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Biomedical subjects

E Kaplinsky

Publications and source records attributed to E Kaplinsky.

At least 181 records · Page 10Linked to original sources

Spontaneous termination of reentry ventricular tachycardia in the late myocardial infarction period: an experimental study in the dog.

Forty episodes of induced ventricular tachycardia in the late myocardial infarction period (4-6 days old) were analyzed in 12 dogs in an attempt to identify the possible mechanisms for the termination of reentry tachycardia. Multiple epicardial and endocardial composite electrograms were recorded in and around the central ischemic zone of the infarction. During tachycardia, the earliest site of activation was identified in the epicardial surface of the border or normal zone immediately adjacent to the ischemic zone in 36 of the 40 episodes, suggesting efferent epicardial spread from the site of the activity. In four instances, the efferent pathways were directed to the endocardial surface. Four distinct patterns of activation sequences were observed during spontaneous termination: (a) a shift of the efferent pathways from epicardial to endocardial site (19 instances); (b) a change of the efferent pathways within the endocardium (4 instances); (c) a shift of the earliest site of activation between the left and right ventricles (9 instances); and (d) no apparent change in the epicardial efferent pathways (4 instances). In four other instances, ventricular tachycardia deteriorated into ventricular fibrillation. In patterns (a) and (c), a shift of the efferent pathways resulted in a more rapid and homogeneous activation of the border and normal zone epicardium. These changes were associated with cessation of delayed or continuous activity in the ischemic zone epicardium, resulting in termination of tachycardia.

Animals↗

Two periods of early ventricular arrhythmia in the canine acute myocardial infarction model.

The time course of ventricular arrhythmias in the early period (0--30 minutes) after ligation of the left anterior descending coronary artery was studied in 41 open-chest mongrel dogs anesthetized with pentobarbital sodium (Nembutal). ECGs and seven single and composite electrograms from various regions in and around the ischemic zone were recorded throughout the experiments. Two periods of ventricular arrhythmias were clearly seen. The first occurred 2--10 minutes after coronary ligation, peaking at 5--6 minutes, and was designated as immediate ventricular arrhythmias (IVAs). There was a distinct correlation between incidence, severity, onset and termination of IVA and the degree of local delay and fragmentation of the normal sinus activation spread in the ischemic subepicardial zone. The second wave of ventricular arrhythmias occurred 12--30 minutes after ligation independently of the previous increased delay and fragmentation of activation in the ischemic subepicardium. Delayed ventricular arrhythmias (DVAs) were as severe as IVAs--there were nine instances of ventricular fibrillation during DVA and seven during IVA. While the mechanism of IVA is most probably related to reentry accompanied by delay and fragmentation of ischemic subepicardial activation, the mechanism of DVA remains unclear. Our evidence suggests that DVAs are also reentrant, with the reentry pathways located in deep myocardial structures or involving microscopic pathways at the Purkinje muscle junction.

Acute Disease↗

The beneficial effects of verapamil in chronic atrial fibrillation.

Digitalis preparations frequently fail to control heart rate in many patients who have chronic atrial fibrillation, particularly during physical exertion. The effects of orally administered verapamil, 160 to 240 mg/day, on the heart rate at rest and during mild exercise were studied in 23 digitalized patients with chronic atrial fibrillation of various causes. Verapamil substantially reduced the excessive heart rate response to exercise in well-digitalized patients who had chronic atrial fibrillation.

Aged↗

Patterns of activation in ventricular arrhythmias of late myocardial infarction in dogs.

Ventricular arrhythmias were produced in 12 dogs 4 to 6 days after coronary artery ligation by programmed ventricular stimulation. The electrocardiogram and 7 composite electrograms from endocardial and epicardial surfaces of the ischemic, border and normal zones, as well as from the right ventricle, were recorded during and after programmed ventricular stimulation. The ventricular arrhythmias were preceded and sustained by delayed, fragmented activity in the ischemic epicardial zone bridging diastole. Efferent pathways from the ischemic epicardium led to direct epicardial spread to adjacent normal epicardium in most instances. Efferent pathways into the endocardial regions were also observed, but to a lesser extent. The efferent reentry pathways led to both ventricles, and produced right and left ventricular arrhythmias in 8 of the 12 dogs; they were exclusively of left ventricular origin in the remaining 5. Classification of right and left ventricular arrhythmias may only be related to the exit points and not necessarily to their origin.

Animals↗

Origin of so-called right and left ventricular arrhythmias in acute myocardial ischemia.

The anatomic origin of ventricular arrhythmias occurring immediately after coronary arterial ligation was studied in 32 dogs. The electrocardiogram and seven single or composite bipolar electrograms were recorded from various sites within and surrounding the ischemic area in the left and right ventricles. Delay and fragmentation in the activation of the epicardial ischemic zone of the left ventricle, bridging diastole, preceded the appearance of ventricular arrhythmias and were continuous during the rhythm disorders. So-called left and right ventricular arrhythmias were associated with similar delay and fragmentation in left ventricular ischemic epicardial activity. Multiple and simultaneous activation of both the right and left ventricles produced ventricular fusion premature complexes. Multiple exit points increased before ventricular fibrillation occurred. The ultimate origin of premature ectopic impulse formation in the ventricles is not necessarily related to one or more exit points in either ventricle. Ischemic damage to the heart produces ventricular arrhythmias that appear to originate from both ventricles. The site of origin of ventricular arrhythmias should not be the sole factor in assessing the benign or malignant properties of the arrhythmia.

