Endothelial Dysfunction: Its Clinical Value and Methods of Assessment

Abstract

Endothelial dysfunction (ED) is a systemic disorder characterized by reduced production of nitric oxide. This pathologic condition, which impairs vascular homeostasis, leads to the loss of protective properties of endothelial cells and is related to the pathogenesis of cardiovascular diseases. ED may affect every vascular bed, accounting for several clinical implications, particularly when the coronary bed is affected. Although the reliability of ED as a cardiovascular disease surrogate is still debated, many methods for its assessment have been proposed. In this review, we underline the clinical value of ED in the cardiovascular field and summarize the principal methods currently available for its assessment.

Reciprocal Relationship Between Insulin Resistance and Disturbed Adma/No Axis in Gestational Diabetes Mellitus.

“…Such relationship between NO level and IR could be attributed the fact that insulin metabolic signaling increases endothelial cell NO production, so impaired vascular insulin sensitivity is an early defect leading to impaired vascular relaxation through reduction of NO production by endothelium (44,45) . Moreover, IR induces pathway-specific impairment in phosphatidylinositol 3-kinase-dependent signaling leading to imbalance between NO production and secretion of endothelin-1 and induces endothelial dysfunction (46) which is characterized by reduced production of NO, thus creating a vicious circle (47) .…”

Assessment of endothelial function by flow-mediated dilation in diabetic patients: Effects of physical exercise

“…In addition, NO also acts inhibiting platelet aggregation, leukocyte adhesion, attenuation of vascular smooth muscle cell proliferation and migration, mitochondrial function, oxidative stress and inflammation. Thus, NO is a fundamental protective element to maintain the integrity of endothelium and the homeostasis of the cardiovascular system (Lundberg et al, 2015;Strisciuglio et al, 2014;Versari, Daghini, Virdis, Ghiadoni, & Taddei, 2009;Zhao et al, 2015).…”

“…This unbalance is believed to be as consequence of reduced NO production and/or its bioavailability to the surrounding tissues (Avogaro et al, 2008;Endemann & Schiffrin, 2004;Strisciuglio et al, 2014). Endothelial dysfunction also causes thromboembolic disease and pro-inflammatory state by NO deficiency.…”

“…Moreover, endothelial dysfunction can be observed in the early stage of CVD, especially atherosclerosis and, has independent prognostic value to acute cardiovascular events for subjects with or without CAD (Halcox et al, 2002;Yang et al, 2010). Thus, early detection of endothelial dysfunction is essential in preventing and even identification of a reversible step in the development of these cardio-metabolic disorders (Park & Park, 2015;Strisciuglio et al, 2014;Widlansky, Gokce, Keaney Jr., & Vita, 2003).…”

Folate therapy improves the stress-to-rest mean LV volume ratio in myocardial perfusion imaging in patients with diabetes

“…An abnormally high stress-to-rest mean left ventricular volume (SRLVV) ratio is also one of the stress-induced abnormalities in myocardial perfusion imaging (MPI) that may be unrelated to obstructive coronary artery disease [7]. High SRLVV ratio-transient ischemic dilatation (TID)-is a prognostic factor in cardiovascular disease in persons with diabetes mellitus [8] and correlates with difference in stress and rest LV ejection fractions [9], which is a risk factor for future cardiac events [10]. Considering the simultaneous correlation of ED and TID by abnormalities of MPI which may occur in the absence of obstructive coronary artery disease, we speculate ED may associate with TID through microvascular mechanisms [6,7].…”