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Biomedical subjects

F Morady

Publications and source records attributed to F Morady.

At least 325 records · Page 18Linked to original sources
PubMed1986

Intravenous propafenone for termination of reentrant supraventricular tachycardia. A placebo-controlled, randomized, double-blind, crossover study.

To assess the antiarrhythmic efficacy of intravenous propafenone, 20 patients with inducible sustained supraventricular tachycardia received propafenone, 2 mg/kg body weight, or placebo in a double-blind, randomized, crossover study. Three patients had intra-atrial reentrant tachycardia, 3 had atrioventricular nodal reentrant tachycardia, and 14 had atrioventricular reciprocating tachycardia associated with the Wolff-Parkinson-White syndrome. Termination of supraventricular tachycardia occurred in 15 of the 20 patients receiving propafenone but 0 of the 11 patients receiving placebo (p less than 0.01). Propafenone prolonged refractoriness and slowed conduction of the atrium, the atrioventricular node, and accessory atrioventricular bypass tracts, and these effects provided antiarrhythmic action to halt tachycardia. No adverse effects were observed in any patient. We conclude that intravenous propafenone is safe and effective in the acute treatment of various forms of reentrant supraventricular tachycardia.

Adult↗
PubMed1986

The evaluation of syncope with electrophysiologic studies.

An electrophysiologic study is appropriate in patients with syncope that remains unexplained after a complete clinical, neurologic, and non-invasive cardiovascular evaluation. However, not all abnormalities demonstrated by electrophysiologic testing can be assumed to be related to syncope. The findings that have a high and low probability of being clinically significant are summarized in Table 2. If patients with the carotid hypersensitivity syndrome are screened out before electrophysiologic testing, the most common clinically significant abnormality in patients with structural heart disease is inducible unimorphic ventricular tachycardia, which is found in approximately 30 per cent of patients. The overall yield of clinically significant findings in patients with unexplained syncope is 40 per cent. In contrast, the overall yield of clinically significant abnormalities in patients who do not have structural heart disease is extremely low, less than 10 per cent. Because the yield is low, an electrophysiologic study is not indicated in patients without structural heart disease unless the syncope is recurrent and problematic or there is a specific reason to suspect an arrhythmia as the cause of syncope. However, in patients who have structural heart disease, an electrophysiologic study is appropriate after even one episode of unexplained syncope, because of the importance of identifying those patients in whom a potentially lethal arrhythmia may be the cause of syncope.

Electrodiagnosis↗
PubMed1985

A prevalent misconception regarding wide-complex tachycardias.

In response to a questionnaire, 59% of 196 physicians indicated that they were influenced by a patient's blood pressure and clinical status when attempting to distinguish ventricular tachycardia (VT) from paroxysmal supraventricular tachycardia with bundle-branch block. A sizable proportion of physicians are unaware that VT need not be associated with shock. More emphasis should be placed on making physicians aware that the differentiation of VT from paroxysmal supraventricular tachycardia should be based on electrocardiographic findings and not on the patient's blood pressure or clinical status.

Aged↗
PubMed1985

Effects of high stimulation current on the induction of ventricular tachycardia.

Programmed stimulation at 2 right ventricular sites with 1 to 3 extrastimuli was performed at current strengths of twice diastolic threshold (1.0 +/- 0.2 mA, mean +/- standard deviation) and 10 mA in 41 patients undergoing an electrophysiologic study because of sustained ventricular tachycardia (VT) (11 patients), nonsustained VT (19 patients) or unexplained syncope (11 patients). In 26 patients, VT was not induced by programmed stimulation at twice diastolic threshold. Programmed stimulation at 10 mA induced VT or ventricular fibrillation in 16 of these 26 patients (62%). In 4 of 16 patients, the coupling intervals of the extrastimuli that induced VT/ventricular fibrillation at 10 mA were all equal to or longer than the shortest coupling intervals resulting in ventricular capture at twice diastolic threshold. Fifteen patients had inducible VT at twice diastolic threshold. Programmed stimulation at 10 mA induced a similar VT in 12 of these patients, but resulted in no VT induction in 3 of 15 patients (20%), despite ventricular capture at the same coupling intervals that had induced VT at twice diastolic threshold. This study shows that programmed stimulation at a high current strength may either facilitate or prevent induction of VT. Facilitation of VT induction usually is attributable to a shortening of ventricular refractoriness and the ability of extrastimuli at 10 mA to capture the ventricle at shorter coupling intervals than possible at twice diastolic threshold. However, in 25% of cases, the facilitation of VT induction by 10-mA stimuli is not explained by a shortening of ventricular refractoriness.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1985

Cardiac arrest and sudden death in patients treated with amiodarone for sustained ventricular tachycardia or ventricular fibrillation: risk stratification based on clinical variables.

