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Biomedical subjects

B Surawicz

Publications and source records attributed to B Surawicz.

At least 55 records · Page 3Linked to original sources
PubMed1987

Effects of antiarrhythmic drugs on premature action potential duration in canine ventricular muscle fibers.

The range of premature action potential duration (APDs) during the first 100 ms of electrical restitution was determined in canine ventricular muscle fibers (VM) in the presence of lidocaine (4 and 8 micrograms/ml), mexiletine (8 micrograms/ml), flecainide (2 and 4 micrograms/ml), procainamide (50 micrograms/ml), quinidine (10 micrograms/ml), and disopyramide (10 micrograms/ml). The drug effects on the characteristics of action potential at the basic cycle lengths (BCLs) of 500 and 1,000 ms were similar to those reported previously. At control, the range of premature APDs was approximately 40 ms at BCL of 1,000 ms and approximately 30 ms at BCL of 500 ms. It was decreased 26-52% by lidocaine, mexiletine, and flecainide, not changed significantly by procainamide, and increased 17-53% by quinidine and disopyramide. The range of premature APDs at control and in the presence of drugs in ventricular muscle was smaller than in Purkinje fibers at the same or lower drug concentrations (Varro et al., J Pharmacol Exp Ther 1985;233:304). The four factors influencing the premature APD range in the Purkinje fibers operated in the VM as follows: The difference between the duration of effective refractory period (ERP) and the APD at BCL (APDb) (i.e., the ERP-APDb interval) was increased by lidocaine, mexiletine, and flecainide; normalized restitution curve was shifted toward longer premature APD values only by flecainide; the kinetics of restitution were slowed only by procainamide; and APD at BCL of 1,000 ms was shortened by lidocaine and mexiletine, and prolonged at BCLs of 1,000 and 500 ms by the other four drugs.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗
PubMed1987

The QT interval and cardiac arrhythmias.

The relation between the QT interval, ventricular arrhythmias, and dispersion of ventricular repolarization is reviewed. Conditions associated with prolonged QT interval in clinical practice are listed and discussed briefly. There is no conclusive evidence that prolonged QT is an independent prognostic marker in patients with coronary and other types of heart disease.

Arrhythmias, Cardiac↗
PubMed1986

Electrocardiographic diagnosis of chamber enlargement.

The purpose of this article is to review the changing role of the electrocardiogram in the diagnosis of cardiac chamber enlargement. Electrocardiographic criteria for the diagnosis of ventricular hypertrophy and atrial enlargement are reviewed in relation to autopsy, angiographic, echocardiographic and imaging findings. The electrocardiographic theory underlying the recognition of hypertropphy or dilation incorporates a number of sound physical principles that may lead to meaningful correlations with the tissue mass, chamber diameter and intracardiac blood volume. However, there are limiting factors related to the variable orientation of the heart in the chest, variable extracardiac factors and nonspecificity of each depolarization and repolarization abnormality used in the diagnosis of hypertrophy or dilation. This explains the superiority of the new noninvasive methods, in particular echocardiography, in the diagnosis of hypertrophy. Echocardiography is superior to electrocardiography in the detection of mild hypertrophy, and is more useful in the serial follow-up of changes during progression or regression of chamber enlargement.

Autopsy↗
PubMed1986

ST-segment, T-wave, and U-wave changes during myocardial ischemia and after myocardial infarction.

This review deals with the pathogenesis of ischemia-related abnormalities of ventricular repolarization. The most common repolarization abnormality during acute myocardial ischemia is the deviation of ST segment from the baseline due to diastolic and systolic currents of injury. The patterns of primary and reciprocal ST deviations during and after myocardial infarction are discussed. A very tall upright or a deeply inverted T wave, and shortened QT interval are transient phenomena followed by postischemic T wave abnormalities associated with QT lengthening. These changes are associated with lengthening of the ventricular action potentials at the border of infarction. Persistence of ST elevation after myocardial infarction is usually associated with ventricular dyskinesia. The differential diagnosis of this pattern and its possible mechanism are discussed. Also the mechanisms of ST alternans, T alternans and negative U waves, i.e. less common manifestations of myocardial ischemia are discussed. Studies of exercise-induced T wave normalization suggest that the behavior of primary T wave abnormalities after exercise does not alter the interpretation of the ischemic changes. T wave abnormalities are frequently non-specific but the post myocardial infarction T wave changes persist after administration of isoproterenol while various functional and neurogenic T wave abnormalities are corrected by isoproterenol.

