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Biomedical subjects

M Jazayeri

Publications and source records attributed to M Jazayeri.

At least 55 records · Page 3Linked to original sources
PubMed1989

Cryoablation of refractory sustained ventricular tachycardia due to coronary artery disease.

Thirty-nine patients with medically refractory sustained monomorphic ventricular tachycardia (VT) due to coronary artery disease underwent map-guided cryosurgery. Locations of prior myocardial infarctions had been inferior in 22, anterior in 16 and combined in 1. Mean age was 61 +/- 9 years and the mean number of drug trials per patient before surgery was 3.8 +/- 1.4. Intraoperative endocardial mapping induced 67 tachycardias in 35 patients. Each patient received 6 to 18 (11 +/- 3) endocardial cryothermic applications (15 mm, -60 degrees C, 2 minutes) at areas of earliest activation during VT. Encircling endocardial cryoablation was performed in 4 patients who had unsuccessful mapping. In addition, 11 patients had subendocardial resection of their well-demarcated septal scars as well as cryosurgery. There were 2 in-hospital deaths. At postoperative programmed ventricular stimulation, 28 of the 37 patients (76%) had no inducible or spontaneous VT before hospital discharge. Six patients (16%) with spontaneous or inducible VT had a single morphology and were controlled with antiarrhythmic drugs that had previously failed. Therefore, surgery alone or in combination with drugs was efficacious in 92% of the population surviving surgery. The remaining 3 patients (8%) received automatic implantable cardioverter defibrillators. No significant difference in surgical outcome was seen between patients who had cryosurgery alone and those who had subendocardial resection together with cryoablation. Mean left ventricular ejection fractions before and after surgery were 33 and 39%, respectively (p less than 0.01). Clinical follow-up ranged from 2 to 36 months (18 +/- 12). One patient died of heart failure and another underwent heart transplantation.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

Sustained bundle branch reentry as a mechanism of clinical tachycardia.

The incidence of sustained bundle branch reentrant (BBR) tachycardia as a clinical or induced arrhythmia or both continues to be underreported. At our institution, BBR has been the underlying mechanism of sustained monomorphic ventricular tachycardia in approximately 6% of patients, whereas mechanisms unrelated to BBR were the cause in the rest. Data gathered from 20 consecutive patients showed electrophysiologic characteristics that suggest this possibility. These include induction of sustained monomorphic tachycardia with typical left or right bundle branch block morphology or both and atrioventricular dissociation or ventriculoatrial block. On intracardiac electrograms, all previously published criteria for BBR were fulfilled, and in addition, whenever there was a change in the cycle length of tachycardia, the His to His cycle length variation produced similar changes in ventricular activation during subsequent complexes with no relation to the preceding ventricular activation cycles. Compared with patients with ventricular tachycardia due to mechanisms unrelated to BBR, patients with BBR had frequent combination of nonspecific intraventricular conduction defects and prolonged HV intervals (100% vs. 11%, p less than 0.001). When this combination was associated with a tachycardia showing a left bundle branch block pattern, BBR accounted for the majority compared with mechanisms unrelated to BBR (73% vs. 27%, p less than 0.01). The above finding in patients with dilated cardiomyopathy should raise the suspicion of sustained BBR because dilated cardiomyopathy was observed in 95% of the patients with BBR. Twelve of the 20 patients were treated with antiarrhythmic agents, and the other eight were managed by selective catheter ablation of the right bundle branch with electrical energy. Our data suggest that sustained BBR is not an uncommon mechanism of tachycardia; it can be induced readily in the laboratory and is amendable to catheter ablation by the very nature of its circuit. The clinical and electrophysiologic features outlined in this study should enable one to correctly diagnose this important arrhythmia.

Adult↗
PubMed1989

Electrophysiologic spectrum of concealed intranodal conduction during atrial rate acceleration in a model of 2:1 atrioventricular block.

