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作者：Laurie Barclay, MD  
出處：WebMD醫學新聞

　　September 16, 2009 — 根據一項9月8日發表於線上循環期刊（Circulation）的前瞻性世代研究結果，女性的代謝症候群（MetS）與未來罹患周邊動脈血管疾病（PAD）有關。
　　
　　麻州波士頓哈佛大學醫學院與布萊根婦女醫院心臟疾病預防中心的David Conen醫師與其同事們表示，MetS與心肌梗塞及中風事件有關，也與亞臨床發炎反應有關。然而，關於MetS及未來發生PAD的前瞻性研究數據並不多，且很少有研究檢驗發炎反應的角色。我們因此評估MetS、發炎與PAD事件之間的關係。
　　
　　這項研究族群包括27,111位試驗前沒有心血管疾病危險因子，且收納到女性健康研究的女性。在後續追蹤中（平均時間為13.3年），114位女性發生有症狀的PAD事件。以Cox比例風險模式分析罹患MetS與沒有MetS女性發生PAD的風險。
　　
　　為了確認MetS與亞臨床發炎反應的關係，研究者們測量高敏感度C反應蛋白（hsCRP）、可溶細胞內貼附因子（sICAM-1），並使用多變項模式校正這些指標。
　　
　　罹患MetS女性，日後發生PAD的風險增加了62%（危險比值[HR]為1.62；95%信賴區間[CI]為1.10-2.38）。MetS在經過多變項校正後，仍然顯著與PAD有關（校正HR為1.48；95% CI為1.01-2.18）。每增加一個MetS定義特徵（腹部肥胖、高血壓、低高密度脂蛋白、高三酸甘油酯以及異常葡萄糖代謝），風險增加21%（校正HR為1.21；95% CI為1.06-1.39）。
　　
　　罹患MetS女性的hsCRP濃度中位數為4.0 mg/L，沒有MetS的女性則是1.5 mg/L（P< 0.001）。在sICAM-1方面，濃度分別為374 ng/ml與333 ng/ml。MetS相關風險顯著下降，且當hsCRP與sICAM-1加入多變項模式後，就不再達到統計上顯著差異（HR為1.14；95% CI為0.75-1.73）。
　　
　　研究作者們寫到，罹患MetS女性與之後發生有症狀PAD的風險增加有關。這些風險顯然絕大部分由發炎與內皮細胞活化效應所調控。
　　
　　這項研究的限制包括，收納一群主要是高加索人種的女性，限制了其應用性，且排除了亞臨床PAD患者。除此之外，這些分析使用修改過後的官方成人治療專家小組III的MetS定義。
　　
　　研究者們的結論是，非常需要來自其他族群的前瞻性研究數據，不僅是確認我們的研究，還要進一步釐清這個疾病發生與群聚危險因子的機轉連結。
　　
　　國家心臟、肺臟、與血液機構；國家癌症機構；Donald W. Reynolds基金會贊助這項研究。Conen博士接受瑞士國家科學基金會的經費贊助。資深作者Paul M. Ridker醫師名列於布萊根婦女醫院與心臟血管疾病相關發炎性生物標記專利所有人清單。

Metabolic Syndrome in Women Linked to Increased Risk for PAD

By Laurie Barclay, MD
Medscape Medical News

September 16, 2009 — Metabolic syndrome (MetS) in women is associated with an increased risk for future symptomatic peripheral artery disease (PAD), according to the results of a prospective cohort study reported online in the September 8 issue of Circulation.

"...MetS is associated with incident myocardial infarction and stroke and is linked with subclinical inflammation," write David Conen MD, MPH, from the Center for Cardiovascular Disease Prevention, Brigham and Women's Hospital and Harvard Medical School in Boston, Massachusetts, and colleagues. "However, prospective data pertaining to MetS and future...PAD are sparse with few studies examining the role of inflammation. We therefore evaluated the relationship between MetS, inflammation, and incident PAD."

The study cohort consisted of 27,111 women who had no cardiovascular disease at baseline and who were enrolled in the Women's Health Study. During follow-up (median duration, 13.3 years), 114 women went on to have incident symptomatic PAD. Risk for PAD among women with and without MetS was compared with use of Cox proportional hazards models.

To determine associations between MetS and subclinical inflammation, the investigators measured high-sensitivity C-reactive protein (hsCRP) and soluble intercellular adhesion molecule-1 (sICAM-1) and used multivariable models to adjust for these biomarkers.

Risk for future PAD was increased by 62% in women with MetS (hazard ratio [HR], 1.62; 95% confidence interval [CI], 1.10 - 2.38). MetS remained significantly associated with PAD after multivariable adjustment (adjusted HR, 1.48; 95% CI, 1.01 - 2.18). For each additional MetS-defining trait (abdominal obesity, high blood pressure, low high-density lipoprotein cholesterol levels, high triglyceride levels, and abnormal glucose metabolism), there was a 21% increase in risk (adjusted HR, 1.21; 95% CI, 1.06 - 1.39).

Median levels of hsCRP were 4.0 mg/L in women with MetS and 1.5 mg/L (P < .0001) in women without MetS (P < .0001). For sICAM-1, levels were 374 ng/mL and 333 ng/mL, respectively. The risk associated with MetS was markedly decreased and was no longer significant when hsCRP and sICAM-1 were added to multivariable models (HR, 1.14; 95% CI, 0.75 - 1.73).

"MetS is associated with an increased risk of future symptomatic PAD in women," the study authors write. "This risk appears largely mediated by the effects of inflammation and endothelial activation."

Limitations of this study include a study cohort of women who are of predominantly Caucasian origin, limiting generalizability, and exclusion of subclinical PAD. In addition, this analysis used a modified version of the official Adult Treatment Panel III MetS definition.

"Prospective data from other cohorts are greatly needed not only to corroborate our results but also to further elucidate mechanistic links between risk factor clustering and onset of this disease," the study authors conclude.

The National Heart, Lung, and Blood Institute; the National Cancer Institute; and the Donald W. Reynolds Foundation supported this study. Dr. Conen was supported by a grant from the Swiss National Science Foundation. Senior author Paul M. Ridker, MD, MPH, is listed as a coinventor on patents held by the Brigham and Women's Hospital that relate to the use of inflammatory biomarkers in cardiovascular disease.

Circulation. Published online September 8, 2009.