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Biomedical subjects

A Keren

Publications and source records attributed to A Keren.

At least 109 records · Page 6Linked to original sources
PubMed1983

Effect of exercise on cerebral circulation.

The effect of supine physical exercise on cerebral blood flow (CBF) was measured in 30 normal subjects with the 133Xe inhalation technique. The CBF measurements were correlated to changes in PCO2, heart rate, and blood pressure, and to cardiac output and right atrial pressure in 10 of the subjects who underwent Swan-Ganz catheterization. No significant change was found in CBF during physical exercise, although a marked increase in cardiac output, blood pressure, and right atrial pressure and a mild decrease in PCO2 were found. Cerebrovascular resistance increased by 38%, in contrast to a decrease of 33% in the peripheral vascular resistance. The factors that affect the mechanism of cerebrovascular autoregulation during exercise are discussed.

Adult↗
PubMed1983

Exercise-induced S-T segment elevation in variant angina.

3 patients with co-existing effort angina and Prinzmetal's variant angina are described, who had also 'atypical' manifestations of variant angina, i.e. chest pain and S-T segment elevation also during treadmill exercise testing. Because of these unusual manifestations the proper diagnosis was delayed and the patients continued with inappropriate therapy (propranolol and only low-dose nitrates). After the correct diagnosis of variant angina with 'atypical' manifestations was made, application of high-dose nitrates and nifedipine resulted in complete relief of symptoms. Repeat treadmill testing during this therapy did not provoke attacks of chest pain with S-T elevation.

Angina Pectoris, Variant↗
PubMed1982

Origin of both coronary arteries from the same sinus of Valsalva: report of two cases.

Origin of both coronary arteries from the same sinus of Valsalva was found in two patients. In one patient the right coronary artery opened from the left sinus of Valsalva, coursed between the pulmonary artery and aorta, disclosed a 95% obstruction in its proximal third with good runoff. The portion of the artery between the aorta and pulmonary artery showed cyclic narrowing during systole. In the second patient the left coronary opened from the right sinus of Valsalva, the left main trunk crossed anteriorily the pulmonary artery conus, and both the circumflex and the left anterior descending branches showed significant narrowing. In both patients the arteries shared a common sinus with two separate orifices, both had bicuspid aortic valve, and in both, nonaberrant coronary vessels also had stigmata of atherosclerosis.

Aged↗
PubMed1982

Comparison of right atrial pacing soon after myocardial infarction with treadmill testing 6 months later.

Seventy-four patients recovering from acute myocardial infarction underwent right atrial pacing before hospital discharge, and treadmill exercise testing 6 months later. The early right atrial pacing test was positive in 32 patients (43 percent) and the late treadmill test was positive in 32 patients (42 percent). The results of the two tests were concordant in 77 percent of the patients, 23 with an ischemic response and 34 with a normal response on both tests. In nine patients a positive right atrial pacing test was followed by a negative treadmill test, and in eight patients a negative pacing test was followed by a positive treadmill test. A positive right atrial pacing test at hospital discharge had an 81.0 percent predictive accuracy for a positive late treadmill test; chest pain, congestive heart failure or increased cardiothoracic ratio at discharge had a predictive value of only 52.9, 42.8 and 42.8 percent, respectively. Both the early right atrial pacing test and the late treadmill test were positive in a significantly higher proportion of patients with inferior or subendocardial infarction than of patients with anterior myocardial infarction. During early right atrial pacing the mean maximal heart rate achieved was higher than that during late treadmill testing (148 versus 133 beats/min) and the mean systolic blood pressure was lower (137 versus 162 mm Hg), but the pressure-rate product was similar on the two tests (20,282 versus 21,455 mm Hg/min). This finding may explain the similar frequency of ischemic responses to the two tests. These results indicate that the response to right atrial pacing soon after myocardial infarction is a good predictor for the presence or absence of an ischemic response to treadmill testing 6 months later. Thus, early right atrial pacing at the time of hospital discharge may be used to determine the pace of rehabilitation and short-term prognosis.

Adult↗
PubMed1982

Initiation of ventricular tachycardia by supraventricular beats.

9 patients (6 males and 3 females, age 5-69 years) with ventricular tachycardia induced by supraventricular beats are reported. 3 patients had had previous myocardial infarction, 1 patient had mitral valve prolapse and in 5 patients no organic heart disease could be demonstrated. Ventricular tachycardia was initiated by a single atrial premature beat in 4 patients, double atrial premature beats in 3 patients (in 1 of them following exercise), by nonsustained AV nodal tachycardia in 1 patient, by rapid atrial pacing in 3 patients and exercise-related ectopic atrial tachycardia in 1 patient. Programmed ventricular stimulation induced ventricular tachycardia in all patients in whom the tachycardia was induced by atrial stimulation. Verapamil abolished sustained ventricular tachycardia in 1 of the 3 patients in whom this drug was administered. Hypotheses are made on the electrophysiological mechanisms of the arrhythmias and clinical implications are listed.

Adult↗
PubMed1982

Atypical ventricular tachycardia (torsade de pointes) induced by amiodarone: arrhythmia previously induced by quinidine and disopyramide.

