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Biomedical subjects

L Zaman

Publications and source records attributed to L Zaman.

At least 19 recordsLinked to original sources
PubMed1991

Paired comparisons of efficacy of intravenous and oral procainamide in patients with inducible sustained ventricular tachyarrhythmias.

Thirty-eight patients who had inducible sustained ventricular tachycardia during baseline programmed electrical stimulation underwent electrophysiologic testing after both intravenous and oral administration of procainamide. Each had presented clinically with documented sustained ventricular tachycardia or out of hospital cardiac arrest not associated with acute myocardial infarction. In 23 patients (61%) (Group I) the arrhythmia became noninducible during an intravenous infusion of procainamide. Oral procainamide was subsequently administered and retesting was carried out after dose titration to match plasma concentration at the end of the intravenous study. Among the 23 patients in Group I the mean (+/- SD) plasma procainamide level was 7.2 +/- 2.8 micrograms/ml after intravenous dosing and 7.9 +/- 2.5 micrograms/ml after oral dosing (p = 0.09). In 15 (65%) of the 23 patients, sustained ventricular arrhythmia was inducible on oral therapy with comparable plasma procainamide levels (intravenous = 6.3 +/- 2.1 micrograms/ml, oral = 7.5 +/- 2.1 micrograms/ml). The other eight patients (35%) had concordant responses to repeat testing with comparable intravenous (mean 9.0 +/- 3.3 micrograms/ml) and oral (8.8 +/- 3.1 micrograms/ml) plasma procainamide levels. In the additional 15 patients (Group II) sustained ventricular tachyarrhythmia remained inducible on intravenous procainamide therapy and the patients were retested on oral therapy with similar plasma concentration (p = 0.05). In seven patients (47%) sustained ventricular tachyarrhythmia was noninducible on treatment with oral procainamide (mean plasma level 7.6 +/- 2.7 micrograms/ml) after failure of intravenous procainamide (mean plasma level 10.3 +/- 2.3 micrograms/ml).(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1991

Decrease in pulmonary artery pressure with slow release nifedipine in Saudi patients with primary pulmonary hypertension.

We studied the acute and short-term hemodynamic effects of vasodilators in three Saudi patients with primary pulmonary hypertension. The study protocol included the measurement of pulmonary artery pressure, resistance and cardiac output at baseline and at 15, 30, 45 and 60 minutes after 10 mg sublingual nifedipine. These hemodynamic studies repeated at 3 and 6 months follow-up. A 24 hour profile of pulmonary artery and aortic pressures were recorded to evaluate the effect of 20 mg of slow release nifedipine, after 25 mg of captopril and 5 mg of sublingual isordil. After nifedipine there was a marked reduction in systolic pulmonary artery pressure from 85 +/- 18 to 55 +/- 8 mmHg and the pulmonary resistance decreased from 1422 +/- 367 to 954 +/- 69 dynes-sec/cm-5. The cardiac output increased from 2.9 +/- 0.2 to 0.2 to 4.0 +/- 0.4 l/min after nifedipine. The patients were discharged on nifedipine 10 mg qid, except for patient #3 who was a non-responder. At follow-up there was a symptomatic improvement and a favourable hemodynamic response was maintained, though patient #2 required a higher dose of nifedipine. The pulmonary artery 24 hour pressure profile revealed that 20 mg slow release adalat reduced pulmonary artery pressure for a 6 hour period. Whereas, regular nifedipine decreased pulmonary artery pressure for a period of less than 90 minutes. There was no favourable hemodynamic response to either captopril 25 mg oral of isordil 5 mg administered sublingually. We conclude that slow release nifedipine decreases the pulmonary artery pressure for longer periods compared to regular nifedipine in patients with primary pulmonary hypertension.

Adolescent↗
PubMed1990

Right atrial, right ventricular and left ventricular thrombi in (incomplete) Behçet's disease.

