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Biomedical subjects

L B Liem

Publications and source records attributed to L B Liem.

At least 19 recordsLinked to original sources
PubMed1992

Relation between repolarization and refractoriness in the human ventricle: cycle length dependence and effect of procainamide.

The cycle length dependence of the action potential duration and the effective refractory period of the right ventricular endocardium were investigated in 24 patients undergoing electrophysiologic studies for suspected ventricular tachycardia. The action potential duration at 90% repolarization and the effective refractory period at twice diastolic threshold strength were measured at the same catheter site at steady state cycle lengths of 350 to 600 ms. Both measurements decreased linearly with decreasing cycle length, maintaining a parallel relation. When the relation between action potential duration and effective refractory period was expressed as the effective refractory period-action potential duration difference, nearly constant values (range -12 to -15 ms) were obtained at all cycle lengths. To determine whether sodium channel blocking drugs influence the effective refractory period-action potential duration relation in humans, measurements of these two variables were obtained in 15 patients before and during the infusion of procainamide. Procainamide prolonged the action potential duration at each cycle length by a near constant amount over baseline values (p less than 0.001). Procainamide also increased the effective refractory period at each cycle length but with a greater incremental increase at the shorter cycle lengths. The rate-dependent increase in the effective refractory period-action potential duration difference became significant at cycle lengths less than or equal to 400 ms; at these high rates, the effective refractory period-action potential duration difference became positive (1.6 ms, p less than 0.01 compared with baseline). Thus, in the human ventricle, the action potential duration and the effective refractory period have a close relation that remains fixed over a wide range of cycle lengths.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗
PubMed1991

Mixed venous oxygen saturation for differentiating stable from unstable tachycardias.

Current antitachycardia systems are incapable of adequately distinguishing stable from unstable tachycardias. Previously, integration of a pressure sensor or an impedance sensor, together with electrogram analysis, has been investigated as an improved method of identifying unstable arrhythmias. A mixed venous oxygen saturation sensor was investigated for differentiating stable from unstable paced and induced tachycardias in 10 patients. During rapid pacing at 600, 500, 400, 350, 300, and 250 msec cycle lengths, mixed venous oxygen saturation decreased as cycle length decreased. For any given cycle length, rapid ventricular pacing tended to result in greater mixed venous oxygen desaturation compared with atrial pacing. Mixed venous oxygen saturation decreased similarly during induced ventricular tachycardias at cycle lengths greater than 230 msec. However, ventricular tachycardias at cycle lengths less than or equal to 230 msec and ventricular fibrillation had no effect on mixed venous oxygen saturation until after termination. Subsequently, a mixed venous oxygen saturation-tiered therapy algorithm (cycle length less than or equal to 230 msec = unstable; cycle length greater than 230 msec and MVO2 greater than or equal to 6% over 30 seconds = unstable) was developed and was tested retrospectively in 113 paced and induced tachyarrhythmias in these 10 patients for detecting unstable tachycardias (defined as a decrease from baseline systolic arterial pressure of greater than or equal to 50 mm Hg at 15 seconds). The mixed venous oxygen algorithm had 93% sensitivity and 96% specificity compared with rate-only (rate greater than or equal to 170 beats/min) detection with 93% sensitivity and 71% specificity.(ABSTRACT TRUNCATED AT 250 WORDS)

Algorithms↗
PubMed1991

Biosensor applications to antitachycardia devices.

Current arrhythmia detection algorithms are unable to adequately distinguish stable from unstable tachycardias; therefore application of a biosensor to antitachycardia devices has been proposed to improve their performance. Right heart pressures and impedance have been investigated for incorporation into these systems. Integration of other parameters (oxygen saturation, preejection period, pH, cardiac output, flow, and temperature) into these devices might also prove useful. The status of these biosensor arrhythmia detection algorithms and their application to antitachycardia devices are described below.

Algorithms↗
PubMed1990

A hemodynamically responsive antitachycardia system. Development and basis for design in humans.

