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Biomedical subjects

J A Kastor

Publications and source records attributed to J A Kastor.

At least 19 recordsLinked to original sources
PubMed1979

Nifedipine in the treatment of Prinzmetal's (variant) angina.

The clinical response to therapy with the calcium-blocking agent nifedipine was assessed in 12 patients with variant angina pectoris who were 44 to 67 years old. Five patients had vasospasm of the left anterior descending coronary artery, and seven had spasm of a dominant right coronary artery. Before nifedipine therapy, the frequency of anginal attacks per 24 hour period ranged from 1 to 12, with ventricular tachycardia accompanying ischemic episodes in 7 of 12 patients and high grade atrioventricular block occurring in 2 patients. After therapy with nifedipine, 11 of 12 patients had initial relief of symptoms, and 7 of the 11 had long-term relief. Withdrawal of nifedipine led to recurrence of angina on six occasions in four patients. Provocative testing in the cardiac catheterization laboratory by means of the cold pressor test in one patient and ergonovine maleate in another before and after nifedipine administration showed that this agent can block both alpha adrenergic- and regonovine-induced vasospasm. Nifedipine may have a significant role in the therapy of angina caused by coronary spasm.

Adult↗
PubMed1979

Relationship of atrial fibrillatory wave amplitude to left atrial size and etiology of heart disease. An old generalization re-examined.

It is commonly stated that coarse f waves in atrial fibrillation suggest the presence of rheumatic heart disease and large left atrial size, whereas fine f waves indicate non-rheumatic disease and small left atrial size. Using echocardiography as a more reliable indicator of left atrial size, 37 consecutive patients with chronic atrial fibrillation were evaluated. The correlation coefficients between left atrial size and maximum f wave amplitude was -0.12 and -0.07, using average f wave amplitude. Only 53 per cent (9 of 17) of patients with rheumatic heart disease had f wave greater than 1 mm. and 56 per cent (10 of 18) of patients with f wave size less than or equal to 1 mm. had non-rheumatic disease. This study refutes the contention that the f wave amplitude in atrial fibrillation is correlated with either left atrial size or etiology of heart disease. It is possible that an intra-atrial conduction defect is responsible for coarse f wave morphology.

Atrial Fibrillation↗
PubMed1979

Coronary hemodynamic and myocardial metabolic alterations accompanying coronary spasm.

Arterial pressure, coronary sinus blood flow with the thermodilution technique and calculated coronary vascular resistance were measured and coronary arteriography performed at rest and after the administration of ergonovine in 14 patients with atypical chest pain (group 1) and 6 patients with variant angina (group II). Mild diffuse narrowing of the left coronary bed in group I was not accompanied by S-T segment shifts, and coronary vascular resistance did not change significantly. In contrast, severe focal spasm (greater than 90 percent narrowing) of the left anterior descending coronary artery in group II patients was accompanied by S-T elevation and a marked overall increase in coronary vascular resistance (from 0.65 +/- 0.07 to 1.14 +/- 0.10 mm Hg/ml per min) (P less than 0.005). In addition, the myocardial arteriovenous oxygen difference increased and net lactate extraction changed to lactate production in the two patients in group II in whom these measurements were made. Thus, thermodilution coronary sinus blood flow measurement may be a sensitive method for detecting primary increases in coronary vascular resistance due to a high grade focal spasm in the left anterior descending coronary artery.

Adult↗
PubMed1979

The mechanism of apparent right bundle branch block after transatrial repair of tetralogy of Fallot.

The electrocardiographic pattern of right bundle branch block (RBBB) is routinely observed after transatrial repair of tetralogy of Fallot even though no ventriculotomy has been performed. The mechanism of this conduction disturbance was studied in 16 patients with tetralogy of Fallot and one patient with infundibular pulmonic stenosis. Preoperative ECGs and vectorcardiograms showed right ventricular hypertrophy and no RBBB. Epicardial activation maps were obtained before and after total surgical repair in all patients and after infundibular resection but before closure of ventricular septal defect (VSD) in four of these patients. After infundibular resection, RBBB appeared and activation was markedly delayed (greater than 30 msec) over the pulmonary outflow tract, but was unchanged over the body of the right ventricle. No further changes in ventricular activation occurred after closure of the VSD. This study shows that RBBB after transatrial repair of tetralogy of Fallot is usually produced by infundibular resection, but not by VSD closure, and is associated with delayed activation of the pulmonary outflow tract and base of the right ventricle which results from damage to portions of the right ventricular conduction system.

Adolescent↗
PubMed1979

The effects of coronary artery disease on the ventricular fibrillation threshold in man.

