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Circulating CD34~+/KDR~+ endothelialprogenitor cells are reduced in chronicheart failure patients as a functionof Type D personality

机译:循环CD34〜+ / KDR〜+内皮脯蜂窝细胞减少了计时的患者作为D型人格的功能

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The aim of the present study was to assess whether EPC (endothelial progenitor cell) number/function might be an explanatory factor for the observed relationship between Type D personality (a joint tendency towards negative affectivity and social inhibition) and poor cardiovascular prognosis. We also assessed whether the effect of a single exercise bout on EPC number/function was affected by Type D personality. A total of 35 sedentary men with CHF (chronic heart failure; left ventricular ejection fraction <=45 %) underwent CPET (cardiopulmonary exercise testing) and personality assessment with the 14-item Type D scale. CD34~+/KDR (kinase insert domain-containing receptor)~+ cells were quantified by flow cytometry before and immediately after CPET. Migration of early EPC towards VEGF (vascular endothelial growth factor) and SDF-1alpha (stromal-cell-derived factor-1alpha) was investigated. Type D (n= 10) and non-Type D (n = 25) patients were comparable with regards to demographics, disease severity and Framingham risk factor score. Circulating EPC numbers were reduced by 54% in Type D compared with non-Type D patients (0.084 + 0.055 and 0.183 + 0.029% of lymphocytes respectively; P = 0.006). Exercise led to a 60% increase in EPC in Type D patients, whereas the EPC number remained unchanged in the non-Type D group (P - 0.049). Baseline migratory capacity was related to disease severity, but was not different between Type D and non-Type D patients. Exercise induced a highly significant enhancement of migratory capacity in both groups. In conclusion, reduced EPC numbers might explain the impaired cardiovascular outcome in Type D patients. The larger increase in circulating EPCs observed in these patients suggests that acute exercise elicits a more pronounced stimulus for endothelial repair.
机译:本研究的目的是评估EPC(内皮祖细胞)数/功能是否可能是观察到的D人物之间观察到的关系的解释性因素(对负面情感和社会抑制的关节趋势)和差的心血管预后。我们还评估了单次运动Bout对EPC号/功能的影响是否受到D型人格的影响。共有35名久坐不动的男性,CHF(慢性心力衰竭;左心室喷射分数<= 45%)接受CPET(心肺运动测试)和具有14项D级的人格评估。通过在CPET之前和在CPET之后通过流式细胞术来量化CD34〜+ / KDR(含激酶嵌入结构域受体)〜+细胞。研究了早期EPC迁移到VEGF(血管内皮生长因子)和SDF-1α(基质细胞衍生因子-1Alpha)的迁移。 D型(n = 10)和非型D(n = 25)患者与人口统计,疾病严重程度和伪装风险因子分数相当。与非D型患者(0.084±0.055和0.183 + 0.029%的淋巴细胞)相比,D循环EPC数减少了54%; P = 0.006)。锻炼导致D型患者EPC增加了60%,而EPC号在非型D组中保持不变(P - 0.049)。基线迁徙能力与疾病严重程度有关,但D型和非型患者之间没有差异。运动诱导两个群体中迁徙能力的高度显着提高。总之,降低EPC号码可以解释D型患者的心血管结果受损。在这些患者中观察到的循环EPC的增加表明,急性运动引发了一种更明显的内皮修复刺激。

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