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Biomedical subjects

F Morady

Publications and source records attributed to F Morady.

At least 37 records · Page 2Linked to original sources

Atrioventricular node properties in patients with accessory pathways.

A study during the era of surgical ablation suggested that atrioventricular (AV) nodal conduction is faster in patients with accessory pathways than in controls. In the present study, AV nodal characteristics were studied in 30 patients who underwent radiofrequency ablation of an accessory pathway and compared to 23 control patients. Sinus cycle length, AH and HV intervals, AV block cycle length, ventriculoatrial (VA) block cycle length, AV nodal effective refractory period, and VA effective refractory periods were measured in control and postablation accessory pathway patients before and after autonomic blockade with 0.04 mg/kg of atropine and 0.2 mg/kg of propranolol. The mean sinus cycle length in the control and accessory pathway groups did not differ significantly at baseline (798 +/- 211 and 766 +/- 156 msec, respectively) or after autonomic blockade (654 +/- 98 and 649 +/- 108 msec, respectively). The mean AH interval in the accessory pathway group (77 +/- 15 msec) was significantly shorter than in the control group (91 +/- 22 msec; p < 0.05) at baseline; however, there was no difference after autonomic blockade. No other significant differences were observed between the accessory pathway and control groups. These results demonstrate that AV nodal properties of patients with accessory pathways are not significantly different from controls and suggest that previously reported differences may have been due to selection bias.

Adult

Comparison of atrial-His intervals in patients with and without dual atrioventricular nodal physiology and atrioventricular nodal reentrant tachycardia.

The purpose of this study was to compare the atrial-His intervals generated during programmed atrial stimulation in patients with and without dual atrioventricular nodal physiology and with and without inducible atrioventricular nodal reentrant tachycardia. Programmed atrial stimulation at a basic-drive cycle length of 500 to 600 msec was performed in 180 patients. The minimum atrial-His interval was defined as the atrial-His interval of the basic-drive beats. The maximum atrial-His interval was defined as the longest A2H2 interval. The criterion for dual atrioventricular nodal physiology was an increment of 50 msec in the A2H2 interval in association with a 10 msec decrement in the A1A2 interval. The minimum atrial-His interval was significantly shorter (106 +/- 34 msec vs 116 +/- 29 msec; p < 0.05) and the maximum atrial-His interval significantly longer (304 +/- 101 msec vs 222 +/- 56 msec; p < 0.001) in the 87 patients who had atrioventricular nodal reentry than in the 93 patients who did not. Among the 87 patients who had atrioventricular nodal reentry, the maximum atrial-His interval was significantly longer in 53 patients who had dual atrioventricular nodal physiology than in 34 patients who did not (340 +/- 105 msec vs 249 +/- 62 msec; p < 0.001). Among the 66 patients who had dual atrioventricular nodal physiology, the maximum atrial-His interval was significantly longer in 53 patients who had atrioventricular nodal reentry than in 13 patients who did not (340 +/- 105 msec vs 268 +/- 61 msec; p < 0.01). The insensitivity of the conventional dual atrioventricular nodal physiology criterion for the detection of dual atrioventricular nodal pathways is in part attributable to a lesser degree of slowing of conduction in the slow pathway relative to the fast pathway in some patients who have atrioventricular nodal reentry. The inability to demonstrate atrioventricular nodal reentry despite the presence of dual atrioventricular nodal physiology in some persons may be attributable in part to an inadequate degree of conduction delay in the slow pathway.

Atrioventricular Node

Comparison of the ages of tachycardia onset in patients with atrioventricular nodal reentrant tachycardia and accessory pathway-mediated tachycardia.

