Search PubMed⌕ Search

Biomedical subjects

F Morady

Publications and source records attributed to F Morady.

At least 289 records · Page 16Linked to original sources
PubMed1988

Significance of ST segment depression during paroxysmal supraventricular tachycardia.

During paroxysmal supraventricular tachycardia, patients frequently experience chest pain and marked ST segment depression suggesting acute myocardial ischemia. The purpose of this study was to assess whether ST depression during supraventricular tachycardia is caused by myocardial ischemia as reflected by net myocardial lactate production. Twenty-five patients (14 men, 11 women) who had a history of paroxysmal supraventricular tachycardia and a mean age (+/- SD) of 38 +/- 14 years underwent electrophysiologic testing. Twenty-four of these patients had no evidence of coronary disease, whereas one patient had undergone previous coronary bypass surgery. Nineteen patients had orthodromic and six patients had atrioventricular node reentrant tachycardias. A 12 lead electrocardiogram and simultaneous femoral artery and coronary sinus blood samples for lactate determinations were obtained at baseline and at 5 and 10 min of supraventricular tachycardia. Mean baseline heart rate of 83 +/- 12 beats/min increased to 180 +/- 25 beats/min during supraventricular tachycardia. All patients had 1 to 8 mm of ST segment depression in 1 to 9 of the 12 leads. Chest pain occurred in 64% of patients during supraventricular tachycardia. Baseline myocardial lactate extraction was 28 +/- 13% with no significant change at 5 or 10 min of tachycardia. In contrast, in a comparison group of seven patients with known coronary artery disease, atrial pacing at 168 +/- 26 beats/min in five patients resulted in greater than or equal to 1 mm ST depression in 2 to 7 of the 12 leads and a change in lactate extraction from a baseline of 29 +/- 13% to -27 +/- 20% (p less than 0.05) indicating net myocardial lactate production.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

Antagonism of quinidine's electrophysiologic effects by epinephrine in patients with ventricular tachycardia.

The purpose of this study was to determine whether pharmacologically induced elevations in the plasma epinephrine concentration within reported physiologic limits alter the response to quinidine during electropharmacologic testing. Twenty-one patients with coronary artery disease and a history of unimorphic ventricular tachycardia were found to have inducible sustained unimorphic ventricular tachycardia that was suppressed by treatment with oral quinidine gluconate. Epinephrine was then infused at a rate of either 25 or 50 ng/kg per min and testing was repeated. These infusion rates of epinephrine were previously demonstrated to result in elevations of the plasma epinephrine concentration in the range of concentrations that occur during a variety of stresses. Quinidine significantly lengthened the ventricular refractory periods and the QRS duration at a ventricular pacing cycle length of 350 ms, which was used as an index of intraventricular conduction. Epinephrine partially or completely reversed the effects of quinidine on ventricular refractory periods, but had no effect on QRS duration. During electropharmacologic testing of quinidine, no ventricular tachycardia was inducible in 12 patients, and only nonsustained ventricular tachycardia, 8 to 48 beats in duration, was inducible in 9 patients. Retesting during infusion of epinephrine demonstrated inducible sustained unimorphic ventricular tachycardia in 2 of the 12 patients in whom quinidine had completely suppressed the induction of ventricular tachycardia and in 8 of the 9 patients in whom only nonsustained ventricular tachycardia had been inducible during testing of quinidine. In conclusion, physiologic elevations in the plasma epinephrine concentration may reverse quinidine-induced prolongation of ventricular refractoriness but not intraventricular conduction.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1988

Electrophysiologic demonstration of an atriofascicular accessory pathway.

Evidence of an atriofascicular accessory pathway has not been reported previously. In the patient presented in this case report, an electrophysiology study demonstrated a constant left bundle branch block QRS configuration despite varying degrees of ventricular preexcitation, in association with a constant artrioventricular interval during incremental atrial pacing and programmed atrial stimulation. The presence of an atrioventricular, nodoventricular, nodofascicular, and atrial-His accessory pathway was ruled out. The findings are best explained by the presence of an underlying left bundle branch block and an atriofascicular accessory pathway connecting the atrium and right bundle. The atriofascicular accessory pathway was a passive bystander during an atrial tachycardia and was not directly involved in the generation of the tachycardia. To our knowledge, this is the first report of an atriofascicular accessory pathway.