Concealed anterograde penetration of the atrioventricular (AV) node has been used to explain a wide variety of electrocardiographic findings. The effects of atrial rate acceleration on this phenomenon remain undefined. To examine the dynamic interrelations between conducted and nonconducted beats at different atrial rates, a unique atrial pacing protocol of functional 2:1 AV block was used in 10 patients. The pacing protocol involved abrupt transitions from 2:1 to 1:1 AV conduction and enabled quantification of conduction delay produced by nonpropagated impulses over extremes of atrial rate. Stable 2:1 AV conduction was maintained over a mean range of atrial paced cycle lengths of 289 +/- 29.6 to 223 +/- 33.0 msec, respectively. The mean AV conduction time during 2:1 and corresponding 1:1 drives at the longest atrial paced rates were 169 +/- 33.5 and 136.5 +/- 26.9 msec, respectively--revealing a significant effect of nonpropagated impulses on subsequent conduction. Surprisingly, at the shortest atrial paced rates, the mean AV conduction times were 191.5 +/- 31.8 and 161.0 +/- 23.3 msec, respectively. The lack of significant changes in conduction time between 2:1 and 1:1 drives at the extremes of atrial rate (32.5 vs. 30 msec, p = NS) suggests that the effect of concealed conduction is "fixed" and independent of rate. Clinical implications and postulated electrophysiologic mechanisms are discussed.

Adult↗
PubMed1989

Psychological support and psychiatric management of patients with automatic implantable cardioverter defibrillators.

There are well over 6,000 automatic implantable cardioverter defibrillators (AICD) that have been implanted in the United States since 1980. The device clearly reduces arrhythmic mortality in high risk patients. Many AICD patients have other cardiac diseases, most commonly, coronary artery disease with associated prior myocardial infarctions. These patients have special psychosocial stresses that may make them vulnerable to depression and other psychological disturbances. Psychological support together with psychiatric treatment, if needed, should be provided to these patients. Use of psychotropic medications should be closely monitored, especially in this population, as many of these drugs can exacerbate ventricular tachyarrhythmias. Special precautions should also be taken when administering electroconvulsive therapy in these patients.

Adjustment Disorders↗
PubMed1989

Use of calcium channel entry blockers in the treatment of cardiac arrhythmias.

In clinical arrhythmias, the main therapeutic role of calcium channel entry blockers is related to their effect on the sinus and atrioventricular (AV) node. Consequently, in cardiac arrhythmias where the AV node is part of the reentry circuit, a beneficial effect of diltiazem and verapamil can be demonstrated. These include AV nodal reentry and orthodromic tachycardia in patients with Wolff-Parkinson-White syndrome. In addition, the ventricular response by the AV node during atrial tachycardias can also be controlled with these agents. A specific type of ventricular tachycardia seen in the absence of structural heart disease has also been reported to respond to intravenous and oral verapamil. Calcium channel blockers have no proven depressant effect on accessory pathway conduction. Similarly, the value of these agents in the treatment of ventricular tachycardia in association with chronic coronary artery disease and idiopathic dilated cardiomyopathy is rather limited. The use of calcium entry blockers in patients with wide QRS tachycardia, therefore, is to be discouraged unless it can be proved that supraventricular tachycardia with aberrant conduction is the underlying basis.

Anti-Arrhythmia Agents↗
PubMed1988

Role of adrenergic stimulation by isoproterenol in reversal of effects of encainide in supraventricular tachycardia.

