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Title: Limitation of left ventricular dysfunction after acute myocardial infarction
Author: Hargreaves, Allister D.
Awarding Body: University of Edinburgh
Current Institution: University of Edinburgh
Date of Award: 1993
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Myocardial infarction remains an important cause of death and disability in Scotland. Although initial mortality is largely a consquence of arrhythmias, after the first few hours mortality and morbidity is closely related to the extent of myocardial damage and subsequent ventricular dilatation. This thesis discusses means of reducing left ventricular dysfunction after myocardial infarction. The first two sections describe a placebo controlled double blind clinical trial of oral therapy with captopril or isosorbide mononitrate initiated early after myocardial infarction and continued for 28 days. Left ventricular function and volume as assessed by echocardiography, radionuclide ventriculography or magnetic resonance imaging was similar in the placebo and vasodilator groups at 5 weeks. Even the placebo group showed a trend to a decrease in ventricular diameter. In contrast to many similar studies most of these patients (88% ) received thrombolysis, perhaps resulting in a population with little tendency to ventricular dilatation. Clinical outcome (death, cardiogenic shock) was significantly better in the captopril group, suggesting this agent may have a role for high risk patients (possibly those with persisting coronary occlusion). However there was no evidence that vasodilator therapy reduced infarct size as quantified by tomographic radionuclide imaging. In addition the acute inflammatory response, as reflected by measures of neutrophil activation and free radical lipid attack, was not modified by vasodilator therapy. The last two sections focus on coronary artery reperfusion. A detailed study of 17 patients with myocardial infarction found streptokinase therapy caused complement and neutrophil activation, particularly in those that did not reperfuse. This inflammatory activation may lead to a detrimental increase in infarct size. The pattern of complement activation was consistent with plasmin mediated proteolytic activation rather than an antigen-antibody reaction.
Supervisor: Not available Sponsor: Not available
Qualification Name: Thesis (M.D.) Qualification Level: Doctoral
EThOS ID:  DOI: Not available