Bundle-Branch Block↗
PubMed1988

The maximum effect of an increase in rate on human ventricular refractoriness.

The purpose of this study was to determine the maximum shortening of ventricular refractoriness that occurs following an increase in rate and to quantitate the duration of ventricular pacing required to obtain this maximum shortening of refractoriness. The subjects of the study consisted of 41 patients who underwent a clinically indicated electrophysiologic study. Ventricular refractory periods were measured with an extrastimulus (S2) at basic cycle lengths of 600 and 400 ms by Method A (8 beat basic drive trains and 4 second intertrain paue and Method B (drive train duration of 3 minutes, then an S2 after every eighth basic drive beat, with no pause after the S2). In 23 subjects, the mean ventricular effective refractory period determined by Method B was 12 +/- 7 ms (+/- standard deviation) shorter than when determined by Method A at a basic drive cycle length of 600 ms (p less than 0.0001) and 33 +/- 9 ms shorter at a basic drive cycle length of 400 ms (p less than 0.001). In these 23 subjects, the drive train duration required for maximum shortening of ventricular refractoriness was estimated by counting the number of drive train beats preceding ventricular capture by an S2 inserted after every fourth basic drive beat at a coupling interval fixed at 5 ms longer than the ventricular effective refractory period determined in that subject by Method B. The mean number of basic drive beats preceding capture by S2 was 114 +/- 84 beats at a basic drive cycle length of 600 ms and 233 +/- 85 beats at a BDCL of 400 ms. In six subjects the ventricular effective refractory period was measured by Methods A and B before and after autonomic blockade with propranolol and atropine, and the amount of shortening in the ventricular effective refractory period with Method B was not affected by autonomic blockade. In conclusion, the basic drive train has a cumulative effect on ventricular refractoriness in humans, and a drive train duration substantially longer than 50 beats often is required to obtain the maximum shortening of ventricular effective refractory period after an increase in rate. Therefore, ventricular effective refractory periods determined conventionally using 8 beat drive trains and a 4 second intertrain pause often may be overestimates of the actual ventricular effective refractory period. The shortening of ventricular refractoriness with long drive train durations is probably related to a prolonged duration of pacing required to obtain a steady-state action potential duration after an increase in rate.

Action Potentials↗
PubMed1988

Accentuated antagonism between beta-adrenergic and vagal effects on ventricular refractoriness in humans.

The purpose of this study was to determine whether there is accentuated antagonism between sympathetic and vagal effects on ventricular refractory periods (VRPs) in humans. The effects of 0.04 mg/kg of atropine on the right ventricular effective and functional refractory periods were determined in the setting of beta-adrenergic blockade by propranolol (0.15 mg/kg loading dose, then 0.1 mg/min continuous infusion, group 1) and in the setting of beta-adrenergic stimulation by 25 or 50 ng/kg/min isoproterenol (groups 2 and 3, respectively). Groups 4 to 6 served as control groups. In group 4, VRPs were determined on three occasions separated by 10 min each in the absence of drug. VRPs also were determined on two occasions after infusion of propranolol (group 5) or 25 ng/kg/min of isoproterenol (group 6). Groups 1 to 4 consisted of 10 subjects each, and groups 5 and 6 consisted of five subjects each. VRPs were determined with the use of basic drive cycle lengths of 600, 500, 400, and 350 msec. Because of sinus tachycardia, sufficient data for comparison of groups 1 to 3 were available only at drive cycle lengths of 400 and 350 msec. Atropine significantly shortened the VRPs in groups 1 to 3, but the magnitude of atropine's effects in group 3 (5.3% to 5.8% shortening at drive cycle length of 350 msec) was significantly greater than in group 1 (2.6% to 3.0% shortening, p less than .05) Data from the control groups demonstrated that there was no effect of time on measurement of VRPs either in the drug-free state or in the presence of propranolol or isoproterenol. The results of this study indicate that cholinergic tone lengthens VRPs in the absence of background sympathetic activity and that this lengthening of VRPs may become accentuated during beta-adrenergic stimulation.

