Search PubMed⌕ Search

Biomedical subjects

F Morady

Publications and source records attributed to F Morady.

At least 307 records · Page 17Linked to original sources
PubMed1987

Effect of propranolol on ventricular rate during atrial fibrillation in the Wolff-Parkinson-White syndrome.

Atrial fibrillation was induced during an electrophysiology study in 10 patients with the Wolff-Parkinson-White (WPW) syndrome, after determination of baseline properties of the accessory atrioventricular (AV) connection; intravenous propranolol (0.2 mg/kg) was then administered. Atrial fibrillation terminated during the drug infusion in three patients, allowing determination of propranolol's effects on conduction and refractoriness during sinus rhythm, before atrial fibrillation was reinduced. In these three patients propranolol had no effect on refractoriness or conduction properties of the accessory AV connection during sinus rhythm. The mean ventricular rate during atrial fibrillation was slowed by 15-56 beats/min in six patients, had no effect on the mean rate in three patients, and markedly increased the ventricular rate (203 to 267 beats/min) in one patient. In this patient, 54% of QRS complexes during atrial fibrillation were narrow, compared to 0-25% in the other patients. Propranolol reduced the percentage of QRS complexes that were narrow from 13 +/- 16% to 1 +/- 2% (mean +/- standard deviation, p less than 0.05). We conclude that propranolol may slow the ventricular rate during atrial fibrillation in some patients with the WPW syndrome, probably by blocking the effects of adrenergic activation. However, propranolol should not be used in patients with the WPW syndrome who have atrial fibrillation, if most QRS complexes during atrial fibrillation are preexcited. When a large percentage of QRS complexes are narrow, propranolol may increase the ventricular rate, probably by eliminating concealed retrograde conduction in the accessory AV connection.

Adult↗
PubMed1987

Supraventricular tachycardia induced by swallowing: a case report and review of the literature.

A 64-year-old man who complained of palpitations brought on by swallowing was found to have short runs of paroxysmal supraventricular tachycardia (SVT) induced by swallowing. Electrophysiology studies suggested that the SVT was an automatic atrial tachycardia. An esophageal manometric study demonstrated that the tachycardia was coincident with relaxation of the upper esophageal spincter and preceded peristaltic activity in the esophageal body. Atropine and bethanechol did not affect the swallow-induced tachycardia. The patient's symptoms were controlled by verapamil and quinidine. After five months, these medications were discontinued, with no recurrence of symptoms. Based on analysis of ten prior cases and the present case, it appears that swallow-induced SVT generally occurs in men between the ages of 45-75 years who have no evidence of structural heart disease or an esophageal disorder. The SVT is usually either a nonsustained automatic atrial tachycardia or atrial fibrillation. The mechanism is conjectural, but the most likely possibility is a vagally-mediated neural reflex, probably involving a neurotransmitter other than acetylcholine.

Deglutition↗
PubMed1987

Catheter ablation of ventricular tachycardia with intracardiac shocks: results in 33 patients.

