Department of Clinical Sciences, Lund University, Malmö, Sweden.
Department of Oncology, Skåne University Hospital, Lund, Sweden.
PLoS One. 2022 Mar 9;17(3):e0264376. doi: 10.1371/journal.pone.0264376. eCollection 2022.
Chronic obstructive pulmonary disease (COPD) and coronary artery disease (CAD) are leading causes of global morbidity and mortality. There is a well-known comorbidity between COPD and CAD, which is only partly explained by smoking and other known common risk factors. In order to better understand the relationship between COPD and CAD, we analyzed myocardial perfusion, pulmonary function and novel cardiovascular biomarkers in patients with symptoms suggesting myocardial ischemia.
A total of 396 subjects from the Swedish Biomarkers and Genetics CardioPulmonary Physiology Study (BiG CaPPS) were included, all of whom had been referred to myocardial perfusion imaging due to suspected myocardial ischemia. Subjects performed myocardial perfusion imaging (MPI), pulmonary function tests (PFT) and analysis of 92 proteomic biomarkers, previously associated with cardiovascular disease. Linear regression was used to study the relationship between MPI and PFT results and proteomic biomarkers.
Subjects with CAD (n = 159) had lower diffusing capacity (DLCO) than patients without CAD (6.64 versus 7.17 mmol/(minkPal); p = 0.004) in models adjusted for common covariates such as smoking, but also diabetes and brain natriuretic peptide (BNP). The association remained significant after additional adjustment for forced expiratory volume in one second (FEV1) (p = 0.009). Subjects with CAD, compared with subjects without CAD, had higher total airway resistance (0.37 vs 0.36 kPa/(l/s); p = 0.036). Among 92 protein biomarkers, nine were associated with a combined diagnosis of CAD and airflow obstruction: VSIG2, KIM1, FGF-23, REN, XCL1, GIF, ADM, TRAIL-R2 and PRSS8.
Diffusing capacity for carbon monoxide is decreased in patients with CAD, independently of decreased FEV1, diabetes, and elevated BNP. Several cardiovascular biomarkers are associated with co-existent CAD and airflow obstruction, but none with airflow obstruction only. The current findings indicate that the interaction between CAD and lung function is complex, including mechanisms beyond the known association between CAD and reduced ventilation.
慢性阻塞性肺疾病（COPD）和冠状动脉疾病（CAD）是全球发病率和死亡率的主要原因。 COPD 和 CAD 之间存在众所周知的合并症，而这种合并症仅部分归因于吸烟和其他已知的共同危险因素。为了更好地了解 COPD 和 CAD 之间的关系，我们分析了有心肌缺血症状的患者的心肌灌注、肺功能和新型心血管生物标志物。
共纳入来自瑞典生物标志物和遗传学心肺生理学研究（BiG CaPPS）的 396 名患者，所有患者均因疑似心肌缺血而接受心肌灌注成像检查。患者进行心肌灌注成像（MPI）、肺功能检查（PFT）和 92 种蛋白质组生物标志物分析，这些标志物先前与心血管疾病相关。线性回归用于研究 MPI 和 PFT 结果与蛋白质组生物标志物之间的关系。
CAD 患者（n = 159）的弥散量（DLCO）低于无 CAD 患者（6.64 与 7.17 mmol/（minkPal）；p = 0.004），在调整了吸烟等常见混杂因素后，但也调整了糖尿病和脑钠肽（BNP）。在进一步调整了一秒用力呼气容积（FEV1）后，该关联仍然显著（p = 0.009）。与无 CAD 患者相比，CAD 患者的总气道阻力更高（0.37 与 0.36 kPa/（l/s）；p = 0.036）。在 92 种蛋白质生物标志物中，有 9 种与 CAD 和气流阻塞的联合诊断相关：VSIG2、KIM1、FGF-23、REN、XCL1、GIF、ADM、TRAIL-R2 和 PRSS8。
一氧化碳弥散量在 CAD 患者中降低，与 FEV1 降低、糖尿病和 BNP 升高无关。一些心血管生物标志物与并存的 CAD 和气流阻塞相关，但没有与仅气流阻塞相关的生物标志物。目前的研究结果表明，CAD 和肺功能之间的相互作用很复杂，包括除了已知的 CAD 和通气减少之间的关联之外的机制。
