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Biomedical subjects

C S Kuo

Publications and source records attributed to C S Kuo.

At least 37 records · Page 2Linked to original sources
PubMed1993

Effect of verapamil on an accessory pathway manifesting as "fatigue phenomenon" in Wolff-Parkinson-White syndrome.

Electrophysiologic study was performed in a 52-year-old man with type A ventricular preexcitation. An accessory atrioventricular pathway with no ventriculoatrial conduction was localized to the posteroseptal region. "Fatigue phenomenon," defined as suppression of atrioventricular conduction following rapid pacing, was observed to be provoked by atrial pacing in a rate- and duration-dependent manner. Administration of 5 mg of intravenous verapamil during sinus rhythm abolished the delta waves. These observations may indicate that pathologic changes in the accessory pathway are responsible for these phenomena.

Cardiac Pacing, Artificial↗
PubMed1992

Carbamazepine-induced cardiac dysfunction. Characterization of two distinct clinical syndromes.

A patient with sinus bradycardia and atrioventricular block, induced by carbamazepine, prompted an extensive literature review of all previously reported cases. From the analysis of these cases, two distinct forms of carbamazepine-associated cardiac dysfunction emerged. One patient group developed sinus tachycardias in the setting of a massive carbamazepine overdose. The second group consisted almost exclusively of elderly women who developed potentially life-threatening bradyarrhythmias or atrioventricular conduction delay, associated with either therapeutic or modestly elevated carbamazepine serum levels. Because carbamazepine is widely used in the treatment of many neurologic and psychiatric conditions, the recognition of the latter syndrome has important implications for the use of this drug in elderly patients.

Bradycardia↗
PubMed1991

Increased risk of death and cardiac arrest from encainide and flecainide in patients after non-Q-wave acute myocardial infarction in the Cardiac Arrhythmia Suppression Trial. CAST Investigators.

This report examines whether in the Cardiac Arrhythmia Suppression Trial death and cardiac arrest from encainide, flecainide and moricizine during the titration phase and from encainide and flecainide during the follow-up phase were related to presence (Q-wave acute myocardial infarction [Q-AMI]) or absence (non-Q-AMI) of pathologic Q waves. In all, 2,371 patients (70% with Q-AMI, 26% with non-Q-AMI, and 4% unknown) entered the titration phase, starting 117 +/- 163 days after index AMI and lasting for an average of 21 days. For the titration phase, no significant differences existed between Q-AMI and non-Q-AMI patients for death and cardiac arrest rate, ventricular premature complex suppression rate, and nonrandomization rate. A total of 1,498 patients entered the follow-up phase of an average of 10 months (starting 129 +/- 158 days after the index AMI), and were randomized to encainide or flecainide, or their matching placebos. In the placebo group, non-Q-AMI patients had a significantly lower rate of death and cardiac arrest than Q-AMI patients (1.0 and 4.6%, respectively; p = 0.04). Encainide and flecainide significantly elevated death and cardiac arrest rate in both non-Q-AMI patients (8.7%, p less than 0.01) and Q-AMI patients (7.8%, p = 0.04). The relative risk for encainide or flecainide over placebo in the non-Q-AMI patients was 8.7, which was significantly higher than 1.7 observed for the Q-AMI patients (p = 0.03). None of the baseline characteristics had any significant interaction with encainide or flecainide.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiac Complexes, Premature↗
PubMed1991

Pre-excited RR intervals during atrial fibrillation in the Wolff-Parkinson-White syndrome: influence of the atrioventricular node refractory period.

The ventricular rate and percent of pre-excited QRS complexes during atrial fibrillation were compared in two groups of patients with the Wolff-Parkinson-White syndrome. Group A consisted of 22 patients whose anterograde effective refractory period of the accessory pathway was longer than that of the atrioventricular (AV) node. Group B consisted of 23 patients in whom this relation was reversed. No patient had organic heart disease. Both groups had a similar effective refractory period of the accessory pathway (288 +/- 37 vs. 280 +/- 26 ms), whereas that of the AV node was shorter in group A than group B (242 +/- 25 vs. 285 +/- 27 ms, p = 0.0001). Patients in group A had a lower percent of pre-excited QRS complexes during atrial fibrillation (39 +/- 43% vs. 93 +/- 20%, p = 0.0001). In the 21 patients whose refractory period was measured, the difference was plotted against the percent of pre-excited QRS complexes; there was a significant correlation between the two (r = -0.83, p less than 0.001). In patients in whom pre-excited RR intervals were present, the pre-excited RR intervals were compared between the two groups. Both groups had similar effective refractory periods of the accessory pathway (265 +/- 22 vs. 280 +/- 27 ms) and ventricle (200 +/- 17 vs. 211 +/- 26 ms). The effective refractory period of the AV node was shorter in group A (248 +/- 22 vs. 285 +/- 28 ms, p = 0.0005). The shortest pre-excited RR interval did not show any difference (244 +/- 37 vs. 265 +/- 41 ms). However, both the average (328 +/- 39 vs. 397 +/- 56 ms, p = 0.001) and longest (495 +/- 109 vs. 666 +/- 205 ms, p = 0.02) pre-excited RR intervals were shorter in group A.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1989

Relationship between respiratory muscle function and age, sex, and other factors.

