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Biomedical subjects

L B Liem

Publications and source records attributed to L B Liem.

At least 37 records · Page 2Linked to original sources
PubMed1994

Efficacy of adenosine in terminating catecholamine-dependent supraventricular tachycardia.

The purpose of this study was to determine if adenosine is equally effective in terminating catecholamine-dependent and independent supraventricular tachycardia (SVT). The effect of adenosine on termination of SVT was studied in 21 patients: 12 with atrioventricular (AV) reciprocating tachycardia, and 9 with AV node reentrant tachycardia. Group 1 comprised 13 patients who had SVT induced in the absence of exogenous catecholamines, whereas group 2 comprised 8 who needed isoproterenol (1.6 +/- 0.4 micrograms/min) for induction. There was no statistical difference between the 2 groups regarding age, weight, mean arterial pressure during sinus rhythm and SVT, cycle length of SVT, or norepinephrine and epinephrine levels during sinus rhythm and SVT. Cycle length during sinus rhythm was significantly decreased in group 2. The mean dose of adenosine needed to terminate SVT was 52 +/- 6 micrograms/kg of body weight in group 1, and 61 +/- 12 micrograms/kg in group 2 (p > 0.05). In addition to isoproterenol not altering the minimal dose of adenosine necessary to terminate SVT, there was also no correlation between the dose of adenosine (mean 55 +/- 6 micrograms/kg) of each patient, and the corresponding endogenous epinephrine (273 +/- 59 pg/ml) (r = -0.19) and norepinephrine (400 +/- 58 pg/ml) (r = 0.01) levels during SVT, or cycle length of SVT (323 +/- 9 ms) (r = -0.35). The results show that adenosine is equally effective in terminating catecholamine-dependent and independent SVT; higher adenosine doses should not be needed to manage catecholamine-dependent SVT.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine↗
PubMed1993

Implantable cardioverter-defibrillator therapy in survivors of out-of-hospital sudden cardiac death without inducible arrhythmias.

OBJECTIVES: The aim of this study was to determine the efficacy of implantable cardioverter-defibrillator (ICD) therapy in survivors of sudden cardiac death in whom no ventricular arrhythmias can be induced with programmed electrical stimulation. BACKGROUND: Survivors of sudden cardiac death in whom ventricular arrhythmias cannot be induced with programmed electrical stimulation remain at risk for recurrence of serious arrhythmias. Optimal protection to prevent sudden death in these patients is uncertain. This study compares survival in the subset of survivors of sudden cardiac death with that of patients treated with or without an ICD. METHODS: A retrospective study was performed on 194 consecutive survivors of primary sudden death who had < or = 6 beats of ventricular tachycardia induced with programmed electrical stimulation with at least three extrastimuli. Ninety-nine patients received an ICD and 95 did not. RESULTS: There were no significant differences between the two groups in presenting rhythm, number of prior myocardial infarctions or use of antiarrhythmic agents. Patients treated with an ICD were younger (55 +/- 16 vs. 59 +/- 11 years, p = 0.03) and had a lesser incidence of coronary artery disease (48% vs. 63%, p = 0.04) and a lower ejection fraction (0.43 +/- 0.16 vs. 0.48 +/- 0.18, p = 0.04). There were no significant differences between the groups in the use of revascularization procedures or antiarrhythmic agents after the sudden cardiac death. Patients treated with an ICD had an improvement in sudden cardiac death-free survival (p = 0.04) but the overall survival rate did not differ from that of the patients not so treated (p = 0.91). A multivariate regression analysis that adjusted for the observed differences between the groups did not alter these results. CONCLUSIONS: Survivors of sudden cardiac death in whom no arrhythmias could be induced with programmed electrical stimulation remained at risk for arrhythmia recurrence. Although the proportion of deaths attributed to arrhythmias was lower in the patients treated with an ICD, this therapy did not significantly improve overall survival.

Actuarial Analysis↗
PubMed1993

Ventricular fibrillation in patients without significant structural heart disease: a multicenter experience with implantable cardioverter-defibrillator therapy.

OBJECTIVES: This study was undertaken to characterize the outcome of survivors of ventricular fibrillation with no or minimal structural heart disease who received an implantable cardioverter-defibrillator. BACKGROUND: The prognosis among survivors of ventricular fibrillation with minimal or no structural cardiac abnormalities remains unclear. Since the advent of implantable cardioverter-defibrillators, this question takes on added importance. METHODS: This 10-center retrospective study provided information on 28 survivors of ventricular fibrillation (mean age 42 years) with minimal or no structural abnormalities who were treated with an implantable cardioverter-defibrillator. RESULTS: Ventricular tachyarrhythmias (polymorphic in all but one patient) were induced during baseline programmed stimulation in 39% of patients. During a median 30.6-month follow-up period after implantable cardioverter-defibrillator implantation, there were no cardiac deaths and two noncardiac deaths. Sixteen patients experienced 36 shock episodes (total 88 shocks). The majority of shocks were classified as "indeterminate"; one patient received 47 "spurious" shocks during one shock episode and each of four patients received one "appropriate" shock. Ventricular arrhythmias were not inducible in any of these latter four patients. CONCLUSIONS: Survivors of ventricular fibrillation with minimal or no structural cardiac abnormalities receiving an implantable cardioverter-defibrillator have an excellent 3-year survival rate. The occurrence, albeit infrequent, of appropriate implantable cardioverter-defibrillator shocks in this group suggests that these patients have a potential risk of recurrent cardiac arrest whose fatal outcome may be avoided by implantable cardioverter-defibrillator therapy.

Actuarial Analysis↗
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↗