An 18-year-old man presented with a history of oral sores and presence of high fever, scrotal ulcerations and haemoptysis. Multiple mural cardiac masses were present in the right atrium, right ventricle and left ventricle. Furthermore, pulmonary vasculitis with aneurysm formation and venous thrombosis involving the superior sagittal sinus and right transverse sinus were found, and the diagnosis was made of (incomplete) Behçet's disease. While receiving anticoagulation and later, treatment with prednisone and cyclophosphamide, the cardiac thrombi gradually disappeared. We stress the importance of early echocardiography to evaluate cardiac abnormalities in Behçet's disease.

Adolescent↗
PubMed1989

Changes in spontaneous sinus node rate as an estimate of cardiac autonomic tone during stable and unstable ventricular tachycardia.

Changes in sinus node rate were measured as an estimate of reflex control of cardiac autonomic tone during 32 episodes of stable ventricular tachycardia (without loss of consciousness) and 21 episodes of unstable ventricular tachycardia (loss of consciousness requiring electrical cardioversion) in 32 patients without retrograde ventriculoatrial conduction. Sinus node rate was measured before induction of ventricular tachycardia (at 5 s intervals during tachycardia) and 5 s after termination of ventricular tachycardia. It increased from 85 +/- 12 beats/min to a maximum of 109 +/- 25 beats/min during stable ventricular tachycardia (p less than 0.001) and from 82 +/- 15 beats/min to a maximum of 105 +/- 34 beats/min during unstable ventricular tachycardia (p less than 0.001). During unstable ventricular tachycardia, the increase in sinus rate was more abrupt and was followed by a sharp decrease beginning before termination of the tachycardia and resulting in a slower rate after termination (56 +/- 15 beats/min) than before tachycardia (p less than 0.001). Stable ventricular tachycardia resulted in a continuous increase of sinus node rate, which remained higher after termination (102 +/- 15 beats/min) than before tachycardia (p less than 0.001). Autonomic mechanisms responsible for changes in sinus rate were evaluated by reinducing the ventricular tachycardia after beta-adrenergic blockade by propranolol in 10 patients. Intravenous propranolol (mean dose 11 +/- 4 mg) had no effect on the magnitude of increase in sinus rate (+18 +/- 6 beats/min before and +17 +/- 7 beats/min after propranolol).(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1989

The clinical implication of changing unbound quinidine levels.

Pharmacodynamic and pharmacokinetic aspects pertinent to the potential clinical application of unbound quinidine levels were studied. Following heparin administration during electrophysiologic testing in 10 patients receiving quinidine, there were significant increases in the mean (+/- SD) right ventricular effective refractory period (266 +/- 24 versus 279 +/- 23; p less than 0.025), free fatty acid concentration (515 +/- 213 versus 1071 +/- 359 mmol/L; p less than 0.001), and unbound quinidine concentration (0.3 +/- 0.1 to 0.6 +/- 0.1 microgram/ml; p less than 0.001) but no changes in heart rate, corrected QT interval, or total plasma quinidine concentration. Ten control patients showed no change in the right ventricular effective refractory period following heparin administration. These findings were consistent with a heparin-induced increase in unbound drug concentration and activity that was limited to the vascular compartment. Eleven patients studied on day 3 (+/- 1) and day 10 (+/- 3) during an acute myocardial infarction showed a significant decrease in unbound quinidine fraction (12 +/- 4% versus 9 +/- 4%; p less than 0.02) accompanied by a decrease, rather than the predicted increase, in half-life (7.1 +/- 2.7 versus 6.3 +/- 2.1 hours; p less than 0.02). Volumes of distribution remained stable while the mean quinidine clearance tended to increase. Half-life correlated with albumin changes (r = -0.71; p less than 0.02). Apparently, improvement in clinical status (assumed) and drug clearance (measured) negated the direct effects of the decrease in unbound quinidine fraction. Although unbound drug concentrations should correlate best with drug dynamic and kinetic information, full knowledge of the clinical context of such measurements is needed for appropriate interpretation.

Adult↗
PubMed1989

Time to first shock and clinical outcome in patients receiving an automatic implantable cardioverter-defibrillator.