Catheter electrical ablation of ventricular tachycardia (VT) was attempted in 33 patients who had recurrent unimorphic VT refractory to 3.7 +/- 1.2 (mean +/- SD) antiarrhythmic drugs. Their mean age was 56 +/- 14 years. Twenty-two patients had coronary artery disease, six had other types of heart disease, and five had no structural heart disease. The mean left ventricular ejection fraction was 0.34 +/- 0.17. Thirty patients had only one documented morphologic type of spontaneous VT, whereas three patients had more than one. One to four shocks of 100 to 300 J each were delivered to the endocardial exit site of VT, as identified by endocardial activation mapping and pace-mapping. In each patient endocardial activation at the exit site of VT preceded the onset of the QRS complex (mean activation time -50 +/- 30 msec). Pace-mapping was possible in 26 patients, and in all but two patients the QRS complexes during VT and during pacing at the exit site of VT were very similar in at least 10 of 12 electrocardiographic leads. In 29 patients, shocks were delivered between an endocardial electrode (cathode) and a patch electrode on the chest wall (anode). Seven patients (including three who first received shocks using an external anode) whose VT originated in the septum received transseptal shocks between two electrodes positioned on either side of the septum. The procedure was successful in 15 patients (45%), who had no recurrence of VT either on no antiarrhythmic therapy or on the same regimen that was ineffective before ablation, over a follow-up period of 15.5 +/- 10 months (range 5 to 35). The ablation attempt was unsuccessful in 18 patients (55%). There were no significant differences in clinical and electrophysiologic variables between patients with and without a successful outcome. Seven nonfatal complications occurred in six patients: sustained nonclinical VT immediately after the shock, ventricular fibrillation on days 5 and 6 after ablation, neurologic deficits (n = 2), atrioventricular block (n = 2), and brachial artery thrombosis. In conclusion, catheter electrical ablation of VT has modest efficacy and is relatively safe in a selected group of patients who have predominantly one configuration of unimorphic VT.

Cardiac Catheterization↗
PubMed1987

Hemodynamic and electrophysiologic effects of encainide in patients with bundle branch block.

Electrophysiologic studies were performed in 6 consecutive patients with bundle branch block and organic heart disease. All were studied after intravenous (0.9 mg/kg) encainide and 3 of the 6 after 36-72 hours of oral encainide (50 mg every 6 hours). After intravenous encainide, mean H-Q increased from 51 +/- 20 msec to 58 +/- 25 msec (14% p less than or equal to .05). After oral encainide (3 patients) H-Q increased to 90 +/- 39 msec (56% p less than or equal to .05, compared to baseline). Programmed ventricular stimulation was performed in 5. In 1 patient without spontaneous ventricular tachycardia, tachycardia was non-inducible before and after encainide. Of 5 patients with spontaneous arrhythmia, 3 had ventricular tachycardia induced before and after intravenous encainide at mean cycle lengths of 287 +/- 130 msec and 407 +/- 261 msec, (not significant) respectively, while 1 had ventricular tachycardia induced only after encainide. Four patients began chronic treatment with oral encainide (2 patients with inducible rapid ventricular tachycardia after encainide were excluded). All suffered major adverse outcomes. One died suddenly after an electrophysiology study demonstrated inducible ventricular tachycardia, which occurred only after encainide. One experienced new syncope after baseline H-Q increased 75% after encainide. Two patients developed new sustained atrial tachycardias and 1 patient developed persistent ventricular tachycardia on encainide.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1986

Prognostic usefulness of programmed ventricular stimulation in idiopathic dilated cardiomyopathy without symptomatic ventricular arrhythmias.

Twenty-four patients, mean age 42 years, with idiopathic dilated cardiomyopathy (DC) and no history of symptomatic ventricular arrhythmias underwent right ventricular programmed stimulation with up to 3 extrastimuli. Ventricular tachycardia (VT) was induced in 8 patients and ventricular fibrillation (VF) in 2. The VT was unimorphic in 2 and polymorphic in 6. No significant differences were noted between patients in whom arrhythmias were inducible and and those in whom they were not with regard to age, symptomatic class, arrhythmia severity or hemodynamic indexes. Over a mean follow-up of 12 months, 4 patients died, 3 suddenly and 1 with progressive heart failure. Only 1 of the 3 who died suddenly had inducible VT. One other patient with induced sustained unimorphic VT later presented with spontaneous sustained VT similar in rate and configuration to induced VT. In conclusion, VT or VF may be induced in approximately 40% of patients with DC and no history of symptomatic VT or VF. Inducibility of polymorphic VT or VF does not correlate with clinical or hemodynamic variables or with the risk of sudden death. However, induction of unimorphic VT may predict later occurrence of spontaneous unimorphic VT.

Adult↗
PubMed1986

Immediate reproducibility of clinical and nonclinical forms of induced ventricular tachycardia.