Atrioventricular nodal reentrant tachycardia and accessory pathway-mediated tachycardia may have different ages of tachycardia onset. Symptom onset data were obtained in 519 patients (atrioventricular nodal reentrant tachycardia, 231, accessory pathway-mediated tachycardia, 288). The mean age of the patients at the time of evaluation was 47 +/- 17 years (atrioventricular nodal reentrant tachycardia) and 37 +/- 15 years (accessory pathway-mediated tachycardia). The mean age of symptom onset was 32 +/- 18 years for atrioventricular nodal reentrant tachycardia and 23 +/- 14 years for accessory pathway-mediated tachycardia. A significantly greater proportion of patients with atrioventricular nodal reentrant tachycardia had the initial onset of symptoms after the age of 20 years (atrioventricular nodal reentrant tachycardia, 67% vs accessory pathway-mediated tachycardia, 41%, p < 0.001). In summary, there is a different mean age of symptom onset for patients with atrioventricular nodal reentrant tachycardia and accessory pathway-mediated tachycardia.

Adult

Evaluation and extraction of the Accufix atrial J lead.

The Accufix (Telectronics Pacing Systems, Englewood, Colo.) atrial active fixation pacemaker lead has a preformed J stiff retention wire that can fracture and erode through the atrium. We screened 85 patients with digital fluoroscopy and detected 18 (21%) lead fractures. Fourteen (16%) leads were successfully extracted by percutaneous techniques. The mean time for extraction and placement of a new atrial lead was 109 +/- 53 min, and a lead > 1 year old but not in the presence of a fracture was associated with a significantly longer extraction time. There were two extraction complications. One patient had a fever following the extraction, and one patient had a focal sensory deficit 1 week after the extraction probably caused by a paradoxical embolus. Standard percutaneous extraction tools can be used for successful and safe removal of a fractured Accufix lead.

Aged

Use of isoproterenol during programmed ventricular stimulation in patients with coronary artery disease and nonsustained ventricular tachycardia.

Twenty-three consecutive patients (20 men and 3 women) with coronary artery disease and nonsustained ventricular tachycardia (VT) in whom sustained VT was not inducible in a baseline electrophysiology test underwent repeated testing during isoproterenol infusion to determine the inducibility of sustained monomorphic VT. After the baseline study, each patient received a 2 to 4 microgram/min infusion of isoproterenol (mean 2.5 +/- 0.8 microgram/min). The sinus cycle length shortened by a mean of 29% +/- 9% and programmed stimulation was repeated. Nineteen patients had no inducible sustained, monomorphic VT, two patients had only inducible nonsustained VT, and two patients had ventricular fibrillation. Patients were followed up for 10 to 20 months (mean 14.4 +/- 2.9 months) and had no syncope, sustained monomorphic VT, or sudden death. Isoproterenol infusion during programmed stimulation in patients with coronary heart disease and nonsustained VT does not facilitate the induction of sustained monomorphic VT.

Aged

Slow pathway ablation in patients with documented but noninducible paroxysmal supraventricular tachycardia.

OBJECTIVES: The purpose of this study was to assess the clinical efficacy of radiofrequency ablation of the slow pathway in patients with documented but noninducible paroxysmal supraventricular tachycardia (PSVT) who have evidence of dual atrioventricular (AV) node pathways. BACKGROUND: Patients with a documented history of PSVT at times do not have inducible PSVT in the electrophysiology laboratory. Because dual AV node pathways serve as the substrate for AV node reentrant tachycardia (AVNRT), ablation of the slow pathway potentially may be useful in these patients. METHODS: The subjects in this prospective study were seven consecutive patients who underwent an electrophysiologic procedure because of documented PSVT and were found to have dual AV node physiology or inducible single AV node echo beats, but no inducible PSVT despite the administration of isoproterenol and atropine. Their mean (+/- SD) age was 33 +/- 13 years, and they had been symptomatic for 12 +/- 12 years. The frequency of the episodes of PSVT ranged from > or = 1/day to 1/month. The rate of the documented episodes ranged from 170 to 260 beats/min, and discrete P waves were not apparent. Slow pathway ablation was performed with 9 +/- 4 applications of radiofrequency energy using a combined anatomic and electrogram mapping approach. RESULTS: All evidence of dual AV node pathways was eliminated in six patients, and dual AV node physiology remained present in one patient. During a mean follow-up period of 15 +/- 10 months (range 8 to 27), no patient had a recurrence of symptomatic tachycardia (success rate 95% confidence interval 65% to 100%). CONCLUSIONS: Slow pathway ablation may be clinically useful in patients with documented but noinducible PSVT who have evidence of dual AV node pathways.