Acute Disease↗
PubMed1985

Use-dependent effects of amiodarone on Vmax in cardiac Purkinje and ventricular muscle fibers.

Superfusion with 5 micrograms/ml amiodarone for 3-4 h induced use-dependent Vmax block in dog Purkinje and guinea pig ventricular muscle fibers. The recovery from block was exponential with tau of 289 +/- 30 ms in Purkinje (n = 7) and 282 +/- 47 ms in muscle (n = 6) fibers. The onset of frequency-dependent Vmax block was rapid, i.e. reached steady state after 4.2 +/- 0.5 beats (n = 5). The combination of rapid interaction with sodium channel and the reported action potential lengthening make amiodarone unique among Class I antiarrhythmic drugs.

Action Potentials↗
PubMed1985

Effects of hyperkalemia on the electrocardiogram of patients receiving digitalis.

In a prospective and a retrospective study, the effects of hyperkalemia on the electrocardiogram (ECG) of patients treated with customary maintenance doses of digoxin were examined and the results were compared with the effects of hyperkalemia in patients not receiving digitalis. The prospective study included 11 patients treated and 11 not treated with digitalis, and the retrospective study 27 patients treated and 61 not treated with digitalis. In all patients serum potassium concentrations (Ks) were determined within 1 hour of the recorded electrocardiogram. Serum digoxin concentrations, measured in 11 patients in the prospective and in 4 in the retrospective study, ranged from 0.7 to 5.0 ng/ml, and exceeded 2.0 ng/ml in 10 of 15 patients. Since the results of the prospective and of the retrospective study were similar, they were combined. In patients treated with digitalis, Ks ranged from 5.5 to 6.6 mEq/liter in 21 patients, from 6.7 to 7.5 mEq/liter in 17 and from 7.6 to 8.5 mEq/liter in 6; the Ks was 9.1 mEq/liter in 1 patient. The ventricular rate in patients treated with digitalis ranged from 48 to 140 beats/min, and was not significantly different from that in untreated patients within each range of Ks. Atrioventricular (AV) junctional rhythm occurred more frequently in the electrocardiograms of digitalis-treated patients (15 of 45 vs 2 of 76, p less than 0.001). The average PR intervals were longer in patients treated with digitalis who had Ks greater than 6.6 mEq/liter, but no patient in the study had greater than first-degree AV block, and no patient required a pacemaker.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1985

Factors affecting tolerance to digitalis.

A review of factors altering the safety margin between a therapeutic and a toxic dose of digitalis includes the consideration of: clinical conditions to which digitalis action may be undesirable, allergy and hypersensitivity to digitalis, physiologic factors modifying tolerance to digitalis, factors that change the amount of digitalis in the body, nervous and metabolic factors modifying tolerance to digitalis, modifications of digitalis tolerance produced by the status of the myocardium, and modifications of digitalis tolerance produced by diseases of other organs. The problems related to digitalis toxicity are more common than those of resistance to treatment. The most important factors contributing to decreased tolerance and risk of toxicity are: heart disease, poor renal function, hypokalemia and hypothyroidism. The roles of impaired liver function, chronic lung disease, acid-base disturbances, anesthesia, autonomic imbalance, calcium and magnesium are less important and less well established.

Adult↗
PubMed1985

Ventricular fibrillation.