This prospective study assessed the immediate reproducibility of clinical and nonclinical forms of ventricular tachycardia (VT) induced by programmed ventricular stimulation. Twenty-three clinical VTs were unimorphic and previously documented and 22 nonclinical VTs (17 polymorphic and 5 unimorphic) were induced in patients with either no documented or suspected history of VT, or documented VT that had a configuration different from that of the induced VT. The stimulation protocol included 1 to 3 ventricular extrastimuli, 2 drive cycle lengths, and 2 right ventricular stimulation sites. Each VT was induced on the first attempt, then the stimulation protocol was repeated twice in the drug-free state. After the first VT induction, 21 of 23 clinical VTs (91%) and 17 of 22 nonclinical VTs (77%) were reinduced on the second attempt. After 2 VT inductions, 21 of 21 clinical VTs (100%) and 15 of 17 nonclinical VTs (88%) were reinduced on the third attempt. The reinduction rates of the clinical and nonclinical VTs were not significantly different. Among the clinical VTs, the reproducibility of the induction technique was 81% after 1 induction and 88% after 2 inductions with the same technique. These results imply that acute drug testing can be reliably performed after 2 inductions but not 1 induction of clinical VT; reproducibility is not helpful in determining whether an induced VT is clinical or nonclinical; and changes in induction technique during drug testing should be interpreted with caution because changes may occur in the absence of drugs.

Adult↗
PubMed1986

Comparison of coupling intervals that induce clinical and nonclinical forms of ventricular tachycardia during programmed stimulation.

Coupling intervals of extrastimuli that induced 57 previously documented unimorphic ventricular tachycardias (VTs) were compared with coupling intervals that induced 57 episodes of polymorphic VT or ventricular fibrillation (VF) in patients without a documented or suspected history of polymorphic VT or VF. Programmed stimulation was performed with the patient in the drug-free state, with 1 to 3 extrastimuli and 2 basic drive cycle lengths (600 or 500 ms, and 400 ms) at 2 right ventricular sites; stimuli were twice diastolic threshold. The mean coupling intervals of the first, second and third extrastimuli that induced nonclinical VT/VF (241 +/- 19, 185 +/- 19 and 173 +/- 24 ms, respectively, mean +/- standard deviation) were significantly shorter than the corresponding coupling intervals that induced the clinical VTs (266 +/- 25, 228 +/- 32 and 214 +/- 27 ms, respectively, p less than 0.001 for each). Regardless of the basic drive cycle length, the shortest coupling interval required to induce a clinical VT was 180 ms. Depending on the drive cycle length, 29 to 70% of nonclinical VT/VF induced by 3 extrastimuli required a coupling interval of less than 180 ms to induce. Therefore, a lower limit of coupling intervals may be identified below which only nonclinical VT/VF is induced by programmed stimulation. Restriction of coupling intervals to this lower limit may allow for significant improvement in specificity without compromise in the sensitivity of programmed ventricular stimulation protocols.

Aged↗
PubMed1986

Interrelationships between serum levels of amiodarone, desethylamiodarone, reverse T3 and the QT interval during long-term amiodarone treatment.

The interrelationships between serum levels of amiodarone, desethylamiodarone, and reverse T3, and changes in the corrected QT interval (delta QTc) were examined in 22 patients during long-term treatment with amiodarone. At 1, 3, and 6 months of follow-up, the correlation coefficient between serum levels of amiodarone or desethylamiodarone and reverse T3 ranged from 0.01 to -0.2 (p greater than 0.4). At the same time intervals, the correlation coefficient between both amiodarone and desethylamiodarone levels and delta QTc ranged from 0.1 to -0.1 (p greater than 0.6), and the correlation coefficient between reverse T3 and delta QTc also ranged between 0.1 to -0.1 (p greater than 0.5). Substituting percent delta QTc for delta QTc also did not reveal a significant correlation. These data demonstrate that serum levels of reverse T3 cannot be used as a substitute for serum levels of amiodarone in monitoring patients being treated with amiodarone. The absence of a correlation between serum reverse T3 levels and delta QTc suggests that the delay in repolarization which occurs during amiodarone therapy is not secondary to an amiodarone-induced abnormality in thyroid hormone metabolism.

