HF Unit, St Vincent's University Hospital, Elm Park, Dublin, Ireland.
Clin Ther. 2012 Jan;34(1):91-100. doi: 10.1016/j.clinthera.2011.11.002. Epub 2011 Dec 9.
The role of statin therapy in heart failure (HF) is unclear. The amino-terminal propeptide of procollagen type III (PIIINP) predicts outcome in HF, and yet there are conflicting reports of statin therapy effects on PIIINP.
This study determined whether there was an increase in serum markers of inflammation, fibrosis (including PIIINP), and B-type natriuretic peptide (BNP) in patients with systolic HF and normal total cholesterol and determined the effects of long-term treatment with atorvastatin on these markers.
Fifty-six white patients with systolic HF and normal cholesterol levels (age 72 [13] years; 68% male; body mass index 27.0 [7.3] kg/m(2); ejection fraction 35 [13]%; 46% with history of smoking) were randomly allocated to atorvastatin treatment for 6 months, titrated to 40 mg/d (A group) or not (C group). Age- and/or sex-matched subjects without HF (N group) were also recruited. Biomarkers were measured at baseline (all groups) and 6 months (A and C groups).
Serum markers of collagen turnover, inflammation, and BNP were significantly elevated in HF patients compared with normal participants (all P < 0.05). There were correlations between these markers in HF patients but not in normal subjects. Atorvastatin treatment for 6 months caused a significant reduction in the following biomarkers compared with baseline: BNP, from median (interquartile range) 268 (190-441) pg/mL to 185 (144-344) pg/mL; high-sensitivity C-reactive protein (hs-CRP), from 5.26 (1.95 -9.29) mg/L to 3.70 (2.34-6.81) mg/L; and PIIINP, from 4.65 (1.86) to 4.09 (1.25) pg/mL (all P < 0.05 baseline vs 6 months). Between-group differences were significant for PIIINP only (P = 0.027). There was a positive interaction between atorvastatin effects and baseline hs-CRP and PIIINP (P < 0.01).
Long-term statin therapy reduced PIIINP in this small, selected HF population with elevated baseline levels. Further evaluation of statin therapy in the management of HF patients with elevated PIIINP is warranted.
他汀类药物治疗心力衰竭（HF）的作用尚不清楚。III 型前胶原氨基末端肽（PIIINP）可预测 HF 的预后，但他汀类药物对 PIIINP 的治疗效果存在相互矛盾的报告。
本研究旨在确定收缩性 HF 患者血清中炎症、纤维化（包括 PIIINP）和 B 型利钠肽（BNP）标志物是否增加，并确定阿托伐他汀长期治疗对这些标志物的影响。
56 例收缩性 HF 且胆固醇水平正常的白人患者（年龄 72 [13]岁；68%男性；体重指数 27.0 [7.3]kg/m2；射血分数 35 [13%]；46%有吸烟史）被随机分为阿托伐他汀治疗组 6 个月，滴定至 40mg/d（A 组）或不治疗（C 组）。还招募了年龄和/或性别匹配的无 HF 患者（N 组）。所有组均在基线（所有组）和 6 个月（A 和 C 组）时测量生物标志物。
与正常参与者相比，HF 患者的胶原代谢、炎症和 BNP 血清标志物均显著升高（均 P < 0.05）。HF 患者的这些标志物之间存在相关性，但在正常受试者中不存在相关性。与基线相比，阿托伐他汀治疗 6 个月后，以下标志物显著降低：BNP，从中位数（四分位距）268（190-441）pg/mL 降至 185（144-344）pg/mL；高敏 C 反应蛋白（hs-CRP），从 5.26（1.95-9.29）mg/L 降至 3.70（2.34-6.81）mg/L；和 PIIINP，从 4.65（1.86）降至 4.09（1.25）pg/mL（均 P < 0.05，基线 vs 6 个月）。仅 PIIINP 组间差异有统计学意义（P = 0.027）。阿托伐他汀的作用与基线 hs-CRP 和 PIIINP 之间存在正交互作用（P < 0.01）。
在基线水平升高的小部分选择的 HF 人群中，长期他汀类药物治疗降低了 PIIINP。进一步评估他汀类药物在治疗 PIIINP 升高的 HF 患者中的作用是必要的。
