Plasma Homocysteine, Aortic Stiffness, and Renal Function in Hypertensive Patients

Abstract

Abstract-Hyperhomocysteinemia has been associated with both vascular structure alterations and vascular clinical end points. To assess the relation between plasma homocysteine, structure and function of large arteries, and the presence of clinical vascular disease, we investigated a population of 236 hypertensive patients. We estimated arterial stiffness by measuring the carotid-femoral pulse wave velocity. Total plasma homocysteine was determined by fluorometric high-performance liquid chromatography. The presence of cardiovascular disease was defined on the basis of clinical events, including coronary heart disease, cerebrovascular disease, and peripheral vascular disease. In this population, pulse wave velocity was positively correlated with homocysteine, even after adjustments for age, mean blood pressure, extent of atherosclerosis, and creatinine clearance (Pϭ0.016). Analysis of variance showed statistically significant differences between the mean values of homocysteine, creatinine clearance, and pulse wave velocity according to the extent of atherosclerosis, with an increase in these 3 parameters concomitant with an increase in the number of vascular sites involved with atherosclerosis. In conclusion, in hypertensive patients the levels of homocysteine are strongly and independently correlated to arterial stiffness measured by aortic pulse wave velocity. Plasma homocysteine, creatinine clearance, and aortic pulse wave velocity are higher in patients presenting with clinical vascular disease. These results suggest that the evaluation of aortic distensibility and homocysteine levels can help in cardiovascular risk assessment in hypertensive populations. Key Words: homocysteine Ⅲ arteries Ⅲ blood flow velocity Ⅲ vascular diseases Ⅲ hypertension, renovascular C ardiovascular (CV) disease (CVD) is a major cause of morbidity, dependence, and mortality worldwide. Besides the well-accepted CV risk factors such as smoking, diabetes mellitus, dyslipidemia, and hypertension, hyperhomocysteinemia is emerging as an independent and graded risk factor for stroke, myocardial infarction, and CV death. [1][2][3] Although there is considerable epidemiological evidence for a relationship between plasma homocysteine and CVD, not all prospective studies have supported such a relationship. 4 -8 Moreover, it is not known whether a reduction in plasma homocysteine will reduce CVD risk. 9,10 Experimental studies have demonstrated that hyperhomocysteinemia can induce smooth muscle cell proliferation, 11 endothelial dysfunction, 12 collagen synthesis, and deterioration of elastic material of the arterial wall. 13 In humans, plasma homocysteine levels were found to be positively correlated with carotid artery intimalmedial wall thickness 14 and with extracranial carotid artery stenosis. 15 Regarding the relationships between homocysteine and hypertension, 2 studies noted a synergistic effect of these parameters on CV risk, 16,17 and Sutton-Tyrrell et al 18 reported an independent relationship between high homocysteine levels and is...

Total plasma homocysteine is associated with hypertension in Type I diabetic patients

“…Recently, an inverse relation between a range of tHcy concentrations and endothelium-dependent coronary blood flow was documented [32]. Furthermore, it was shown that increased tHcy concentrations in patients with essential hypertension are strongly and independently correlated to stiffness of the aortic artery measured by aortic pulse wave velocity (adjusted for GFR) [33]. Thus, longstanding, mild to moderate hyperhomocysteinaemia could contribute to the development of hypertension through interference with the nitrovasodilator system and could therefore promote microvascular and macrovascular complications, which are mainly determined by hypertension.…”

Circulating homocysteine and large arterial stiffness and thickness in a population-based sample of middle-aged and elderly men

“…12,14 The fact that other studies observed a significant association between tHcy levels and PWV is probably due to the fact that those studies were performed in subjects who were at a markedly increased risk of cardiovascular events. 11,27,28 Two other studies reported that acute rises in tHcy after oral methionine caused increased aortic stiffness. 29,30 We believe that this finding does not conflict with our results as these effects of tHcy were attained at concentrations that are not comparable to the epidemiological observations.…”

D919G polymorphism of methionine synthase gene is associated with blood pressure response to benazepril in Chinese hypertensive patients

“…Since only nitric oxide-mediated vasodilation is damaged, the impact of Hcy on endothelium function may have small influence on blood pressure reduction response to benazepril. Finally, a high-plasma Hcy level might be associated with increased arterial stiffness as well as thickness (Bortolotto et al 1999;Malinow et al 1993;Nestel et al 2003; Smilde et al 1998), which may lead to a poor response to benazepril. But whether blood pressure can be directly affected by an increased arterial stiffness resulting from hyperhomocysteinemia remains to be elucidated (Davis et al 2001;Nestel et al 2003).…”