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Biomedical subjects

J M Desai

Publications and source records attributed to J M Desai.

15 recordsLinked to original sources

Orthogonal electrode catheter array for mapping of endocardial focal site of ventricular activation.

Precise location of the endocardial site of origin of ventricular tachycardia may facilitate surgical and catheter ablation of this arrhythmia. The endocardial catheter mapping technique can locate the site of ventricular tachycardia within 4-8 cm2 of the earliest site recorded by the catheter. This report describes an orthogonal electrode catheter array (OECA) for mapping and radiofrequency ablation (RFA) of endocardial focal site of origin of a plunge electrode paced model of ventricular activation in dogs. The OECA is an 8 F five pole catheter with four peripheral electrodes and one central electrode (total surface area 0.8 cm2. In eight mongrel dogs, mapping was performed by arbitrarily dividing the left ventricle (LV) into four segments. Each segment was mapped with OECA to find the earliest segment. Bipolar and unipolar electrograms were obtained. The plunge electrode (not visible on fluoroscopy) site was identified by the earliest wave front arrival times of -30 msec or earlier at two or more electrodes (unipolar electrograms) with reference to the earliest recorded surface ECG (I, AVF, and V1). Validation of the proximity of the five electrodes of the OECA to the plunge electrode was performed by digital radiography and RFA. Pathological examination was performed to document the proximity of the OECA to the plunge electrode and also for the width, depth, and microscopic changes of the ablation. To find the segment with the earliest LV activation a total of 10 +/- 3 (mean +/- SD) positions were mapped. Mean arrival times at the two earlier electrodes were -39 +/- 4 msec and -35 +/- 3 msec. Digital radiography showed the plunge electrode to be within the area covered by all five electrodes in all eight dogs. The plunge electrode was within 1 cm2 area of the region of RFA in all eight dogs. The width and depth of ablation were 5 +/- 3.5 and 7 +/- 3.5 mm, respectively. Microscopic changes revealed coagulative necrosis, hemorrhage, and inflammatory changes in all RFAs. In conclusion, the OECA can map the endocardial focal site of origin of paced ventricular activation within 1 cm2 area in a canine model. RFA from the OECA can cause discrete ablations representing all five electrodes or cross-shaped ablation connecting central electrode to all four peripheral electrodes. This catheter holds promise for extending surgical and clinical catheter ablation procedures.

Animals↗

Two phase radiofrequency catheter ablation of isolated ventricular endomyocardium.

UNLABELLED: This report describes a two phase radiofrequency (TPRF) energy source producing two radiofrequency sinusoidal voltages of similar frequency but different phase angles between three points of wire. When delivered through an orthogonal electrode catheter array (OECA) TPRF energy produces a square-shaped lesion of the area covered by the five electrodes (0.8 cm2). The purposes of the study were: to create square-shaped lesions using TPRF energy; to compare the size of lesions created by single phase radiofrequency (SPRF) to that of TPRF energy; and to study the depth of such lesions and to create lesions of desired size by adjacent placement of the OECA using TPRF energy. Ablations were created in nine isolated bovine hearts using three power settings (10, 20, and 40 watts) and three pulse durations (5, 10, and 20 seconds). Pathological examination was performed to document the length, width, depth, and the microscopic changes of ablations. TPRF energy increases the size of lesion (P less than 0.001) and utilizes less power (P less than 0.008) at the same power setting and pulse duration compared to SPRF energy. This is possibly related to earlier rise in impedance with TPRF compared to SPRF ablations. The largest lesion for both SPRF (0.51 +/- 0.08 cm2) and TPRF (1.03 +/- 0.18 cm2) ablations were observed at 20 watts for 20 seconds. By adjacent placement of the OECA and TPRF energy desired size (6 cm2) lesions were created. There was no significant difference between the depth of SPRF versus TPRF ablations at comparable power setting and pulse duration. Pathological examination revealed the shape of lesions were elliptical or cross-shaped for SPRF and square for TPRF ablations. Microscopic examination revealed coagulation necrosis, edema, and few necrotic cardiac muscle strands. CONCLUSIONS: TPRF energy can cause 1.2 cm2 lesions. TPRF compared to SPRF energy causes larger lesions but depth of lesions are not different than SPRF energy at the same power setting and pulse duration. By adjacent placement of OECA and TPRF energy desired size lesion can be created (6 cm2).

Animals↗

Ventricular fibrillation following elective cardioversion in a patient with permanent pacemaker.

Elective cardioversion was undertaken in a patient with a VVI pacemaker and atrial tachyarrhythmia after converting the pacemaker to a VOO mode of function. The cardioverter output energy was unwittingly synchronized to the pacemaker output pulses that were falling randomly in various portions of the cardiac cycle. This resulted in the cardioverter DC shock being discharged in the ST segment of the native QRS with consequent ventricular fibrillation.

Aged↗

Mitral valve surgery in children.