Current automatic implantable cardioverter-defibrillators detect tachyarrhythmias primarily by rate-only algorithms and cannot adequately distinguish hemodynamically stable from unstable tachyarrhythmias. The responses of right atrial (mean) and right ventricular pressures (mean, systolic, diastolic, and pulse) to 64 induced and paced supraventricular and ventricular tachyarrhythmias were studied in 10 patients (left ventricular ejection fraction of 32 +/- 6%) to develop an algorithm capable of differentiating stable from unstable rhythms. Tachyarrhythmias were defined as hemodynamically unstable when mean arterial pressure decreased by 25 mm Hg or more during 15 seconds. Mean right atrial, right ventricular systolic, and right ventricular pulse pressures were found to be useful in distinguishing the hemodynamic significance of a tachyarrhythmia. A combined detection algorithm was developed that identified a hemodynamically unstable rhythm when the heart rate was 150 beats/min or more and mean right atrial pressure increased by 4 mm Hg or more and right ventricular systolic pressure decreased by 5 mm Hg or more during 15 seconds. This algorithm was then applied to the next 20 consecutive patients (left ventricular ejection fraction of 34 +/- 4%) and compared with the current rate-only algorithm (heart rate of 150 beats/min or more) in 143 tachyarrhythmias, and the sensitivity and specificity for detection of hemodynamically unstable tachyarrhythmias were determined. The rate-only detection algorithm had 100% sensitivity but only 68% specificity for detection of unstable tachyarrhythmias, whereas the combined rate-mean right atrial pressure-right ventricular systolic pressure detection algorithm had sensitivity and specificity of 100%. Therefore, the performance of an antitachycardia system may be significantly improved by detection algorithms that integrate hemodynamic and rate criteria.

Blood Pressure↗
PubMed1990

Arrhythmias and clinical electrophysiology of the transplanted human heart.

The denervated transplanted heart has given us numerous opportunities to assess normal and abnormal electrophysiology and the influence of the autonomic system on these parameters. Observation of baseline electrophysiology of the denervated heart and its response to various physiologic and pharmacologic stimuli has emphasized the role of the parasympathetic system on heart rate and arrhythmia modulation in the normal population. In the transplant patients, the denervated hearts lack the full spectrum of physiologic responses due to the absence of vagally mediated neurostimuli. This results in a higher resting heart rate, sluggish rate response to exercise, and perhaps inadequate response to some commonly used drugs such as atropine and digitalis. Nevertheless, the heart's overall response to physiologic demands and various pharmacologic maneuvers including beta-antagonists and antagonists remains relatively normal and the patient's overall cardiac performance appears to be quite adequate. Thus, despite its shortcomings, the denervated heart provides near normal functional integrity and overall improved quality of life. Arrhythmias are generally a minor problem in these patients. Although there appears to be a high prevalence of various forms of arrhythmias, most present as isolated and insignificant problems. The more severe arrhythmias consist primarily of atrial tachyarrhythmias that are usually associated with acute rejection, and treatment for these arrhythmias never pose serious difficulty. However, sudden death remains an intriguing issue. Clearly, serious ventricular tachyarrhythmias can occur in these patients, arguing against the concept of a primary role of an intact autonomic nervous system for the generation of arrhythmia.(ABSTRACT TRUNCATED AT 250 WORDS)

Arrhythmias, Cardiac↗
PubMed1989

Frequency-dependent effect of quinidine, mexiletine, and their combination on postrepolarization refractoriness in vivo.

Combination therapy with mexiletine and quinidine has been shown to enhance antiarrhythmic efficacy. To assess further the underlying electrophysiological mechanism, the effect of therapeutic concentrations of mexiletine and quinidine, and of their combination, on action potential duration (at the level of 90% repolarization, APD90), effective refractory (ERP), and the relationship between these two parameters (ERP-APD90) was determined in 21 in vivo canine hearts. The frequency dependence of these effects was assessed over a range of paced steady-state cycle lengths from 250-600 ms. A modified contact electrode technique allowed measurements of both APD90 and ERP simultaneously and at the same ventricular site. In the drug-free state, both APD90 and ERP shortened linearly with shorter cycle lengths, maintaining a constant relationship (ERP-APD90) difference = -9 +/- 2 ms) at all cycle lengths. Quinidine prolonged APD90 by a near constant amount of 11 +/- 1 ms over the entire range of cycle lengths, while mexiletine tended to shorten it. Both mexiletine and quinidine increased ERP and ERP-APD90 in a rate-dependent fashion, the effect increasing with shorter cycle lengths. When used in combination, mexiletine attenuated the lengthening effect of quinidine on APD90 but augmented the rate-dependent increase in ERP, thereby producing greater postrepolarization refractoriness than either drug alone. This effect may explain the clinically favorable antiarrhythmic efficacy of mexiletine and quinidine combination therapy.

Action Potentials↗
PubMed1989

Update: cardiac antiarrhythmic drugs.

The last ten years have been a period of extensive research and development of new agents for the treatment of cardiac rhythm abnormalities. Several new subclass Ic agents have been developed, and more recently the class III agents have become the focus of attention. These new agents are all remarkable for their potency and potential for producing side effects. While none of these agents offers the perfect cure for the treatment or prevention of cardiac arrhythmias, they all offer advantages and options that are valuable for clinical management of patients.

Amiodarone↗
PubMed1988

Value of electropharmacologic testing in idiopathic dilated cardiomyopathy and sustained ventricular tachyarrhythmias.