Adult

2:1 atrioventricular block during atrioventricular node reentrant tachycardia.

OBJECTIVES: The purpose of this study was to determine the incidence and to clarify the mechanism of 2:1 atrioventricular (AV) block during AV node reentrant tachycardia induced in the electrophysiology laboratory. BACKGROUND: In patients with 2:1 AV block during AV node reentrant tachycardia, the absence of a His bundle potential in the blocked beats has been considered evidence of intranodal, lower common pathway block. METHODS: In consecutive patients with AV node reentrant tachycardia, the incidence of 2:1 AV block and the response to atropine and a single ventricular extrastimulus was observed. RESULTS: Persistent 2:1 AV block occurred in 13 of 139 patients with AV node reentrant tachycardia. A His bundle deflection was present in the blocked beats in eight patients and absent in five. Patients with 2:1 AV block had a shorter tachycardia cycle length than did patients without such block (mean +/- SD 312 +/- 32 vs. 353 +/- 55 ms, p < 0.01). Atropine did not alter the 2:1 block in any patient. In every patient, a single ventricular extrastimulus introduced during the tachycardia converted the 2:1 block to 1:1 conduction. CONCLUSIONS: The incidence of induced 2:1 AV block during AV node reentrant tachycardia is approximately 10%. The lack of a response to atropine and the consistent conversion of 2:1 block to 1:1 conduction by a ventricular extrastimulus indicate that, regardless of the presence or absence of a His bundle potential in blocked beats, 2:1 block during AV node reentrant tachycardia is due to functional infranodal block.

Adult

Incidence of lead system malfunction detected during implantable defibrillator generator replacement.

Implantable cardioverter-defibrillator (ICD) generator replacement due to a depleted battery is a frequently performed procedure. The frequency with which sensing and defibrillation system failures are identified during device replacement procedures has not been previously described. Therefore, the purpose of this study was to prospectively determine the frequency of lead system malfunction detected at the time of device replacement in 55 consecutive patients undergoing ICD generator replacement. The mean age of the patients was 63 +/- 10 years and 40 of them were men. Forty-nine patients had an epicardial lead system, and six patients had a nonthoracotomy lead system. Four [7%] of these 55 patients were noted to have previously undetected lead system failure, either sensing (n = 3) or defibrillation (n = 1), necessitating system revision. The lead systems that failed were 40 +/- 6 months old (33-49 months). In summary, during ICD generator replacement, previously undetected problems with sensing or defibrillation may be identified in approximately 10% of patients. Therefore, a comprehensive evaluation of the sensing and the defibrillation functions should be an essential component of the ICD generator replacement procedure.

Defibrillators, Implantable

Temperature and impedance monitoring during slow pathway ablation in patients with AV nodal reentrant tachycardia.

INTRODUCTION: Successful radiofrequency ablation of an accessory pathway has been demonstrated to be associated with an electrode-tissue interface temperature of approximately 60 degrees C or an impedance change of -5 to -10 omega. However, the temperature and impedance changes associated with ablation of AV nodal reentrant tachycardia (AVNRT) using the slow pathway approach have not been reported. Therefore, the purpose of this study was to define the temperature and impedance changes achieved during ablation of AVNRT: METHODS AND RESULTS: The study included 35 consecutive patients with AVNRT undergoing radiofrequency ablation of the slow pathway with a fixed power output of 32 W, and using a catheter with a thermistor bead embedded in the distal 4-mm electrode. The procedure was successful in each patient. The steady-state electrode-tissue interface temperature during successful applications of energy was 48.5 +/- 3.3 degrees C (range 42 degrees to 56 degrees C), and the steady-state temperature during ineffective applications was 46.8 degrees +/- 5.5 degrees C (P = 0.03). The mean impedance change during all applications of energy was -1.4 +/- 2.8 omega, and did not differ significantly during effective and ineffective applications. Coagulum formation resulted during five applications (2.7%) in two patients (5.7%). There were no recurrences during 114 +/- 21 days of follow-up. CONCLUSIONS: Successful ablation of AVNRT using fixed power output is achieved at an electrode-tissue interface temperature of approximately 48 degrees C and is associated with a drop in impedance of 1 to 2 omega. These findings suggest that slow pathway ablation requires less heating at the electrode-tissue interface than does accessory pathway or AV junction ablation.

