Provocation of coronary artery spasm by the cold pressor test. Hemodynamic, arteriographic and quantitative angiographic observations.
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Biomedical subjects
Publications and source records attributed to R J Luchi.
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The assess whether the magnitude of exercise induced ST segment depression improves the predictive values of symptom limited exercise tests, and helps in the recognition of patients with more severe coronary heart disease, 90 consecutive patients with positive treadmill tests who also underwent selective coronary arteriography were reviewed. The predictive value improved progressively with the increasing ST depression and was most reliable in a select group of patients with normal electrocardiographic baseline who were not receiving digitalis (73% with ST depression greater than or equal to 1 mm to 100% with ST depression greater than or equal to 4 mm). The incidence of 2 and 3 vessel disease increased from 61% with ST depression greater than or equal to 1 mm in the overall population to 100% with ST depression greater than or equal to 4 mm in the select group, and the incidence of left main trunk lesions increased, respectively from 6 to 30%. The prediction of 2 and 3 vessels disease was found to be significantly greater when patients were dichotomized into those with ST depression greater than or equal to 4 mm compared to less than 4 mm. It is concluded that the magnitude of ST segment depression definitely improves the predictive values of exercise tests as well as the ability to recognize the patients with more severe disease. However, the markedly positive exercise tests cannot be utilized to accurately predict the presence of 2 or 3 vessel disease in individual cases unless ST depression attains 4 mm or more in patients with normal electrocardiographic baseline who are not taking digitalis. In this group, the ability to predict left main trunk lesion is approximately 30%.
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Coronary artery spasm is an important pathogenetic mechanism in some forms of myocardial ischemic disease. Factors that may be important in the genesis of spasm include the autonomic nervous system, prostaglandins, endoperoxides, thromboxanes, and the calcium availability to the contractile apparatus. Spasm results in myocardial ischemia with attendant chest pain and electrocardiographic and hemodynamic changes; it is the primary pathogenetic mechanism in Prinzmetal's variant angina and has been found in association with classic angina pectoris and acute myocardial infarction. Diagnosis of coronary artery spasm is firmly made only by coronary angiography. Treatment includes the use of both short- and long-acting nitrates and the slow-channel blocking agents such as verapamil, nifedipine, and perhexiline.
An equation was derived from which the turnover time of individual muscle proteins could be calculated from measurements made at a single time interval in individual animals after initiation of constant intravenous infusion of labelled amino acid. The calculation requires only the specific radioactivities of the amino acid in plasma, in the intracellular fluid and in the protein under study. Pool sizes were not required. When the equation was applied to adult guinea-pig cardiac myosin, the average turnover time was 16 +/- 1 days.
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We have reported an instance of fracture of a temporary bipolar electrode catheter with embolization of the distal fragment to the lung. The patient had no untoward effects for 45 days before death. Autopsy revealed no thrombosis proximal or distal to the catheter fragment. The inability of the catheter to withstand the stress of usage questions the efficacy of its design. Careful inspection of the catheter before its use might have prevented this complication.
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Little is known of the clinical significance of myocardial bridges, which may be recognized angiographically as systolic coronary artery narrowing (SCAN). A retrospective review of a 1 year's experience (313 consecutive coronary arteriograms) revealed 5 patients with SCAN, an incidence of 1.6%. SCAN involved the proximal and/or middle segments of the left anterior descending coronary artery in all patients. It is of particular note that the administration of nitroglycerin noticeably accentuated the SCAN phenomenon in each of 3 patients to whom it was administered. Four of the 5 patients had left ventricular hypertrophy due to hypertrophic cardiomyopathy (2), aortic stenosis (1), and hypertension (1). All 5 patients with the SCAN phenomenon had anginal chest pains, and critical obstructive coronary atherosclerosis was observed in only 2 cases. The other 3 patients showed, otherwise normal coronary arteriograms. Thus, myocardial bridges appear to be angiographically manifest predominantly in patients with cardiac hypertrophy. Nitroglycerin, which accentuates SCAN, might be useful as a provocative test to enhance the angiographic recognition of this phenomenon. The possible role of myocardial bridges in the production of myocardial ischemia warrants further investigation.
Two hundred consecutive patients with a history of chest pain undergoing cardiac catheterization, coronary angiography and atrial pacing have been analyzed to assess the clinical significance of Mobitz I atrioventricular (A-V) block developing with the stress of atrial pacing. Of 160 patients with coronary artery disease, 26 (16%) developed Mobitz I A-V block at rates below 140 beats/min. Eighteen of these 26 patients (69%) had electrocardiographic evidence of old inferior wall myocardial infarction, compared to only 34 of the remaining 134 patients (29%) (P = less than 0.01). During the mean follow-up of 29.5 months (range 18-50 months) none of the 26 patients has developed spontaneous second or third degree A-V block. Twenty-three of the 26 patients had an exercise test within one week of the pacing study. No A-V block was noticed during or immediately following exercise, although the mean heart rate attained during exercise was higher than the mean pacing rate at which the A-V block occurred (136 +/- 5 vs 122 +/- 3, P = less than 0.01). Eighteen of these 23 achieved heart rates equal to or higher than the pacing rate at which A-V block developed. Nineteen (83%) shortened their P-R interval during exercise and 4 (17%) did not change the P-R length. Although atrial pacing-induced Mobitz I A-V block may indicate a latent A-V nodal conduction abnormality in some cases, its demonstration does not necessarily predict the occurrence of spontaneous advanced A-V block. Exercise should not be restricted in these patients on the basis of such a finding during a pacing study.
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A patient with classical clinical and roentgenographic features of congenital absence of the left pericardium is described. On physical examination in the supine position, the precordial apical impluse was markedly displaced laterally. In the left lateral decubitus position, however, the apical impulse was felt in a mor medial location. This apparently paradoxical movement of the apical impulse was not found in persons with normal hearts or with left ventricular enlargement of hypertrophy, and may be characteristic of the pericardial defect. Further, with echocardiography we were able to demonstrate the absence of a pericardial echo on the lateral surface of the heart. Thus, echocardiography may be a useful noninvasive tool in the diagnosis of this defect.
A number of serum enzymes increase after strenuous exercise. However, there is no information concerning these enzymes after routine treadmill testing, SGOT, CPK and LDH were determined before, immediately after, at 4 and 24 h postexercise in 100 subjects undergoing this test. When the group was considered as a whole, only the SGOT showed a slight but statistically significant elevation immediately after exercise. The mean values of the SGOT at 4 and 24 h, as well as the mean values for the CPK and LDH at all times after exercise, were not significantly increased. SGOT increased more significantly immediately after exercise in those patients who exercised more than 6 min. This group of patients also showed modest but statistically significant elevations of their CPK immediately after completion of the exercise test. Analyses of the data in relation to the presence or absence of ischemic ST shifts and presence or absence of documented coronary obstruction, failed to show any significant correlation. The effect of conditioning on the serum enzyme changes postexercise was not demonstrable.