To investigate the effects of gender and age on respiratory muscle function, 160 healthy volunteers (80 males, 80 females) were divided into four age groups. Twenty-eight of the male subjects were smokers. After the subjects were familiarized with the experimental procedure, respiratory muscle strength, inspiratory muscle endurance, and spirometric function, including forced vital capacity (FVC), forced expiratory volume in 1 s (FEV1), FEV1/FVC, tidal volume, breathing rate, and duty cycle, were measured. The respiratory muscle strength was indicated by the maximal static inspiratory and expiratory pressures (PImmax and PEmmax). Inspiratory muscle endurance was determined by the time the subject was able to sustain breathing against an inspiratory pressure load on a modified Nickerson-Keens device. The results showed that 1) except for inspiratory muscle endurance and FEV1/FVC, men had greater respiratory muscle and pulmonary functions than women, 2) respiratory muscle function and pulmonary function decreased with age, 3) smoking tended to lower duty cycle and FEV1/FVC and to enhance PE,mmax, and 4) inspiratory muscle endurance was greater in men who were physically active than in those who were sedentary. Therefore we conclude that there are sexual and age differences in respiratory muscle strength and pulmonary function and that smoking or physical activity may affect respiratory muscle function.

Adult↗
PubMed1988

Fatal amiodarone hepatoxicity.

The antiarrhythmic agent amiodarone is associated with numerous adverse effects, but clinically significant liver disease is rare. A patient is described who presented with muscle weakness, hepatomegaly, and ascites following 28 months of amiodarone usage. His condition deteriorated despite discontinuation of amiodarone therapy. A postmortem liver biopsy demonstrated necrosis, fibrosis, hyalin, and phospholipid-laden lysosomal lamellar bodies. Resolution of hepatic dysfunction may not necessarily occur on withdrawal of amiodarone if irreversible damage is already established. We speculate as to the reasons for the reportedly low incidence of overt liver disease, and suggest that hepatic enzyme levels, as well as other indicators of hepatic function, such as the serum albumin concentration, be monitored indefinitely in all patients while taking amiodarone.

Aged↗
PubMed1985

Asystole during treatment with amiodarone in a patient with persistent atrial tachycardia.

During treatment with amiodarone, digoxin and nadolol, asystole occurred repeatedly in a patient with chronic persistent automatic atrial tachycardia. Asystole did not occur after discontinuation of drug therapy, and rechallenge with amiodarone alone produced marked overdrive suppression of all pacemakers resulting in asystole. Amiodarone serum level was within therapeutic range. The possible electrophysiologic mechanisms by which amiodarone might suppress both normal and abnormal pacemakers are discussed. The occurrence of asystole at therapeutic serum concentration of amiodarone suggests that this drug should be used with caution.

Adult↗
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↗
PubMed1984

Treatment of ventricular tachycardia using an automatic scanning extrastimulus pacemaker.

A patient with recurrent sustained ventricular tachycardia that was resistant to both conventional and experimental antiarrhythmic agents was treated with a programmable automatic scanning extrastimulus pacemaker. The antitachycardia pacemaker was implanted only after many episodes of spontaneous and laboratory-induced ventricular tachycardia were reliably and reproducibly terminated with programmed ventricular extrastimuli. In the 6 months since implantation of the automatic scanning pacemaker, all episodes of ventricular tachycardia have been terminated successfully by the pacemaker. Acceleration of rate of ventricular tachycardia or induction of ventricular fibrillation did not occur at any time during attempted termination of ventricular tachycardia by the pacemaker. The advantages of the automatic scanning extrastimulus pacemaker over other antitachycardia pacemakers are discussed.

Electrocardiography↗
PubMed1984

Effect of amiodarone on electric induction, morphology, and rate of ventricular tachycardia and its relation to clinical efficacy.

Using His bundle electrograms and programmed ventricular stimulation, the effects of chronic amiodarone treatment on induction, morphology, and the rate of ventricular tachycardia (VT) were studied in 17 consecutive patients treated with amiodarone for control of recurrent sustained VT or ventricular fibrillation. Studies were done before and after treatment with amiodarone for an average duration of 5.3 (range 2 to 18) months. During the control study, sustained VT could be induced in 16 patients. VT was initiated by single or double right ventricular (RV) extrastimuli in 14 patients, by double left ventricular (LV) extrastimuli in 1 patient, and by RV burst pacing in 1 patient. Only one pattern (morphology) of VT similar to that of spontaneous VT was induced in 12 patients and two patterns of VT in 4 patients. The average cycle length (CL) (mean +/- SD) of induced VT was 325.8 +/- 61.2 ms. After amiodarone, VT could be induced in 7 of 17 patients and was initiated by single RV extrastimuli in 5 patients, double RV extrastimuli in 1 patient, and RV burst pacing in 1 patient. In 3 of 5 patients in whom VT could be initiated by single RV extrastimuli, initiation of VT required double RV or double LV extrastimuli in the control study; in 1 of 5 patients VT could not be induced in the control study. Amiodarone induced nonclinical, polymorphic VT in 4 patients in whom only clinical VT could be induced during the control study. Compared to control, the CL of induced VT was significantly longer (322 +/- 65.7 vs 416 +/- 41.5 ms; P less than 0.001).+

Adult↗
PubMed1984

Effect of amiodarone on retrograde conduction and refractoriness of the His-Purkinje system in man.

The effects of long term treatment with oral amiodarone on retrograde conduction ( S2H2 interval) and refractoriness of the His-Purkinje system were studied in 11 patients using His bundle electrograms and the ventricular extrastimulus method. Ten patients had ventricular tachycardia and one supraventricular tachycardia. Electrophysiological studies were carried out before and after the patients had been taking their maintenance dose for a mean duration of 84 days. After amiodarone treatment the HV interval was prolonged in seven patients and unchanged in four. At comparable S1S2 intervals, the S2H2 intervals were longer after treatment with amiodarone in all patients than before. Similarly, the longest S2H2 intervals achieved after amiodarone were longer than the control values. Amiodarone significantly increased the relative, effective, and functional refractory periods of the His-Purkinje system. Thus amiodarone exerts important effects on the His-Purkinje system.

Adult↗
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↗