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Biomedical subjects

A Maseri

Publications and source records attributed to A Maseri.

At least 415 records · Page 23Linked to original sources
PubMed1977

Coronary vasospasm in angina pectoris.

Coronary angiography was performed during 34 angina attacks in thirty patients admitted because of recurrent angina at rest. Nineteen (seventeen with S-T segment elevation and two S-T depression) had angiograms during a spontaneous attack, eleven (nine with S-T elevation and two with S-T depression) during an attack induced by intravenous ergonovine maleate. Control coronary angiograms showed a wide range of atherosclerotic obstruction, from normal vessels to severe triple-vessel disease. During the anginal attack, all patients with S-T segment elevation had vasospasm localised to one of the major branches, often resulting in complete occlusion. Attacks with S-T segment depression were seen only in patients with double or triple vessel disease, and here the vasospasm generally affected coronary branches without causing complete occlusion. When appropriately searched for, vasospastic angina seems to be common.

Adult↗
PubMed1977

Possibilities, limitations, and technique for the study of regional myocardial perfusion in man by Xenon-133.

The theoretical possibilities and the practical limitations of the Xenon-133 (133Xe) method for the study of regional myocardial perfusion in man are discussed. The techniques for data acqusition and processing developed over the past 5 years are described in detail. Illustrative examples of experimental findings are reported. The practical interpretation of the data, at the light of the influence of injection site, initial tracer distribution, constancy of counting geometry, spatial resolution, and Xenon retention in fat, is presented.

Coronary Circulation↗
PubMed1977

Regional myocardial perfusion in patients with atherosclerotic coronary artery disease, at rest and during angina pectoris induced by tachycardia.

We studied regional myocardial perfusion by scintigraphic computer-assisted analysis of initial distribution, washout rates, and residual activity of 133Xe injected into the left coronary artery of four patients with normal arteriograms and 14 patients with coronary stenosis. At rest, residual activity in poststenotic regions was always greater than in control regions, but initial washout rates were not slower. During angina, following xenon injections, the amount of indicator distributed to the poststenotic regions was markedly reduced; the increase of the initial washout rates was smaller than in control regions relative to rest, and residual activity was higher. Initial washout rates did not differ as much as from those of normal myocardium because in severe ischemia too little indicator is deposited initially in these regions to produce a change of any magnitude. Indeed, when angina was induced immediately after the xenon injection, poststenotic washout rates became much slower during angina than at rest, a finding that implicates functional factors in impairing poststenotic myocardial perfusion during angina.

Adult↗
PubMed1976

Pathophysiologic studies of the pulmonary and coronary circulations in man.

Studies of the pulmonary circulation in normal man, performed with external radiation detectors, have shown that pulmonary blood volume is about 10% of total blood volume. Pulmonary blood volume was unchanged in patients with acute or chronic left atrial hypertension and in normal persons during expansion of total blood volume in spite of marked increases in pulmonary vascular pressures. However, pulmonary blood volume was greatly increased in patients with polycythemia rubra vera and a large total blood volume and in patients with a left to right shunt but normal pulmonary intravascular pressure. Studies of regional myocardial perfusion with injection of xenon-133 solution into the left coronary artery revealed localized areas of ischemia distal to stenotic lesions even when the patient was at rest. During angina produced by pacing, more severe ischemia occurred, thus suggesting that functional factors reduce local perfusion below resting levels. In patients with "variant" angina, intravenous injection of thallium-201 chloride during spontaneous attacks has revealed large cold areas in myocardial scintigrams not present under control conditions, thus suggesting severe transmural reduction of perfusion in heart muscle corresponding to S-T segment elevation in the electrocardiogram.

Angina Pectoris↗
PubMed1976

Transient transmural reduction of myocardial blood flow demonstrated by thallium-201 scintigraphy, as a cause of variant angina.

In previous studies we demonstrated that variant angina could not be attributed to increased myocardial demands. In order to investigate whether a reduction of regional myocardial blood supply could be responsible for these ischemic episodes, we studied regional myocardial perfusion in six patients admitted to our coronary care unit. Myocardial scintigrams, obtained 5-7 min following i.v. injection of 1 mCi of thallium-201, performed during an episode of ST-segment elevation, showed transmural deficits of tracer uptake in the heart wall corresponding to the leads showing ST-segment elevation. These regional deficits ahd disappeared by 2 hours because of late uptake in previously ischemic myocardium. One week later, following injections performed in the absence of acute ischemia, no deficit was apparent. Tracer uptake in ischemic areas was 60% to 85% of that observed a week later. After adjusting for thallium-201 kinetics and counting geometry promblems., these scintigrams actually represent large underestimations of actual flow reduction. Thus variant angina appears to be caused by massive transmural reduction of myocardial blood supply.

Adult↗
PubMed1976

Systemic and coronary haemodynamic effects of the new hypotensive drug L 6150.

The acute systemic and coronary haemodynamic effects of a new hypotensive drug L 6150 (3-hydrazino-6-[N,N-bis(2-hydroxyethyl)amino]pyridazine) have been studied in six patients with renal or essential hypertension. The drug, administered intravenously at a dose of 2-9 mg, caused a marked hypotension and increase of cardiac output in five cases. Though left ventricular work was reduced or unchanged after the drug, myocardial blood flow increased markedly, coronary resistance decreased and coronary A-V oxygen difference decreased by about 50% indicating coronary vasodilation. When compared with the available data on the effects of hydrazinophthalazine, L 6150 appeared to have qualitatively similar effects, but a somewhat greater direct coronary vasodilator effect.

Aged↗