Reversal of the electrophysiologic effects of oral encainide with isoproterenol was evaluated in 16 patients with atrioventricular (AV) nodal reentry (group A) and in another 16 patients with Wolff-Parkinson-White syndrome (group B). Sustained AV nodal reentry was induced in all group A cases before administration of encainide, in 2 cases after oral encainide, and in 12 patients during infusion of isoproterenol. Among group B cases, 14 of 16 had sustained AV reentry during control, 6 of 16 after receiving encainide, and 8 of 16 with addition of isoproterenol. During a mean follow-up of 19 +/- 10 months in group A and 17 +/- 9 months in group B, clinical tachycardia recurred in 8 patients (4 from each group). These 8 patients were among the 20 patients who demonstrated (1) isoproterenol-induced reversibility of encainide-suppressed tachycardia, or (2) acceleration of tachycardia rate slowed by encainide. No recurrences were seen among any of the 12 cases in which isoproterenol failed to reverse the encainide-induced tachycardia suppression. Patients with clinical recurrences were controlled with a variety of means, which included beta blockers in 3 and nonpharmacologic methods in the remaining 5. In patients with AV junctional tachycardia treated with oral encainide, our findings suggest that lack of tachycardia inducibility with isoproterenol predicts freedom from clinical recurrences. Furthermore, addition of a beta blocker to oral encainide may prevent clinical recurrence in some who demonstrate adrenergic reversal of encainide effect.

Administration, Oral↗
PubMed1988

Wide QRS complex tachycardia. Reappraisal of a common clinical problem.

BACKGROUND AND PURPOSE: Despite available criteria, diagnosis of the mechanisms of wide complex tachycardia is often incorrect. We aimed in this study to identify reasons for misdiagnoses and the value and limitations of clinical and surface electrocardiographic criteria. DATA IDENTIFICATION: The analyzed data of 150 consecutive patients with wide QRS tachycardia from this study and a literature search of key papers in English since 1960 on clinical and surface electrocardiographic criteria form the basis of this report. The final correct diagnosis was made with intracardiac electrograms. DATA EXTRACTION AND ANALYSIS: Among the 150 patients, 122 had ventricular tachycardia, 21 had supraventricular tachycardia with aberrant conduction, and 7 had accessory pathway conduction. Only 39 of 122 patients with ventricular tachycardia were correctly diagnosed initially. In others, the diagnoses were supraventricular tachycardia with aberrant conduction (43 of 122) or simply a wide QRS tachycardia (40 of 122). Misdiagnosis in patients with aberrant or accessory pathway conduction was also common. Standard electrocardiographic criteria for ventricular tachycardia had unacceptable sensitivity, poor specificity, or both. Collectively such criteria allowed a correct diagnosis of ventricular tachycardia in 92% of cases. Diagnosis of ventricular tachycardia was also suggested by its association with structural heart disease. Criteria suggestive of ventricular tachycardia included atrioventricular dissociation, positive QRS concordance, axis less than -90 deg to +/- 180 deg, combination of left bundle branch block and right axis, QRS duration of greater than 140 ms with right bundle branch block and greater than 160 ms with left bundle branch block and, a different QRS during tachycardia compared to baseline preexisting bundle branch block. CONCLUSIONS: Ventricular tachycardia is the commonest underlying mechanism for wide QRS tachycardia. A correct diagnosis can usually be made from clinical and surface electrocardiographic criteria.

Adolescent↗
PubMed1988

Automatic implantable cardioverter defibrillators and survival of patients with left ventricular dysfunction and malignant ventricular arrhythmias.

STUDY OBJECTIVE: To assess survival after insertion of automatic implantable cardioverter defibrillators in high-risk patients who have malignant ventricular arrhythmias and left ventricular dysfunction. DESIGN: Actual survival time compared with arrhythmia-free time in a single group of patients. SETTING: Inpatient services of a tertiary referral center and outpatient follow-up. PATIENTS: Seventy consecutive patients with clinical sustained ventricular tachycardia or fibrillation whose arrhythmia could not be controlled by medication as determined by programmed electrical stimulation, and who had an automatic cardioverter defibrillator implanted. INTERVENTION: All patients received an implantable defibrillator. MEASUREMENTS AND MAIN RESULTS: Two-year survival was 93.4% (95% CI, 87 to 99.8) and projected survival based on recurrence of malignant arrhythmias was 60.3% (CI, 47.3 to 73.3; P less than 0.001). In the 25 patients with left ventricular ejection fraction less than 30%, actual survival was 86.7% (CI, 72.3 to 91.1) and projected survival was 56.9% (CI, 35.9 to 77.9; P = 0.025). Projected survival percentages are similar to survival figures reported in the literature for such high-risk patients. There was only one sudden death; the remaining deaths were not arrhythmic in nature. Of the 65 patients who were alive at the end of follow-up, 13 were in New York Heart Association Class I; 44, Class II; 5, Class III; and 3, Class IV. CONCLUSIONS: The automatic implantable cardioverter defibrillator is probably highly effective in preventing arrhythmic mortality even in high-risk patients. Such treatment does not appear to significantly impair a patient's functional status.

