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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For the greater part of the 20th century, the pathophysiology of acute myocardial infarction regarding whether thrombosis was either present or primary was debated until 1973 when pathologists and clinicians met and by consensus, finally decided that the data supported that transmural infarction (what we now refer to as ST elevation myocardial infarction or STEMI) was caused by thrombus in the vessel supplying the infarcted territory. As the data for this consensus came from pathological analysis, it took another 7 years until angiographic and interventional data in humans with acute presentations of transmural infarction convincingly indicated that thrombus was indeed responsible. Subsequently, in patients presenting with either syndromes of unstable angina or nontransmural (later called non-ST elevation) myocardial infarction, it was established through angiographic and other interventional approaches that thrombus formation was also causative in a substantial proportion of these patients. This article reviews the history and this search for causation of myocardial infarction that now has resulted in present therapies that have saved innumerable lives over the last 30 to 40 years.
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Patients presenting to the emergency department with consideration of an acute coronary syndrome (ACS) are risk-stratified with sensitive troponin assays. Among many patients who present with symptoms other than chest pain, they are admitted for observation if the troponin assay is above the upper reference limit of that specific assay. ⋯ As such, the clinician is often confused about the optimal treatment at hospital discharge. More studies should address the value of specific known therapies in this cohort that have been shown to improve outcomes in patients with an acute coronary syndrome or type 1 myocardial infarction.
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The definition of severe aortic stenosis has undergone significant change casting a wider net to avoid missing patients who could benefit from valve replacement. The presence or absence of symptoms remains the key decision-making element; however, individuals presently undergoing evaluation are older, more likely asymptomatic, and have lower gradients. Due to numerous potential measurement errors, attention to detail when performing diagnostic testing and understanding their limitations are necessary to render appropriate treatment. ⋯ The amount of aortic valve calcification adds useful information when the degree of aortic stenosis is uncertain. A good history and physical integrated with high-quality imaging data allows for appropriate clinical treatment decisions for patients with aortic stenosis. The goal is simultaneously to provide aortic valve replacement for patients in need while avoiding overdiagnosis and performance of unnecessary procedures.
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The role of targeted hypothermia in patients with coma after cardiac arrest has been challenged in a recent randomized clinical trial. ⋯ Targeted temperature management was not associated with improved survival or neurological outcomes compared with normothermia in comatose patients after cardiac arrest. Further studies are warranted to further clarify the value of targeted hypothermia compared with targeted normothermia.