Multivariate analysis of 11 clinical variables was performed in 104 patients with sustained, symptomatic ventricular tachycardia (VT) or ventricular fibrillation treated with amiodarone to determine variables predictive of subsequent cardiac arrest or sudden death. Twenty-five patients (24%) had fatal or nonfatal cardiac arrest after 7.3 +/- 6.2 months (mean +/- standard deviation) of therapy. Multivariate analysis identified an ejection fraction of less than 0.40, syncope or cardiac arrest before amiodarone therapy, and VT (3 or more consecutive ventricular premature complexes) during predischarge ambulatory electrocardiographic monitoring as variables associated with a high risk of subsequent fatal or nonfatal cardiac arrest (p less than 0.03). Patients who had these 3 clinical variables had a much higher predicted incidence of cardiac arrest at 6 months (62%) and 12 months (76%) than did patients with an ejection fraction greater than 0.40, without syncope or cardiac arrest before amiodarone therapy, and without VT during predischarge ambulatory electrocardiographic monitoring (2% and 5%, respectively) (p less than 0.02). Risk stratification using clinical variables can predict which patients are at high risk of recurrent cardiac arrest or sudden death during amiodarone therapy.

Aged↗
PubMed1985

Clinical significance of ventricular fibrillation-flutter induced by ventricular programmed stimulation.

Two hundred twenty-four patients underwent ventricular programmed stimulation (VPS) without prior documentation of the clinical occurrence of sustained ventricular tachycardia (VT) or ventricular fibrillation-flutter (VF). Indications for VPS were: palpitations or nonsustained VT during ambulatory monitoring (85 patients), syncope or presyncope (137 patients), and a family history of sudden death (two patients). Sustained VF requiring transthoracic defibrillation was initiated by VPS in 18 patients (8.0%). Four patients were treated for inducible VF with antiarrhythmic agents directed by electropharmacologic testing; five patients were treated empirically; nine patients received no therapy. No patient has had a cardiac arrest or sudden death during a follow-up period 25.2 +/- 13.8 months (mean +/- standard deviation). VF was initiated by two ventricular extrastimuli in three patients and by three extrastimuli in 15 patients. The incidence of VF was similar in patients with and without previous symptoms (8.8% vs 6.9%) or heart disease (7.1% vs 9.6%). It was significantly higher when VPS at three ventricular sites with a current of 5 mA (pulse width 2 msec) was compared to programmed stimulation at two ventricular sites with a current twice diastolic threshold (pulse width 2 msec) (15.2% vs 3.0%, p less than 0.05). VF initiated by VPS in patients without prior VT or VF appears to be a nonspecific finding. Antiarrhythmic therapy for VF may not be necessary in these patients.

Adult↗
PubMed1985

Rate-dependent effects of intravenous lidocaine, procainamide and amiodarone on intraventricular conduction.

In this study, the duration of the QRS complex during ventricular pacing was used as an index of intraventricular conduction to quantitate the rate-dependent effects of intravenous lidocaine, procainamide and amiodarone. Right ventricular apical pacing (15 to 20 beats) was performed at cycle lengths of 600, 500, 400, 350, 300, 275 and 250 ms, before and 5 minutes after the intravenous administration of lidocaine in 11 patients (serum level 3.2 +/- 0.8 micrograms/ml [mean +/- SD] ), procainamide in 14 patients (serum level 8.2 +/- 1.9 micrograms/ml) and amiodarone in 12 patients (serum level 3.9 +/- 1.2 micrograms/ml). Electrocardiographic recordings were made at a paper speed of 150 mm/s. QRS duration was measured in a blinded fashion, with reproducibility within 5%. In the control state, QRS duration was the same at all paced cycle lengths. After lidocaine, procainamide and amiodarone administration, the shortest paced cycle length with complete ventricular capture was 250 +/- 0, 275 +/- 38 and 264 +/- 20 ms, respectively. At a paced cycle length of 600 ms, the increase in QRS duration compared with the control state was 1 +/- 2% with lidocaine (p greater than 0.05), 21 +/- 7% with procainamide (p less than 0.001) and 6 +/- 6% with amiodarone (p less than 0.05). At the shortest paced cycle length with complete capture, the increase in QRS duration compared with the control state was 20 +/- 6% with lidocaine (p less than 0.001), 42 +/- 11% with procainamide (p less than 0.001) and 26 +/- 4% with amiodarone (p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1985

Coexistent posteroseptal and right-sided atrioventricular bypass tracts.