Actuarial Analysis↗
PubMed1988

Mechanisms of clinical tachycardias.

Animal data suggest that cardiac arrhythmias can result from a variety of mechanisms. In clinical settings, arrhythmias that are easily initiated and terminated with programmed electrical stimulation are often designated as reentry tachycardias. However, proof of reentry is contingent upon demonstration of the entire circuit; this relation has been proposed for arrhythmias associated with large circuits, such as those seen in the Wolff-Parkinson-White syndrome. Reentry has also been proposed as the mechanism responsible for a variety of other tachycardias, including bundle branch and atrioventricular nodal reentry tachycardia, permanent junctional reentrant tachycardia, reentry tachycardia associated with nodoventricular Mahaim fibers and inducible atrial and ventricular tachycardia. Documentation of triggered rhythms as the mechanism responsible for clinical arrhythmias has been even more difficult. Examples of arrhythmias resulting from triggered activity may include those associated with digitalis toxicity arising from the atria, the atrioventricular junction or the ventricles. Clinical arrhythmias due to triggered activity in the absence of digitalis have also been described. Cardiac arrhythmias that cannot be induced by electrical stimulation are presumably due to normal or abnormal automaticity. Examples of normal automaticity in the human heart are sinus rhythm and junctional and idioventricular escape rhythms. Tachycardias by abnormal automaticity have seldom been investigated for the purpose of documenting the mechanism and therefore the limited data available make it difficult to draw any final conclusions.

Animals↗
PubMed1988

Marked Q-T prolongation due to encainide therapy.

Encainide is a type Ic antiarrhythmic agent. During encainide therapy, mild Q-T interval prolongation can be seen, usually associated with prolongation of the Q-R-S interval. The present case report describes an unusual and marked prolongation of the Q-T interval with no Q-R-S interval prolongation in a patient who was treated with encainide for atrioventricular nodal reentrant tachycardia. The drug metabolite profile in this patient's serum indicated an unusual elevation of the 3-methoxy-O-demethyl encainide metabolite, versus O-demethyl encainide. This elevated metabolite level suggests that 3-methoxy-O-demethyl encainide has a significant effect on prolongation of repolarization. An abnormal metabolism of encainide may be the underlying mechanism by which some patients would manifest an unusual prolongation of Q-T interval during encainide therapy.

Anilides↗
PubMed1988

Absence of significant postdefibrillation bradyarrhythmias in patients with automatic implantable defibrillators.

Because postdefibrillation bradycardia or asystole is of clinical concern in patients with implanted automatic cardioverter defibrillators, we analyzed the cardiac rhythm after 157 intraoperative defibrillations in 50 patients undergoing implantation of the device. Factors that could influence the heart rhythm immediately after defibrillation were also analyzed. The postdefibrillation heart rate and the duration of postdefibrillation asystole did not correlate with age, conduction abnormalities, type or duration of arrhythmia before defibrillation, delivered energy, lead system, or left ventricular ejection fraction, but they did correlate with the resting preoperative heart rate and the concomitant performance of coronary artery bypass surgery at the time of defibrillator implantation. Temporary pacing (for prolonged asystole) was required in only two patients, both of whom had also undergone bypass surgery. Fourteen patients being treated with amiodarone had slower resting and postdefibrillation heart rates, but the mean duration of posdefibrillation asystole was similar to that seen in patients not receiving any antiarrhythmic medication. On follow-up, 25 monitored and 178 unmonitored automatic defibrillator discharges occurred in 24 patients, without evidence of symptomatic postdefibrillation bradyarrhythmias. Thus significant postdefibrillation bradyarrhythmias were uncommon, but when such a propensity existed it could not be predicted reliably on clinical grounds alone.

