Biomedical subjects
Publications and source records attributed to R W Dhurandhar.
Aortic dissection was found in a woman, her 2 sons, and 1 of her 3 daughters, and the 3 affected children and a granddaughter had patent ductus arteriosus. The pattern of inheritance of this unique syndrome probably is an autosomal dominant one.
We report a patient who developed anterior ST segment elevation following angioplasty of the right coronary artery in which a right ventricular branch became occluded. Several similar reports were found in the literature as well as a putative mechanism for the electrocardiographic changes. Cathet. Cardiovasc. Intervent. 47:327-330, 1999.
We describe pacemaker pauses and pseudohysteresis resulting from sensing of retrograde P waves in a patient with an implanted AV sequential universal pacemaker. Although retrograde P waves are usually followed by a ventricular spike and therefore create the possibility for "endless loop tachycardia," in our patient some retrograde P waves which followed premature ventricular contractions or junctional beats produced pacemaker pauses. The reason for the occurrence of this phenomenon is that the sum of the VA conduction time and the AV delay is shorter than the pacemaker's hardware rate limit. Therefore, the ventricular spike that should follow the retrograde P wave is inhibited. In the pacemaker used by us, the atrial refractory period is only initiated by an atrial event, allowing the pacemaker to sense retrograde P waves occurring after premature junctional or ventricular depolarizations. Although no therapy is needed for the phenomenon described, it is important to understand its true significance and to avoid unnecessary surgical procedures.
A retrospective analysis compared the sensitivity, specificity, and predictive value of two methods using noninvasive Doppler ultrasound for detecting the severity of carotid artery disease. Doppler spectral analyses were used in determining the peak systolic frequency (PF) found within the stenosis, as well as the ratio of the peak systolic frequency distal to the stenosis, to the peak systolic frequency within the stenosis (f2/f1). The results of the noninvasive tests were compared with carotid arteriography. The sensitivity of the two methods were similar, but the specificity of f2/f1 was much higher (98%) than PF (88%) with stenosis greater than 50%, and marginally better, 97 and 94%, respectively, with stenosis greater than 75%. The positive predictive value was also better for f2/f1 than PF; 91% and 71% for stenosis greater than 50%, and 77% and 67%, respectively for stenosis greater than 75%. The use of Doppler frequency ratio in conjunction with peak frequency measurements provide a quantitative and fairly accurate evaluation of the severity of carotid artery disease.
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Ventricular fibrillation has been only rarely observed as a complication of cardiac pacing after the advent of demand pacemakers. Automatic AV sequential pacing (DDD) may provide the setting for ventricular fibrillation in patients with junctional rhythms. In this report we present two patients with implanted DDD pacemakers in whom ventricular pacemaker spikes were seen occurring on top of the T wave during episodes of junctional rhythm. This apparent lack of sensing of QRS complexes does not represent pacemaker malfunction, but rather, is the result of physiologic lack of sensing (blanking) which occurs 56 to 100 msec. following the output of the atrial and ventricular channels. During junctional rhythm when the atrial spike occurs at the beginning of a QRS complex the ventricular channel is blanked and does not sense the intrinsic ventricular activity and thus, ventricular output occurs during repolarization. Increasing the maximum pacemaker rate and decreasing the AV delay will reduce the chance occurrence of this phenomenon.
This case report describes myopotential interference with an automatic AV sequential pacemaker (DDD) producing repetitive firing of the ventricular channel up to a rate of 160 and occasional suppression of the ventricular output. A silastic boot which covered the pacemaker did not prevent sensing of electromyopotentials. The problem was partially corrected by decreasing the sensitivity of the ventricular channel. The ventricular response to myopotentials sensed by the atrial channel was limited by decreasing the maximum programmed rate to 120/minute.
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Pseudo second degree atrioventricular block resulting from blocked His premature beats was successfully treated with quinidine. The diagnosis was proved by His bundle electrogam which showed both blocked and conducted His premature beats. The blocked His prematures produced second degree atrioventricular block by making the atrioventricular junction refractory. Quinidine abolished both conducted and blocked His extrasystoles. There has been no recurrence of arrhythmia during a one-year follow-up.
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Nine patients who had recurrent ventricular fibrillation following acute myocardial infarction or angina were given bretylium tosylate in a dose of 5 mg./kg. intramuscularly every eight hours after other measures had proved ineffective. Provided the patients were not in shock or in heart failure, there was a considerable reduction in the episodes of ventricular fibrillation.A second group of nine patients who developed recurrent ventricular fibrillation following open heart surgery were given bretylium intravenously, which controlled the arrhythmia in every instance.Bretylium did not completely abolish ventricular premature beats but the latter did not initiate ventricular fibrillation even when they occurred on the T wave.
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