Biosynthesis of oxanthromicin.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to J Desai.
Explore the source record for details and available documents.
His bundle electrograms were obtained in 313 patients with chronic bundle branch block who were followed for a mean period of almost 3 years. The infranodal conduction time (H-Q interval) was less than 55 ms in 97 patients (Group I), 55 to 69 ms in 99 patients (Group II), and greater than or equal to 70 ms in 117 patients (Group III). There was a higher incidence of organic heart disease in patients in Group III, but the groups were otherwise comparable. On follow-up study, mortality and the incidence of sudden death were similar among the groups, but patients in Group III had a greater incidence of progression to high degree atrioventricular block (HDB) than did those in Groups I and II (14 of 117 [12%] versus 4 of 97 [4%] and 2 of 99 [2%], p less than 0.01, respectively). High degree block was found in 4 of 17 (24%) patients with an H-Q interval (H-Q) greater than or equal to 100 ms. Sixty-two patients underwent permanent prophylactic pacemaker insertion at the discretion of the referring physician and were compared with 231 patients who did not. Paced patients had a higher incidence of transient neurologic symptoms and prolonged H-Q, but the groups were otherwise comparable. On follow-up study, mortality and the incidence of sudden death were similar among the groups, but symptom relief was significantly more common among patients with pacemakers. In conclusion, in our population (1) H-Q greater than or equal to 70 ms was an independent risk factor for progression to HDB, (2) H-Q greater than or equal to 100 ms identified a subgroup at particularly high risk, and (3) prophylactic pacemakers relieved neurologic symptoms but did not prolong life.
Intracardiac electrophysiologic studies were performed in two patients who had recurrent sustained ventricular tachycardia. In both, the tachycardia was repeatedly terminated by carotid massage. In one patient, intracardiac electrophysiologic studies revealed ventricular tachycardia with 2:1 retrograde ventriculoatrial (VA) block. Carotid massage resulted in alternate Wenckebach retrograde VA conduction terminated by ventricular echo beats. When ventricular echo beats occurred at a coupling interval of 340 - 400 msec, the tachycardia was terminated. Similarly, induced atrial depolarizations (during ventricular tachycardia) produced ventricular capture and terminated the tachycardia when the resultant ventricular coupling interval was 330 - 395 msec. In the second patient, progressively premature atrial or ventricular depolarizations did not terminate the tachycardia. carotid massage had no consistent effect on retrograde VA conduction during ventricular tachycardia, but usually resulted in gradual increases in the tachycardia cycle length (50 - 100 msec) before abrupt termination of the tachycardia. This is the first report documenting termination of ventricular tachycardia by carotid massage alone (i.e., without prior drug intervention); hence, tachycardia termination by simple carotid sinus massage does not prove a supraventricular origin. The mechanism of tachycardia termination was due to ventricular echo beats from retrograde atrioventricular nodal reentry in one patient and to direct vagal effects on either the ventricular muscle or the ventricular specialized conduction system in the other.
Seventeen patients with first-degree or Mobitz I atrioventricular (AV) block and narrow QRS complexes underwent electrophysiologic drug testing before and after i.v. administration of disopyramide. Disopyramide did not significantly change the mean sinus cycle length (895 +/- 131 vs 877 +/- 119 msec), mean maximal sinus node recovery time (1134 +/- 160 vs 1133 +/- 13 msec), mean atrial effective refractory period (314 +/- 72 vs 307 +/- 54 msec), mean AV nodal conduction time (187 +/- 79 vs 180 +/- 73 msec) or the mean paced cycle length at which AV nodal Wenckebach conduction occurred (545 +/- 144 vs 497 +/- 130 msec) after disopyramide. The mean AV nodal effective refractory period decreased significantly (from 535 +/- 137 to 521 +/- 122 msec), and both infranodal conduction time and the paced ventricular cycle length producing ventriculoatrial block increased significantly (from 56 +/- 12 to 63 +/- 13 msec and from 625 +/- 158 to 655 +/- 157 msec, respectively). We conclude that i.v. disopyramide administered in a dose resulting in therapeutic blood levels showed no adverse effects on AV nodal conduction in patients with AV nodal dysfunction. In contrast, i.v. disopyramide depressed retrograde AV conduction.
Since disopyramide was introduced 5 years ago, the therapeutic spectrum of this drug in treating patients with ventricular and atrial arrhythmias has been found to be similar to that of the other type I antiarrhythmic drugs, quinidine and procainamide. Disopyramide has the potential to suppress sinus node function and, therefore, must be used cautiously in patients with the sick sinus syndrome. The available data indicate that it can be used safely in patients with bundle branch block and first-degree or type I second-degree atrioventricular block. Disopyramide has been found at times to precipitate ventricular tachycardia or ventricular fibrillation. Because this drug often causes decompensation in patients with congestive heart failure, it must be used very cautiously, if at all, in such patients.
