Perioperative myocardial infarction after coronary bypass surgery.
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Biomedical subjects
Publications and source records attributed to M Ray.
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A 44-yr-old man suffering fro exertional, emotional and spontaneous angina underwent coronary arteriography. During the examination he had a spontaneous attack of angina with ST elevation in the anterior leads. Injection of a contrast medium in the left coronary artery during pain showed marked spasm with anterior descending artery occlusion. The spasm was quickly relieved by nitroglycerin. Intravenous administration of 0.4 mg of ergonovine maleate reproduced the anginal episode with pain, ST elevation in the anterior leads and coronarographic patterns of a spasm occluding the anterior descending artery at the same level. After nitroglycerin, the pain disappeared and the electrocardiographic and coronarographic findings returned to basal conditions.
In 10 patients with supraventricular tachycardia who underwent an electrophysiological study the ectopic atrial origin of the tachycardia could be demonstrated by the intracavitary localization of the earliest depolarized point (six cases in the right atrium and four cases in the left). Vagal stimulation and/or the i.v. infection of ATP induced or increased the degree of AV block during tachycardia; in five cases ATP interrupted the tachycardia. On the basis of their clinical and electrophysiological behavior, the patients were divided into two groups. In the first one (6 patients) tachycardia was persistent, started following late atrial beats with the same morphology of the subsequent and showed a progressive initial rate increase (warm-up phenomenon); programmed atrial stimulation failed to start and interrupt it. In the second group (4 patients) tachycardia was paroxysmal or repetitive, started following early atrial beats and could be induced and interrupted by programmed atrial stimulation. With respect to the electrophysiological characteristics of each group the authors try to define the possible mechanism responsible for the tachycardia (automaticity and micro-reentry).
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To evaluate hyaluronidase's effect in reducing post-infarction myocardial necrosis, we randomized 91 patients with anterior infarction to control (45) or to hyaluronidase-treatment (46) groups. A 35-lead precordial electrocardiogram was recorded on admission and seven days later. Hyaluronidase was administered intravenously after the first electrocardiogram and every six hours for 48 hours. QRS-complex changes were analyzed to assess the drug's effect. Precordial sites with ST-segment elevation (larger than or equal to 0.15 mV) on the initial electrocardiogram that retained an R wave were considered vulnerable for the development of electrocardiographic signs of necrosis. The sum of R-wave voltages of vulnerable sites fell more in the control group than in the hyaluronidase group (70.9 +/- 3.6 per cent [+/- 1 S.E.M.] vs 54.2 +/- 5.0 per cent P less than 0.01). Q waves appeared in 59.3 +/- 4.9 per cent of the vulnerable sites in control versus 46.4 +/- 4.9 per cent in hyaluronidase-treated patients (P less than 0.05). Thus, hyaluronidase reduced the frequency of electrocardiographic signs of myocardial necrosis.
This paper reports two patients with a ring 22 chromosome which has been confirmed by Q-banding. The literature contains 19 patients with a ring G-group chromosome which has been shown by chromosome banding to be a ring 22. The most commonly reported features in affected patients have included: retardation with disproportionate verbal delay, reduced head circumference, hypotonia, unsteady gait, large ears with abnormal configuration, and epicanthic folds. The importance of these, as well as other, less often noted findings, is discussed in relation to a possible r(22) syndrome.
An infant who died in the perinatal period with the unusual association of trisomy 18 and cebocephaly is described. It is suggested that this association may be more common than is generally recognised because the majority of such infants are stillborn or live only briefly and often do not have chromosome studies performed.
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Two cases of paroxysmal supraventricular tachycardia sustained by an atrioventricular junctional reentry mechanism are presented. During the electrophysiological study it was possible to induce paroxysms of tachycardia showing 3:2 Lucianai-Wenckebach type and 2:1 atrioventricular block. The site of the block, its functional nature and the possible involvement of an anterogradely blocked atrio-nodal or atrio-His accessory pathway in the reentry circuit are discussed.
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UDP-glucose 4-epimerase from Saccharomyces fragilis is rapidly inactivated by heating at 42 degrees C for 7 min and at 45 degrees C for 4 min. The effector site, specific for sugar phosphates, is destroyed still earlier. The enzyme is inactivated by the dissocation of NAD from it leaving the dimeric structure unaffected. It can be reactivated by mercaptoethanol and NAD, both of which are essential for reactivation, and NAD becomes associated with the dimeric protein moiety.
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