Ventricular fibrillation is the most common mechanism of sudden unexpected cardiac death in persons with asymptomatic or symptomatic coronary artery disease. The electrophysiologic mechanisms reviewed in this article include: automaticity of pacemaker fibers, transformation of nonpacemaker into pacemaker fibers, "injury" currents and reentry. Some of the conditions facilitating ventricular fibrillation include bradycardia, long QT syndrome, electrocution, electrolyte imbalance, drugs, sympathetic stimulation and myocardial ischemia. Electrophysiologic studies during acute myocardial ischemia suggest that the earliest activity at the onset of arrhythmia may originate at the sites of the surviving Purkinje fibers or at the epicardial rim. Reentrant arrhythmias arising in ischemic myocardium are attributed to nonhomogeneous distribution of local hyperkalemia and acidosis.

Anti-Arrhythmia Agents↗
PubMed1985

Effect of uniformly prolonged, and increased basic dispersion of repolarization on premature dispersion on ventricular surface in dogs: role of action potential duration and activation time differences.

Strong experimental evidence links ventricular fibrillation to an increased temporal dispersion of the recovery of excitability. The effect of an overall prolongation of repolarization and an increased basic dispersion of repolarization on premature dispersion was studied on ventricular surface in 10 dogs. Our observations reveal the operation of several fundamental electrophysiologic mechanisms controlling the conduction and the refractoriness in the ventricular myocardium in vivo. Action potential (AP) duration was influenced by the heart rate, the duration of the preceding AP and the proximity to the repolarization of the preceding AP. These effects can both slow, or enhance ventricular conduction, during propagation of premature impulses. This model may be applicable to several clinical situations where APs are prolonged (hypothermia, drug effects, changes in electrolytes) or when dispersion of refractoriness is increased (long QT-time syndrome, neural imbalance of the heart with and without heart disease.

Animals↗
PubMed1985

Mechanism of ventricular arrhythmias caused by increased dispersion of repolarization.

To explain the mechanism of arrhythmias dependent predominantly on increased dispersion of repolarization, we created a model in which increased dispersion was induced by means of generalized hypothermia (29 degrees C) and regional warm blood (38-43 degrees C) perfusion (RWBP) via a coronary artery branch. In 23 open-chest dogs, hypothermia plus RWBP increased maximum dispersion of repolarization from 13 +/- 10 to 111 +/- 16 ms (P less than 0.001) due predominantly to the increased monophasic action potential duration (MAP) difference of six simultaneously recorded MAP's from the ventricular surface, from 10 +/- 15 to 97 +/- 16 ms (P less than 0.001). The maximal difference between activation times was not significantly changed while QRS duration increased from 47 +/- 6 to 52 +/- 7 ms (P less than 0.01). Ventricular arrhythmia (VA) did not occur spontaneously but was induced by a single ventricular premature stimulus (VPS) in all 23 dogs during hypothermia plus RWBP when dispersion reached a critical magnitude. The requirement of this critical magnitude of dispersion for the induction of VA was documented in 16 dogs by means of stepwise increments or decrements of dispersion. In four dogs an increase in atrial pacing rate by 24 beats/min-1 prevented induction of VA by decreasing dispersion from a critical magnitude of 103 +/- 5 ms to a nonarrhythmogenic value of 86 +/- 9 ms (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 MAPD. In all dogs VA was inducible only by VPS from the region with short MAPD.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

Dispersion of ventricular repolarization and arrhythmia: study of two consecutive ventricular premature complexes.

The effect of two consecutive ventricular premature stimuli (S1S2) during atrial pacing on dispersion of repolarization and inducibility of ventricular arrhythmias was studied in 16 dogs under control conditions and in four dogs in the presence of an increased dispersion of repolarization during atrial pacing induced by general hypothermia and regional warm blood perfusion via selective cannulation of the distal branch of left anterior decending coronary artery. Dispersion of repolarization was measured as the maximal difference between the ends of six simultaneously recorded monophasic action potentials (MAPs) from anterior ventricular surface, and consisted of MAP duration difference and activation time difference. Dispersion of repolarization during atrial pacing at control was 29 +/- 7 msec (activation time difference 4 +/- 6 msec, MAP duration difference 25 +/- 8 msec), that after S1 at paraseptal the site was 81 +/- 8 msec (activation time difference 73 +/- 12 msec, MAP duration difference 8 +/- 5 msec), and that after S1S2 was 148 +/- 27 msec (activation time difference 103 +/- 21, MAP duration difference 44 +/- 26 msec). Neither S1 nor S1S2 induced ventricular arrhythmia. Hypothermia and regional warm blood reperfusion increased dispersion of repolarization during atrial pacing to 70 +/- 22 msec (activation time difference 9 +/- 3 msec, MAP duration difference 61 +/- 19 msec). During hypothermia and regional warm blood reperfusion, S1 produced a dispersion of repolarization of 149 +/- 29 msec (activation time difference 85 +/- 8 msec, MAP duration difference 64 +/- 23 msec) and did not induce ventricular arrhythmia.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

