Kishimoto Shinji, Kajikawa Masato, Maruhashi Tatsuya, Iwamoto Yumiko, Matsumoto Takeshi, Iwamoto Akimichi, Oda Nozomu, Matsui Shogo, Hidaka Takayuki, Kihara Yasuki, Chayama Kazuaki, Goto Chikara, Aibara Yoshiki, Nakashima Ayumu, Noma Kensuke, Higashi Yukihito
Department of Cardiovascular Medicine, Graduate School of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.
Department of Gastroenterology and Metabolism, Institute of Biomedical and Health Sciences, Graduate School of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.
Int J Cardiol. 2017 Mar 15;231:181-187. doi: 10.1016/j.ijcard.2017.01.024. Epub 2017 Jan 5.
Endothelial dysfunction and abnormal vascular structure may be involved in the pathogenesis of chronic heart failure (HF). The purpose of this study was to evaluate simultaneously vascular function and vascular structure in patients with heart failure with preserved ejection fraction (HFpEF).
We measured flow-mediated vasodilatation (FMD) and nitroglycerine-induced vasodilation as indices of vascular function and intima-media thickness (IMT) as an index of vascular structure of the brachial artery in 41 patients with HFpEF (23 men and 18 women; mean age, 66±12yr) and 165 patients without HF (95 men and 70 women; mean age, 54±16yr).
FMD was significantly smaller in patients with HFpEF than in patients without HF (2.9±2.1% versus 4.6±2.7%, P=0.0002). Nitroglycerine-induced vasodilation was significantly smaller in patients with HFpEF than in patients without HF (9.3±4.1% versus 12.9±4.9%, P<0.0001). Brachial artery IMT was significantly larger in patients with HFpEF than in patients without HF (0.35±0.06mm versus 0.31±0.07mm, P=0.0002). After adjustment for age, sex, hypertension, dyslipidemia, and diabetes mellitus, the associations remained significant between HFpEF and FMD (odds ratio, 0.79; 95% confidence interval, 0.66-0.92; P=0.0032), nitroglycerine-induced vasodilation (odds ratio, 0.88; 95% confidence interval, 0.80-0.96; P=0.0039), and brachial artery IMT (odds ratio, 1.08; 95% confidence interval, 1.01-1.17; P=0.033).
These findings suggest that both endothelial dysfunction and abnormal vascular structure may contribute to the pathogenesis and maintenance of HFpEF. Endothelial function and vascular structure may be potential therapeutic targets for HFpEF.
内皮功能障碍和血管结构异常可能参与慢性心力衰竭（HF）的发病机制。本研究的目的是同时评估射血分数保留的心力衰竭（HFpEF）患者的血管功能和血管结构。
我们测量了41例HFpEF患者（23例男性和18例女性；平均年龄66±12岁）和165例无HF患者（95例男性和70例女性；平均年龄54±16岁）的肱动脉血流介导的血管舒张（FMD）和硝酸甘油诱导的血管舒张作为血管功能指标，以及内膜中层厚度（IMT）作为血管结构指标。
HFpEF患者的FMD显著小于无HF患者（2.9±2.1%对4.6±2.7%，P=0.0002）。HFpEF患者硝酸甘油诱导的血管舒张显著小于无HF患者（9.3±4.1%对12.9±4.9%，P0.0001）。HFpEF患者的肱动脉IMT显著大于无HF患者（0.35±0.06mm对0.31±0.07mm，P=0.0002）。在调整年龄、性别、高血压、血脂异常和糖尿病后，HFpEF与FMD（优势比，0.79；95%置信区间，0.66-0.92；P=0.0032）、硝酸甘油诱导的血管舒张（优势比，0.88；95%置信区间，0.80-0.96；P=0.0039）和肱动脉IMT（优势比，1.08；95%置信区间，1.01-1.17；P=0.033）之间的关联仍然显著。
这些发现表明，内皮功能障碍和血管结构异常可能都有助于HFpEF的发病机制和维持。内皮功能和血管结构可能是HFpEF的潜在治疗靶点。