Explore the source record for details and available documents.
A 27-year-old man with primary oxalosis and extensive visceral involvement was maintained on long-term chronic hemodialysis. He had an episode of presyncope associated with electrocardiographic findings of an erratic atrial rhythm, atrioventricular dissociation due to an accelerated junctional rhythm and right bundle branch block. Electrophysiologic studies showed irregular atrial depolarizations probably associated with multiple atrial pacemakers, atrial inexcitability, atrioventricular dissociation and infranodal conduction delay. These findings correlated well with extensive oxalate infiltration of the sinoatrial node and its approaches, the atrial preferential pathways, the approaches to the atrioventricular node, the atrioventricular node, and the His bundle and bundle branches. This is the first reported case of cardiac electrophysiologic abnormalities due to oxalate infiltration in a patient with primary oxalosis.
A patient was admitted to the hospital with wide complex tachycardia and a history of recurrent palpitations. Electrophysiologic studies showed evidence of dual atrioventricular (AV) accessory pathways. One proved to be an anteroseptal (possible right anterior) pathway probably capable of only unidirectional conduction. The other pathway was in the posterior septum and conducted only in the retrograde direction. The tachycardia circuit involved anterograde conduction via either the AV node-His axis or the anteroseptal pathway and retroconduction over the posteroseptal accessory pathway. In addition, enhanced AV nodal conduction coupled with two accessory AV nodal pathways has rarely been described in English medical literature. Previous reports have carefully described anatomic, electrocardiographic, and electrophysiologic evidence of more than one accessory pathway in patients with the Wolff-Parkinson-White syndrome. The introduction of surgical techniques for ablation of an accessory pathway demands precision in the electrophysiologic evaluation of patients with ventricular preexcitation. Reported herein is a patient with the unique finding of two extranodal accessory pathways and enhanced atrioventricular (AV) nodal conduction (or AV nodal bypass).
Three hundred fifty-eight of 429 (83%) consecutive patients with acute myocardial infarction (MI) and a normal PR interval received various antiarrhythmic drugs (AD), including lidocaine and/or procainamide, quinidine, digoxin, propranolol or disopyramide. There was no significant difference in the incidence of progression to any degree of atrioventricular (AV) block or to higher degrees of AV block (Mobitz II or third-degree AV block) between those treated and not treated with AD: 38 of 358 (11%) and six of 358 (1.7%) with AD vs 11 of 71 (15%) and two of 71 (2.8%) in the untreated group, respectively. Similarly, there was no significant difference in progression between treated and untreated patients with anterior MI, 14 of 144 (10%) vs five of 32 (16%); inferior MI, 21 of 111 (19%) vs five of 26 (19%), or subendocardial MI, three of 103 (3%) vs one of 12 (8%). Bundle branch block (BBB) (without AV block) was initially present in 89 of 249 (21%). The incidence of AV block (seven of 24, 30%) was higher in treated patients with newly acquired BBB (27 patients) than in the untreated patients (none of three, p less than 0.05). The commonly used ADs did not adversely affect AV conduction in patients with acute MI with narrow QRS and either normal, first-degree, or Mobitz I AV block. Moreover, no subset of patients grouped by infarct location, specific AD used, or BBB (except perhaps for those with newly acquired BBB) appeared to be at risk of development of AV block during AD therapy.
Consistent His bundle pacing was accomplished in one of 60 consecutive patients. Intracardiac electrophysiologic studies in this patient revealed rapid atrioventricular nodal conduction (AH = 55 msec). While the relative refractory period of the His-Purkinje system as a whole determined by His bundle pacing (using the extrastimulus technique) was identical to that determined by atrial pacing, changes in right bundle branch refractoriness differed. An atrial extrasystolic interval of 370 msec resulted in right bundle branch block, whereas direct His pacing at a shorter extrasystolic interval (360 msec) failed to produce a bundle branch block pattern. The effective refractory period of the His-Purkinje system could not be determined by atrial pacing because of atrial refractoriness, but was obtained by His bundle pacing. Theoretically, direct His bundle pacing may be of value in determining His-Purkinje system refractoriness when this parameter is unobtainable due to either atrial or atrioventricular nodal refractoriness. This technique appears to have limited clinical usefulness, however, because of the very small success rates. Finally, His-Purkinje system refractoriness may differ, depending on site of stimulation, presumably due to differing inputs into the His-Purkinje system.
