49 THỬ NGHIỆM LÂM SÀNG KHẲNG ĐỊNH: ACID FOLIC LÀM GIẢM HUYẾT ÁP, BỆNH TIM MẠCH VÀ HOMOCYSTEIN MÁU

Introduction

Prospective previous researches had confirmed a solid, graded, and independent positive association between blood pressure and risk of stroke and cardiovascular disease (CVD) (Chobanian et al., 2003). The latest epidemiological data showed that hypertension is the biggest single contributor to the global burden of disease, leading to approximately nine million deaths each year (Lim et al., 2012), which was largely mediated through CVD and stroke (Poulter et al., 2015). Furthermore, the numbers of subjects suffered from hypertension and the morbidity of high blood pressure worldwide were predicted to increase over the next decade (Kearney et al., 2005). What is more, hyperhomocysteinemia has also emerged as an independent risk factor for CVD and stroke. A recent meta-analysis showed that folic acid supplementation to lower total homocysteine (tHcy) concentrations could effectively reduce the risk of stroke in primary prevention (Wang et al., 2007). Meanwhile, it was interesting to note that several carefully conducted studies to date have showed hyperhomocysteinemia often accompany with hypertension in many experimental models, as well as in patients with primary hypertension, especially systolic blood pressure (SBP) (Lim and Cassano, 2002; Huo et al.,2015). In addition, some randomized, placebo-controlled trials (RCTs) of tHcy-lowering therapy had shown that such intervention was associated with a decrease in blood pressure (Mangoni et al., 2002). However, although Hyperhomocysteinemia associated hypertension patients (HT/HHcy) are common in clinic, the precise mechanism by which tHcy results in vascular dysfunction and contributes to hypertension are largely unknown (Sen et al., 2010). To date, several mechanisms have been proposed. Hyperhomocysteinemia related changes in vascular biology such as increased arterial stiffness, vascular smooth muscle cell proliferation and endothelial dysfunction could easily lead to an increase in blood pressure (Stehouwer and van Guldener, 2003).

The evidence from observational studies suggested that HT/HHcy levels were associated with increased danger of CVD and stroke compared with hypertension alone (Wang et al., 2007). Stanger and colleagues displayed that tHcy lowering may have intrinsic vasoprotective effects principally independent of folic acid supplementation (Stanger et al., 2002). Two meta-analyses reported that folic acid administration may be good for CVD prevention in patients with kidney disease, especially in patients without a history of grain fortification with folic acid, with lower percent baseline diabetes (Jardine et al., 2012; Qin et al., 2013). In addition, folic acid supplementation was effective in stroke prevention in populations with no or partial folic acid fortification (Huo et al., 2012). On the contrary, Zhou et al reported that folic acid did not impact on the incidence of CVD, stroke or all-cause mortality based on the 16 RCTs (Zhou et al.,2011). Taken together, multiple clinical trials had now been performed investigating folic acid administration for the prevention of CVD and stroke outcomes in HT/HHcy patients. However, there were still no meta-analysis concerns on tHcy-lower therapy in HT/HHcy. Our purpose was thus to do a meta-analysis focusing on efficacy of folic acid plus antihypertensive combination therapy among patients with HT/HHcy.