a new lidocaine-like antiarrhythmic drug.

The 2,6-dimethylanilide of quinuclidine-3-carboxylic acid hydrochloride (EO-122), a new structural analog of lidocaine, has been shown to possess potent antiarrhythmic activity in experimentally induced arrhythmias in animals. Restoration of normal sinus rhythm and suppression of ouabain-induced arrhythmia in cats and dogs, and of coronary occlusion-induced arrhythmia in dogs, followed a single IV injection of 1--3 mg/kg, with an onset of 2 minutes and a duration of 20--240 minutes. Occlusion-induced arrhythmia was likewise suppressed after an oral dose of 10--20 mg/kg, with an onset of 11--65 minutes and a duration of 25--120 minutes. Under similar conditions, lidocaine was either totally ineffective or of ultra-short duration. The bioavailability of EO0122 by the oral route exceeded 80% of the oral dose. Therapeutic blood concentrations were in the range 0.5--7 microgram/ml. At about 5 microgram/ml there was a slight depression of cardiac function in the anesthetized cat, but not in the conscious dog. In cats, complete A-V block occurred at concentrations of 60--70 microgram/ml. The IV LD50 in mice was 22 mg/kg, and in rabbits 8.5 mg/kg. No overt signs of neurotoxicity could be observed at any dose of EO-122. The pharmacokinetic profile of the drug fits a two-compartment open model, with t1/2 congruent to 150 min and Vd (SS) congruent to 1.5 l/kg.

Animals↗
PubMed1980

Overdrive pacing in quinidine syncope and other long QT-interval syndromes.

Prolongation of QT interval is associated with repetitive paroxysm of a particular ventricular tachycardia. It is a typical complication of quinidine therapy but may occur in various other conditions. We used endocardial pacing in nine patients with prolongation of the QT interval who suffered from bouts of ventricular tachycardia and fibrillation. In six patients, the syndrome was due to quinidine and in three, to prenylamine. Acceleration of heart rate resulted in immediate suppression of all arrhythmias. Pacing was continued until the condition producing the QT prolongation disappeared. In one case, a permanent pacemaker was implanted, as the QT prolongation was congenital and permanent. The absolute QT interval was shortened by overdrive pacing from a mean value of 0.65 s to 0.50 s. The corrected QT interval remained prolonged (about 0.56 s). Thus, the arrhythmia was associated with the duration of the actual QT interval, and overdrive pacing was able to suppress it without shortening the corrected QT interval.

Adult↗
PubMed1979

Inefficacy of digitalis in the control of heart rate in patients with chronic atrial fibrillation: beneficial effect of an added beta adrenergic blocking agent.

The role of digoxin and the new beta adrenergic blocking agent, timolol, in controlling heart rate at rest and during exercise was investigated in 28 patients with chronic atrial fibrillation. Digoxin failed to prevent excessively rapid heart rates during mild to moderate exercise. Increasing digoxin blood levels from a mean of 0.6 to 1.8 ng/ml had no effect on heart rate either at rest or during exercise. The addition of timolol, 20 to 30 mg/day, resulted in a satisfactory and significant attenuation of the rapid heart rates both at rest and during exercise. Heart rates at rest were 91 and 98 beats/min in the patients with low and high digoxin dosage and rose to 135 and 139 beats/min, respectively, during exercise. Timolol reduced the heart rate to 67 at rest and to 92 beats/min during exercise. The effect of beta adrenergic blockade at rest was less pronounced in patients whose initial heart rates were below 90 beats/min. Digoxin alone may not suffice to control excessive heart rate in patients with chronic atrial fibrillation. The additional beta adrenergic blockade actually normalizes the heart rate response in these patients.

Adrenergic beta-Antagonists↗