Electrophysiologic studies in 64 patients with idiopathic dilated cardiomyopathy who had sustained ventricular tachycardia or ventricular fibrillation were performed. A sustained ventricular tachyarrhythmia was induced in 43 patients (67%). Electropharmacologic testing predicted an antiarrhythmic drug effective in 15 of 35 patients in whom sustained monomorphic ventricular tachycardia could be induced reproducibly (43% of tested patients, 23% of all patients). During median follow-up of 1.6 years, there were 32 arrhythmia recurrences and 24 cardiac arrests. Multivariate regression analysis identified treatment with a drug predicted to be effective at electropharmacologic testing as the only predictor of freedom from arrhythmia recurrence (p = 0.01); and treatment with a drug predicted to be effective at electropharmacologic testing and lower New York Heart Association functional class as independent predictors of freedom from cardiac arrest (p = 0.03 and p = 0.02, respectively). At median follow-up, the incidences of freedom from arrhythmia recurrence and from cardiac arrest were both 100% during treatment with a drug predicted to be effective at electropharmacologic testing versus 54 +/- 8% and 62 +/- 7%, respectively, during other treatments. These findings indicate that results of electropharmacologic testing accurately predict freedom from arrhythmia recurrence and cardiac arrest in patients with idiopathic dilated cardiomyopathy and sustained ventricular tachyarrhythmias.

Adolescent↗
PubMed1988

Effect of flestolol on ventricular rate during atrial fibrillation in Wolff-Parkinson-White syndrome.

The ultrashort-acting beta blocker flestolol was studied during atrial pacing and atrial fibrillation (AF) in 10 patients with Wolff-Parkinson-White syndrome. Flestolol was given as a 100-micrograms/kg bolus followed by a 10-micrograms/kg/min infusion for 15 minutes. The drug did not alter the antegrade effective refractory period of the accessory pathway or the atrial paced cycle length at which block occurred in the accessory pathway. After flestolol, the percent of preexcited QRS complexes during AF increased (60 +/- 10 vs 87 +/- 5%, p = 0.01). Despite this, the ventricular rate slowed, with increases in mean RR interval (382 +/- 20 vs 416 +/- 22 ms, p = 0.02) and in the shortest interval between preexcited QRS complexes (251 +/- 18 vs 270 +/- 17 ms, p less than 0.01). The effect of isoproterenol 3 to 5 micrograms/min was studied in 5 patients. During atrial pacing, isoproterenol decreased the antegrade refractory period and the atrial paced cycle length of block in the accessory pathway (p less than or equal to 0.05). During AF, it decreased the percent of preexcited QRS complexes, mean RR interval and shortest interval between preexcited QRS complexes (p less than 0.05). Flestolol reversed the effects of isoproterenol both during atrial pacing and AF. Thus, flestolol does not alter conduction over the accessory pathway during atrial pacing, but during AF it slows conduction over the accessory pathway and prevents isoproterenol-mediated increases in ventricular rate. This suggests that in patients with Wolff-Parkinson-White syndrome sympathetic stimulation after the onset of AF enhances conduction over the accessory pathway and is an important determinant of ventricular rate.

Adrenergic beta-Antagonists↗
PubMed1988

Strength-interval relation for ventricular functional refractoriness.

Successful initiation and termination of presumed reentrant ventricular tachycardia frequently depends on the ability to deliver closely coupled impulses to the region of the tachycardia origin. To evaluate systematically the relative influence of local latency and large-scale conduction delay in limiting the delivery of closely coupled impulses, the strength-interval relation of the effective refractory period (RP), and the local and remote functional RP in 35 patients at paced cycle length of 500 ms were measured. The pacing threshold was less than or equal to 0.25 mA in all patients. The drive-train (S1) and the extrastimulus (S2) were applied from the same site, the right ventricular (RV) apex, in 25 patients, and from separate sites (RV apex and RV outflow tract) in 10 patients. The effect of procainamide (plasma concentration 10.1 +/- 2.3 micrograms/ml) on the strength-interval relations in 10 patients was also assessed. Although effective RP decreased significantly with each successive increase in current strength (p less than 0.001), local functional RP decreased only up to current strength of 4 mA, and remote functional RP decreased only up to 2 mA. Procainamide shifted the effective RP and local and remote functional RP strength-interval curves uniformly to the right without altering their relation. These data indicate that large-scale conduction delay provides the principal limitation for using increasing current strengths of a single extrastimulus to initiate or terminate ventricular tachycardia.

Adult↗
PubMed1988

Pharmacodynamics of procainamide in patients with ventricular tachyarrhythmias.