Adult↗
PubMed1986

Effect of programmed ventricular stimulation on myocardial lactate extraction in patients with and without coronary artery disease.

The arterial-coronary sinus lactate difference was measured in 17 patients after each step of a programmed ventricular stimulation protocol consisting of single, double, and triple extrastimuli, first at a basic drive cycle length of 600 msec, then at 400 msec, with an inter-train interval of 4 seconds. Four patients had no structural heart disease, four had an idiopathic dilated cardiomyopathy, and nine had coronary artery disease with a significant stenosis in at least one branch of the left coronary artery. Net myocardial lactate production during programmed ventricular stimulation was observed in three patients with coronary artery disease, but not in any patient without coronary artery disease. Among the patients who had coronary artery disease, net myocardial lactate production generally occurred in the patients who had more severe coronary artery disease. Exercise-induced ischemia, as demonstrated by a stress thallium-201 test, did not correlate with myocardial lactate production during programmed ventricular stimulation. Programmed ventricular stimulation, with a stimulation protocol typically used in many electrophysiology laboratories, is capable of inducing myocardial ischemia in at least some patients who have coronary artery disease. This finding suggests that myocardial ischemia may potentially influence the results of programmed ventricular stimulation in some patients with coronary artery disease.

Adult↗
PubMed1986

Plasma levels of immunoreactive atrial natriuretic factor increase during supraventricular tachycardia.

A significant diuretic and natriuretic response occurs during paroxysmal supraventricular tachycardia (SVT). Although the diuresis may be secondary to suppression of vasopressin secretion, the etiology of the natriuresis remains unexplained. To determine if atrial natriuretic factor (ANF) could contribute to the polyuric response during SVT, 10 patients were studied: five during spontaneous SVT and five during simulated SVT produced by rapid simultaneous atrial and ventricular pacing. Plasma immunoreactive ANF (IR-ANF) levels measured by radioimmunoassay were obtained at baseline (before and/or 24 to 48 hours after SVT) and after at least 15 minutes of SVT in all patients. During spontaneous and simulated SVT, IR-ANF was significantly elevated (mean +/- SE; 275 +/- 68 pmol/L) compared to baseline (28 +/- 7 pmol/L; p = 0.0036). Similar increases in IR-ANF were noted during both simulated and spontaneous SVT. To determine if this IR-ANF release was related to the increase in heart rate or the rise in right atrial pressure during SVT, IR-ANF levels were also measured in five patients with sinus tachycardia and in six patients with congestive heart failure. IR-ANF was significantly related to right atrial pressure (r = 0.93; p = 0.0009) but not to heart rate (r = 0.46). Thus, IR-ANF is elevated during SVT and may contribute to the natriuretic response. The stimulus to IR-ANF secretion during SVT appears to be related to the rise in right atrial pressure rather than to the increase in heart rate.

Adult↗
PubMed1986

Effects of magnesium sulfate on cardiac conduction and refractoriness in humans.

