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Biomedical subjects

C P Reddy

Publications and source records attributed to C P Reddy.

At least 19 recordsLinked to original sources
PubMed1989

Amiodarone.

Amiodarone is an antiarrhythmic agent with unique electrophysiological and pharmacokinetic properties and a wide spectrum of antiarrhythmic activity. Its clinical efficacy is not confined to ventricular arrhythmias but extends to supraventricular arrhythmias including those associated with Wolff-Parkinson-White Syndrome. Though a highly effective drug, amiodarone causes significant side effects. In this article, the electrophysiologic and pharmacokinetic properties, the clinical efficacy, and the adverse effects of amiodarone are reviewed.

Amiodarone↗
PubMed1989

Clinical approach to antiarrhythmic therapy in patients with ventricular arrhythmia.

Ventricular arrhythmias can be categorized into three broad groups, namely, benign, malignant, and potentially malignant based on the presence or absence and the severity of underlying heart disease. The benign group does not require treatment, the benefits of treatment in the potentially malignant group are unproven, and the malignant group benefits the most from antiarrhythmic therapy. Because there is no ideal antiarrhythmic drug and all drugs have limitations, selection of an antiarrhythmic drug should be based on the therapeutic goal and the relative efficacies and toxicity profiles of various agents. In the absence of demonstrated beneficial effect from suppression of ventricular arrhythmia in many cardiac patients, antiarrhythmic drug therapy should be confined to patients with serious symptoms, patients with recurrent sustained ventricular tachycardia, and those resuscitated from cardiac arrest.

Anti-Arrhythmia Agents↗
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

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↗
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↗
PubMed1979

Gap phenomenon in "the right and left bundle branch systems" during retrograde conduction in man.

Gap phenomenon in right and left bundle branch systems during retrograde conduction is described in two patients with manifest reentry within the His-Purkinje System (V3 phenomenon). In this form of gap the premature impulse (S2) initially blocked in the right bundle branch system and conducted retrogradely via the left bundle branch system as manifested by sudden prolongation of S2H2 interval and appearance of V3. At close coupling intervals S2 impulse encountered retrograde block in the left bundle branch system and resumed retrograde conduction via the right bundle branch system with S2H2 intervals shorter than critical value and was not followed by V3. However, on further shortening the S1S2 intervals S2 impulse blocked again in right bundle branch system and resumed conduction via the left bundle branch system with S2H2 intervals longer than critical values and V3 reappeared. The mechanism of these gaps is not clear but we believe is similar to the one proposed in Types I and II gaps in antegrade bundle branch conduction and involves proximal delay allowing distal recovery. The similarities and differences between the gap phenomenon in bundle branches during antegrade and retrograde conduction are discussed.

Adolescent↗
PubMed1978

Study of the temporal effects on conduction and refractoriness of the His-Purkinje system in man.

Temporal effects on refractoriness within the His-Purkinje system (HPS) were studied in 14 patients in whom effective refractory period (ERP) of HPS could be determined, using His bundle electrograms, incremental atrial pacing, and atrial extrastimulus method. His-Purkinje conduction times (H-V interval) and relative (R), effective (E), and functional (F) refractory periods (RP) of HPS were measured during the control period and repeat measurements were made after a 30 minute interval. H-V intervals were unchanged from control in all patients. Although changes of the magnitude of 5 to 25 msec. in either direction from control values commonly occurred, on the average, no statistically significant changes were seen in RRP, ERP, or FRP of HPS. The results of the present study confirm the stability of refractoriness of HPS over a 30 minute period and provide baseline data for future investigations of cardiovascular drugs which act primarily on the distal part of the A-V conduction system.

Adult↗
PubMed1978

Abolition and modification of reentry within the His-Purkinje system by procainamide in man.

