Hyperhomocysteinemia and its relations to conventional risk factors for cardiovascular diseases in adult Nigerians: the REMAH study

Abstract

Background Evidence linking homocysteine (Hcy) with cardiovascular diseases (CVD) or its risk factors are limited in a sub-Saharan black population. Objective We set out to evaluate the association between Hcy and hypertension and other CVD risk factors in a population of adult Nigerians. Methods Data of 156 adults aged 18–70 years was accessed from the North Central study site of the REmoving the MAsk on Hypertension (REMAH) study. Homocysteine, blood glucose and lipid profile in whole blood/serum were measured using standard laboratory methods. Hypertension was diagnosed if average of 5 consecutive blood pressure (BP) measurements obtained using a mercury sphygmomanometer was equal to or higher than 140 systolic and/or 90 mmHg diastolic or the individual is on antihypertensive medication. Hyperhomocysteinemia (HHcy) was defined as Hcy > 10 µmol/L. Results Of the 156 participants, 72 (43.5%) were hypertensive, of whom 18 had HHcy. Subjects with HHcy were significantly (p < 0.05) older (41.5 vs. 40.6yrs), had lower HDL-cholesterol (0.6 vs. 0.8 mmol/L) and higher systolic (145.5 vs. 126.0 mmHg) and diastolic BP (92.9 vs. 79.6 mmHg), compared to those without HHcy. Intake of alcohol and a 1 yr increase in age were respectively and significantly (p < 0.05) associated with a 1.54 and 0.10 µmol/L increase in Hcy. In a multivariable model adjusted for age, sex and body mass index, a 1 µmol/L increase in Hcy, was associated with a 1.69 mmHg and 1.34 mmHg increase in systolic and diastolic pressure (p < 0.0001) respectively; and a 0.01 mmol/L decrease in HDL-cholesterol (p < 0.05). Conclusion HHcy occurs among hypertensive Nigerians and it is independently associated with age, HDL-cholesterol, systolic and diastolic BP.

Differential effects of hyperhomocysteinemia on the lipid profiles and lipid ratios between patients with and without coronary artery disease: A retrospective observational study

“…There were also some invaluable clinical observations that demonstrated the possible link between Hcy and lipid metabolism pathways. Consistent research findings suggest that Hcy is significantly and negatively correlated with HDL-C and ApoAI in community-based or health physical examination populations, [12–17] and these correlations also exist in patients with diagnosed CAD. [19–21] It is well known that HDL and ApoAI exert antiatherogenic effects by transporting cholesterol from cells into peripheral tissues, [32] reducing oxidative stress and suppressing inflammatory pathways.…”

“…HHcy acts through various mechanisms, including vascular endothelial damage, stimulation of smooth muscle cell proliferation, and thrombosis activation. [10,11] Previous studies have shown that HHcy and serum Hcy are positively correlated with serum TC, LDL-C, and TG levels [12,13] and negatively correlated with serum HDL-C [12–17] and ApoAI [17] levels in physical examination populations or community-based populations. However, the VLDL-21 study [18] failed to find an association between HHcy and lipid profiles in a large population.…”

Lipid Profile Alterations and Predisposing factors associated with Cardiovascular Diseases at Kibagabaga District Hospital, Rwanda: A cross sectional study

“…It is estimated that the number of deaths associated with CVDs will increase from 17.5 million to 25 million by 2030 [3]. Lipid profiles are studied or tested in hospitals or by researchers to detect the risk of heart disease or cardiovascular diseases.…”

Plasma Cotinine Is Positively Associated with Homocysteine in Smokers but Not in Users of Smokeless Tobacco

“…Plasma total homocysteine (tHcy) is primarily considered to be a biomarker of functional vitamin B12 and folate status, and has also been demonstrated to be useful as a general risk marker of cardiovascular disease (CVD) [1,2]. tHcy is associated with cardiovascular risk factors [3] and correlates with the Framingham cardiovascular risk score [4]. Smoking is one of the strongest established risk factors for CVD.…”