Magnesium has been used empirically for several decades in the treatment of atrial and ventricular arrhythmias in patients with normal and decreased serum magnesium levels. However, a systematic evaluation of the effects of magnesium on cardiac conduction and refractoriness in humans has not been described. In this study, the electrocardiographic and electrophysiologic effects of magnesium were determined in 10 patients with normal baseline serum magnesium and other electrolyte levels. Six grams of magnesium sulfate was administered intravenously over 6 minutes followed by a continuous infusion of 1 additional gram over 1 hour. Serum magnesium levels rose significantly from a baseline of 2.0 +/- 0.2 to 5.4 +/- 0.4 mg/dl (p less than 0.001). No significant change occurred in heart rate at rest, or in duration of the QRS complex or QT or QTc intervals during sinus rhythm. There were significant increases in sinus node recovery time (1,000 +/- 211 to 1,106 +/- 223 ms, p less than 0.01) and corrected sinus node recovery time (279 +/- 87 to 336 +/- 104 ms, p less than 0.05). Significant increases occurred in atrioventricular (AV) node conduction time during sinus rhythm (82 +/- 22 to 97 +/- 17 ms, p less than 0.02), in the atrial paced cycle length at which AV node Wenckebach block occurred (350 +/- 46 to 419 +/- 65 ms, p less than 0.01) and in the AV node relative refractory period (397 +/- 27 to 422 +/- 18 ms, p less than 0.05), functional refractory period (395 +/- 41 to 415 +/- 33 ms, p less than 0.05) and effective refractory period (306 +/- 67 to 338 +/- 38 ms, p less than 0.05).

Adult↗
PubMed1986

The plasma catecholamine response to ventricular tachycardia induction and external countershock during electrophysiologic testing.

Adrenergic activation during electrophysiologic study could potentially alter the electrophysiologic properties of the arrhythmia substrate. However, the catecholamine response to ventricular tachycardia induction and termination during electrophysiologic testing has to date not been quantitated. Therefore, in 13 patients undergoing electrophysiologic study, arterial plasma norepinephrine and epinephrine were measured before, during and 1, 3, 5, 10 and 15 minutes after ventricular tachycardia induced by programmed stimulation and terminated by a single 100 J external countershock. Sinus rate and the effective refractory period at the right ventricular apex at a basic drive cycle length of 400 ms were measured after the countershock at the same time intervals used for the catecholamine measurements. The mean ventricular tachycardia cycle length (+/- SD) was 187 +/- 30 ms, and the mean duration of ventricular tachycardia was 18 +/- 4 seconds. Plasma norepinephrine and epinephrine increased, respectively, from a baseline of 286 +/- 141 and 119 +/- 40 pg/ml to 770 +/- 330 (169%) and 597 +/- 467 pg/ml (402%), (p less than 0.01) at 1 minute after the countershock. The mean plasma norepinephrine and epinephrine levels during ventricular tachycardia and at times greater than 1 minute after the shock did not differ significantly from baseline levels. Sinus rate increased from a baseline of 74 +/- 13 to 103 +/- 26/min (39%) at 1 minute after the shock (p less than 0.05) and then returned to baseline.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1986

Acute and chronic effects of amiodarone on ventricular refractoriness, intraventricular conduction and ventricular tachycardia induction.

In eight patients, the right ventricular effective refractory period, rate-dependent changes in intraventricular conduction (as reflected by QRS duration during ventricular paced cycle lengths of 600 to 250 ms) and results of programmed ventricular stimulation were determined in the control state, 5 minutes after the intravenous infusion of 10 mg/kg body weight of amiodarone and after 2 months of treatment with oral amiodarone. The right ventricular effective refractory period was 230 +/- 30 ms (mean +/- SD) in the control study, 248 +/- 27 ms after intravenous amiodarone (p less than 0.001) and 296 +/- 26 ms after oral amiodarone (p less than 0.001). In the control state, QRS duration was constant at all paced cycle lengths. Intravenous amiodarone resulted in a rate-dependent prolongation of QRS duration. This rate-dependent prolongation was markedly accentuated by oral amiodarone in six patients who had an elevated serum level of reverse triiodothyronine (T3) after 2 months of oral treatment, but it was not more pronounced than the effects of intravenous amiodarone in two patients with a normal reverse T3 serum level after oral therapy. Both intravenous and oral amiodarone either suppressed or modified the induction of ventricular tachycardia by programmed stimulation in some patients, but in a discordant fashion. The relative effects of intravenous and oral amiodarone on ventricular refractoriness and conduction and on ventricular tachycardia induction did not correlate with serum amiodarone levels. Chronic amiodarone therapy results in a marked prolongation in ventricular refractoriness compared with the relatively small but significant increase that occurs after intravenous amiodarone.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1986

An analysis of post-pacing R-R intervals during atrial fibrillation.

