二尖瓣环钙化(MAC)可能是生物衰老的潜在标志。然而,MAC与非心血管测量的关联,包括骨矿物质密度(BMD),肾衰竭,痴呆症,和非心血管死亡率,在多种族队列中没有得到很好的研究。在动脉粥样硬化的多种族研究中,我们使用了6,814名参与者(平均年龄:62.2±10.2岁;52.9%-女性)的数据,这些参与者在基线时没有心血管疾病。在研究基线时用非对比心脏计算机断层扫描评估MAC。使用多变量调整线性和逻辑回归,我们评估了MAC与BMD和步行速度的横断面相关性.此外,使用Cox比例风险,我们评估了MAC与肾衰竭的相关性,痴呆症,和全因死亡率。此外,我们使用竞争风险回归法评估了MAC与心血管和非心血管死亡率的相关性.MAC的患病率为9.5%,女性(10.7%)高于男性(8.0%)。MAC与低BMD(系数:-0.04;95CI:-0.06--0.02)相关,性别之间存在显着的相互作用(p相互作用:0.035)。MAC是,然而,与步行速度受损无关(比值比:1.09;95CI:0.89-1.33)。与没有MAC的个人相比,患有MAC的患者发生肾衰竭的风险增加,尽管不显著(风险比[HR]:1.18;95CI:0.95~1.45),但痴呆的风险显著更高(HR:1.36;95CI:1.10~1.70).此外,MAC患者的全因风险更高(HR:1.47;95CI:1.29-1.69),心血管(子分布HR:1.39;95CI:1.04-1.87),和非心血管死亡率(细分HR:1.35;95CI:1.14-1.60),与没有MAC的人相比。MAC≥100vs<100与BMD降低显著相关,肾衰竭,痴呆症,所有原因,心血管,和非心血管死亡率。总之,MAC与降低BMD和痴呆有关,以及所有原因,心血管,和非心血管死亡率在这个多种族队列。因此,MAC可能不仅是动脉粥样硬化负担的标志物,而且是其他代谢和炎症因子的标志物,这些因素会增加非心血管疾病结局和其他原因死亡的风险。
Mitral annular calcification (MAC) may be a potential marker of biologic aging. However, the association of MAC with noncardiovascular measures, including bone mineral density (BMD), incident renal failure, dementia, and noncardiovascular mortality, is not well-studied in a multiracial cohort. We used data from 6,814 participants (mean age: 62.2 ± 10.2 years, 52.9% women) without cardiovascular disease at baseline in the Multi-Ethnic
Study of Atherosclerosis. MAC was assessed with noncontrast cardiac computed tomography at
study baseline. Using multivariable-adjusted linear and logistic regression, we assessed the cross-sectional association of MAC with BMD and walking pace. Furthermore, using Cox proportional hazards, we evaluated the association of MAC with incident renal failure, dementia, and all-cause mortality. In addition, we assessed the association of MAC with cardiovascular and noncardiovascular mortality using competing risks regression. The prevalence of MAC was 9.5% and was higher in women (10.7%) than in men (8.0%). MAC was associated with low BMD (coefficient -0.04, 95% confidence interval [CI] -0.06 to -0.02), with significant interaction by gender (p-interaction = 0.035). MAC was, however, not associated with impaired walking pace (odds ratio 1.09, 95% CI 0.89 to 1.33). Compared with participants without MAC, those with MAC had an increased risk of incident renal failure, albeit nonsignificant (hazard ratio [HR] 1.18, 95% CI 0.95 to 1.45), and a significantly higher hazards of dementia (HR 1.36, 95% CI 1.10 to 1.70). In addition, participants with MAC had a substantially higher risk of all-cause (HR 1.47, 95% CI 1.29 to 1.69), cardiovascular (subdistribution HR 1.39, 95% CI 1.04 to 1.87), and noncardiovascular mortality (subdistribution HR 1.35, 95% CI 1.14 to 1.60) than those without MAC. MAC ≥100 versus <100 was significantly associated with reduced BMD, incident renal failure, dementia, all-cause, cardiovascular, and noncardiovascular mortality. In conclusion, MAC was associated with reduced BMD and dementia and all-cause, cardiovascular, and noncardiovascular mortality in this multiracial cohort. Thus, MAC may be a marker not only for atherosclerotic burden but also for other metabolic and inflammatory factors that increase the risk of noncardiovascular outcomes and death from other causes.