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Biomedical subjects

B Surawicz

Publications and source records attributed to B Surawicz.

At least 73 records · Page 4Linked to original sources
PubMed1983

Cycle length effect on restitution of action potential duration in dog cardiac fibers.

Electrical restitution of action potential duration (APD) was determined in Purkinje (n = 8) and ventricular muscle (n = 6) fibers at two different basic cycle lengths (BCL, 1,500 and 500 ms). Restitution curves, normalized for the longest APD (the plateau of restitution), fitted the sum of a fast (T1) and a slow (T2) exponential component. The T1 was shorter in ventricular muscle than Purkinje fibers (89 +/- 5 and 143 +/- 9; mean +/- SE, P less than 0.05), whereas the T2 did not differ (1,448 +/- 231 and 1,439 +/- 211). The BCL altered the APD value during the plateau of restitution but did not change the two exponential components. In both fiber types, the relation between APD and BCL during steady state fitted a hyperbolic curve that predicts the achievement of the maximum APD at long BCL. The restitution curves crossed the steady-state curve at two points outlining three different zones of APD intervals: early premature, late premature, and postmature. The APD during restitution was longer than the steady state in the late premature zone and shorter than the steady-state APD in the post-mature and early premature zones. The APD per se, independent of BCL, did not influence the kinetics of restitution in Purkinje fibers.

Action Potentials↗
PubMed1983

Characteristics and possible mechanism of ventricular arrhythmia dependent on the dispersion of action potential durations.

The arrhythmogenic role of increased dispersion of repolarization (dispersion) was studied in 23 open-chest dogs using six simultaneously recorded monophasic action potentials (MAPs) from the ventricular surface and programmed ventricular premature stimulation (VPS). Increased dispersion was induced by generalized hypothermia (29 degrees C) and regional warm blood (38-43 degrees C) perfusion through a coronary artery branch. Hypothermia and regional warm blood perfusion increased maximum dispersion from 13 +/- 10 to 111 +/- 16 msec (p less than 0.001), predominantly because of the increased MAP duration difference (10 +/- 15 vs 97 +/- 16 msec, p less than 0.001). The maximal difference between activation times was not significantly changed, but the QRS duration increased from 47 +/- 6 to 52 +/- 7 msec (p less than 0.01). Ventricular arrhythmia did not occur spontaneously but was induced by a single VPS in all 23 dogs during hypothermia and regional warm blood perfusion when dispersion reached a critical magnitude. The critical magnitude of dispersion required to induce ventricular arrhythmia was documented in 16 dogs by stepwise increments or decrements of dispersion. In four dogs, an increase in atrial pacing rate of 24 beats/min prevented induction of ventricular arrhythmia by decreasing dispersion from a critical magnitude of 103 +/- 5 msec to a nonarrhythmogenic value of 86 +/- 9 msec (p less than 0.05). In six dogs, we compared the stimulation site-dependent effects of VPS applied in the region with short and long MAPs. In all dogs, ventricular arrhythmia was inducible only by VPS from the region with a short MAP. Premature impulses from this region propagated more slowly than those from the region with a long MAP. Our results show that the large dispersion of repolarization facilitates the development of a conduction delay necessary to induce sustained arrhythmia by an early premature stimulus applied at the site with a short MAP.

Action Potentials↗
PubMed1982

Role of calcium-blocking agents in treatment of cardiac arrhythmias related to myocardial ischemia.

Potential antiarrhythmic effects of calcium (slow-channel)-blocking drugs ca be indirect or direct. The indirect effect would affect ischemia-induced arrhythmias by improving myocardial perfusion or decreasing myocardial oxygen consumption. The direct effect would affect the electrical activity of the sinoatrial (SA) and atrioventricular (AV) nodes and any type of cardiac fibers depolarized to a level at which the slow inward current becomes activated. Although myocardial ischemia could become a setting of slow-channel-dependent conduction or automaticity, or both, there is no conclusive evidence that slow-channel-blocking drugs suppress ischemia-induced ventricular arrhythmias. Thus the principal usefulness of slow-channel-blocking drugs may be expected in the treatment of supraventricular arrhythmias and in the prevention of arrhythmogenic ischemia.

Animals↗
PubMed1982

Negative U wave: a highly specific but poorly understood sign of heart disease.

A negative U wave is highly specific for the presence of heart disease and is associated with other electrocardiographic abnormalities in more than 90 percent of patients. The three most common conditions associated with a negative U wave are systemic hypertension, aortic and mitral regurgitation and ischemic heart disease. The U wave vector is directed opposite to the QRS axis in the horizontal plane in patients with both left and right ventricular hypertrophy. In patients with ischemic heart disease, the U wave vector tends to be directed away from the site of the akinetic or dyskinetic region. The change from a negative to an upright U wave after a reduction in blood pressure, renal transplantation, insertion of a valve prosthesis or a coronary arterial bypass graft procedure is associated with a decrease in the QRS amplitude but with no consistent changes in T wave polarity. The timing of the U wave apex is dependent on the duration of ventricular repolarization but not on the duration of the QRS complex. This finding and other electrocardiographic observations are explained better by the ventricular relaxation than by the Purkinje fiber repolarization theory of U wave genesis.

Aortic Valve Insufficiency↗
PubMed1982

Idiopathic long QT syndrome: association of ventricular tachycardia with alternating left and right bundle branch block.

A case of sporadic long QT syndrome with ventricular tachycardia characteristic of torsades de pointes is presented. The ECG revealed sinus rhythm with marked prolongation (less than 140%) of QT interval and alternating periods of left and right bundle branch block. The onset of ventricular tachycardia was associated with alternating left and right bundle branch block and the disappearance of bundle branch block coincided with the resolution of ventricular tachycardia. This observation suggests the possibility that heterogeneous repolarization of the bundle branch system contributed to ventricular tachycardia either alone or in combination with dispersion of refractoriness of the ventricular myocardium.