Adult

The mechanisms responsible for lack of reproducible induction of atrioventricular nodal reentrant tachycardia.

INTRODUCTION: AV nodal reentrant tachycardia (AVNRT) is not always reproducibly inducible. The purpose of this study was to determine the mechanisms responsible for the lack of reproducible induction of AVNRT. METHODS AND RESULTS: The induction of AVNRT was assessed with atrial burst pacing, and with atrial and ventricular programmed stimulation, each with one and two extrastimuli, in 103 patients with AVNRT. The stimulation protocol was repeated 10 times in the baseline state, during isoproterenol infusion, and after atropine administration, or until AVNRT was induced in 7 of 10 attempts. The mechanisms responsible for < 7 of 10 inductions were classified as: (1) the inability to achieve critical AH prolongation; (2) fast pathway block; and (3) slow pathway block. The induction endpoint was achieved in 90 patients: 55 in the baseline state, 34 during isoproterenol infusion, and 1 after atropine. The mechanism of noninducibility in the baseline state (n = 48) was the inability to achieve a critical AH interval in 20%, fast pathway block in 49%, and slow pathway block in 31% (P = 0.02). During isoproterenol administration (n = 14) and after atropine administration (n = 13), the three mechanisms were equally responsible for nonreproducible induction of AVNRT. CONCLUSIONS: The induction of AVNRT is poorly reproducible in approximately 10% of patients. In the baseline state, the most common reason for the inability to reproducibly induce AVNRT is fast pathway block. In the presence of isoproterenol or atropine, each of the three mechanisms was equally responsible for noninducibility of AVNRT.

Adrenergic beta-Agonists

Randomized comparison of two techniques for titrating power during radiofrequency ablation of accessory pathways.

INTRODUCTION: The purpose of this study was to prospectively compare the value of impedance and temperature monitoring during accessory pathway ablation. Temperature and impedance monitoring can be used during radiofrequency ablation of accessory pathways to titrate power to achieve adequate but not excessive tissue heating. METHODS AND RESULTS: One hundred thirty-two patients with a single accessory pathway were randomly assigned to undergo ablation using either impedance monitoring or temperature monitoring. During impedance monitoring, the endpoint for titration of power was a 5- to 10-omega decrease in the measured impedance while for temperature monitoring the endpoint was to achieve a temperature of 58 degrees to 62 degrees C. Two protocols were used. In protocol 1 (90 patients), impedance monitoring was performed with a nonthermistor catheter and temperature monitoring was performed with a thermistor catheter. In protocol 2 (42 patients), a thermistor catheter was used in all patients. In protocol 1, the success rate (93% vs 93%; P = 1.0), ablation procedure duration (57 +/- 56 vs 41 +/- 41 min), fluoroscopy time (48 +/- 29 vs 41 +/- 23 min; P = 0.3), number of applications (6.2 +/- 4.7 vs 5.7 +/- 4.6; P = 0.8), and the number of applications associated with coagulum formation (0.1 +/- 0.3 vs 0.3 +/- 0.6; P = 0.1) were similar in the two groups. In protocol 2, as in protocol 1, there were no differences in the success rate (91% vs 95%; P = 1.0), ablation procedure duration (49 +/- 37 vs 62 +/- 55 min; P = 0.4), fluoroscopy time (46 +/- 24 vs 49 +/- 36 min; P = 0.8), number of applications (6.8 +/- 7.0 vs 7.8 +/- 12.1; P = 0.7), or number of applications associated with coagulum formation (0.3 +/- 0.6 vs 0.2 +/- 0.7; P = 0.6), between the impedance and temperature monitoring groups. CONCLUSION: Temperature and impedance monitoring are equally effective in optimizing the results of accessory pathway ablation.

Adult