Adult↗
PubMed1988

Transvenous catheter ablation of a posteroseptal accessory pathway in a patient with coexistent posteroseptal and right-sided accessory pathways.

Transvenous catheter ablation techniques have recently been used successfully in blocking posteroseptal accessory pathways in patients with Wolff-Parkinson-White syndrome (WPWS). We report the case of a patient in the People's Republic of China who had WPWS and posteroseptal and right anterolateral accessory pathways, and who had failed to respond to conventional antiarrhythmic drug therapy. The posteroseptal accessory pathway was ablated successfully. During 23 months of follow-up there were no complications; this led us to conclude that this technique can be used to achieve successful long-term ablation of this accessory pathway. This technique obviates the need for drug therapy and direct surgical ablation; it offers, as well, the advantages of shorter hospitalization, lower cost, a much shorter convalescence, and less discomfort to the patient.

Journal Article↗
PubMed1987

Value of programmed ventricular stimulation in presumed carotid sinus syndrome.

This study determines the results of programmed stimulation in patients with syncope or near-syncope presumed to have the carotid sinus syndrome based on the finding of carotid sinus hypersensitivity and the absence of any other apparent cause for syncope or near-syncope after clinical evaluation. Fourteen patients had coronary artery disease, 1 had dilated cardiomyopathy and 18 patients did not have structural heart disease. Programmed simulation was performed at 2 basic drive cycle lengths and 2 right ventricular sites with 1 to 3 extrastimuli. Sustained unimorphic ventricular tachycardia (VT) was induced in 5 of 15 patients who had structural heart disease, and in none of the 18 patients who did not (p less than 0.05). Polymorphic VT or ventricular fibrillation (VF) was induced in 5 of 15 patients (33%) who had structural heart disease, and in 5 of 18 patients (27%) who did not (p greater than 0.05). Patients who had inducible unimorphic VT were treated with antiarrhythmic drugs that suppressed the induction of VT, and 4 of 5 patients also received a pacemaker; no patient had a recurrence of syncope during follow-up. Patients who had inducible polymorphic VT and VF (n = 10) or no inducible VT (n = 18) received treatment directed at only carotid sinus syndrome. Two patients with inducible VT or VF and 1 patient without inducible VT had recurrent syncope during follow-up, but none had cardiac arrest or died suddenly.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1987

Effects of chronic amiodarone therapy on ventricular tachycardia induced by programmed ventricular stimulation.

Several studies have reported upon the inducibility of ventricular tachycardia (VT) with programmed ventricular stimulation (PVS) during chronic amiodarone therapy; however, few studies have systematically described and compared the morphology, duration, and cycle length of VT induced by PVS before and after amiodarone. In this study, 26 patients with symptomatic VT or ventricular fibrillation were evaluated by PVS by means of one to three extrastimuli (ES) before treatment and after 2 months of amiodarone therapy. Before amiodarone, sustained unimorphic VT was induced in 21 patients (group A) and symptomatic, nonsustained VT was induced in five patients (group B). After 65 +/- 8 days of amiodarone (total dose 64.5 +/- 8.9 gm, mean +/- S.D.), 15 of 21 patients (71%) in group A had sustained VT, five patients (24%) had nonsustained VT, and one patient had no VT induced. Four of five patients (80%) in group B had sustained VT and one patient had no VT induced. VT was induced by the same or by fewer number of ES in 79% of cases. When the morphologies of the VT induced before and after amiodarone were compared, the morphology of VT induced after amiodarone was the same in only 8 of 24 patients (33%), unimorphic but different in 14 patients (58%), and polymorphic in the remaining two patients. No correlation was found between the serum concentrations of amiodarone, desethylamiodarone, tetraiodothyronine, triiodothyronine, or reverse triiodothyronine, and similarities or differences in VT morphology, VT cycle length, or the relative number of ES required to induce VT after treatment with amiodarone.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1987

The interplay between endogenous catecholamines and induced ventricular tachycardia during electrophysiologic testing.

