COPD is a common respiratory disease with high morbidity and is becoming a growing social health problem. This chronic inflammation is mainly characterized by chronic inflammation of the airways, lung parenchyma, and pulmonary blood vessels. Cigarette smoking is the major risk factor for COPD. Fabbri et al  proposed that cigarette smoke induced airway and lung inflammation and at the same time caused systemic cellular and humoral inflammation, oxidative stress, altered endothelial function, and enhanced circulating concentrations of several procoagulant factors. Cigarette smoke can also cause other systemic diseases such as cardiovascular and metabolic diseases. Common comorbidities of COPD include skeletal muscle abnormalities, hypertension, diabetes, coronary artery disease, heart failure, lung infection, cancer, and pulmonary vascular disease . Atherosclerosis is the most common complication of COPD.
This study showed that subjects with AECOPD + CAC had significantly higher FEV1%pred and PaO2 than the AECOPD group. Although increasing trends were observed for FVC, FVC%pred, FEV1, and FEV1/FVC, the differences were not statistically significant. Previous studies have shown that lung function in patients with COPD complicated with coronary heart disease was lower than that in COPD [6, 10–11]. Jia et al  found that low-dose aspirin can reduced blood viscosity, improved gas exchange in the lungs, and improved lung function and arterial blood gas levels. Yao et al  had shown that statins can promoted blood gas improvement and reduced hypoxemia in patients with COPD. Melo et al  used elastase to prepared a mouse model of emphysema and treated the animals with atorvastatin. Notably, the numbers of elastic and collagen fibers in the lungs of the treated group were significantly increased compared with the untreated group, demonstrating that statins could significantly repaired lung tissue in injured mice. To further analyze the effects of oral medications on AECOPD, we subdivided the AECOPD + CAC subjects into two subgroups according to whether oral aspirin and statins were administered. There were no significant differences in FVC, FEV1, FVC%pred and FEV1/FVC among the three groups, but levels were higher in the AECOPD + CAC medication group compared to the AECOPD and AECOPD + CAC non-medication groups. The lack of significance was likely due to the small sample size, and a larger study is needed to verify our findings. PaO2 in the AECOPD + CAC medication group was significantly improved compared with the AECOPD group, and the difference was statistically significant. Jia et al  found that aspirin can inhibited cyclooxygenase activity, thereby reducing arachidonic acid production of prostaglandins, leading to decreased production of its metabolite thromboxane A2, which normally induces platelet aggregation and vasoconstriction. Aspirin can dilate blood vessels by reducing thromboxane A2, improving gas exchange in the lungs, increase oxygen partial pressure, and improve lung function. Emphysema is a major pathological feature of COPD; it leads to different degrees of hypoxemia by reducing capillaries, increasing ineffective cavity volume, and producing an imbalance between ventilation and blood flow. Notably, some of the indicators in the AECOPD + CAC group were significantly improved compared with the AECOPD group, probably due to the effects of statins and aspirin.
The Lym% was significantly higher in AECOPD patients with CAC compared to the AECOPD group, and lymphocyte numbers showed an increasing (but nonsignificant) trend. COPD is a systemic inflammatory disease , and the most common exacerbating factor is infection. Atherosclerosis is also an inflammatory state . The combination of AECOPD and CAC can cause lymphocyte and neutrophil numbers to rise. We found the WBC and Neu numbers were significantly lower in the AECOPD + CAC group than those of AECOPD group. Some previous studies [6, 10–11, 17] reported that patients with AECOPD and CAC have higher WBC and Neu than those with only AECOPD. Others have shown that oral aspirin and statins can reduce neutrophils in sputum and peripheral blood from patients with COPD. To further analyze the effects of oral drugs on AECOPD, the AECOPD + CAC group was subdivided into two groups according to oral aspirin/statin use. WBC and Neu were significantly lower in AECOPD + CAC who had taken these medications. Hamid  and colleagues selected healthy volunteers to receive placebo or aspirin for 7 days prior to lipopolysaccharide inhalation followed by bronchoalveolar lavage (BAL). They found that aspirin could reduce BAL neutrophilia and secretion of neutrophil-derived enzymes (matrix metalloproteinase-8, -9). Peripheral neutrophils were not significantly reduced by aspirin but exhibited a downward trend, possibly due to the short duration of action. Aspirin treatment did not significantly change the number of lymphocytes in BAL fluid. This indicated that aspirin does not effectively reduce the number of lymphocytes, which is consistent with our results. Statins inhibit 3-hydroxy-3methylglutaryl coenzyme A (HMG-CoA) reductase, which inhibits the intracellular hydroxyvalerate metabolic pathway by competitive inhibition of the enzyme, thereby reducing intracellular cholesterol synthesis. Therefore, the feedback stimulates the increase in the number and activity of low-density lipoprotein receptors on cell membrane surface, which increases serum cholesterol clearance and lowers its level. They are mainly prescribed for lowering cholesterol, which is very beneficial for preventing coronary heart disease. In addition to lipid-lowering effects, statins are also anti-inflammatory, immunosuppressive, and inhibit platelet aggregation. Some studies [19–21] have reported that statins reduced mortality and morbidity in patients with COPD. Potentially important actions of statins in this population include reducing neutrophil numbers, reducing T cell activation and differentiation, and increasing eosinophil apoptosis . Mroz et al  found that statins use was associated with reduced neutrophils in sputum from patients with COPD, and the authors also performed genetic testing. They found decreased expression of genes that regulated immune response and leukocyte activation in statin-treated subjects and speculated that statins reduced neutrophils and reduced inflammation by altering gene expression. However, the relationship between gene and protein levels has not been elucidated. The collective evidence suggested administration of aspirin and statins in patients with AECOPD + CAC can reduced the numbers of neutrophils but not lymphocytes.