Angiopoietin-like protein 4 and cardiovascular function in COPD

Abstract

IntroductionThe coexistence of chronic obstructive pulmonary disease (COPD) and cardiovascular disease (CVD) is frequent and might be inter-related through inflammation-related processes reflected by specific markers. Here, we studied angiopoietin-like protein 4 (ANGPTL4), an upcoming cardiovascular marker, in stable COPD, and its relationship to cardiovascular function with respect to well-known CVD risk factors.MethodsIn a prospective COPD cohort study, we investigated serum ANGPTL4 levels, vascular status (ankle–brachial index (ABI)) and cardiac function (N-terminal pro-B-type natriuretic peptide (NT-proBNP)) as well as airflow limitation, objectively measured physical activity, the metabolic syndrome, high-sensitive C reactive protein (hs-CRP) and other CVD risk factors at 2 time points. We initially studied 74 stable COPD patients and 18 controls. For internal validation, we additionally studied 160 COPD patients of a former visit.ResultsANGPTL4 was significantly elevated in COPD patients compared with controls (p=0.026). After correction for traditional CVD risk factors, including hs-CRP, higher levels of ANGPTL4 were independently associated with lower ABI (p=0.023) and higher NT-proBNP (p<0.001). These findings were confirmed in the internal validation analysis, which included echocardiographic assessments.ConclusionsSerum ANGPTL4 is independently associated with cardiovascular function in COPD and might qualify as a biomarker reflecting a pathogenic link between COPD and CVD.

Cardiovascular disease and COPD: dangerous liaisons?

“…For example, arterial stiffness (as measured by aPWV) has been shown to be predictive of CV events independent of classic CV factors and has been proposed as a surrogate marker of severity [38]. In addition, a prospective cohort study indicated that angiopoietin-like protein 4 was independently associated with CV function in patients with COPD [188].…”

Plasminogen activator inhibitor-1 is elevated in patients with COPD independent of metabolic and cardiovascular function

“…Details regarding the COPD population and the methodology of the study have been published elsewhere 16–18. In the present study, 74 stable outpatients with mild-to-very severe COPD (ie, n=16, 20, 18, and 20 with Global Initiative for Chronic Obstructive Lung Disease [GOLD] Stages I, II, III, and IV, respectively) and 18 nonsmoking controls without any lung disease from the 3-year follow-up visit were included.…”

“…The study was approved by the Ethics Committee of the Medical Association of Schleswig-Holstein, Bad Segeberg, Germany (III/EK 116/05[I]; 185/08[I]), and all the participants provided written informed consent. In this study, the serum levels of PAI-1 were analyzed by using enzyme-linked immunosorbent assay (ELISA; Human Serpin E1/PAI-1 DuoSet ELISA; R&D Systems, Wiesbaden-Nordenstadt, Germany; detection range =0.312–20 ng/mL); metabolic and cardiovascular functions as possible confounders of PAI-1, including triglyceride levels, high-density lipoprotein (HDL) cholesterol, fasting plasma glucose, waist circumference, blood pressure, the presence of the metabolic syndrome (based on the latter five variables according to the criteria of the International Diabetes Federation19), smoking status, and history of coronary artery disease and diabetes, were determined; high-sensitivity C-reactive protein (hs-CRP) was measured as an established marker of systemic inflammation and adiponectin, which is involved in anti-inflammatory, anti-diabetic, and anti-atherogenic processes;20 in addition, global cardiac function by serum levels of N-terminal pro-B-type natriuretic peptide (NT-proBNP) and the presence of atherosclerosis by the ankle–brachial index (ABI) were also determined as previously described 16,18…”

Diagnostic Value of Leptin in Chronic Obstructive Pulmonary Disease of the Iii Degree in Patients with Excessive Body Weight

“…The key elements connecting COPD and overweight involve systemic inflammation and dysfunction of antioxidant mechanisms [10,18,19]. Significant vascularization of lungs, the presence of leptin receptors in alveolar and bronchial epithelial cells, smooth muscular cells and bronchial submucosal membrane, as well as increased blood serum leptin levels in patients with COPD exacerbation, allow suggesting pathogenic contribution of leptin to the disease progression [20,21].…”