Animals↗

Ventricular reentry and automaticity in myocardial infarction. Effect of size of injury.

The effects of the size of acute myocardial infarction on ventricular reentry and automaticity were studied in 36 mongrel dogs. Large transmural myocardial infarctions were produced by ligation of the left anterior descending coronary artery (major ligation; diameter of infarction above 4.0 cm), and small subendocardial or intramural infarctions were produced by ligating a small diagonal branch of the left anterior descending coronary artery (minor ligation; diameter of infarction less than 1.5 cm). Reentrant arrhythmias were induced by rapid ventricular stimulation, and ventricular automaticity was determined during vagal stimulation. Ventricular automaticity became enhanced only 30 to 45 minutes after both major and minor coronary arterial ligations; however, the animals with major ligations attained a higher level of increased automaticity. While automaticity became enhanced in both groups reentrant arrhythmias could never be produced artificially (or observed spontaneously) in the animals with myocardial infarctions. The dependence of the so-called reentrant arrhythmias on the size of the infarction is a major support for the theory of reentry as the basis for these arrhythmias.

Animals↗

Procainamide-induced left anterior hemiblock of the 2:1 type (pseudoelectrical alternans).

A selective defect in cardiac conduction in the anterior division of the left bundle branch was induced in a patient by therapy with procainamide hydrochloride. The defect in conduction, when intermittent, resulted in 2:1 Wencklebach sequences and produced a pattern similar to classic electrical alternans. The prognosis in drug-induced alternans is good, and it is important to differentiate it from true electrical alternans.

Aged↗

Treatment of ruptured interventricular septum with afterload reduction.

Two patients with a ruptured interventricular septum complicating acute myocardial infarction were treated with isosorbide dinitrate. The first patient recovered from cardiogenic shock after sublingual administration of 5 mg of isosorbide dinitrate every two hours and was successfully operated on. The second patient recovered from severe pulmonary edema during the acute stage of the infarction with sublingual isosorbide dinitrate. Moreover, she experienced a considerable symptomatic improvement when a 5 mg sublingual dose of isosorbide dinitrate every three hours was added to her long-term treatment. Analysis of hemodynamic data showed that the most striking change following administration of the drug was the substantial reduction of pulmonary wedge pressure. The striking symptomatic and hemodynamic improvement was achieved by the favorable effect of afterload reduction on left ventricular performance and not by reduction in left to right shunt.

Aged↗

Bradycardia-related (phase 4) left anterior hemiblock.

A case is presented in which left anterior hemiblock (LAH) appeared transiently after the pause terminating atrial pacing, after atrial premature beats and during the slowing of sinus rhythm induced by carotid sinus massage. The transient LAH is attributed to phase-4 block, and is reported in order to add weight to the hypothesis that phase-4 block is a significant factor in the genesis of discrete conduction blocks in the human heart.

Aged↗

Isorhythmic Dissociation--a "physiological" arrhythmia.

The behavior of the sino-atrial mechanism in isorhythmic dissociation (IRD) was studied in 21 patients, nine with spontaneous IRD and 12 with artificially pacemaker-induced IRD following electrode placement for heart block. Successive P-P, R-R and P-R intervals and blood pressure (BP) fluctuations were determined and graphically interrelated at control and during IRD. Several features were observed: a. IRD was present only when the independent ventricular rate was close to the atrial; b. P rate oscillations closely followed the P-R interval-dependent BP fluctuations (mean difference 30 mmHg) during IRD. In cardiogenic shock and in severe hypertension IRD could not be achieved easily; c. While during complete dissociation or during 1:1 A-V conduction the sinus rate was remarkably constant (2-4 beats/min variations), it showed marked oscillations (differences of 6-19, mean 13, beats/min) during IRD. All the data and calculations support the theory that in most instances of IRD, the arrhythmia is sustained by the normal physiologically active baroreceptor reflex arc.

Aged↗

Beta-adrenergic blockade as adjunctive oral therapy in patients with chronic atrial fibrillation.

In many patients with chronic atrial fibrillation, it is difficult to prevent an excessive ventricular rate under stress, even with high levels of digoxin in the blood. The effect of adding beta-adrenergic blockade with practolol to digoxin on the heart rate at rest and during low-grade controlled exercise was investigated in 28 patients with chronic atrial fibrillation and in ten normal control subjects who were receiving maintenance dosages (0.25 to 0.75 mg) of digoxin. In atrial fibrillation, therapy with practolol decreased the mean heart rate at rest from 99.8 beats per minute to 77.5 beats per minute (23 percent reduction; P less than 0.01) and during mild exercise from 148.9 beats per minute to 105.4 beats per minute (29 percent) reduction (P less than 0.001). Fifteen patients had clinically significant heart failure; therapy with practolol did not worsen it. Reversible side effects were detected in two patients. When therapy with digoxin is not sufficient to control atrial fibrillation, the addition of a beta-adrenergic blocking agent is recommended as adjunctive treatment in selected patients.

Administration, Oral↗

The Wenckebach phenomenon between electric pacemaker and ventricle.

Two cases which exhibited a Wenckebach form of exit conduction between an electrical pacemaker and the ventricular myocardium are presented. This manifests with increasing latency (stimulus to QRS intervals) and ultimate stimulus failure (block). The cycle then repeats itself. The QRS duration also increases progressively within each cycle. The phenomenon connotes an adverse prognosis. Several postulates regarding the mechanism are discussed.

Female↗