Plasma epinephrine and norepinephrine concentrations were measured before, during, and shortly after induced ventricular tachycardia (VT) in 22 selected patients. Sustained, unimorphic VT was induced by programmed ventricular stimulation and terminated after 45 to 384 seconds by overdrive pacing in all patients. In no patient did VT result in loss of consciousness. The baseline plasma catecholamine concentrations did not correlate with the baseline right ventricular effective refractory period, the cycle length of induced VT, or the number of extrastimuli required to induce VT. Induced VT was not associated with a significant increase in the mean plasma epinephrine concentration. In contrast, the plasma norepinephrine concentration increased from a mean baseline level of 317 +/- 136 pg/ml (mean +/- standard deviation) to 418 +/- 220 pg/ml during VT (p less than 0.01) and increased further to 569 +/- 387 pg/ml shortly after VT (p less than 0.01). The plasma norepinephrine concentration shortly after VT correlated with the rate and duration of VT and with the magnitude of decrease in mean blood pressure during VT (p less than 0.05 for each). In eight patients the same configuration of VT was induced on two sequential attempts; in five patients the same number of extrastimuli were required for the second induction of VT as for the first, whereas in three patients fewer extrastimuli were required. Plasma catecholamine concentrations were not higher in patients requiring fewer extrastimuli to induce the second episode of VT, either shortly after the first episode of VT or shortly after the second episode of VT.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1987

The hemodynamic effects of ventricular pacing with and without atrioventricular synchrony in patients with normal and diminished left ventricular function.

The relative hemodynamic effects of heart rate, inotropic state, and atrioventricular (AV) synchrony during ventricular pacing were evaluated in 10 patients with normal left ventricular ejection fraction (LVEF) (0.66 +/- 0.07, mean S.D.) and in eight patients with a diminished LVEF (0.34 +/- 0.18). Hemodynamics were measured at AV intervals of 130, 0, and -130 msec during ventricular pacing at a baseline rate that was 10 pulses/min greater than the resting heart rate, at 130 pulses/min alone, and at 130 pulses/min during continuous intravenous infusion of dobutamine. During baseline ventricular pacing and during ventricular pacing at 130 pulses/min with and without dobutamine, both groups of patients had a significant decrease in cardiac index, stroke volume index, and stroke work index when the AV pacing interval was decreased from 130 to 0 msec. The observed decrease in these three hemodynamic variables was similar when patients with diminished LVEF were compared to patients with normal LVEF. No further significant decrease in cardiac index, stroke volume index, and stroke work index occurred in either group when the AV interval was changed from 0 to -130 msec during baseline ventricular pacing or during ventricular pacing at 130 with and without dobutamine. Beneficial hemodynamic effects occur during ventricular pacing when AV synchrony is maintained at resting heart rates and during increases in heart rate and inotropic state in patients with normal and diminished LVEF.

Adult↗
PubMed1987

Natural history and determinants of conduction defects following coronary artery bypass surgery.

Ninety-three consecutive patients undergoing coronary artery bypass grafting (CABG) were followed prospectively to ascertain the natural history and determinants of new postoperative conduction defects. Each patient was followed in the postoperative period with serial electrocardiograms and continuous monitoring. In the last 70 patients, a technetium pyrophosphate scan was obtained 48 to 72 hours after operation. Postoperatively, new bundle-branch or fascicular block developed in 42 patients (45%) and third-degree atrioventricular (AV) block, in 4 (4%). The occurrence was compared with patient age, preoperative bundle-branch block or fascicular block, number of diseased arteries, number of bypassed arteries, total time of cardiopulmonary bypass, aortic cross-clamping time, occurrence of a preoperative or perioperative myocardial infarction, and presence of disease in the left anterior descending or right coronary artery. Only the number of bypassed arteries, the total time of cardiopulmonary bypass, and the aortic cross-clamping time were related to the development of postoperative conduction defects (all, p less than .05). The conduction defect resolved partially or completely by the time of hospital discharge in 54% of patients. In the 4 patients with third-degree AV block, AV block resolved on postoperative day 2 in 1 patient and resolved transiently for up to 5 days or persisted in 3 patients. At two months of follow-up, all 3 patients discharged in third-degree AV block with a permanent pacemaker were no longer in AV block. In conclusion, following CABG, the occurrence of new AV conduction defects is related to the number of vessels bypassed, the cardiopulmonary bypass pump time, and the aortic cross-clamping time.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiopulmonary Bypass↗
PubMed1987

