Lerman Joseph B, Joshi Aditya A, Chaturvedi Abhishek, Aberra Tsion M, Dey Amit K, Rodante Justin A, Salahuddin Taufiq, Chung Jonathan H, Rana Anshuma, Teague Heather L, Wu Jashin J, Playford Martin P, Lockshin Benjamin A, Chen Marcus Y, Sandfort Veit, Bluemke David A, Mehta Nehal N
From National Institutes of Health, National Heart, Lung, and Blood Institute, Bethesda, MD (J.B.L., A.A.J., A.C., T.M.A., A.K.D., J.A.R., T.S., J.H.C., A.R., H.L.T., M.P.P., M.Y.C., V.S., D.A.B., N.N.M.); Department of Dermatology, Kaiser Permanente Los Angeles Medical Center, CA (J.J.W.); and DermAssociates, Silver Spring, MD (B.A.L.).
Circulation. 2017 Jul 18;136(3):263-276. doi: 10.1161/CIRCULATIONAHA.116.026859. Epub 2017 May 8.
Psoriasis, a chronic inflammatory disease associated with an accelerated risk of myocardial infarction, provides an ideal human model to study inflammatory atherogenesis in vivo. We hypothesized that the increased cardiovascular risk observed in psoriasis would be partially attributable to an elevated subclinical coronary artery disease burden composed of noncalcified plaques with high-risk features. However, inadequate efforts have been made to directly measure coronary artery disease in this vulnerable population. As such, we sought to compare total coronary plaque burden and noncalcified coronary plaque burden (NCB) and high-risk plaque (HRP) prevalence between patients with psoriasis (n=105), patients with hyperlipidemia eligible for statin therapy under National Cholesterol Education Program-Adult Treatment Panel III guidelines (n=100) who were ≈10 years older, and healthy volunteers without psoriasis (n=25).
Patients underwent coronary computed-tomography angiography for total coronary plaque burden and NCB quantification and HRP identification, defined as low attenuation (<30 hounsfield units), positive remodeling (>1.10), and spotty calcification. A consecutive sample of the first 50 patients with psoriasis was scanned again 1 year after therapy.
Despite being younger and at lower traditional risk than patients with hyperlipidemia, patients with psoriasis had increased NCB (mean±SD: 1.18±0.33 versus 1.11±0.32, =0.02) and similar HRP prevalence (=0.58). Furthermore, compared to healthy volunteers, patients with psoriasis had increased total coronary plaque burden (1.22±0.31 versus 1.04±0.22, =0.001), NCB (1.18±0.33 versus 1.03±0.21, =0.004), and HRP prevalence beyond traditional risk (odds ratio, 6.0; 95% confidence interval, 1.1-31.7; =0.03). Last, among patients with psoriasis followed for 1 year, improvement in psoriasis severity was associated with improvement in total coronary plaque burden (β=0.45, 0.23-0.67; <0.001) and NCB (β=0.53, 0.32-0.74; <0.001) beyond traditional risk factors.
Patients with psoriasis had greater NCB and increased HRP prevalence than healthy volunteers. In addition, patients with psoriasis had elevated NCB and equivalent HRP prevalence as older patients with hyperlipidemia. Last, modulation of target organ inflammation (eg, skin) was associated with an improvement in NCB at 1 year, suggesting that control of remote sites of inflammation may translate into reduced coronary artery disease risk.
银屑病是一种与心肌梗死风险增加相关的慢性炎症性疾病,为体内研究炎症性动脉粥样硬化提供了理想的人体模型。我们假设,银屑病患者心血管风险增加部分归因于由具有高危特征的非钙化斑块组成的亚临床冠状动脉疾病负担增加。然而,在这一易感人群中,直接测量冠状动脉疾病的工作做得还不够。因此,我们试图比较银屑病患者(n = 105)、符合美国国家胆固醇教育计划成人治疗小组III指南且适合他汀类药物治疗的高脂血症患者(n = 100,年龄约大10岁)和无银屑病的健康志愿者(n = 25)之间的冠状动脉总斑块负担、非钙化冠状动脉斑块负担(NCB)和高危斑块(HRP)患病率。
患者接受冠状动脉计算机断层扫描血管造影,以量化冠状动脉总斑块负担和NCB,并识别HRP,HRP定义为低衰减(<30亨氏单位)、正性重构(>1.10)和点状钙化。对首批50例银屑病患者进行连续抽样,在治疗1年后再次扫描。
尽管银屑病患者比高脂血症患者年轻且传统风险较低,但银屑病患者的NCB增加(均值±标准差:1.18±0.33对1.11±0.32,P = 0.02),HRP患病率相似(P = 0.58)。此外,与健康志愿者相比,银屑病患者的冠状动脉总斑块负担增加(1.22±0.31对1.04±0.22,P = 0.001),NCB增加(1.18±0.33对1.03±0.21,P = 0.004),且HRP患病率超出传统风险(比值比,6.0;95%置信区间,1.1 - 31.7;P = 0.03)。最后,在随访1年的银屑病患者中,银屑病严重程度的改善与冠状动脉总斑块负担(β = 0.45,0.23 - 0.67;P < 0.001)和NCB(β = 0.53,0.32 - 0.74;P < 0.001)超出传统风险因素的改善相关。
银屑病患者的NCB更大,HRP患病率高于健康志愿者。此外,银屑病患者的NCB增加,HRP患病率与老年高脂血症患者相当。最后,靶器官炎症(如皮肤)的调节与1年后NCB的改善相关,这表明控制远处炎症部位可能转化为降低冠状动脉疾病风险。