The ventricular fibrillation threshold (VFT) was measured in 28 patients at the time of cardiac surgery. The VFT was measured with a 100 Hz train of 24 rectangular pulses positioned across the ST segment and T wave. Current was applied to the epicardial surface of either ventricle with a bipolar electrode probe. In six patients, the normal right VFT was 24.3 +/- 5.2 mA, and in 10 patients the normal left VFT was 33.6 +/- mA (p less than 0.05). In 12 patients with greater than or equal to 75% obstruction of the left anterior descending coronary artery, the left VFT was 18.6 +/- 6.9 mA. This value was significantly less than the left VFT in patients without coronary artery disease (p less than 0.001). This study shows that the VFT can be measured in man and that coronary artery disease reduces this parameter.

Adult↗
PubMed1979

Tricuspid valvular incompetence and rupture of the ventricular septum caused by nonpenetrating trauma.

A young adult involved in an automobile accident had tricuspid valvular incompetence and rupture of the ventricular septum owing to blunt trauma. He had a successful repair of the ventricular septal defect and replacement of the tricuspid valve. Tricuspid valvular incompetence owing to nonpenetrating trauma is uncommon. Blunt trauma resulting in rupture of the ventricular septum is rare. Rupture of the membranous portion of the ventricular spetum is extremely rare. This is the first report of a patient having a combination of these lesions.

Adult↗
PubMed1978

Fascicular conduction distrubances after coronary bypass surgery.

Two hundred patients underogoing coronary bypass graft surgery were studied to determine the frequency and significance fo new fascicular conduction distrubances. The follow-up period ranged from 13 to 39 months. New disturbances developed in 39 patients (20 percent). Isolated right bundle branch block (6 percent) and left anterior hemiblock (6 percent) were the most common disturbances. Righ bundle branch block was usually transient and was not associated with further complications in the follow-up period. However, patients with either transient or persistent left bundle branch block or left anterior hemiblock, or both, had (1) increased later mortality compared with patients without new fascicular conduction disturbances (5 of 26 versus 11 of 161; P less than 0.02), and (2) increased late myocardial infarction (2 of 26 versus 2 of 161; P less than 0.05). New left fascicular conduction disturbances after coronary surgery identified a subset of patients with more extensive ischemic heart disease, suggesting that these patients require close follow-up care.

Adult↗
PubMed1978

Paroxysmal supraventricular tachycardia in patients with mitral valve prolapse.

The mechanism of supraventricular tachycardia was evaluated in twelve patients with mitral valve prolapse utilizing standard intracardiac recording and stimulation techniques. Eight patients had normal electrocardiograms, three had a short PR interval and normal QRS (Lown-Ganong-Levine syndrome) and one had Wolff-Parkinson-White type A. Six of the eight patients with normal electrocardiograms were demonstrated to have atrioventricular bypass tracts. Five patients had A-V nodal re-entrant supraventricular tachycardia. In two patients the bypass tract could be demonstrated to conduct antegradely when the left atrium was paced via the coronary sinus, while in four the bypass tract only conducted retrogradely. In all seven patients with atrioventricular bypass tracts, the accessory pathway was left-sided. We conclude that a) supraventricular tachycardia in the mitral valve prolapse syndrome appears related to a high frequency of bypass tracts; b) electrophysiological studies are required to diagnose these bypass tracts; and c) the atrioventricular bypass tracts may be related to the mitral valve abnormality since they are always left-sided.

Adolescent↗
PubMed1978

Recurrent sustained ventricular tachycardia. 1. Mechanisms.

The mechanism of recurrent sustained ventricular tachycardia (VT) was evaluated in 21 patients. Re-entry as the mechanism for VT was suggested by a) the reproducible initiation (19) and termination (15) of the arrhythmia by programmed stimulation. The rate, ventricle of origin, and stimulation site determined the method of termination. One VPD was usually required with VT rates less than 175/min and/or ventricle of origin ipsilateral to the stimulation site, while two VPDs were usually required for VT with faster rates originating in a contralateral ventricle. The proximal His-Purkinje system (HPS) was not required for initiation or maintenance of VT. Evidence localizing the site of re-entry to a small portion of the ventricles included: a) ventricular capture by ventricular premature depolarizations (VPDs) or pacing (VP) without terminating VT (5), b) sinus capture following VPDs and/or supraventricular fusions without terminating VT (12), and c) atrial pacing normalizing the QRS and H-V intervals without terminating VT (5).

Adolescent↗
PubMed1978

Recurrent sustained ventricular tachycardia. 2. Endocardial mapping.