Differentiation of ventricular tachycardia from supraventricular tachycardia with aberration: value of the clinical history.

The purpose of this study was to assess whether the clinical history is of any value in the differentiation in the emergency department of ventricular tachycardia (VT) from supraventricular tachycardia (SVT) with aberration. The records of 84 patients who presented with a wide-complex tachycardia and who were able to provide a history were reviewed. The wide-complex tachycardia was proven by a later electrophysiologic study to be VT in 62 patients and SVT with aberration in 22 patients. History of prior myocardial infarction, history of congestive heart failure, and history of recent angina pectoris all had positive predictive values for VT of greater than 95%, but had sensitivities of 66%, 24%, and 24%, respectively. Age greater than 35 years had a sensitivity of 92% and a positive predictive value of 85% for VT. None of the clinical characteristics was strongly predictive for SVT; the best was age less than or equal to 35 years, which had a positive predictive value of 70%. We conclude that clinical variables may be helpful in the emergency department diagnosis of wide-complex tachycardias. If a patient with a wide-complex tachycardia has a history of myocardial infarction, congestive heart failure, or recent angina pectoris, the tachycardia has a high likelihood of being ventricular in origin. However, there are no clinical variables that are highly predictive of SVT with aberration.

Adult↗
PubMed1987

Electrophysiologic testing in patients with unexplained syncope: clinical and noninvasive predictors of outcome.

To assess whether the level of risk of having significant electrophysiologic abnormalities can be determined, 29 clinical variables were analyzed in 104 patients with unexplained syncope who underwent electrophysiologic testing. A positive electrophysiologic study was defined as: a sinus node recovery time greater than or equal to 3 seconds; HV interval greater than or equal to 100 ms; infranodal block during atrial pacing; unimorphic ventricular tachycardia; and supraventricular tachycardia associated with hypotension. Thirty-one patients had a positive study, with inducible ventricular tachycardia being the most common finding (71% of positive studies). A left ventricular ejection fraction less than or equal to 0.40 was the most powerful predictor of a positive electrophysiologic study (p less than 0.00001), followed by the presence of bundle branch block (p less than 0.00003), coronary artery disease (p less than 0.0003), remote myocardial infarction (p less than 0.00006), use of type 1 antiarrhythmic drugs (p less than 0.00003), injury related to loss of consciousness (p less than 0.01) and male sex (p less than 0.01). A negative electrophysiologic study was associated with an ejection fraction greater than 0.40 (p less than 0.00001), the absence of structural heart disease (p less than 0.00001), a normal electrocardiogram (ECG) (p less than 0.0001) and normal ambulatory ECG monitoring (p less than 0.0001). The probability of a negative study increased as the number and duration of syncopal episodes increased.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1987

Coexistent Mahaim and Kent accessory connections: diagnostic and therapeutic implications.

Six patients with coexistent Mahaim and Kent accessory connections are described. Two had left nodoventricular Mahaim connections, the first reported cases demonstrating these findings. In neither were the left-sided Mahaim connections components of a tachycardia and their presence was incidental. In two of four with nodoventricular connections, associated atrioventricular (AV) node conduction and coexistent posteroseptal accessory pathways were found. One of these had the unusual finding of a right-sided Mahaim connection arising from a "fast" AV node pathway. In only one patient did the tachycardia incorporate the Mahaim connection. In this patient, anterograde conduction during tachycardia occurred over a right nodoventricular connection whereas retrograde conduction occurred through a concealed right free wall Kent connection. Two patients had fasciculoventricular connections that were associated with either septal (one patient) or left free wall (one patient) Kent connections. The latter also had evidence of enhanced AV node conduction. This report is unique in that it describes in detail two patients with left nodoventricular connections (Mahaim) inserting in or near the left posterior fascicle. Combined Kent and Mahaim connections, present in the six patients, appear to occur in approximately 5% of patients with the Wolff-Parkinson-White syndrome. Precise identification of bypass connections critical for reentrant circuits is essential for intelligent application of treatment options.

