Evidences from epidemiologic studies demonstrate that heart rate is an independent risk factor for cardiovascular disease events within a wide range of subjects. An increase in the resting heart rate predisposes to cardiometabolic abnormalities and is closely associated with them. Heart rate is also closely associated with inflammation, endothelial function, plaque formation and progression, eventually plaque rupture, and cardiovascular death indicating that heart rate is associated with every process of atherosclerosis. Postprandial dysmetabolism induced by excessive intake of high-calorie diet generates oxidative stress leading to inflammation, sympathoexitation, and heart rate elevation. While the heart rate accelerates atherosclerosis via sympathetic nervous system, heart rate per se promotes atherosclerosis independent of sympathoexitation. Elevated heart rate accelerates the frequency of vascular wall stress, and low or oscillatory shear stress found downstream of non-target lesion, resulting in structural changes in the vascular wall and endothelial dysfunction. Evidence of heart rate lowering strategy for patients with coronary artery disease is considered mainly to be attributed to lowering the frequency of flow oscillation found downstream of non-target lesion. This local effect of heart rate-lowering strategy is a unique one that no other drugs have. Heart rate provides us a lot of information about the patients cardiovascular risk status. Moreover, heart rate per se could be an independent risk factor and might be an important therapeutic target.
Keywords: Atherosclerosis, cardiovascular disease, heart rate, risk factor, postmenopausal women, carotid artery stenosis, dyslipidemia, dysmetabolism, Sympathoexcitation, Inflammation
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