Objective To evaluate the relationship between COPD and atherosclerosis, and analyze the risk factors of atherosclerosis among COPD patients. Methods A total of 40 COPD patients and 43 normal subjects were enrolled in the study. Carotid intima-media thickness (IMT) and plaques were detected in both groups. Blood samples were collected to measure the concentration of high sensitive C-reactive protein (hs-CRP) , fibrinogen (Fbg) , total cholesterol (TC) , triglyceride (TG) , high density lipoprotein cholesterol (HDL-C) , low density lipoprotein cholesterol (LDL-C) , while smoking index was recorded. Multiple regression analysis was performed to evaluate the correlative factors of IMT among COPD patients. According to whether luminal stenosis appeared, the COPD patients were allocated into group A ( without luminal stenosis) and group B ( with luminal stenosis) . Age, gender, hs-CRP, Fbg, TC, TG, HDL-C, LDL-C, and smoking index of the two groups were compared respectively. Results Hs-CRP, Fbg, thickness of IMT, plaques detection rate, and smoking index in the COPD group were significantly higher than those in the control group ( Plt;0.05) . TC, HDL-C, LDL-C in the COPD group were significantly lower than those in the control group ( Plt;0. 05) .Multiple regression analysis of IMT correlative factors among COPD patients showed that age, hs-CRP, Fbg, TC, TG, LDL-C, HDL-C, and smoking index were in linear relationship with IMT thickening. Age, hs-CRP, TC, and smoking index were positively correlated with IMT ( Plt;0.05) . Hs-CRP and smoking index in the group A were lower than those in the group B ( Plt;0. 05) .While TC, TG, LDL-C, and HDL-C in the group A were higher than those in the group B ( Plt;0.05) . Conclusions Age, smoking index, hs-CRP, and TC are risk factors for thickening of carotid artery IMT in COPD patients. Furthermore, smoking index, hs-CRP, TC, TG, LDL-C, and HDL-C are related to the severity of IMT thickening. The ultrasound detection of carotid artery IMT can be a valuble tool to screen atherosclerosis in patients with COPD.
Objective
To explore the relationship between thrombocytosis and all-cause in-hospital mortality in patients with chronic obstructive pulmonary disease (COPD) and low-risk pulmonary embolism (PE).
Methods
In a multicenter retrospective study on clinical characteristics, COPD patients with proven acute PE between October 2005 and February 2017 were enrolled. The patients in risk classes III-V on the basis of the PESI score were excluded. The patients with COPD and low-risk PE were divided into two groups of those with thrombocytosis and without thrombocytosis after extracting platelet count on admission. The clinical characteristics and prognosis of the two groups were compared. Multivariate logistic regression was performed to reveal an association between thrombocytosis and all-cause in-hospital mortality after confounding variables were adjusted.
Results
A total of 874 consecutive patients with COPD and PE at low risk were enrolled in which 191 (21.9%) with thrombocytosis. Compared with those without thrombocytosis, the thrombocytopenic group had significantly lower body mass index [(20.9±3.3) kg/m2 vs. (25.1±3.8) kg/m2, P=0.01], lower levels of forced expiratory volume in one second (FEV1) [(0.9±0.4) L vs. (1.3±0.3) L, P=0.001] and lower partial pressure of oxygen in the arterial blood (PaO2) [(7.8±1.2) kPa vs. (9.7±2.3) kPa, P=0.003]. The COPD patients with thrombocytosis had a higher proportion of cardiovascular complications as well as higher level of systolic pulmonary arterial pressure (sPAP) [(46.5±20.6) mm Hg vs. (34.1±12.6) mm Hg, P=0.001]. Multivariate logistic regression analysis after adjustment for confounders revealed that thrombocytosis was associated with all-cause mortality in hospitalized patients with COPD and low-risk PE (adjusted OR=1.53, 95%CI 1.03–2.29), and oral antiplatelet treatment was a protective factor (adjusted OR=0.71, 95%CI 0.31–0.84).
Conclusions
Thrombocytosis is an independent risk factor for all-cause in-hospital mortality in COPD patients with PE at low risk. Antiplatelet therapy may play a protective role in the high-risk cohort.