The effects of intravenous procainamide infusion of 10--14 mg/kg body weight (i.e., 750 mg) of procainamide (PA) on reentry within the His-Purkinje system (HPS) were studied in 13 patients using His bundle electrograms and ventricular extrastimulus method. PA abolished reentry in eight patients (group 1) and decreased the width of reentry zone in the remaining five (group 2). At comparable S1S2 intervals, the S2H2 intervals after PA were longer than control in all patients. In group 1 patients, after PA, reentry did not occur even at S2H2 intervals that were significantly longer than control critical S2H2 intervals. In two of eight patients in group 1, PA abolished reentry by converting unidirectional block into bidirectional block in the antegrade limb (right bundle) of the reentry circuit. In the remaining six patients reentry was abolished because of consistent retrograde block of S2 impulse at some point between the site of stimulation and the His bundle recording site. In group 2, reentry was initiated after PA at approximately the same S1S2 intervals as in control, but required significantly longer S2H2 intervals; in these patients the zone of reentry was shortened due to increase in effective refractory period of the ventricular muscle. PA significantly increased the functional refractory period of HPS and the effective refractory period of ventricular muscle. The results of this study differ from the previously reported effects of lower concentrations of PA which facilitated reentry within the same circuit. We conclude that the effects of PA on reentry are dose-related and can both facilitate and suppress reentry, depending on critical changes in conduction and refractoriness of the HPS.

Adult↗
PubMed1977

Ventricular septal motion and left ventriclular dimensions during abnormal ventricular activation.

To determine the effect of abnormal ventricular activation on ventricular septal motion, left ventricular endocardial motion and left ventricular dimensions, 12 patients with normal motion were studied with echocardiography during incremental pacing of the right ventricular apex, outflow and inflow regions. Three types of abnormal ventricular septal motion were seen: The type I pattern was characterized by an early rapid preejection posterior ventricular septal motion followed by another posterior systolic motion that lasted throughout ejection, both of which were associated with septal thickening. In the type II pattern an early rapid preejection posterior ventricular septal motion was followed by an anterior ejection motion; the latter was not accompanied by septal thickening. The type III pattern consisted of an early preejection posterior ventricular septal motion followed by a mid and late systolic posterior motion: the latter motion extended through diastole. During right ventricular apical pacing, 8 of 11 patients showed a type 1 pattern, 1 a type II pattern and 2 a normal septal motion. During right ventricular outflow pacing,seven of nine patients showed a type II pattern, one a type III pattern and one a type I pattern. During right ventricular inflow pacing, eight of nine patients showed a type II pattern and one a type III pattern. At faster pacing rates patterns of types I and III changed to a type II pattern (five patients). End-diastolic dimensions decreased significantly during incremental right ventricular pacing when compared with those during sinus rhythm. End-systolic dimensions decreased significantly only during right ventricular apical and outflow pacing at maximal rates. In the seven patients who had pacing from all three sites, the decrease in left ventricular dimensions did not significantly differ when the three pacing sites were compared. These findings suggest that (1) abnormal ventricular septal motion during right ventricular pacing (induced left bundle branch block patterns) is dependent on the sequence of ventricular activation; (2) ventricular septal motion during right ventricular outflow and inflow pacing is similar to that seen in spontaneous left bundle branch block, whereas the pattern of septal motion during right ventricular apical pacing is different from that of spontaneous left bundle branch block; and (3) changes in left ventricular dimension are dependent on ventricular pacing rate but independent of pacing site.

Adult↗
PubMed1977

Induction of iatrogenic electrocardiographic patterns during electrophysiologic studies.

Indwelling cardiac catheters by producing local mechanical stimulation or trauma can induce electrocardiographic (ECG) patterns which simulate known electrophysiologic phenomena. Catheter-induced ECG patterns were analyzed in 447 consecutive patients undergoing electrophysiologic studies. Iatrogenic nature of these patterns was suggested by 1) absence prior to placement of catheter; 2) sudden appearance with catheter placement and disappearance with catheter repositioning; 3) reoccurrence with remanipulation of catheters; and 4) simulation (in some cases) by programmed electrical stimulation from the catheter. Common catheter-induced patterns were 1) right bundle branch block (RBBB) lasting less than 24 hours occurred in 19 patients; 2) transient third degree atrioventricular block in His-Purkinje system developed in 3/13 patients with pre-existing left BBB; 3) catheter-induced ventricular pre-excitation which simulated ECG patterns of type B Wolff-Parkinson-White syndrome; 4) fortuitous synchronization of right ventricular excitation from the catheter, and left ventricular excitation from sinus beat resulted in normalization of the QRS complexes in 5/68 patients with pre-existing RBBB; 5) premature beats from the atria, right ventricle, and His bundle, which were common, resulted in complex ECG patterns. These iatrogenic ECG patterns must be identified in order to avoid errors in interpretation.

Arrhythmias, Cardiac↗