Endocardial ventricular mapping of 21 ventricular tachyardias (VT) in 17 patients was performed using electrode catheters. Activation at multiple left and right ventricular sites was utilized to determine the site of origin of the VT. Eleven VT had a left bundle branch block pattern (VT-LBBB) and 10 VT had right bundle branch block pattern (VT-RBBB). In all VT-RBBB the earliest site of activation was in the LV or septum. In VT-LBBB the earliest site was RV (4/11), LV (5/11) and septum (2/11). All ventricular tachycardias with QRS less than 140 msec arose in the septum. In patients with an aneurysm, the site of origin of ventricular tachycardia was always in the aneursm. All VT-LBBB arising from the left ventricle originated in an aneurysm involving the septum. QRS changes during ventricular tachycardia were associated with alterations in the patterm of ventricular activation without alteration of the site of origin. In three patients the site of origin predicted by endocardial ventricular mapping was confirmed intraoperatively by epi- and/or endocardial mapping. We conclude that endocardial ventricular mapping demonstrates the limitations of the surface electrocardiogram in localizing the site of origin of ventricular tachycardia. The method may provide important data upon which the surgical therapy of ventricular tachycardia is based.

Adolescent↗
PubMed1978

Fixed coupling: different mechanisms revealed by exercise-induced changes in cycle length.

Fixed coupled ventricular premature depolarizations (VPDs) are usually considered reentrant; recent experimental models have demonstrated that parasystolic rhythms may also appear in fixed coupled patterns. To analyze the mechanisms of fixed coupled VPDs, 60 exercise tests were chosen to evaluate the response of VPD coupling intervals to changes in cycle length of the dominant supraventricular rhythm. Selection criteria included the presence of frequent, unifocal VPDs that were fixed coupled (variation less than or equal to 80 msec) at any one cycle length, with the persistence of VPDs at several different cycle lengths. Three patterns of response of coupling intervals to changes in cycle length were noted: 1) 32 patients with a direct linear relation (r greater than or equal to 0.9) of coupling intervals to cycle length; 2) 16 patients with coupling intervals fixed, independent of cycle length; and 3) 12 patients with no consistent relation over a wide range of cycle lengths. Two patients in group 2 and four in group 3 fulfilled criteria for parasystole with interectopic intervals that remained constant at different cycle lengths. These results suggest that VPDs in group 1 are reentrant, while some patients with group 2 or 3 responses have evidence for parasystolic rhythms. We conclude that 1) fixed coupling of VPDs is not diagnostic of reentry, and 2) changes in cycle length induced with exercise may be useful in the analysis of mechanisms of VPDs.

Adolescent↗
PubMed1978

His-Purkinje conduction during retrograde stress.

The pattern of retrograde His-Purkinje conduction was evaluated in 28 patients using ventricular extrastimuli. In each patient progressive prolongations of His-Purkinje conduction (S2H2) which appeared as ventricular extrastimuli were induced at closer coupling intervals (S1S2). There was an inverse linear relationship of S2H2 to S1S2 which was cycle length-dependent: i.e., at any S1S2 interval the resultant S2H2 was less at shorter drive cycle lengths. The degree of S2H2 delay varied widely (from 30 to 340 ms) and was unrelated to the presence of bundle branch block, H-V intervals, or capability of ventriculoatrial conduction. Prolongation of S2H2 was independent of intraventricular (muscle) conduction delay; such delay was usually absent at most, and occasionally all, S1S2 coupling intervals during which S2H2 was lengthening. Furthermore, in two patients both left and right ventricles were activated before the timed depolarization of the His bundle occurred, demonstrating that under the stress of extrastimuli, the impulse conducts through ventricular muscle with less delay than through the His-Purkinje system. We conclude that the His-Purkinje system typically displays slow conduction response to ventricular stress. The site of this conduction delay is probably at the distal "gate".

Arrhythmias, Cardiac↗
PubMed1977

Supraventricular tachycardia in Lown-Ganong-Levine syndrome: atrionodal versus intranodal reentry.

The mechanism of the abbreviated atrioventricular (A-V) nodal conduction time and paroxysmal supraventricular tachycardia in the Lown-Ganong-Levine syndrome was evaluated in six patients. In each the A-H interval increased in response to rapid atrial pacing and atrial extrastimuli; typical dual A-V nodal pathways were demonstrated. In five patients studied at two cycle lengths prolongation of conduction and refractoriness of the "fast" pathway was noted at the shorter basic cycle length. Propranolol prolonged conduction and refractoriness of the "fast" pathway in three patients and in one produced Wenckebach conduction during atrial pacing which did not occur prior to its administration. In three patients the atrium did not appear necessary to sustain supraventricular tachycardia. These findings suggest that preferential rapidly conducting A-V nodal fibers and intranodal reentry are the responsible mechanisms in those patients with Lown-Ganong-Levine syndrome and reciprocating tachycardia.

Adolescent↗