A 4-year-old girl with acute DiGuglielmo's syndrome exhibited an unusually malignant erythropoietic proliferation as evidenced by an extremely high number of actively dividing nucleated erythroid cells in the peripheral blood and the bone marrow. The ransfusion of erythrocytes to the patient resulted in a marked decrease in the size of the liver, spleen, and the number of nucleated erythroid cells. These clinical and hematological events were associated with a reduction in the activity of plasma erythropoietin. The above findings suggested that the neoplastic nature of the erythroid elements and their lack of autonomy are not mutually exclusive.
Over five years, 13 patients with episodic apparent type II atrioventricular (AV) block associated with sinus slowing were seen. This phenomenon occurred only transiently during an acute illness in eight patients (group I) but recurred chronically in five (groupII). For the group as a whole, the mean spontaneous cycle length was 42% longer during the period of AV block compared with periods of 1:1 AV conduction (800 +/- 116 msec to 1138 +/- 489 msec) (P less than 0.05). Electrophysiologic studies in four group I patients showed no abnormalities, whereas abnormalities in AV nodal conduction and refractoriness or provocation of intranodal Mobitz type II AV block (during carotid massage) were observed in three patients in group II and were totally abolished by atropine. In group I patients, apparent type II AV block was self-limited. In the chronic group, recurrent symptoms required insertion of permanent pacemakers in two patients. Simultaneous type II block and sinus slowing appeared to be related to the effects of increased vagal tone on both nodal structures. Intracardiac pacing is not indicated for patients with transient episodes associated with an acute illness, but may be required for symptomatic patients with recurrent episodes.
Primary mitral valve tumors are rare. We describe the transesophageal appearances of a papillary fibroelastoma (Lambl's giant excrescence) of the anterior mitral valve leaflet causing partial mitral valve obstruction. Transesophageal echocardiography proved particularly useful in identifying the limited attachment of the tumor to the anterior mitral valve leaflet and excluding its attachment to the interatrial septum. These features helped to exclude the possibility of the tumor being a left atrial myxoma, the primary differential diagnosis of the lesion. Transesophageal echocardiography enabled the planned surgical option to be mitral valve repair and also allowed intraoperative monitoring to assess the results of the surgical repair.
Transesophageal echocardiography is the method of choice for investigating suspected intracardiac masses. It also plays a valuable role in the detection of central pulmonary artery embolism. We present a case that highlights the use of transesophageal echocardiography for imaging of a mass in the right atrium and the right pulmonary artery.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Brain damage remains a significant cause of post-operative morbidity following open-heart surgical procedures. Though cerebral ischaemia and micro-embolic damage are considered the main causative factors, further understanding of this particular clinical problem has been hampered by the lack of an acceptably sensitive experimental model. Recent development of a biochemical marker model using cerebrospinal fluid levels of creatine kinase enzyme and its B brain specific isoenzyme have been used in the present study designed to investigate the effect of corticosteroid pre-treatment of dogs submitted to 60 minutes of normothermic cardiopulmonary bypass. Identical vials containing methylprednisolone 30 mg/kg body weight or placebo were administered intravenously to the dog before the period of bypass was begun. The cisterna magna was cannulated in order to obtain appropriate cerebrospinal fluid samples. The results indicate a rise in the enzyme and isoenzyme levels in cerebrospinal fluid during the period of perfusion for both total creatine kinase enzyme and its B isoenzyme. Analysis of the results following completion of the study indicated that the levels of enzyme and isoenzyme rise in the steroid treated group were always lower than the levels obtained in the group receiving placebo. Though this difference was consistent it did not achieve statistical significance. Analysis of the distribution of the rise in enzyme levels in the individual dogs in the two groups suggested, however, that the group of dogs receiving methylprednisolone were possibly protected from excessive degrees of enzyme release indicating a possible protective effect of steroid pre-treatment.(ABSTRACT TRUNCATED AT 250 WORDS)
Paroxysmal supraventricular tachycardia can usually be managed without any specific therapy or with an appropriate drug program. Some patients, however, are resistant to conventional therapy. In the past decade, the electrophysiologic pathogenic mechanisms of this rhythm disorder have been elucidated, and this, coupled with progress in intracardiac instrumentation, has enabled the physician to induce specific rhythm disorders and to map them to determine an ideal, specially tailored method of treatment. As a result, the use of radiofrequency pacing and surgery are becoming increasingly important in the treatment of patients with paroxysmal supraventricular tachycardia, especially those with arrhythmias related to Wolff-Parkinson-White syndrome.