Adult↗
PubMed1988

Useful clinical criteria for the diagnosis of ventricular tachycardia.

Misdiagnosis occurs upon initial presentation to medical attention in a considerable number of patients referred for evaluation of wide QRS tachycardia. In order to improve diagnostic accuracy (ventricular versus supraventricular tachycardia), the answers to two key bedside questions were prospectively evaluated: (1) Had the patient experienced a prior myocardial infarction? (2) Did symptoms of tachyarrhythmia start only after the infarction? A patient presenting with a wide QRS tachycardia was considered to have ventricular tachycardia if he or she answered in the affirmative to both of these questions. Of 31 consecutive patients referred with electrocardiographically documented sustained wide QRS tachycardia that was reproduced in the electrophysiology laboratory, the diagnoses made when the patients first presented to medical attention were ventricular tachycardias in 17 patients and supraventricular tachycardias in 14 patients. Following electrophysiologic evaluation, 29 were diagnosed as having ventricular tachycardia and two as supraventricular tachycardia. If the diagnoses were made solely on the basis of responses to the bedside questions mentioned earlier, 28 of the 29 patients having a final diagnosis of ventricular tachycardia would have been correctly identified. It is concluded that the use of these two questions can be very helpful in improving the clinical diagnosis of ventricular tachycardia.

Adult↗
PubMed1988

Efficacy of cryosurgery alone for refractory monomorphic sustained ventricular tachycardia due to inferior wall infarction.

The efficacy of cryosurgery alone was evaluated in 15 patients with refractory monomorphic sustained ventricular tachycardias related to inferior wall infarction. Patients were 64 +/- 9 (SD) years old and had a mean left ventricular ejection fraction of 39.2 +/- 11.2%. Thirty different tachycardias were mapped with the origin localized to the septum or inferior wall in 20 (67%), near the mitral valve anulus in 6 (20%) and at the base of the posterior papillary muscle in 4 (13%) tachycardias. Endocardial cryoablation of these sites was performed with 6 to 13 (mean 9.2 +/- 1.8) cryolesions per heart. No mitral valve replacement was performed. There was one postoperative death as a result of sepsis. Cryoablation abolished inducible ventricular tachycardia in 11 patients. Of the other three patients, the tachycardia in two was controlled with a single antiarrhythmic agent that had previously failed to suppress inducible ventricular tachycardia. Thus, clinical success was obtained in 13 (93%) of 14 patients. The remaining patient received an automatic implantable cardioverter defibrillator. Ejection fraction remained unchanged or improved after surgery in 14 patients (93%). There have been no late deaths, recurrence of sustained ventricular tachycardia or significant mitral regurgitation during a mean follow-up period of 19 +/- 7 months. These results compare quite favorably with those previously reported for subendocardial resection alone, and indicate that cryosurgery is highly effective, does not result in deterioration of left ventricular function and preserves mitral valve competence when cryoablation of the posterior papillary muscle is necessary.

Aged↗
PubMed1988

Atriofascicular connection or a nodoventricular Mahaim fiber? Electrophysiologic elucidation of the pathway and associated reentrant circuit.

