Department of Laboratory Medicine & Pathology University of Minnesota Minneapolis MN.
Division of Biostatistics School of Public Health University of Minnesota Minneapolis MN.
J Am Heart Assoc. 2020 Feb 4;9(3):e013934. doi: 10.1161/JAHA.119.013934. Epub 2020 Jan 30.
Background While elevated homocysteine has been associated with calcification in several studies, its importance as a cardiovascular risk factor remains unclear. This study examines the relationship between homocysteine and vascular and valve calcification in the MESA (Multi-ethnic Study of Atherosclerosis) cohort. Methods and Results MESA participants with baseline homocysteine measurements and cardiac computed tomography scans were included (N=6789). Baseline and follow-up assessment of vascular (coronary artery [CAC], descending thoracic aorta [DTAC]) and valve (aortic valve [AVC], mitral annular [MAC]) calcification was performed. Prevalence ratio/relative risk regression was used to assess the relationship of homocysteine with prevalent and incident calcification, and multivariable logistic regression was used to assess associations between homocysteine and calcification progression. Elevated homocysteine was associated with greater relative risk of prevalent and incident CAC and incident DTAC. We also identified a strong association between elevated homocysteine and CAC and DTAC progression. Elevated homocysteine was found to confer a >2-fold increased risk of severe CAC progression (defined as ΔCAC ≥100/year) and an ≈1.5-fold increased risk for severe DTAC progression (defined as ΔDTAC ≥100/year). Conclusions To our knowledge, this is the first study demonstrating an association between elevated homocysteine and both incidence and progression of coronary and extra-coronary vascular calcification. Our findings suggest a potential role for elevated homocysteine as a risk factor for severe vascular calcification progression. Future studies are warranted to further assess the utility of homocysteine as a biomarker for vascular calcification incidence and progression. Clinical Trial Registration https://www.clinicaltrials.gov/. Unique identifier: NCT00005487.
虽然几项研究表明同型半胱氨酸水平升高与钙化有关，但它作为心血管风险因素的重要性仍不清楚。本研究在 MESA（动脉粥样硬化的多民族研究）队列中检查了同型半胱氨酸与血管和瓣膜钙化之间的关系。
纳入了基线时具有同型半胱氨酸测量值和心脏计算机断层扫描的 MESA 参与者（N=6789）。对血管（冠状动脉[CAC]、降主动脉[DTAC]）和瓣膜（主动脉瓣[AVC]、二尖瓣环[MAC]）钙化进行了基线和随访评估。使用患病率比/相对风险回归来评估同型半胱氨酸与现患和新发钙化的关系，使用多变量逻辑回归来评估同型半胱氨酸与钙化进展之间的关系。同型半胱氨酸升高与 CAC 和 DTAC 现患和新发的相对风险增加相关。我们还发现同型半胱氨酸与 CAC 和 DTAC 进展之间存在很强的关联。同型半胱氨酸升高与严重 CAC 进展（定义为ΔCAC≥100/年）的风险增加超过 2 倍和严重 DTAC 进展（定义为ΔDTAC≥100/年）的风险增加约 1.5 倍相关。
据我们所知，这是第一项表明同型半胱氨酸升高与冠状动脉和非冠状动脉血管钙化的发生和进展之间存在关联的研究。我们的研究结果表明，同型半胱氨酸升高可能是严重血管钙化进展的一个潜在风险因素。未来的研究需要进一步评估同型半胱氨酸作为血管钙化发生和进展的生物标志物的效用。
