Abstract
Ischemic heart disease still represents a large burden on individuals and health care resources worldwide. By conventions, it is equated with atherosclerotic plaque due to flow-limiting obstruction in large–medium sized coronary arteries. However, clinical, angiographic and autoptic findings suggest a multifaceted pathophysiology for ischemic heart disease and just some cases are caused by severe or complicated atherosclerotic plaques. Currently there is no well-defined assessment of ischemic heart disease pathophysiology that satisfies all the observations and sometimes the underlying mechanism to everyday ischemic heart disease ward cases is misleading. In order to better examine this complicated disease and to provide future perspectives, it is important to know and analyze the pathophysiological mechanisms that underline it, because ischemic heart disease is not always determined by atherosclerotic plaque complication. Therefore, in order to have a more complete comprehension of ischemic heart disease we propose an overview of the available pathophysiological paradigms, from plaque activation to microvascular dysfunction.
Highlights
Over the last years clinical practice strategies have evolved optimizing prevention and treatment for ischemic heart disease (IHD), the consequences of this condition represent a significant burden on human health, in terms of mortality and morbidity [1]
IHD occurs as the result of multiple altered regulating vascular pathways that include severe atherosclerosis just in some cases
They suggest that microvascular disease plays an important role in the etiology of IHD, by regulating blood flow and oxygen and energetic substrates delivery, in the microcirculation–myocardium interaction
Summary
Over the last years clinical practice strategies have evolved optimizing prevention and treatment for ischemic heart disease (IHD), the consequences of this condition represent a significant burden on human health, in terms of mortality and morbidity [1]. Basic, translational, and clinical data have provided a massive amount of information about the etiology of myocardial ischemia. Both clinical, angiographic and autoptic findings suggest a complex pathophysiology of IHD [2,3,4,5,6,7,8], which goes beyond the conventional and simplistic role of atherosclerosis. For this reason, it is necessary to overcome the concept that IHD is always an atherosclerotic disease synonym. The vasodilatory effects of shear stress are mediated by endothelial-dependent vasodilatation
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