Accessory pathways showing decremental properties and inserting into the right ventricle have been frequently described as "nodoventricular" or Mahaim pathways. However, conclusive evidence for a nodal origination of such pathways is lacking. The patient in this study had characteristics typical of such a pathway. Antegradely, the pathway showed decremental, nodelike conduction properties. With the aid of right bundle branch recordings, the pathway was demonstrated to insert directly into the right bundle branch. Atrioventricular reciprocating tachycardia could be readily initiated by atrial or ventricular pacing. The QRS morphology was normal during sinus rhythm and demonstrated a left bundle branch block pattern with normal axis during tachycardia. The reentrant circuit involved antegrade conduction over the accessory pathway and retrograde conduction via the bundle branches, His bundle, and the atrioventricular node. More significantly, late atrial stimuli delivered during tachycardia could preexcite the ventricle via the accessory pathway despite their inability to enter the atrioventricular node. Thus, the upper "turn around" of the reentrant circuit involved atrial tissue and the accessory pathway originated directly from the right atrium independent of the atrioventricular node. In view of these new findings and other recent observations during surgical resection of similar pathways, a reassessment of previous descriptions of "nodoventricular" fibers may be necessary. Many of these pathways may actually represent atriofascicular or atrioventricular connections with decremental properties.

Adolescent↗
PubMed1988

Transcatheter electrical ablation of right bundle branch. A method of treating macroreentrant ventricular tachycardia attributed to bundle branch reentry.

The present study describes the clinical and electrophysiological characteristics of sustained bundle branch reentrant ventricular tachycardia treated with electrical ablation of the right bundle branch. Seven patients presented with syncopal episodes, and six of the seven had documented episodes of ventricular tachycardia. All patients had depressed left ventricular ejection fraction with cardiomegaly. Six of the seven had dilated cardiomyopathy in the absence of significant coronary disease. Twelve-lead electrocardiograms in all seven patients during sinus rhythm were remarkably similar; six demonstrated intraventricular conduction defect resembling left bundle branch block, and one showed left anterior fascicular block. All patients showed prolonged His-to-ventricle intervals during sinus rhythm. Sustained ventricular tachycardia (with atrioventricular dissociation) because of bundle branch reentry was induced in all patients during baseline electrophysiological study. The His-to-ventricle intervals during tachycardia were similar to those seen during sinus rhythm. Electrical ablation of the right bundle branch was accomplished in each patient with delivery of two electrical shocks (170-310 J) through electrode catheters. Right bundle branch block developed on their surface electrocardiogram immediately after the ablation. Follow-up electrophysiological studies showed no inducible ventricular tachycardia. Clinical follow-up showed no recurrence of syncope or ventricular tachycardia. From the data presented, the following can be concluded. First, right bundle branch ablation is a safe and promising means of treating ventricular tachycardia because of bundle branch reentry and can obviate the need for antiarrhythmic drug therapy and its frequent undesirable side effects. Second, there are common clinical and electrophysiological characteristics that are frequently seen in patients with this tachycardia, and the recognition of these common characteristics should alert the physician to a bundle branch reentrant mechanism of ventricular tachycardia.

Aged↗
PubMed1988

Modulation of conduction and refractoriness in atrioventricular junctional reentrant circuit. Effect on reentry initiated by atrial extrastimulus.

The importance of activation sequence of an atrioventricular junctional reentrant (AVJRe) circuit, before delivery of an extrastimulus, has received little attention in studies concerned with clinical tachycardias. In this study a change in activation sequence was accomplished using bidirectional activation (V-A sequential pacing) during the basic drive (V1A1-V1A1). It was noted that, compared with an atrial extrastimulus (A2) after an atrial drive (A1-A1), earlier activation (by V1 impulse of the V1A1-V1A1 drive) consistently improved conduction, or decreased refractoriness, or both, in the anterograde as well as the retrograde pathway of the AVJRe circuit. In all patients, five with AV nodal reentry and six with Wolff-Parkinson-White syndrome, reentrant tachycardia could be prevented during V-A sequential pacing. In four of eleven patients, reentry was prevented despite achieving the so-called critical atrioventricular nodal delays that had previously caused reentry during control study. This finding suggested that conduction delay necessary for reentry was related to the site of block, which in turn was affected by V-A sequential pacing. We concluded that changing the activation sequence during basic drive modulates conduction and refractoriness in AVJRe circuits, and allows the study of a wide range of electrophysical factors that prevent or permit reentry.

Adult↗