Twelve patients with a posteroseptal accessory pathway underwent complete electrophysiologic studies, and four were found to have a second atrioventricular (AV) bypass tract that was right anterior, right anteromedial or right anterolateral in location. In two of these four patients, the presence of the right-sided AV bypass tract was confirmed by intraoperative epicardial mapping or after catheter-induced abolition of retrograde conduction through the posteroseptal bypass tract. In three of the four patients with a dual AV bypass tract, the delta wave pattern was clearly atypical of the pattern seen with an isolated posteroseptal accessory pathway. Instead of a transition from an isoelectric or slightly positive delta wave in lead V1 to markedly positive delta waves in leads V2 to V6, the delta waves were negative or only slightly positive in leads V2 to V5. However, in a fourth patient with dual AV bypass tracts, the only atypical electrocardiographic finding was an intermittently positive delta wave in lead II; at times this patient's electrocardiogram was consistent with an isolated posteroseptal bypass tract, with negative delta waves in the inferior leads. There appears to be an association between posteroseptal and right-sided accessory pathways. In patients with a posteroseptal accessory pathway who are candidates for catheter or surgical bypass tract ablation, a complete mapping study of the tricuspid anulus is mandatory, even when the electrocardiogram is typical of an isolated posteroseptal bypass tract.

Adolescent↗
PubMed1985

Long-term management of recurrent paroxysmal tachycardia by cardiac burst pacing.

Sixteen patients with either recurrent symptomatic supraventricular tachycardia (SVT) (ten) or ventricular tachycardia (VT) (six) unresponsive to drug treatment underwent insertion of chronic overdrive cardiac pacing devices for arrhythmia control. All patients with SVT followed for longer than 2.5 years required concomitant drug therapy for rhythm control. In addition, one of the ten patients required amiodarone and three required nonpharmacologic therapy (catheter ablation of the atrioventricular junction (one), surgical ablation of the Kent bundle and/or bundle of His (two). In the six patients with VT, only one patient used the device successfully. In the other five patients, either the arrhythmia failed to respond to burst overdrive pacing (three) or overdrive acceleration resulted (two). One death in the latter group was related to induction of rapid VT followed by ventricular fibrillation. Long-term follow-up of patients with paroxysmal SVT shows that virtually all require concomitant drug therapy and may require aggressive medical or surgical procedures for arrhythmia control. Use of ventricular overdrive pacing for those with VT appeared singularly disappointing in that pacing proved either ineffective (three) or resulted in overdrive acceleration (two) in 5/6 patients.

Adult↗
PubMed1985

Electrophysiologic testing in patients with the long QT syndrome.

Electrophysiologic studies were performed in 15 patients with syncope and/or cardiac arrest who had the long QT syndrome and 11 control subjects who had normal QT intervals. The syndrome was familial in five patients and idiopathic in 10. All patients had a prolonged QT (546 +/- 68 msec, mean +/- SD) and corrected QT (550 +/- 51 msec). Incremental atrial pacing at cycle lengths of 600 to 400 msec resulted in shortening of the QT interval, but there was no significant difference in the magnitude or percent of shortening of the QT interval between patients with the long QT syndrome and control subjects. Intravenous propranolol did not influence the QT interval measured at fixed atrial-paced cycle lengths in patients with either the familial or idiopathic form of the syndrome. Programmed right and left ventricular stimulation with up to three extrastimuli before and during isoproterenol infusion did not induce sustained ventricular tachycardia or ventricular fibrillation in any of the patients. However, rapid polymorphic nonsustained ventricular tachycardia was induced in six of the 15 patients (40%). Neither the inducibility of nonsustained ventricular tachycardia nor the results of electropharmacologic testing with beta-blockers proved to be of any prognostic value during the mean follow-up period of 28 +/- 17 months. Electrophysiologic studies are of limited value in the diagnosis and treatment of patients with the long QT syndrome.

Adolescent↗
PubMed1985

Efficacy and safety of transcatheter ablation of posteroseptal accessory pathways.

Eight patients with a posteroseptal accessory pathway and symptomatic atrial fibrillation and/or orthodromic reciprocating tachycardia underwent attempted transcatheter ablation of the accessory pathway. A quadripolar electrode catheter was positioned within the coronary sinus such that the proximal pair of electrodes straddled the os. This proximal pair of electrodes was made electrically common and connected to the cathodal output of a defibrillator. A patch electrode placed over the midthoracic spine was connected to the anodal sink of the defibrillator. Two to three transcatheter shocks were delivered, with a cumulative energy of 600 to 900 J. Immediately after the shocks were delivered, retrograde accessory pathway conduction was absent in each patient. Anterograde conduction through the posteroseptal accessory pathway was absent in six patients. In one patient, retrograde accessory pathway conduction was absent and anterograde conduction was present but was slower than at baseline. In this patient, orthodromic tachycardia was no longer inducible and the ventricular rate during induced atrial fibrillation was 150 beats/min, compared with 220 beats/min before the attempted ablation. He has remained asymptomatic without antiarrhythmic drug therapy for 18 months. In one patient, the transcatheter shocks had no long-term effect on accessory pathway conduction. The shocks delivered at the os of the coronary sinus were well tolerated.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1985

Sudden death after catheter-induced atrioventricular junctional ablation.

