Department of Internal Medicine, Glostrup Hospital, University of Copenhagen, DK-2600 Glostrup, Denmark.
J Hypertens. 2011 May;29(5):997-1004. doi: 10.1097/HJH.0b013e328344daa3.
To investigate whether in-treatment measurements of subclinical organ damage (SOD) assessed by elevated urine albumin/creatinine ratio (UACR) or electrocardiographic left ventricular hypertrophy improved the prediction of the composite cardiovascular endpoint of cardiovascular death, nonfatal myocardial infarction and stroke beyond in-treatment Framingham risk score (FRS).
Excluding patients with a composite cardiovascular endpoint within the first year of treatment, 598 endpoints occurred in 6460 patients from the Losartan Intervention For Endpoint reduction in hypertension (LIFE) study with baseline and 1 year values for UACR, left ventricular hypertrophy by electrocardiography and FRS available.
Using Cox-regression analyses, FRS(1year) [hazard ratio=1.006 (0.98-1.04)] did not predict the endpoint independently of history of cardiovascular disease [hazard ratio=1.76 (1.49-2.08)], FRS(baseline) [hazard ratio=1.07 (1.04-1.11)], UACR(baseline) [hazard ratio=1.15 (1.07-1.23), all three P<0.001], Sokolow-Lyon(baseline) [hazard ratio=1.01 (1.006-1.02), P<0.01] and treatment allocation, whereas Cornell product(1year) [hazard ratio=1.01 (1.006-1.02), P<0.001] and to some degree UACR(1year) [hazard ratio=1.05 (0.99-1.10), P=0.09] predicted the endpoint independently of history of cardiovascular disease [hazard ratio=1.71 (1.44-2.02)], FRS(baseline) [hazard ratio=1.08 (1.06-1.10)], Sokolow-Lyon(baseline) [hazard ratio=1.01 (1.007-1.02), both P<0.001], UACR(baseline) [hazard ratio=1.11 (1.03-1.20), P<0.01] and treatment allocation decreasing -2 Log likelihood significantly (P<0.01).Presence of left ventricular hypertrophy by Cornell product(1year) or UACR(1year) at least 1 mmol/l [hazard ratio=1.40 (1.15-1.70), P=0.001] but not FRS(1year) above the median baseline value of 20 [hazard ratio=1.22 (0.94-1.57), not significant] was associated with higher risk of subsequent endpoint after adjustment for history of cardiovascular disease [hazard ratio=1.82 (1.54-2.15)], FRS(baseline) at least 20 [hazard ratio=1.67 (1.30-2.16)], left ventricular hypertrophy by Sokolow-Lyon(baseline) or UACR(baseline) at least 1 mmol/l [hazard ratio=1.61 (1.33-1.94), all P<0.001] and treatment allocation [hazard ratio=0.93 (0.79-1.09), not significant]. In contrast to FRS(1year) at least 20 decreased, SOD(1year) decreased -2Log likelihood significantly (P<0.01).
Cornell product(1year) and UACR(1year) improved in contrast to FRS(1year) risk prediction based on FRS(baseline), Sokolow-Lyon(baseline) and UACR(baseline) significantly in LIFE patients during antihypertensive treatment.
研究在降压治疗期间通过升高的尿白蛋白/肌酐比值（UACR）或心电图左心室肥厚（LVH）评估的亚临床器官损伤（SOD）的治疗中测量值是否能改善Framingham 风险评分（FRS）之外的心血管死亡、非致死性心肌梗死和卒中复合心血管终点的预测。
排除治疗第一年发生复合心血管终点的患者，在 Losartan Intervention For Endpoint reduction in hypertension（LIFE）研究中，共有 6460 例患者基线和 1 年时可获得 UACR、心电图左心室肥厚和 FRS 值，共发生 598 例终点事件。
使用 Cox 回归分析，FRS（1 年）[风险比=1.006（0.98-1.04）]不能独立于心血管疾病病史[风险比=1.76（1.49-2.08）]、FRS（基线）[风险比=1.07（1.04-1.11）]、UACR（基线）[风险比=1.15（1.07-1.23）]，所有三个 P<0.001]、Sokolow-Lyon（基线）[风险比=1.01（1.006-1.02）]和治疗分配预测终点，而 Cornell 乘积（1 年）[风险比=1.01（1.006-1.02）]，在一定程度上 UACR（1 年）[风险比=1.05（0.99-1.10）]，P=0.09]独立于心血管疾病病史[风险比=1.71（1.44-2.02）]、FRS（基线）[风险比=1.08（1.06-1.10）]、Sokolow-Lyon（基线）[风险比=1.01（1.007-1.02）]，所有 P<0.001]、UACR（基线）[风险比=1.11（1.03-1.20）]和治疗分配显著降低 -2Log 似然度（P<0.01）。Cornell 乘积（1 年）或 UACR（1 年）至少 1 mmol/L 存在左心室肥厚[风险比=1.40（1.15-1.70）]，P=0.001，但 FRS（1 年）中位数基线值大于 20[风险比=1.22（0.94-1.57）]，不显著，与心血管疾病病史[风险比=1.82（1.54-2.15）]、FRS（基线）至少 20[风险比=1.67（1.30-2.16）]、Sokolow-Lyon（基线）或 UACR（基线）至少 1 mmol/L 存在左心室肥厚[风险比=1.61（1.33-1.94）]，所有 P<0.001]和治疗分配[风险比=0.93（0.79-1.09）]显著相关。与 FRS（1 年）至少 20 降低相反，SOD（1 年）降低 -2Log 似然度显著（P<0.01）。
在 LIFE 患者的降压治疗期间，与 FRS（基线）、Sokolow-Lyon（基线）和 UACR（基线）相比，Cornell 乘积（1 年）和 UACR（1 年）显著改善了基于 FRS（基线）的风险预测。