Bursts of ventricular pacing at cycle lengths of 350-260 ms were introduced during atrial fibrillation in nine patients, and the post-pacing R-R intervals were compared to the R-R intervals of spontaneous QRS complexes. In eight of nine patients, the mean post-pacing R-R interval was 126-199 ms longer than the mean spontaneous R-R interval (p less than 0.005). Spontaneous runs of aberrantly conducted supraventricular complexes were recorded during atrial fibrillation in one patient. The mean R-R interval following the runs of aberrantly conducted supraventricular complexes was significantly longer than the mean R-R interval of spontaneous narrow QRS complexes (p less than 0.001), but not significantly different than the mean post-pacing R-R interval. The findings of this study suggest that the R-R interval that follows a wide-complex tachycardia during atrial fibrillation is unlikely to be of value in differentiating ventricular tachycardia from aberrantly conducted supraventricular complexes. Analysis of R-R intervals that follow bursts of ventricular pacing suggests that there is likely to be considerable overlap between the R-R intervals that follow runs of ventricular tachycardia and the spontaneous R-R intervals during atrial fibrillation. Furthermore, even when the post-tachycardia R-R interval clearly exceeds the longest spontaneous R-R interval during atrial fibrillation, this is still of little diagnostic value, because a long pause may occur after either a run of ventricular tachycardia or a run of aberrantly conducted QRS complexes of supraventricular origin.

Aged↗
PubMed1986

Effects of incremental doses of procainamide on ventricular refractoriness, intraventricular conduction, and induction of ventricular tachycardia.

The short-term effects of incremental doses of procainamide (7.5, 15, 22.5, and 30 mg/kg) on right ventricular effective refractory period, intraventricular conduction, and induction of ventricular tachycardia were determined in 31 patients who had a history of sustained, unimorphic ventricular tachycardia. QRS duration during incremental ventricular pacing was used as an index of rate-dependent changes in intraventricular conduction. The mean plasma procainamide concentrations corresponding to the incremental doses were 5.5 +/- 1.2 (+/- SD), 9.0 +/- 1.6, 12.6 +/- 2.2, and 16.3 +/- 3.2 mg/liter. Each incremental dose of procainamide up to a dose of 30 mg/kg resulted in a significant increment in right ventricular effective refractory period and each dose up to 22.5 mg/kg potentiated a rate-dependent prolongation of QRS duration. After the 7.5 mg/kg dose of procainamide, induction of ventricular tachycardia was suppressed in eight of 31 patients. After higher doses of procainamide, induction of ventricular tachycardia was suppressed in two additional patients. In three of 10 patients in whom the induction of ventricular tachycardia was suppressed by 7.5, 15, or 22.5 mg/kg of procainamide, sustained unimorphic ventricular tachycardia was again inducible after a higher dose of procainamide. In three of 31 patients, only nonsustained ventricular tachycardia was inducible after a 7.5 to 22.5 mg/kg dose of procainamide; however, in two of these three patients, sustained ventricular tachycardia was again inducible after administration of a higher dose of procainamide. In conclusion, during electropharmacologic testing with procainamide, it is worthwhile to test a dose of 7.5 mg/kg, because this dose is often effective in patients who respond to this drug. However, the results of this study indicate that procainamide may be effective in suppressing the induction of sustained ventricular tachycardia at a relatively low plasma concentration, but not at a higher plasma concentration. Therefore, during long-term therapy with procainamide it may be important to avoid plasma procainamide concentrations not only lower, but also higher than the concentration that results in the suppression of induction of tachycardia.

Acecainide↗