A 44-year-old woman is described in whom amiodarone, disopyramide, and quinidine, administered alone separately, induced atypical ventricular tachycardia (AVT, torsade de pointes). Following a closed mitral valvotomy, she received quinidine, 1.2 g/day, without interruption for 17 years. Because of a recurrence of paroxysmal atrial fibrillation, the dose of the drug was increased to 1.4 g/day; 24 hours later AVT with syncope developed but responded promptly to atropine. Two years later, 24 hours following an increase in the dose of disopyramide from 300 to 600 mg/day, AVT with syncope occurred; isoproterenol abolished the arrhythmia instantly. Amiodarone was the third drug to induce AVT in this patient; she received 200 mg/day six days per week for six months. The dose was subsequently increased to 200 and 400 mg/day on alternate days, six days per week, and two months later AVT occurred. That time the only effective treatment was ventricular pacing.

Adult↗
PubMed1981

Ventricular pacing in atypical ventricular tachycardia.

Ventricular pacing was effective in controlling recurrent bouts of atypical ventricular tachycardia (Torsade de Pointes), in four patients. This arrhythmia was induced by quinidine or disopyramide therapy. Isoproterenol, which is the usually recommended therapy, was ineffective in two of the patients and was considered hazardous in two others. We consider ventricular pacing as a safe and reliable method for treatment of AVT, which should be applied if isoproterenol is ineffective or contraindicated.

Aged↗
PubMed1981

Acute myocardial infarction caused by blast injury of the chest.

A 51-year-old healthy man was hit in the chest by the shock-waves generated by an explosion, without being injured by any physical object. He felt immediate chest pain, but, in spite of electrocardiographic tracings highly suspicious for an acute anteroseptal infarction in the emergency room, he was discharged from hospital. The electrocardiogram recorded three weeks later was pathognomonic of anteroseptal infarction. Coronary arteriography performed four months later showed a complete obstruction of the left anterior descending coronary artery, with retrograde filling from the right coronary artery. It is assumed that the myocardial infarction was caused by the blast injury which induced an intimal tear and/or a subintimal haemorrhage in the left anterior descending artery with subsequent thrombosis. The lack of atherosclerosis in any other coronary arteries in this patient is noteworthy.

Blast Injuries↗
PubMed1981

Relationship between ventricular arrhythmias detected by ambulatory ECG monitoring and subsequent sudden cardiac death.

During the years 1971-1974, ambulatory ECG monitoring (AEM) during everyday activities was done in 888 consecutive subjects. Half of them were patients who suffered from chronic ischemic heart disease (IHD), while in the others no symptoms or signs of this disease were found. Ventricular arrhythmias (VA) were detected in 196 subjects of the former and in 190 of the latter group. The Bureau of Statistics provided information concerning the individuals who died before December 31, 1976, the cause of their death and whether or not the death occurred in hospital or was 'sudden'. We found that during the follow-up period, the rate of sudden cardiac death among the patients with IHD in whom AEM detected VA was higher than in subjects without VA. In the former group, there were 12 sudden cardiac deaths among 196 patients, while in the latter there were only 4 out of 248, a statistically significant difference. Sudden cardiac death was more frequent in individuals without IHD if AEM disclosed VA (4 sudden cardiac deaths among 190 subjects), as compared to individuals without VA (no sudden cardiac deaths among 254 subjects).

Adult↗
PubMed1981

Etiology, warning signs and therapy of torsade de pointes. A study of 10 patients.

Torsade de pointes, also called atypical ventricular tachycardia (AVT), was diagnosed in 10 patients, nine on antiarrhythmic therapy and one with acute central nervous system damage. Four patients received quinidine and five disopyramide, either alone or in combination with amiodarone. AVT was dose-dependent in some, but in others, it started shortly after initiation of drug therapy (idiosyncrasy). All patients had QT prolongation longer than 0.60 second immediately before the onset of AVT. This measurement appeared to be a more sensitive predictor of the development of AVT than QTc prolongation or QRS widening. All patients also showed bradycardia before AVT onset. After therapy, the QT immediately decreased, while QTc and QRS remained prolonged for longer periods. Isoproterenol was effective in five of seven patients, but was contraindicated in two others. Ventricular pacing was used in four patients, including the two who did not respond to isoproterenol, and this abolished AVT promptly. Isoproterenol or pacing appear to be the therapy of choice for AVT, while the conventional drugs used to treat the usual form of ventricular tachycardia are not only ineffective, but even contraindicated.

Adult↗
PubMed1981

Disopyramide-induced Torsade de Pointes.

Recurrent ventricular tachycardia (torsade de pointes) is a serious and sometimes fatal arrhythmia occurring usually with quinidine therapy. Four patients experienced ventricular tachycardia after receiving conventional doses of disopyramide phosphate (600 mg/day) for recurrent atrial fibrillation-two of them in combination with amiodarone hydrochloride. Isoproterenol hydrochloride infusion was effective in three patients, while ventricular pacing promptly abolished ventricular ectopic beats and the ventricular tachycardia in the fourth patient. Torsade de pointes is more likely to occur in patients with severe repolarization delay and sinus bradycardia or atrioventricular block, and its appearance in four patients within a period of nine months after the introduction of disopyramide treatment in our service raises the possibility that this is not a rare complication of this drug, especially if used in combination with other QT interval-prolonging agents.

Aged↗