Effect of antiarrhythmic drugs on the premature action potential duration in canine cardiac Purkinje fibers.

We studied the effect of six class I antiarrhythmic drugs, i.e., quinidine (5 micrograms/ml), disopyramide (10 micrograms/ml), procainamide (30 micrograms/ml), flecainide (4 micrograms/ml), lidocaine (4 micrograms/ml) and mexiletine (4 micrograms/ml), on the durations of the basic action potential (APDb) at a cycle length of 500 ms and on the premature APD (APDt) elicited at progressively increasing diastolic intervals (DI) in canine Purkinje fibers. The difference between APDt elicited at diastolic intervals of 100 msec and the earliest APDt elicited at the onset of effective refractory period was defined as the range of APDt. In control this range was 98 +/- 1.8 ms (n = 59). Disopyramide and procainamide did not change the range significantly but the other four drugs decreased it significantly (P less than .01) as follows: quinidine by 50.2%, lidocaine by 60.2%, mexiletine by 61.6% and flecainide by 61.4%. The following four factors contributed to this decrease in range of APDt: shorter duration of APDb, increased effective refractory period/APD ratio, slower kinetics of APD restitution, and shift of normalized restitution curve toward longer APDt values. The magnitude of the contribution made by each of the above factors varied with different drugs. The greatest contributing factor for quinidine was an increased effective refractory period/APD ratio, for lidocaine a slower restitution and for flecainide and mexiletine the shift of the restitution curve. We concluded that antiarrhythmic drugs belonging to the same class have different effects on the range of premature APD and that these effects cannot be predicted from the effect of the drug on APDb alone.

Action Potentials↗
PubMed1984

The timing of ventricular premature complexes initiating chronic ventricular tachycardia.

Prematurity index (PI), defined as the ratio of the coupling to QT intervals of isolated ventricular premature complexes (VPC) and those initiating ventricular tachycardia (VT) on 24-hour ambulatory ECG recording, was examined in 496 episodes of VT occurring in 122 patients. The PI of VPC initiating VT was less than 1 in only 62 (13%) of the VT episodes and occurred in 14 patients. Although the range of PI was similar for isolated VPC and those initiating VT, for individual patients the PI of VPC initiating VT was significantly longer than the PI of isolated VPC (P less than 0.01). This relationship was not affected by age, sex, presence of absence of heart disease, or drug therapy. The coupling interval of the first VT complex was longer than the first interectopic interval of the VT (VT1-VT2) in 88 (72%) patients; and, the VT1-VT2 interval correlated strongly with the average R-R during VT (r = 0.75), (p less than 0.001). The VT was irregular in 48 patients with 300 episodes of VT. Irregularity of the VT was significantly associated with shorter duration of VT (p less than 0.05). These results show that, for individual patients, the PI of VPC initiating VT tends to be longer than that of isolated VPC, and that the rate of VT is usually predictable from the duration of the first interectopic interval of the VT. These results may have mechanistic implications.

Adolescent↗
PubMed1984

Long QT: good, bad or indifferent?