Atrioventricular (AV) junctional ablation was performed in a 59-year-old woman with recurrent atrial fibrillation refractory to treatment with digoxin, beta-blockers, verapamil, quinidine, procainamide, and amiodarone. She received two shocks of 500 J which produced complete AV block. After six weeks, both 24-hour ECG recordings and an exercise tolerance test showed infrequent premature ventricular complexes, 3 degrees AV block, and paced ventricular rhythm with 100 percent capture. She suddenly collapsed and was found to be in ventricular fibrillation and could not be resuscitated. Serial sections of the conduction system showed marked fatty infiltration of the approaches to the AV node with almost complete separation from the node. A partially fibrosed atrioHisian connection was also present. Fibroelastosis with chronic inflammatory changes was present in the AV node, bundle of His, and right and left bundle branches. In addition, marked inflammatory changes with fibrosis were present in the atrial septum, in the summit of the ventricular septum, with degenerative changes in the tricuspid and aortic valves. The sequelae of these findings outside the conduction system in other patients remains to be determined.

Atrial Fibrillation↗
PubMed1985

Evaluation of the patient with syncope.

Evaluation of the patient who has experienced spontaneous, transient loss of consciousness requires a comprehensive consideration of many disease etiologies. Syncope may be a relatively benign condition with a good prognosis or may be a precursor of subsequent cardiac arrest and sudden death. In this article, the cardiovascular causes of syncope and the role of electrophysiologic testing in the diagnostic evaluation of patients with syncope are discussed.

Bradycardia↗
PubMed1985

Clinical symptoms in patients with sustained ventricular tachycardia.

We questioned 113 patients with subsequently diagnosed sustained ventricular tachycardia (VT) regarding the symptoms that prompted their seeking hospital treatment, eliciting the following: 15% of patients had lost consciousness, 15% had near syncope, 35% had mild lightheadedness and 35% had no cerebral symptoms. Patients with preexisting congestive heart failure or a VT rate of 200 beats per minute or greater more often lost consciousness. Other symptoms included palpitations in 57% of patients, chest pain in 27%, dyspnea in 25%, weakness in 6%, nausea or diaphoresis in 3% each and flushing in 2%. In approximately 50% of patients who had mild lightheadedness or no cerebral symptoms, their condition was incorrectly diagnosed as supraventricular tachycardia based on the absence of severe symptoms during the tachycardia. In some patients, VT may be associated with mild or atypical symptoms. The differentiation of supraventricular from ventricular tachycardia should be based on electrocardiographic criteria and should not be influenced by the nature or severity of a patient's symptoms. The severity of cerebral symptoms is at least partially related to the VT rate and a patient's underlying heart disease.

Adult↗
PubMed1984

Electrophysiologic testing in bundle branch block and unexplained syncope.

Thirty-two patients with bundle branch block and unexplained syncope underwent electrophysiologic testing, including programmed ventricular stimulation with up to triple extrastimuli. The infranodal conduction time (HV) was 70 ms or greater in 12 patients. Pathologic infranodal block during atrial pacing occurred in 2 patients. Unimorphic ventricular tachycardia (VT) was induced in 9 patients (28%) and polymorphic VT in 5 (16%). A permanent pacemaker was implanted in patients with infranodal block during atrial pacing and, generally, in patients with an HV of 70 ms or more. Patients with inducible unimorphic or sustained polymorphic VT were treated with an antiarrhythmic drug. The mean follow-up period was 19 +/- 14 months (+/- standard deviation). Three patients died suddenly: a noncompliant patient with inducible sustained VT; a patient with a normal electrophysiologic study treated empirically with quinidine for premature ventricular complexes; and a patient with an HV of 70 ms and no inducible VT treated with a permanent pacemaker. The actuarial incidence of sudden death was 10% at 45 months of follow-up. Only 2 patients had recurrent syncope; both had a normal electrophysiologic study. Approximately 50% of patients with bundle branch block and unexplained syncope who undergo electrophysiologic testing are found to have a clinically significant abnormality (HV of 70 ms or more, infranodal block during atrial pacing and inducible unimorphic VT), and some patients have more than 1 abnormality. Long-term management guided by the results of electrophysiologic testing generally is successful in preventing recurrent syncope.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