The clinical impact of pulmonary vascular remodeling in smokers

描述(由研究人员提供)：吸烟相关的肺血管疾病已被证明是COPD患者发病率和死亡率的独立预测因子。以往的研究和观察表明，吸烟者可能存在几种类型的病理性肺血管重构。这些症状包括进行性管腔闭塞的炎性重塑，恶性充气区域的异常血管延长，以及严重的肺气肿破坏区域的血管完全丧失。虽然现有的工具可以用来研究这些过程的综合影响，如右心导管术、超声心动图和一氧化碳弥散能力(DLCO)的测量，但没有一种工具可以区分存在的血管重构/变形的类型或它们对临床损害的相对贡献。本研究的目的是提高对吸烟者肺血管重构的临床影响和流行病学相关性的了解。为此，我们将对参加COPD基因研究的所有受试者进行基于CT的纵隔(Aim 1)和实质内血管系统(Aim 2)的定量测量，然后通过超声心动图、心脏MRI和DLCO测量(Aim 3)在临床上验证这些测量。在目标3的最后一步，我们将研究肺和心血管疾病(包括临床诊断的心血管疾病和冠状动脉和胸主动脉钙化)之间的重叠和关联，以及肺血管形态与运动能力、COPD急性加重、症状和死亡率之间的关系。我们相信，这将导致对COPD病理生理学的更好理解，并最终可能改善COPD患者的护理。

DESCRIPTION (provided by investigator): Smoking related pulmonary vascular disease has been demonstrated to be an independent predictor of morbidity and mortality in patients with COPD. Previous investigation and observation suggests that there are several types of pathologic pulmonary vascular remodeling possible in smokers. These range from inflammatory remodeling with progressive luminal occlusion, aberrant vessel elongation in regions of hyperinflation, and outright loss of vasculature in regions of severe emphysematous destruction. While there are existing tools that may be used to investigate the aggregate effect of these processes such as right heart catheterization, echocardiography, and measurements of diffusing capacity for carbon monoxide (DLCO), none can differentiate the types of vascular remodeling/deformation present nor their relative contribution to clinical impairment. The purpose of this investigation is to improve understanding of the clinical impact and epidemiologic associations of pulmonary vascular remodeling in smokers. We will do this by performing CT based quantitative measures of the mediastinal (Aim 1) and intra-parenchymal vasculature (Aim 2) in all subjects enrolled in the COPDGene Study and then clinically validating these measures with echocardiography, cardiac MRI and measures of DLCO (Aim 3). In the final steps of Aim 3 we will examine the overlap and associations between pulmonary and cardiovascular disease (both clinical diagnosed CVD and both coronary and thoracic aortic calcification) and the relationship between pulmonary vascular morphology and exercise capacity, acute exacerbations of COPD, symptoms, and mortality. We believe that this will lead to improved understanding of the pathophysiology of COPD and may ultimately improve the care of patients with COPD.