Do hemophilia A and von Willebrand disease protect against carotid atherosclerosis? A comparative study between coagulopathics and normal subjects by means of carotid echo-color Doppler scan
Do hemophilia A and von Willebrand disease protect against carotid atherosclerosis? A comparative study between coagulopathics and normal subjects by means of carotid echo-color Doppler scan
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DOI：
10.1177/107602969900500405
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发表时间：
1999-10-01
影响因子：
2.9
通讯作者：
Girolami, A
中科院分区：
文献类型：
--
作者：
Bilora, F;Dei Rossi, C;Girolami, A
动脉粥样硬化是由遗传和环境因素引起的多因素疾病，具有重要的临床后遗症。本研究的目的是用回声彩色多普勒扫描评价一组血友病和von Willebrand病患者的颈动脉粥样硬化程度，并与一组明显没有动脉粥样硬化危险因素的正常受试者比较。所有来我科内科(帕多瓦医院)就诊的凝血疾病患者和正常患者均进行了体格检查、血液分析、标准心电图、胸部X线片、回声彩色多普勒扫描和详细的病史检查。我们检查了156名受试者，76名凝血病症患者(46名男性，30名女性)和77名正常人(37名男性，40名女性)。高血压28.9%，糖尿病6.5%，血脂17.1%，吸烟39.4%，肥胖36.8%(p<；0.05)。超声-彩色多普勒扫描显示颈动脉斑块在对照组为27.2%，而在凝血病变组为13.1%(p<；0.05)。血友病患者和患有更严重疾病的von Willebrand病患者的斑块比那些缺陷较轻的患者更少。凝血病理学显示了我们揭示的斑块的23.6%，与76.3%的DF对照组(p<；.01)相比，狭窄程度较轻(p<；.01)。我们的数据表明，血友病A和von Willebrand病患者的颈动脉斑块较少，颈动脉狭窄程度也较同性别和年龄的正常人小。这些数据似乎强化了这样一种假设，即凝血缺陷可能会保护患者免受颈动脉粥样硬化及其后遗症的影响。
Atherosclerosis is a multifactorial disease caused by genetic and environmental factors with important clinical sequelae. The aim of this study was to evaluate the degree of carotid atherosclerosis by echo-color Doppler scan in a group of patients affected by hemophilia A and von Willebrand disease versus a group of normal subjects apparently free of atherosclerotic risk factors. All coagulopathics and normal patients who came to our internal Medicine Department (Padua Hospital) underwent physical exam, blood analysis, standard electrocardiogram, chest x-ray, echo-color Doppler scan, and a thorough history. We examined 156 subjects, 76 coagulopathics (46 men, 30 women) and 77 normals (37 men, 40 women). Coagulopathics were affected by hypertension in 28.9% of cases, diabetes mellitus in 6.5%, dislipidemia in 17.1%, smoke in 39.4%, and obesity in 36.8% (p < .05). Echo-color Doppler scan revealed carotid plaques in 27.2% of control patients versus 13.1% of coagulopathics (p < .05). Hemophilics and subjects with von Willebrand disease with a more serious illness had fewer plaques than those with lighter defects. Coagulopathics showed 23.6% of the plaques we revealed on the whole, versus 76.3% df control subjects (p < .01), with a lighter degree of stenosis (p < .01). Our data demonstrate that patients with hemophilia A and von Willebrand disease have fewer carotid plaques and a smaller degree of carotid stenosis than normal subjects of the same sex and age. These data seem to strengthen the hypothesis that blood coagulation defects may allow protection against carotid atherosclerosis and its sequelae.