The Influence And Mechanism Of Xuezhikang On Arterial Stiffness In Patients With Essential Hypertension

Backgrand: It needs a relatively long process from essential hypertension tocardiovascular events. Effectively control at the beginning of the pathophysiologicalchanges in hypertension, improvement in the early stage of arterial stiffness due tohypertention, might decrease mortality and morbidity of cardiovascular disease. Themain characteristic of early vascular lesion in subjects with hypertension is increasedarterial stiffness. Pluse wave velocity (PWV)—the most commonly used index ofarterial stiffness—has been listed as a routine examination of subclinicalarteriosclerosis in Europe. PWV is one of the risk factors of subclinicalarteriosclerosis in hypertensive patients, and is also an independent predictor ofcardiovascular mortality and morbidity. The improvement of PWV can be used as anevaluation index for antihypertensive therapy. The beneficial effects of statins in theprimary and secondary prevention in cardiovascular disease have been confirmed.Some of the cholesterol-independent or "pleiotropic" effects of statins involvemaintaining vascular function which could decrease cardiovascular events. However,in recent years, the conclusions of statins improving arterial stiffness wereinconsistent. Xuezhikang, an extract of Cholestin, contains a family ofmonacolin-related substances, one of which is a naturally occurring lovastatin.Clinical researches related to Xuezhikang on arterial stiffness are deficient. What arethe mechanism of Xuezhikang on arterial stiffness? Whether Xuezhikang couldprevent or reverse subclinical target organ damage in patients with hypertension?Mathods: This was a randomized, double-blinded, placebo-controlled study. From2010to2011,100essential hypertension patients with normal or lightly elevatedcholesterol levels were randomized to assign to Xuezhikang group and placebo group.Both groups included50individuals. No statistically significant difference in age,gender, taking antihypertensive drugs, blood pressure levels, serum lipid levelsbetween the two groups. Subjects were given Xuezhikang1200mg/d or placebo for6 months. Physical examination, serum lipid spectrum, endothelin-1(ET-1),homocysteine (Hcy),high sensitivity C reactive protein (hs-CRP), matrixmetalloproteinases-9(mmp-9), high-sensitivity cardiac troponin T (hs-cTnT),urinealbumin-creatinine ratio (UACR) were monitored at baseline and6months in allsubjects. Arterial stiffness parameters which included β, Ep, AC, AI and PWVβ weremeasured by Echo Tracking.Results:90cases with completed data were selected at the end of the study. Therewere41males (45.6%) and49females (54.4%), with a mean age of57.7±10.2years.1. Compared with baseline levels, the levels of systolic blood pressure (SBP), pulsepressure (PP), β, Ep, PWVβ were significantly decreased in Xuezhikanggroup(P<0.05).2. Compared with baseline levels, the levels of TG, TC, LDL-C,hs-CRP, Hcy and MMP-9were significantly decreased (P<0.05), the level of HDL-Cwas significantly increased(P<0.05), the levels of ET-1had no change (P>0.05) inXuezhikang group after6months treatment.3. In Xuezhikang group, the changes ofarterial stiffness parameters (△β,△Ep,△PWVβ) were positively related to thechanges of hs-CRP and MMP-9(P<0.05). There were no correlation between thechanges of arterial stiffness parameters and the changes of serim lipidspectrum(P>0.05).4. The prevalence of elevated hs-cTnT(hs-cTNT≥13.3pg/ml)inXuezhikang group was9.1%before treatment, and6.8%after treatment, thedifference had no statistically significant (P>0.05). After treatment, the changes ofUACR had no statistically significant (P>0.05).Conclusions: Xuezhikang effectively improved arterial stiffness in patients withessential hypertension probably through its non-lipid effects which included reductionof the vascular inflammatory process and reduction of the extracellular matrixdegeneration. The mechanism of Xuezhikang improving arterial stiffness wasunrelated with lipid-lowering effects. No effectively improvement of Xuezhikang onsubclinical myocardial damage and microalbuminuria in patients with essentialhypertension.