Palmieri Vittorio, Tracy Russell P, Roman Mary J, Liu Jennifer E, Best Lyle G, Bella Jonathan N, Robbins David C, Howard Barbara V, Devereux Richard B
Weill Medical College of Cornell University, New York, New York 10021, USA.
Diabetes Care. 2003 Oct;26(10):2764-9. doi: 10.2337/diacare.26.10.2764.
To evaluate in adults with type 2 diabetes the extent to which the relation of left ventricular hypertrophy (LVH) to markers of systemic inflammation (fibrinogen and high-sensitivity C-reactive protein [hsCRP]) are affected by microangiopathy.
We selected adults with type 2 diabetes using American Diabetes Association criteria from a population-based cohort, excluding those with medical history or electrocardiographic evidence of coronary heart disease or dialysis-dependent renal failure. LVH was assessed by echocardiogram.
Of the 1299 eligible participants, 384 (29.6%) had LVH, which was associated with higher BMI, hsCRP, fibrinogen, and albuminuria in univariate analyses. After controlling for significant confounders, fibrinogen and albuminuria were higher in the presence of LVH (both P < 0.01), whereas hsCRP was not (P = 0.2), mostly because of the confounding effect of BMI. Adjustment for albuminuria abolished the relation of LVH to higher fibrinogen (P = 0.2). However, fibrinogen was significantly higher in participants with LVH among those without pathologic levels of albuminuria (<30 mg/g creatinuria), but not independent of BMI. Although hsCRP and fibrinogen were moderately correlated, fibrinogen, but not CRP, showed a significant relation with albuminuria.
In adults with type 2 diabetes, echocardiographic LVH is associated with susceptibility to atherothrombosis and increased albuminuria, which is a marker of microangiopathy and endothelial dysfunction that appears in turn to be a relevant pathogenetic link between LVH and inflammation. However, in the absence of significant microalbuminuria, elevated BMI is a relevant pathogenetic factor in the relation of LVH to increased levels of markers of inflammation, potentially preceding development of significant albuminuria. In the presence of microangiopathy, we found that the atherothrombotic risk profile associated with LVH was independent of BMI and possibly reflected the association of LVH with a higher degree of endothelial dysfunction.
评估在2型糖尿病成人患者中，微血管病变对左心室肥厚（LVH）与全身炎症标志物（纤维蛋白原和高敏C反应蛋白[hsCRP]）之间关系的影响程度。
我们根据美国糖尿病协会标准，从一个基于人群的队列中选取2型糖尿病成人患者，排除有冠心病病史或心电图证据或依赖透析的肾衰竭患者。通过超声心动图评估LVH。
在1299名符合条件的参与者中，384名（29.6%）有LVH，在单因素分析中，LVH与较高的体重指数、hsCRP、纤维蛋白原和蛋白尿相关。在控制了显著的混杂因素后，存在LVH时纤维蛋白原和蛋白尿较高（均P<0.01），而hsCRP并非如此（P = 0.2），主要是由于体重指数的混杂效应。对蛋白尿进行校正后，LVH与较高纤维蛋白原之间的关系消失（P = 0.2）。然而，在无病理性蛋白尿水平（<30mg/g肌酐尿）的参与者中，有LVH者的纤维蛋白原显著更高，但并非独立于体重指数。尽管hsCRP与纤维蛋白原中度相关，但纤维蛋白原而非CRP与蛋白尿有显著关系。
在2型糖尿病成人患者中，超声心动图显示的LVH与动脉粥样硬化血栓形成易感性及蛋白尿增加相关，蛋白尿是微血管病变和内皮功能障碍的标志物，而这反过来似乎是LVH与炎症之间的一个相关发病机制联系。然而，在无显著微量白蛋白尿的情况下，体重指数升高是LVH与炎症标志物水平升高之间关系的一个相关发病因素，可能先于显著白蛋白尿的发生。在存在微血管病变的情况下，我们发现与LVH相关的动脉粥样硬化血栓形成风险特征独立于体重指数，可能反映了LVH与更高程度的内皮功能障碍之间的关联。
