The American journal of medicine
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For at least a few centuries, if not millennia, psychological stress has been popularly believed to contribute to heart disease. Does psychological stress really contribute to heart disease? Are anecdotal, patient, and lay press reports that angina, heart attack, and even cardiac death are caused by stress based on fact, or are they just folklore? In this review, the study data supporting associations between stress and cardiovascular risk, as well as potential mechanisms by which psychological stress might contribute to heart disease and precipitate myocardial ischemia and infarction, are critically reviewed and summarized.
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Platelet aggregation and thrombus formation represent the basic mechanism for clinical, electrocardiographic, and biomarker changes consistent with acute coronary syndrome. Various oral and intravenous formulations of platelet function inhibitors have been developed to help decrease platelet aggregation due to acute atherosclerotic plaque rupture. In this article, we review the various mechanisms, pharmacokinetics/pharmacodynamics, and the key clinical trials related to the platelet inhibitors that form the basis for current recommendations of their use in the ST elevation myocardial infarction guidelines by the American College of Cardiology/American Heart Association.