The relation between time to first shock and clinical outcome was studied in 60 patients who received an automatic implantable cardioverter-defibrillator (AICD) from August 1983 through May 1988. The mean (+/- SD) patient age was 64 +/- 10 years, 82% were men and the mean ejection fraction was 33 +/- 13%. During follow-up, 38 patients (63%) had one or more shocks; there were no differences in age, gender distribution or ejection fraction at entry between the shock and no shock groups. Among 51 patients with coronary artery disease, 31 (61%) had one or more shocks, whereas all seven patients with cardiomyopathy had one or more shocks (p less than 0.05). Neither of the two patients with idiopathic ventricular fibrillation had shocks. Of the 13 deaths, 12 occurred during post-hospital follow-up and 1 during the index hospitalization. Of the four sudden post-hospital deaths, only one was due to tachyarrhythmia in the absence of acute myocardial infarction. All four sudden deaths and five of eight post-hospital nonsudden deaths occurred in patients who had had one or more appropriate shocks during follow-up. Eight of the nine first appropriate shocks among patients who subsequently died occurred within the first 3 months of follow-up, but the actual deaths were delayed to a mean of 14.1 +/- 13.9 months (p less than 0.05). The mean time to all deaths was 14.8 +/- 13.1 months. The ejection fraction was significantly lower among patients who died than among patients who survived (25 +/- 7% versus 35 +/- 14%, p less than 0.02), but it did not distinguish risk of first shocks.(ABSTRACT TRUNCATED AT 250 WORDS)

Actuarial Analysis↗
PubMed1988

Characteristics of entrainment during autodecremental atrial and ventricular stimulation.

The entrainment characteristics of orthodromic circus movement tachycardias occurring during autodecremental atrial and ventricular stimulation were studied in 9 patients with manifest Wolff-Parkinson-White syndrome. The phenomenon occurred in 34 of 38 episodes of tachycardia during autodecremental atrial stimulation. It was not seen in 4 episodes because the first impulse penetrating the circuit terminated the arrhythmia. Invariably, the HH and VV intervals were not equal to, but longer than, the stimulus-stimulus intervals, thus not fulfilling the definition of "classic" (constant cycle length) entrainment postulated by Okumura et al. Furthermore, the first 2 of the 3 diagnostic criteria were not demonstrated and the third only could be demonstrated in 7 episodes. Tachycardia termination was achieved in all 38 episodes. Entrainment occurred during autodecremental ventricular stimulation in 79 of 80 episodes, with the AA and H-H- intervals (when visible) being equal to the corresponding paced cycle lengths. Moreover, the intervals between the last paced ventricular beat and the first ventricular beat of the resumed tachycardia were invariably longer than the last stimulus-stimulus intervals. These characteristics were those which Okumura et al attributed to "concealed" entrainment. Tachycardia termination was achieved in 77 of 80 episodes. In summary: (1) autodecremental atrial pacing produced a specific form of entrainment that did not fulfill the "classic" definition of Okumura et al; (2) autodecremental ventricular pacing consistently produced "concealed" entrainment; and (3) autodecremental stimulation was very effective in terminating 115 of 118 (98%) of episodes of circus movement tachycardias.

Cardiac Pacing, Artificial↗
PubMed1988

QRS morphology-dependent pharmacodynamics in multiform ventricular ectopic activity.