A survey of current literature suggests an increasing interest in both the desirable and undesirable implications of a prolonged QT interval, the former perceived to be the beneficial effect of antiarrhythmic drugs that prolong the duration of ventricular action potential, and the latter considered to be a potential marker for sudden cardiac death in patients with ischemic heart disease. In addition, there has been an increasing interest in the congenital long QT syndrome associated with an apparent dysfunction of the autonomic nervous system and serious, potentially lethal ventricular arrhythmias. Circumstantial evidence suggests that these arrhythmias are due to increased dispersion of repolarization which may be aggravated by psychologic and emotional perturbations. In this review, the associations between the long QT interval, autonomic nervous system, dispersion of repolarization, antiarrhythmic drugs and ventricular arrhythmias are examined. Attention is directed to the difficulties of accurate QT measurement, problems related to the correction of the QT interval for heart rate and sex (QTc), the wide range of normal values and the modest QT alterations after various manipulations of the autonomic nervous system. Clinical conditions associated with marked, moderate and occasional QT lengthening are listed and discussed briefly in relation to the disturbances of nervous system, dispersion of ventricular repolarization and ventricular arrhythmias. It is proposed that the absence of relevant animal models of neurogenic or psychogenic QT prolongation hinders the investigation of the neurogenic factors associated with QT lengthening. QT prolongation is most often induced by antiarrhythmic drugs and ischemic heart disease. However, it is not known whether the occurrence of torsade de pointes type of ventricular tachycardia in patients treated with antiarrhythmic drugs is related to a critical drug dose or a critical degree of QTc prolongation. There is no conclusive evidence that QT lengthening has any predictive value either during the acute phase or during convalescence after myocardial infarction. Also, a serious deficiency in current knowledge is the lack of an established relation between the prolonged QT interval and the dispersion of ventricular repolarization. It is concluded that the number of unanswered questions discussed in this review still makes it difficult to judge when a prolonged QT interval is good, bad or indifferent.

Adrenergic beta-Antagonists↗
PubMed1984

Cycle length-dependent action potential duration in canine cardiac Purkinje fibers.

We studied the effects of pharmacologic probes that affect predominantly the Na inward current [tetrodotoxin (TTX), lidocaine], the slow inward current [cobalt, isoproterenol, verapamil], and the potassium currents [tetraethylammonium chloride (TEA), SG-75] on the duration of the action potential (APD) of canine cardiac Purkinje fibers during steady state and restitution. A schema is proposed in which the APD during steady state or restitution is determined by three factors: maximum action potential duration (APDmax), kinetics of restitution, and "memory." The predicted APDmax was 469 +/- 34 (SE) ms (n = 27) in control. It was prolonged (P less than 0.05) by cobalt, verapamil, and TEA and shortened (P less than 0.05) by TTX, lidocaine, isoproterenol, and SG-75. In control, the kinetics of restitution were described by a sum of two exponentials with time constant T1 = 137 +/- 9 ms and T2 = 1,665 +/- 135 ms (n = 27), respectively. T1 was prolonged (P less than 0.05) by TTX, lidocaine, and verapamil but was not changed by other probes. None of the probes studied altered the T2 of restitution or the memory factor, computed at a cycle length of 500 ms from the predicted APDmax and the plateau of restitution. Low temperature (31 degrees C) prolonged APDmax and T1 and reduced the memory. We conclude that each of the proposed three factors is controlled by different mechanisms and that a TTX-sensitive current appears to contribute to the process of restitution of APD.

Action Potentials↗
PubMed1983

Pharmacologic treatment of cardiac arrhythmias: 25 years of progress.

This review of practical and theoretical advances in antiarrhythmic drug therapy consists of four parts. Part 1, on clinical applications, compares the approaches to treatment 25 years ago with those of today, examines the current status of antiarrhythmic drugs used 25 years ago, reports on drugs approved for clinical use during the past 25 years, reviews new experimental drugs and suggests an approach to classification of antiarrhythmic drugs. Part 2 summarizes the contributions of cellular electrophysiology to the understanding of drug action, with emphasis on the drug-induced block of the voltage- and time-dependent properties of the rapid sodium channel. The subsequent section contains a brief discussion of the impact made by the new knowledge and the new diagnostic technology on the contemporary practices. The main conclusions are 1) that the more rational approach to treatment has benefited proportionately more patients with supraventricular than with ventricular arrhythmias, and 2) that new advances have made it possible to design successful treatments for certain patients with problems that could not be resolved in the past.

Action Potentials↗