Yu Qiao, Shang Baoling, Sun Haijiao, Jiang Wei, Cao Qian, Zou Xu
Department of Cardiac Function Center.
Linnan Deng's School of Internal Medicine Inheritance Studio.
Blood Press Monit. 2025 Oct 1;30(5):222-233. doi: 10.1097/MBP.0000000000000766. Epub 2025 Aug 5.
To investigate the associations between phenotypic age acceleration (PhenoAgeAccel) and all-cause/cardiovascular disease (CVD)-related mortality in hypertensive patients.
We analyzed data from 14 352 hypertensive adults (≥20 years) in the National Health and Nutrition Examination Survey 1999-2010. PhenoAge was calculated using chronological age and nine biomarkers (albumin, creatinine, glucose, C-reactive protein, lymphocyte%, mean cell volume, red blood cell distribution width, alkaline phosphatase, and white blood cell count). PhenoAgeAccel was derived as residuals from linear regression of PhenoAge on chronological age. Participants were stratified by PhenoAge [<46.6792 (792-64.774 (T1-T2), ≥64.774 (≥T2)] and PhenoAgeAccel [<-4.3382 (382-0.9896 (T1-T2), ≥0.9896 (≥T2)] tertiles. Cox proportional hazards models assessed mortality risks.
Increased all-cause mortality was observed in hypertensive patients with PhenoAge in T1-T2 group [hazards ratio = 4.38, 95% confidence interval (CI): 3.79-5.06] and greater than or equal to T2 (hazards ratio = 14.22, 95% CI: 12.32-16.43). Significant association between PhenoAgeAccel greater than or equal to T2 and increased risk of all-cause mortality in hypertensive patients (hazards ratio = 1.41, 95% CI: 1.29-1.55) was identified. PhenoAge of T1-T2 (hazards ratio = 5.15, 95% CI: 3.86-6.86) and greater than or equal to T2 (hazards ratio = 20.20, 95% CI: 14.98-27.26) were related to increased CVD-related mortality in hypertensive patients. Increased risk of CVD-related mortality was identified in hypertensive patients with PhenoAgeAccel greater than or equal to T2 (hazards ratio = 1.35, 95% CI: 1.17-1.56).
Elevated PhenoAge and PhenoAgeAccel significantly predict higher all-cause and CVD mortality in hypertension, supporting clinical risk stratification.
探讨表型年龄加速（PhenoAgeAccel）与高血压患者全因/心血管疾病（CVD）相关死亡率之间的关联。
我们分析了1999 - 2010年美国国家健康与营养检查调查中14352名≥20岁的高血压成年患者的数据。使用实际年龄和九种生物标志物（白蛋白、肌酐、葡萄糖、C反应蛋白、淋巴细胞百分比、平均细胞体积、红细胞分布宽度、碱性磷酸酶和白细胞计数）计算PhenoAge。PhenoAgeAccel通过PhenoAge对实际年龄的线性回归残差得出。参与者按PhenoAge [<46.6792（792 - 64.774（T1 - T2），≥64.774（≥T2）]和PhenoAgeAccel [<-4.3382（382 - 0.9896（T1 - T2），≥0.9896（≥T2）]三分位数分层。Cox比例风险模型评估死亡风险。
在T1 - T2组[风险比 = 4.38，95%置信区间（CI）：3.79 - 5.06]以及大于或等于T2组（风险比 = 14.22，95% CI：12.32 - 16.43）的高血压患者中观察到全因死亡率增加。确定PhenoAgeAccel大于或等于T2与高血压患者全因死亡风险增加之间存在显著关联（风险比 = 1.41，95% CI：1.29 - 1.55）。T1 - T2组（风险比 = 5.15，95% CI：3.86 - 6.86）以及大于或等于T2组（风险比 = 20.20，95% CI：14.98 - 27.26）的PhenoAge与高血压患者CVD相关死亡率增加有关。在PhenoAgeAccel大于或等于T2的高血压患者中确定CVD相关死亡风险增加（风险比 = 1.35，95% CI：1.17 - 1.56）。
升高的PhenoAge和PhenoAgeAccel显著预测高血压患者更高的全因和CVD死亡率，支持临床风险分层。