The effect of an infusion of intravenous procainamide on the frequency of ventricular premature complexes (VCPs) of differing QRS morphologies was studied in 20 patients with multiform ectopic activity. In 17 of 20 patients, there was differential suppression of single VPCs with different QRS morphologies. VPCs of the most frequent QRS morphology and the second most frequent QRS morphology were compared with respect to the procainamide level at the escape of VPCs from 85% suppression and the duration of suppression measured from the onset of the procainamide infusion. In 8 patients, VPCs of the most frequent QRS morphology remained suppressed at lower procainamide concentrations and for longer times than did VPCs of the second most frequent QRS morphology (escape procainamide concentration = 2.8 +/- 1.7 versus 5.4 +/- 2.3 micrograms/ml, p less than 0.025; time to escape 244 +/- 138 versus 98 +/- 114 min; p less than 0.05). In 9 other patients, VPCs of the second most frequent QRS morphology remained suppressed at lower procainamide concentrations and for longer times than did VPCs of the most frequent QRS morphology (escape procainamide concentration 2.9 +/- 1.4 versus 8.3 +/- 6.3 micrograms/ml, p less than 0.025; time to escape 317 +/- 114 versus 63 +/- 80 min; p less than 0.001). Thus, in individual patients there are specific patterns of suppression of VPCs of different QRS morphologies which are independent of the frequency of each morphology. There is apparently a differential pharmacologic effect of procainamide on the foci or pathways responsible for the different QRS morphologies of multiform VPCs.

Arrhythmias, Cardiac↗
PubMed1987

Significance of pacing cycle lengths in manifest entrainment of orthodromic circus movement tachycardia by ventricular pacing.

The physiology of entrainment of orthodromic circus movement tachycardia (CMT) was studied using ventricular pacing during 18 episodes of induced CMT in 7 patients with atrioventricular (AV) accessory pathways. The first paced impulse was delivered as late as possible in the tachycardia cycle (mean 88 +/- 5% of the spontaneous cycle length [CL]). Entrainment was demonstrated by the following criteria: 1:1 retrograde conduction via the accessory pathway; capture of atrial, ventricular and His bundle electrograms at the pacing rate; and resumption of tachycardia at its previous rate after cessation of pacing. The number of ventricular paced impulses ranged from 5 to 14 (mean 8 +/- 3), and entrainment occurred in 2 to 7 paced cycles (mean 4 +/- 2). Orthodromic activation of a major part of the reentry circuit (manifest entrainment) was demonstrated during 9 episodes by the occurrence of His bundle electrogram preceding the first CMT QRS at the time anticipated from the last paced beat. In the 9 other episodes, persistent retrograde His bundle activation and AV nodal penetration by each paced impulse caused a delay (mean 79 +/- 25 ms) in activation of the His bundle preceding the first CMT QRS after the last paced beat. The mean pacing CL achieving manifest entrainment was 92 +/- 3% of the tachycardia CL, compared with 84 +/- 3% for retrograde AV nodal penetration (p less than 0.01). In conclusion, manifest entrainment of orthodromic CMT can be demonstrated by ventricular pacing at very long CLs; shorter CLs may cause CMT termination due to retrograde AV nodal penetration.

Adult↗
PubMed1987

Pharmacologic approaches to management of arrhythmias in patients with cardiomyopathy and heart failure.

Interactions between disordered cardiac rhythm and abnormal cardiac hemodynamic function are well recognized. Demonstrations of this relationship include the relationship between prognostic significance of ventricular ectopy and left ventricular ejection fraction, impairment of ventricular function in association with loss of atrial systole in disease states, increased risk of potentially lethal arrhythmias in the myopathic ventricle, and the evolution of advanced grades of ventricular arrhythmias in acute heart failure. With the development of newer and more potent antiarrhythmic agents, in conjunction with drugs that can improve the failing circulation, it is now possible to clarify these interrelationships and perhaps develop new strategies for clinical management.

Anti-Arrhythmia Agents↗
PubMed1987

Recent advances in the diagnosis of fascicular blocks.

The electrocardiographic criteria for the diagnosis of left fascicular blocks have been a subject of debate and speculation. Nevertheless, careful analysis of certain electropathologic studies, extrapolations from animal experiments, and studies resulting from the inadvertent section of the various fascicles and of tracings obtained at the moment that the conduction disturbances appeared or disappeared have led to the acceptance of characteristic patterns. Although the specificity and sensitivity of electrocardiographic criteria of left anterior and left posterior fascicular block still require independent confirmation, there are already some methods that appear promising in this regard.

