The clinical impact of longitudinal measures of cardiac and pulmonary vascular morphology in smokers

项目摘要/摘要： 在美国，COPD影响着多达2400万人，据估计，其中30%到70%的患者 有临床意义的肺血管疾病(PVD)。而观察到的平均肺活量的增加 动脉压倾向于轻度或中度，它们已被证明是医疗保健的独立预测因素 使用率和死亡率。然而，PVD合并继发性肺动脉高压是一种晚期表现。 慢性烟草烟雾暴露与肺血管和心脏的一系列变化 它们反映了疾病的进化。吸烟者大脑实质最早可观察到的变化之一是 肺血管重塑。这些变化已经在肺功能正常的受试者和 被认为是肺气肿破坏实质的前兆。随后的进展 肺气肿和恶性通货膨胀会导致心脏功能受损。左心室舒张期容量 右室缩小和扩大，理论上都是由隐匿性肺血管引起的。 疾病和肺血管阻力升高。我们对这些过程的了解是有限的，因为 它是基于使用一系列调查技术的不同临床研究的集合，如 如心导管术、组织病理学、超声心动图和心脏磁共振成像。这些 工具在很大程度上不能区分血流动力学的显著形态变化的贡献。 吸烟者的肺，如实质过度膨胀区域的血管延长，远端的修剪 小血管，以及肺气肿区域普遍缺乏血管床。我们之前已经 在第一轮COPDgene CT扫描和这次更新中，对这些特征进行了详细的调查 R01 HL0144624的应用，我们建议检查它们随时间的进展，对双室的影响 形态，以及与临床相关结果的相关性。 我们建议进行一项纵向研究，以了解肺血管和 参加COPD基因研究的6000名受试者的心脏形态。为了做到这一点，我们组装了一个 由肺病学家、计算机科学家、流行病学家、放射学家和统计学家组成的多学科团队。我们 将使用4D增强心脏CT扫描和配对来完善我们的心脏表面拟合模型 CARDIA研究中的心脏门控CT扫描和超声心动图。然后，我们将部署这些工具以及 我们在收集的所有第一轮、第二轮和第三轮COPDgene CT扫描中的血管分割算法 在10年的观察期内以标准化的间隔进行。

Project Summary/Abstract: COPD affects up to 24 million people in the United States and it is estimated that 30 to 70% of these patients have clinically significant pulmonary vascular disease (PVD). While the observed increases in mean pulmonary arterial pressure tend to be mild or moderate, they have been shown to be independent predictors of health care utilization and mortality. PVD with secondary pulmonary hypertension, though, is a late stage manifestation of chronic tobacco smoke exposure and there is a continuum of changes to the pulmonary vasculature and heart that reflect the evolution of disease. One of the earliest observable changes in the parenchyma of smokers is pulmonary vascular remodeling. These changes have been described in subjects with normal lung function and are thought to be the precursor to emphysematous destruction of the parenchyma. The subsequent progression of emphysema and hyperinflation then leads to impaired cardiac function. Diastolic volumes of the left ventricle decrease and right ventricle dilates, both of which have been theorized to be due to occult pulmonary vascular disease and elevations in pulmonary vascular resistance. Our knowledge of these processes is limited because it is based upon an aggregation of disparate clinical studies employing an array of investigative techniques such as cardiac catheterization, histopathology, echocardiography, and cardiac magnetic resonance imaging. These tools are largely unable to discriminate the contributions of hemodynamically significant morphologic changes in the lungs of smokers such as vessel elongation in hyperinflated regions of the parenchyma, pruning of the distal small vessels, and widespread absence of a vascular bed due in regions of emphysema. We have previously performed a detailed investigation of these features in the Round 1 COPDGene CT scans and with this renewal application for R01 HL0144624, we are proposing to examine their progression over time, effect on biventricular morphology, and association with clinically relevant outcomes. We are proposing to perform a longitudinal investigation of the clinical relevance of pulmonary vascular and cardiac morphology in 6000 subjects enrolled in the COPDGene Study. To do this we have assembled a multidisciplinary team of pulmonologists, computer scientists, epidemiologists, radiologists, and statisticians. We will refine our surface fitting model of the heart using both 4D contrast enhanced cardiac CT scans and paired cardiac gated CT scans and echocardiograms in the CARDIA Study. We will then deploy these tools as well as our vascular segmentation algorithms in all the Round 1, Round 2 and Round 3 COPDGene CT scans collected at standardized intervals over a 10 year period of observation.