Adolescent↗
PubMed1982

Variable effects of isoproterenol on action potential duration in guinea-pig papillary muscle: differences between nonsteady and steady state; role of extracellular calcium concentration.

The effect of three different isoproterenol (ISP) concentrations (10(-6), 10(-7) and 10(-8) M) on action potential duration (APD) was studied in guinea-pig papillary muscles at low (0.6-0.9 mM), intermediate (1.8 mM) and high (3.6 mM) calcium concentrations (Ca++)0. All three ISP concentrations produced (Ca++)0-dependent changes during both nonsteady (NSS) and steady state (SS). During NSS, initial prolongation of APD occurred in 22 of 22 experiments at low, in 16 of 36 experiments at intermediate and 0 of 15 experiments at high (Ca++)0. In the remaining experiments, APD became progressively shorter. The NSS-APD changes were associated with increase in plateau amplitude attributed to slow inward current (isi). However, we found no correlation between the amplitude of plateau and APD change. This suggests that the (Ca++)0-dependent differences were due more likely to differences in the rat of isi inactivation than to differences in the absolute isi magnitude. The SS-APD was also dependent on (Ca++)0 but, during progression from NSS to SS, plateau amplitude did not change, whereas the force of contraction increased. This supports the hypothesis that the dependence of SS-APD on (Ca++)0 is mediated by the time-independent K conductance controlled by intracellular calcium concentration. Thus, the early and the late ISP effects on APD appeared to differ in their mechanism, but both depended on (Ca++)0.

Action Potentials↗
PubMed1981

Effect of tetraethylammonium chloride on action potential in cardiac Purkinje fibers.

Intracellular loading with 20 mM tetraethylammonium chloride (TEA) diffusing through the cut end of the preparations prolonged action potential duration (APD) in dog Purkinje fibers without changing maximum diastolic potential, overshoot, and dV/dtmax. The APD was prolonged at all rates of stimulation, but, contrary to the normal rules, APD increased more after longer than after shorter interstimulus intervals. TEA increased the number of beats required to achieve the new steady-state APD after an abrupt change in the rate of stimulation. The effect of varying extracellular potassium concentration on maximal diastolic potential suggested that intracellular loading with TEA had no effect on the time-independent "background" outward current (IK1). If we ascribe all observed TEA effects to the reduction of time dependent slow outward current Ix1, we can propose a hypothesis concerning the role of Ix1 in the regulation of APD at slow heart rates.

Action Potentials↗
PubMed1980

Re-entry near the site of the ventricular parasystolic focus: an ECG study of patients with artificial ventricular pacemakers.

Morphology of ventricular ectopic complexes was examined in 1,746 ECGs of 149 patients with permanent ventricular pacemakers. In 20 of 80 patients (25%) the morphology of ventricular ectopic complexes was similar to that of the paced complex. This resulted in a ventricular couplet where the spontaneous premature complex originated at the site of pacing, possibly due to local re-entry. Repeated re-entry (two ventricular ectopic complexes in a row) occurred only in one of these patients, and none had ventricular tachycardia. These observations 1) verify the existence of a mechanism which we have postulated in explaining the association between couplets and ventricular parasystole, and 2) confirm the rare occurrence of repeated reentry in such a setting. Other observations in this studyshow that premature stimulation during right ventricular pacing may alter morphology of the ventricular complex from a left to right bundle branch block pattern in some leads.

Adolescent↗
PubMed1980

Monitoring blood levels of cardioactive drugs.

The availability of specific, sensitive, and convenient analytic methods has simplified determinations of plasma concentrations of several cardioactive drugs. The available data indicate that, although in general the plasma concentrations of cardioactive drugs bear a more consistent relationship to their pharmacologic effects than the doses administered, they cannot substitute for careful clinical observation and judgment. Plasma concentrations of these drugs, following a given dose, are influenced by several factors which include patient's size, renal, hepatic, cardiac, and gastrointestinal function, bioavailability of the drug, and interplay with other concurrently administered drugs. These factors cannot be predicted with any degree of accuracy before starting therapy, but measuring plasma drug concentrations under appropriate conditions can be helpful in determining individual differences in drug disposition. The majority of patients can be treated without the use of plasma concentrations of digitalis and antiarrhythmic drugs. However, the availability of measurements can be helpful in a variety of specific clinical situations discussed in the text. In practice, plasma concentrations have been most valuable in the recognition of digitalis toxicity and as guides to therapy of resistant tachyarrhythmias requiring high dosages of single or multiple antiarrhythmic drugs.

Anti-Arrhythmia Agents↗
PubMed1979

Verapamil plasma levels and ventricular rate response in patients with atrial fibrillation and flutter.

The acute effect of verapamil on the ventricular rate in atrial fibrillation and flutter was studied in 15 patients, 13 of whom had heart rate inadequately controlled with digitalis. Plasma concentrations were measured 5 and 10 min after intravenous doses of 0.075 mg/kg and 0.15 mg/kg verapamil. In 9 patients who were clinically compensated, the 0.075-mg dose alone decreased the ventricular rate to under 100/min (responders); in the remaining 6, who had acute congestive heart failure manifested by orthopnea, rales, and pulmonary congestion, ventricular rates were above 100/min after the 0.075-mg dose (nonresponders). The 6 nonresponders received the 0.15-mg dose 30 min later. In all, the response was greater when plasma drug concentration rose after the high dose, although the rate decrease was smaller than in the 9 compensated patients who received the low dose. These results can be explained by assuming an antagonism of the verapamil effect by sympathetic stimulation in nonresponders.

Adult↗