Endothelial Dysfunction Markers in Low Cardiovascular Risk Individuals: Comparison of Males and Females

Abstract

SummaryBackgroundCardiovascular diseases (CVD) account for approximately 50% of the total deaths in Turkey. Most of them are related with atherosclerotic coronary heart disease. Predictive value of endothelial dysfunction markers related with the earliest stage of atherosclerosis has been getting more attention. We hypothesized that differences in endothelial dysfunction biochemical markers among genders would aid to capture proatherogenic activity that was not diagnosed by conventional risk assessment scoring systems.MethodsWe assessed the endothelial dysfuntion markers in 92 Turkish adults who were in the »low CV risk group« according to ESC (European Society of Cardiology)-Score Risk Charts. We compared the males and females.ResultsWe observed higher endothelial dysfunction rates in males, with higher median and mean levels of e-NOS, ox-LDL before and after adjustment for HDL lowness and obesity (P=0.018, P=0.036 for NOS; P=0.000, P=0.004 for ox-LDL, respectively). Men had higher hs-CRP levels than females before adjustment (P=0.021). Decreased e-NOS levels were related with FMD for females before adjustment for confounders (P=0.028). We also found significant correlation between e-NOS and ox-LDL levels both before (r=0.360, P<0.001) and after adjustment (r=0.366, P<0.01) for confounders which pointed out the nitrosative stress. In multivariate regression analyses, after adjusting for other endothelial dysfunction markers which were not included in the ESC-risk scoring system, decreased e-NOS levels were independently asssociated with impaired flow mediated dilatation for females (odds ratio 0.3; P=0.038).ConclusionsOur results underline the importance of gender in evaluating endothelial dysfunction biochemical markers to assess cardiovascular risk for low CV risk indivuals.

Association of Circulating Levels of ADMA with Carotid Intima-Media Thickness in Patients with CKD: a Systematic Review and Meta-Analysis

“…Accumulating evidences suggested that endothelial dysfunction was one of the critical determinants in pathogenesis of atherosclerotic cardiovascular disease, and angiocardiopathy such as myocardial infarction, stroke, and vascular remodeling was independently associated with endothelial dysfunction [23][24][25][26]. Oxidative stress, inflammatory response and active material imbalance are involved in the progress of vascular endothelial injury [27].…”

Evaluation of endothelial dysfunction and the possibility of its correction at the present stage in patients with cardiovascular diseases

“…Помимо этого, NO тормозит агрегацию тромбоцитов, адгезию лейкоцитов, инфильтрацию и пролиферацию гладкомышечных клеток сосудов. NO препятствует окислительной модификации ЛПНП [10].…”

“…Не потеряла актуальности и точка зрения, что ЭД -это системное расстройство, характеризующееся прежде всего снижением выработки NO, патологическое состояние, ухудшающее сосудистый гомеостаз и приводящее к потере защитных свойств эндотелиальных клеток [6][7][8][9][10]. В противовес NO, как вазодилататору, в организме вырабатывается мощный вазоконстриктор -ЭТ-1 или в ряде литературных источников просто ЭТ [2,4,12].…”

“…Эндокардиальный эндотелий влияет на сократимость кардиомиоцитов через паракринные сигнальные вещества, такие как NO, ЭТ-1, простагландины (PGI2, PGF2, PGE2) и А II. Типичные поражения эндокардиального эндотелия были описаны при фибрилляции предсердий, ишемии / реперфузии, гипертрофии сердца, СН, сепсисе, ИМ, воспалении и тромбозе [3,8,10,16].…”

Effect of Acute Myocardial Infarction on a Disintegrin and Metalloprotease with Thrombospondin Motif 13 and Von Willebrand Factor and Their Relationship with Markers of Inflammation

“…e VWF is synthesised in endothelial cells and is then stored. It mediates platelet aggregation and adhesion [3]. It carries factor VIII in circulation and mediates initial platelets that stick to the sub endothelium following vascular endothelial damage as a result of hyperlipidaemia, smoking, or hypertension [4,5].…”