Bundle of His↗
PubMed1987

Unstable intraventricular conduction disorders.

Unstable bundle branch blocks may be tachycardia dependent, bradycardia dependent, or rate independent. When appearing at the "critical" rates or "critical" cycle lengths they may seem to be rate independent. Conversely, "true" rate-independent blocks may be reversible or irreversible. Determining if a rate-unrelated block may disappear can be difficult because irreversile bundle branch block seems to develop through a slow process in time during which rate-dependent, rate-independent, and even normal conduction alternate in successive electrocardiograms.

Bradycardia↗
PubMed1986

Linking phenomenon during atrial stimulation with accessory pathways.

Linking is an electrophysiologic phenomenon in which each successive impulse entering a macroreentry circuit propagates preferentially along 1 limb because of the functional impedance to conduction in the contralateral limb produced by the previous impulse. Electrophysiologic studies were performed in 12 patients with a bidirectionally conducting accessory pathway. Linking was analyzed while 1:1 atrioventricular conduction took place through the normal pathway. When atrial pacing (at the same cycle length) could be initiated during sinus rhythm in patients with rapidly conducting accessory pathways, linking was dynamically maintained by repetitive local refractoriness (interference). When it could be initiated during the usual type of orthodromic circus movement tachycardia, linking was sustained by actual impulse collision, the underlying mechanism having also been called entrainment. When it could be initiated during sinus rhythm in a patient with a slowly conducting accessory pathway, linking was maintained by impulse collision, but the underlying mechanism could not be called entrainment because stimulation had not been started during tachycardia. This study showed that 2 terms--linking and entrainment--may be applied to the same mechanism and, conversely, that the same name could not be used in reference to the same mechanism when pacing was initiated under different circumstances. However, using the proposed conceptual formulation for linking, it is apparent that seemingly diverse mechanisms associated with macroreentry circuits involving accessory pathways are, in fact, variations on a common electrophysiologic theme.

Adolescent↗
PubMed1986

Cardiac arrest in an adolescent with atrial fibrillation and hypertrophic cardiomyopathy.

A 15 year old youth, who presented with out-of-hospital cardiac arrest due to documented ventricular fibrillation, was found to have nonobstructive hypertrophic cardiomyopathy. Electrophysiologic study demonstrated inducible sustained atrial fibrillation with a rapid ventricular response. This rhythm, associated with hypotension and evidence of myocardial ischemia, spontaneously degenerated into ventricular fibrillation. No ventricular arrhythmias were inducible by programmed ventricular stimulation. Therapy with metoprolol and verapamil slowed the ventricular rate during atrial fibrillation and maintained hemodynamic stability, both during follow-up electrophysiologic study and during a subsequent spontaneous episode.

Adolescent↗
PubMed1986

Attempted entrainment of circus movement tachycardias by ventricular stimulation.

Entrainment was attempted while pacing the right ventricle in 12 patients with circus movement tachycardias. At the onset of stimulation eight patients had short episodes of intraventricular and atrioventricular dissociation during which the paced impulses activated the various ventricular recording sites (right and left), but did not reach the atria. The latter occurred because the ventricular electrograms were recorded from parts of the ventricles which were not essential components of the reentry circuit. Relatively long (greater than 5 s) runs of entrainment were not possible in any case because of the relatively prompt termination of the tachycardias. Whereas in three patients this was due to the abrupt appearance of retrograde block in the accessory pathway, in nine patients it happened when the sequential, anterograde and retrograde, penetration of the AV node resulted in AV nodal block of the subsequent, reentering atrial impulse. The findings in this study showed that, with the methodology used, entrainment of circus movement tachycardias by ventricular stimulation had to be defined conceptually, by the fulfillment of requirements which did not include its occurrence for at least 5 seconds. Furthermore, the results also suggested that entrainment and tachycardia termination were best demonstrated by a technique which allowed the emission of the first stimulus in a constant (late) moment of the cycle, with deliverance of one additional stimulus at the same cycle length in successive pacing runs.

Adolescent↗