Between October 1968 and May 1985, 113 symptomatic pediatric patients (15 years or younger) had operation for rheumatic mitral stenosis or regurgitation. All were in functional classes III and IV of the New York Heart Association classification. The ages ranged from 5 to 15 years. There were 59 female and 50 male children. Nine patients also had grade 1 aortic regurgitation. Seventy-two children with moderately severe to severe mitral stenosis were treated with closed mitral commissurotomy. One patient with preoperative embolization had open commissurotomy while receiving cardiopulmonary bypass. There were two (2.7%) postoperative deaths. Sixty-one (83.5%) had excellent results, and 10 patients (13.7%) had good to fair results. Restenosis occurred in 14 patients (23.0%) over a 15-year period. Of the 40 patients with rheumatic mitral regurgitation, 36 had valve replacement, and mitral valve reconstruction was carried out in four. Six of these were in patients with mitral commissurotomy that was carried out 6, 8, 9, 10, 13, and 15 years earlier. There were four (10.0%) deaths during the postoperative period and one 8 months after operation resulting from a choked valve. Twenty-eight patients (80.0%) had excellent results and seven (20.0%) had fair to good results. Minor episodes of embolization occurred in three patients. All surviving patients were able to perform activities of daily living and showed a normal growth pattern. Three to 13 years' follow-up was available in 61 (85.9%) of 71 patients undergoing mitral commissurotomy who left the hospital and 27 (77.40%) in the mitral valve replacement/reconstruction group.

Adolescent↗

Two-dimensional echocardiography in double orifice mitral valve.

In a patient with endocarditis and significant aortic insufficiency, two-dimensional echocardiography revealed an abnormal mitral valve configuration with division of the valve into two separate orifices. At autopsy, a double orifice mitral valve with two sets of valve leaflets was observed. Appreciation of this echocardiographic abnormality is important because double orifice mitral valve is associated with other congenital anomalies and this echocardiographic configuration may be confused with other cardiac abnormalities.

Adult↗

Electrophysiologic effects on combined autonomic blockade in patients with sinus node disease.

Thirty-two patients were studied before and after i.v. administration of 0.15-0.20 mg/kg of propranolol. Twenty-one of the 32 underwent combined autonomic blockade with the additional infusion of 0.04 mg of atropine. Twenty other patients with sinus node disease underwent electrophysiologic studies both before and after i.v. administration of 0.04 mg of atropine alone. Spontaneous cycle length, maximal corrected sinus node recovery time, sinoatrial conduction time, secondary pauses and intrinsic heart rate were measured. Secondary pauses were more common in those with abnormal intrinsic heart rates, and they did not correlate with changes in maximal corrected sinus node recovery time or sinoatrial conduction time. In patients with normal intrinsic heart rate, abnormal test measurements usually returned to normal after combined blockade (hypervagotonia); however, some patients showed a new abnormality after propranolol that was not reversible with atropine (catecholamine-dependent). Abnormal test responses in patients with abnormal intrinsic heart rate persisted or increased after combined blockade. We conclude that patients with sinus node disease may be categorized as (1) those with intrinsic sinus node disease; (2) those with normal intrinsic sinus node function but either relative hypervagotonia or catecholamine dependency; and (3) those with abnormal intrinsic sinus node function affected by vagal or catecholamine factors.

Adult↗

Cardiovascular collapse associated with disopyramide therapy.

Five patients with severe left ventricular failure, renal insufficiency, and recurrent ventricular tachycardia had cardiovascular collapse and died eight hours to 23 days after initiation of the usual doses of disopyramide. Three patients had recent myocardial infarction (12 to 33 days), and one had severe congestive cardiomyopathy. ECG changes antedated appearance of cardiovascular collapse and consisted of lengthening of the QRS (0.10 plus or minus 0.02 to 0.22 plus or minus 0.09; P less than 0.025) and the QTc duration (0.44 plus or minus 0.04 to 0.56 plus or minus 0.09; P less than 0.05). Sinus bradycardia or varying degrees of atrioventricular block or both occurred in all patients. Terminal disopyramide blood concentration (4.9 and 8.1 micrograms/ml) were available in two patients. A syndrome of progressive lengthening of ventricular depolarization and repolarization terminating in cardiovascular collapse and death associated with disopyramide is described. In addition, a high incidence of sinus bradycardia, atrioventricular conduction disturbances, or both was also noted. Disopyramide is contraindicated in patients with severe heart failure and renal insufficiency. Progressive widening of the QRS complex or the QT interval may presage appearance of severe myocardial dysfunction.

Administration, Oral↗

Electrophysiological effects of disopyramide in patients with bundle branch block.

Electrophysiological studies were performed in 22 patients with intraventricular conduction delay before and after intravenous infusion of disopyramide (Norpace), 2 mg/kg. Mean control maximal sinus node recovery time (1039 +/- 187 msec), atrioventricular nodal conduction time (113 +/- 28 msec), and atrioventricular nodal effective refractory periods (349 +/- 67 msec) did not change significantly after administration of disopyramide (1073 +/- 284 msec, 112 +/- 31 msec, and 342 +/- 42 msec, respectively). Mean spontaneous cycle length (756 +/- 146 msec) decreased significantly 5 minutes after disopyramide (717 +/- 124 msec) (p less than 0.05), but not after 30 minutes (734 +/- 142 msec). A small but statistically significant (p less than 0.05) increase occurred after disopyramide in the mean atrial effective refractory period (259 +/- 51 to 280 +/- 53 msec), ventricular effective refractory period (253 +/- 23 to 275 +/- 33 msec), as well as the relative refractory period of the ventricular specialized conduction system (six patients) 433 +/- 78 to 479 +/- 62 msec). Although mean control infranodal conduction time (67 +/- 35 msec) increased 5 minutes after disopyramide (79 +/- 41 msec) (p less than 0.001) (18%), no spontaneous episodes of second-degree or third-degree atrioventricular block were observed. In six patients with premature ventricular depolarizations (greater than or equal to 1/min), the arrhythmia was totally abolished in four, markedly reduced in one, and remained unchanged in one. Disopyramide resulted in significant prolongation of infranodal conduction time as well as in atrial and ventricular refractoriness, but nevertheless appears to be safe in patients with bundle branch block.

Atrioventricular Node↗