The onset and offset of the electropharmacologic effect of procainamide was studied in nine patients with ventricular arrhythmias. Procainamide was given at a constant infusion rate of 0.27 +/- 0.05 mg/kg/min for 50 to 60 minutes to an average total dose of 15.5 +/- 4.4 mg/kg. The QRS interval (used as an index of electropharmacologic effect) at a paced cycle length of 500 ms, and the plasma procainamide concentration were measured simultaneously every 5 minutes during infusion and at frequent intervals for up to 4 hours during a washout period. The average peak plasma concentration was 15.8 +/- 9.6 micrograms/ml and the average maximum QRS interval prolongation was 23.9 +/- 6.8% from baseline. The temporal and static plasma concentration-effect relationships were evaluated by pharmacodynamic modeling and linear regression. For six patients, there was a minimal (less than 2 minutes) delay in the plasma concentration-effect relationship, and the data fit a linear relationship with an average slope of 3.2 +/- 1.1 msec/microgram/ml. For the other three patients, there was a significant delay (3, 10, and 18 minutes respectively) in the plasma concentration-effect relationship. In most patients, the electropharmacologic effect of procainamide is rapid and proportional to plasma concentration; but in a minority of patients, significant delay occurs and could influence the results and interpretation of electropharmacologic studies.

Adult↗
PubMed1988

Pacing hazards in helicopter aeromedical transport.

A 62-year-old man with third-degree atrioventricular block and hemodynamically unstable ventricular tachycardia had a cardiac arrest during helicopter transport to a specialized cardiac care unit. Before transport, his ventricular tachycardia had been successfully terminated by a rapid overdrive pacing technique. The failure of "burst suppression" and the absence of pacer spike artifact on the electrocardiographic monitor raise questions about the potential hazards of using various pacing techniques during helicopter transports. Most significantly, this case points to the possibility of interference by exogenous electromagnetic signals in the medical compartment of the helicopter.

Aircraft↗
PubMed1988

Cycle length dependence of human action potential duration in vivo. Effects of single extrastimuli, sudden sustained rate acceleration and deceleration, and different steady-state frequencies.

Using a new method for long-term recording of monophasic action potentials from the human heart, we studied in 17 patients the effects on ventricular action potential duration (APD) of three clinically pertinent cycle length perturbations: (1) single extrastimuli, (2) abrupt sustained rate acceleration and deceleration, and (3) different steady-state cycle lengths. Results were: (a) APD after single extrastimuli at progressively longer cycle lengths were related to the extrastimulus cycle length with a biphasic electrical restitution curve which after an initial steep rise and a subsequent transient descent rose again more gradually to a plateau at cycle lengths above 800-1,000 ms. (b) After a sustained step decrease in cycle length, the first APD shortened abruptly while final steady-state adaptation required up to several minutes. The transition between the rapid and slow phase of APD change was characterized by a variable alternans of APD which correlated inversely with the preceding diastolic interval. (c) In the steady state, APD correlated linearly with cycle length, increasing an average of 23 ms per 100 ms cycle length increase (r = 0.995). The divergence between steady-state and non-steady-state APD, and the slowness of steady-state adaptation, are important factors to be considered in clinical electrophysiologic studies and in rate correction algorithms of APD or QT intervals, respectively.

Action Potentials↗
PubMed1987

Electropharmacology of flestolol for supraventricular tachycardia without associated structural heart disease.

Flestolol is an ultrashort-acting beta-blocking drug with a half-life of 6.9 minutes. Its antiarrhythmic efficacy was studied in 21 patients with spontaneous and inducible supraventricular tachycardia: atrioventricular (AV) nodal tachycardia in 6 patients and orthodromic AV reciprocating tachycardia in 15. It increased the effective refractory period of the AV node in all patients with AV nodal tachycardia (fast pathway, p less than 0.02; slow pathway, p less than 0.01), but did not alter the anterograde (n = 8) or retrograde (n = 9) refractory periods of accessory pathways. Flestolol prevented initiation of tachycardia by causing block in anterograde AV nodal conduction. It was more effective in patients with AV nodal tachycardia (5 of 6) than in those with AV reciprocating tachycardia (4 of 15, p less than 0.03). In patients in whom it was ineffective, the mean tachycardia cycle length increased by 54 ms because of an increase in AH interval (p less than 0.0001, n = 11). The cycle length of tachycardia induced 30 minutes after infusion was similar to the cycle length in the control state (354 vs 355 ms, n = 16). Flestolol's kinetics permitted clinically indicated electropharmacologic testing of a second antiarrhythmic drug in 8 patients and control of ventricular rate until arrhythmia surgery in 1 patient with incessant tachycardia. No hypotension or toxicity occurred. Our findings indicate that flestolol's principal antiarrhythmic effects are on the AV node, similar to the effects of other beta-blocking drugs. Its ultrashort duration of action is an advantage during electropharmacologic testing.

Adrenergic beta-Antagonists↗