Chronic inflammation and coronary microvascular dysfunction in patients without risk factors for coronary artery disease
Chronic inflammation and coronary microvascular dysfunction in patients without risk factors for coronary artery disease
复制标题
DOI：
10.1093/eurheartj/ehp205
复制
发表时间：
2009-08-01
影响因子：
39.3
通讯作者：
Camici, Paolo G.
中科院分区：
文献类型：
--
作者：
Recio-Mayoral, Alejandro;Mason, Justin C.;Camici, Paolo G.
为证实慢性炎症可导致冠状动脉微血管功能障碍（CMD），应用正电子发射断层扫描（PET）技术测定了25例系统性红斑狼疮（SLE）或类风湿性关节炎（RA）患者的静息和高血（腺苷140 μ g/kg/min）心肌血流量（MBF）。冠状动脉血流储备（CFR）计算为腺苷/静息MBF。患者在血管造影时冠状动脉正常或病变程度最低（即管腔直径< 20%），无心血管危险因素。25名年龄和性别匹配的健康志愿者作为对照。患者和对照组的静息MBF相似（1.25 +/- 0.27 vs. 1.15 +/- 0.24 mL/min/g; P = 0.15），而患者的充血性MBF较低（2.94 +/- 0.83 vs. 4.11 +/- 0.84 mL/min/g; P < 0.001）和CFR（2.44 +/- 0.78 vs. 3.81 +/- 1.07; P < 0.001）。CFR与病程（r = -0.65; P < 0.001）和SLE疾病活动性（r = -0.69; P = 0.01）呈负相关。7例患者在腺苷治疗期间出现缺血性心电图变化。与无变化的患者相比，他们的疾病持续时间更长（21 +/- 7 vs. 14 +/- 5年; P = 0.03），CFR更低（1.76 +/- 0.81 vs. 2.49 +/- 0.54; P = 0.006）。我们推测，这是长期全身炎症的结果，这可能先于并促成这些患者的早发冠状动脉疾病。
To demonstrate that exposure to chronic inflammation results in coronary microvascular dysfunction (CMD).Using positron emission tomography, resting and hyperaemic (adenosine, 140 mu g/kg/min) myocardial blood flow (MBF) was measured in 25 patients with systemic lupus erythematosus (SLE) or rheumatoid arthritis (RA). Coronary flow reserve (CFR) was calculated as adenosine/resting MBF. Patients had normal or minimally diseased (i.e. < 20% luminal diameter) coronary arteries at angiography and no cardiovascular risk factors. Twenty five age- and gender-matched healthy volunteers served as controls. Resting MBF was similar in patients and controls (1.25 +/- 0.27 vs. 1.15 +/- 0.24 mL/min/g; P = 0.15) while patients had lower hyperaemic MBF (2.94 +/- 0.83 vs. 4.11 +/- 0.84 mL/min/g; P < 0.001) and CFR (2.44 +/- 0.78 vs. 3.81 +/- 1.07; P < 0.001). CFR was inversely related to disease duration (r = -0.65; P < 0.001) and SLE disease activity (r = -0.69; P = 0.01). Seven patients showed ischaemic electrocardiographic changes during adenosine. They had longer disease duration (21 +/- 7 vs. 14 +/- 5 years; P = 0.03) and lower CFR (1.76 +/- 0.81 vs. 2.49 +/- 0.54; P = 0.006) when compared with patients without changes.A reduced CFR in the absence of significant coronary disease is suggestive of CMD. We speculate that this is the consequence of prolonged systemic inflammation, which may precede and contribute to premature coronary artery disease in these patients.