Adult↗
PubMed1987

Determinants of QRS alternans during narrow QRS tachycardia.

This study was designed to prospectively determine the incidence of QRS alternans during various types of narrow QRS tachycardia and to clarify the determinants of QRS alternans. An electrophysiologic study was performed in 28 consecutive patients with a narrow QRS tachycardia. Persistent QRS alternans was observed in 6 (43%) of 14 patients during orthodromic reciprocating tachycardia, 5 (71%) of 7 patients during atrial tachycardia and 3 (43%) of 7 patients during atrioventricular (AV) node reentrant tachycardia. Incremental atrial pacing during sinus rhythm resulted in QRS alternans in patients who had QRS alternans during tachycardia, unless the shortest pacing cycle length associated with 1:1 AV conduction exceeded the tachycardia cycle length. In patients without QRS alternans during narrow QRS tachycardia, incremental atrial pacing during sinus rhythm resulted in persistent QRS alternans in five patients in whom the shortest pacing cycle length associated with 1:1 AV conduction was 60 to 180 ms less than the tachycardia cycle length. In an additional 20 patients without a narrow QRS tachycardia, persistent QRS alternans was observed during incremental atrial pacing in 11 (55%) of the patients. In six of six patients who had QRS alternans during abrupt rapid atrial pacing, QRS alternans was not observed when the same pacing rates were achieved gradually. Among the patients with narrow QRS tachycardia, the mean tachycardia cycle length in those who had QRS alternans (mean +/- SD 288 +/- 44 ms) was significantly shorter than in those who did not (369 +/- 52 ms, p less than 0.001). The presence of QRS alternans was not related to the tachycardia mechanism, relative or functional refractory period of the His-Purkinje system (at a drive cycle length of 500 ms), age, presence of structural heart disease, direction of input into the AV node or concealed retrograde conduction in the His-Purkinje system. In conclusion, QRS alternans during narrow QRS tachycardias is a rate-related phenomenon that depends on an abrupt increase to a critical rate and is independent of the tachycardia mechanism.

Cardiac Pacing, Artificial↗
PubMed1987

Role of myocardial ischemia during programmed stimulation in survivors of cardiac arrest with coronary artery disease.

The role of ischemia in the induction of ventricular tachycardia during programmed stimulation was studied in 19 patients who survived a cardiac arrest and were found to have a significant stenosis in at least one branch of the left coronary artery. The arterial-coronary sinus lactate difference was measured during electrophysiologic testing, before the induction of ventricular tachycardia. Ventricular tachycardia was induced in 15 patients; it was sustained and unimorphic in 6 patients and polymorphic in 9. Myocardial ischemia, as reflected by net myocardial lactate production, was present within 60 seconds before the induction of ventricular tachycardia in 8 of the 15 patients with inducible ventricular tachycardia. In 9 of the 15 patients, programmed stimulation was repeated after a 15 minute rest period, with the same coupling intervals that had induced ventricular tachycardia previously. Net myocardial lactate production was not present in any patient during this repeat attempt. In three patients without evidence of ischemia during the first induction of ventricular tachycardia, the arrhythmia was induced again by the specific coupling intervals that had induced it previously. However, in five of six patients with net myocardial lactate production during the first induction of ventricular tachycardia, the same coupling intervals that had induced the arrhythmia in the presence of ischemia no longer induced it in the absence of ischemia. The results of this study suggest that myocardial ischemia may be a requirement for the induction of ventricular tachycardia in some patients with coronary artery disease who survive a cardiac arrest.

Angioplasty, Balloon↗