Microvascular Responses to Cardiovascular Risk Factors

Abstract

Hypertension, hypercholesterolemia, diabetes and obesity are among a growing list of conditions that have been designated as major risk factors for cardiovascular disease (CVD). While CVD risk factors are well known to enhance the development of atherosclerotic lesions in large arteries, there is also evidence that the structure and function of microscopic blood vessels can be profoundly altered by these conditions. The diverse responses of the microvasculature to CVD risk factors include oxidative stress, enhanced leukocyte-and platelet-endothelial cell adhesion, impaired endothelial barrier function, altered capillary proliferation, enhanced thrombosis, and vasomotor dysfunction. Emerging evidence indicates that a low-grade systemic inflammatory response that results from risk factor-induced cell activation and cell-cell interactions may underlie the phenotypic changes induced by risk factor exposure. A consequence of the altered microvascular phenotype and systemic inflammatory response is an enhanced vulnerability of tissues to the deleterious effects of secondary oxidative and inflammatory stresses, such as ischemia and reperfusion. Future efforts to develop therapies that prevent the harmful effects of risk factor-induced inflammation should focus on the microcirculation.

Increasing fruit and vegetable intake has no effect on retinal vessel caliber in adults at high risk of developing cardiovascular disease

“…Major CVD risk factors such as elevated blood pressure and obesity are known to induce similar phenotypic (pro-oxidative, pro-inflammatory, pro-thrombogenic) changes in all vascular beds including the microcirculation [27] and these factors have also been linked to morphological alteration of the retinal vessels [10,11]. It is possible that vascular reactivity is mediated, in part, by changes in arterial blood pressure.…”

Microcirculatory Disturbances in the Pathogenesis of Acute Pancreatitis

“…This family of membrane proteins consists of CD11a/CD18, CD11b/CD18 and CD11c/ CD18 and interacts with the ICAM-1 endothelial protein whose expression is enhanced by TNFa and IL-1 [16,17]. This interaction fastens the neutrophil to the surface of the endothelial cell and allows the next stage.…”

Heart Failure as a Comorbidity of Diabetes: Role of Dipeptidyl Peptidase 4

“…The primary cause of enhanced platelet aggregation observed in diabetes is hyperglycemia and hyperinsulinemia, leading to platelet activation and oxidative stress [48][49][50] . In addition to macrovascular thrombosis, microvascular thrombosis could occur in diabetes 51) . Therefore, the prothrombotic phenotype may link to an impaired coronary microcirculation and the resultant cardiac dysfunction 7, 52, 53) .…”