Association between blood pressure, inflammation and spirometry parameters in chronic obstructive pulmonary disease.

BACKGROUND/AIMS: Many systems including the cardiovascular system (ischemic heart diseases, heart failure, and hypertension) may act as comorbidities that can be seen during the course of chronic obstructive pulmonary disease (COPD). Comorbidities affect the severity and prognosis of COPD negatively. Nearly 25% of patients with COPD die due to cardiovascular diseases. In this study, we aimed to evaluate the relationship between the blood pressure, inflammation, hypoxia, hypercapnia, and the severity of airway obstruction. METHODS: We included 75 COPD patients in the study with 45 control cases. We evaluated age, sex, body mass index, smoking history, C-reactive protein levels, 24-hour ambulatory blood pressure Holter monitoring, arterial blood gas, and respiratory function tests of the patient and the control groups. RESULTS: In COPD patients, the night time systolic, diastolic blood pressures and pulse per minute and the mean blood pressures readings were significantly elevated compared to the control group (p < 0.05). In the correlation analysis, night time systolic pressure was associated with all the parameters except forced expiratory volume in 1 second (FEV1%). Diastolic blood pressure was associated with pH and HCO3 levels. The mean night time, day time pulse pressures and 24- hour pulse per minute values were also associated with all the parameters except FEV1%. CONCLUSION: In this study we found that parameters of systolic and diastolic blood pressures and pulse pressures were significantly elevated in COPD patients compared to the control groups. Blood pressure was associated blood gas parameters and inflammation parameters in COPD patients. This, in turn, may cause understanding of the pathophysiology of COPD and its complications.

Factors related to microalbuminuria in patients with chronic obstructive pulmonary disease.

BACKGROUND: Chronic obstructive pulmonary disease (COPD) is characterized by inhaled particles and gases inducing chronic inflammation of the airways accompanied by a not fully reversible airflow limitation. Systemic inflammation has an important role in the pathogenesis of COPD. In parallel, several comorbidites can be observed. Microalbuminuria is related to endothelial dysfunction. Microalbuminuria was increased in exacerbation periods of COPD. OBJECTIVES: The aim of the study was evaluate to the presence of microalbuminuria (MA) in patients with chronic obstructive pulmonary disease (COPD) and its relationship to inflammation, arterial blood gas parameters and 24-hour ambulatory blood pressure alterations. MATERIAL AND METHODS: Seventy COPD patients and 40 healthy volunteers were enrolled in the study. 24-h ambulatory blood pressure monitoring (ABPM) results, including pressure and pulse rates of the subjects were recorded and the cases were classified as "dipper" if a normal fall of more than 10% in blood pressure was observed at night and "non-dipper" if not. Routine renal function tests were performed, C-reactive protein (CRP) values were examined and urine samples were obtained to scrutinize the presence of MA. Patients were allocated into two groups, those with and without MA. The spirometry and arterial blood gas results of the patients were recorded. RESULTS: The urinary albumin creatinin ratio (64.8 ± 91.8), CRP (21 ± 14.8), nocturnal systolic and diastolic blood pressure (118 ± 14 and 72 ± 10), nocturnal and diurnal pulse (87 ± 17 and 90 ± 14), nocturnal pulse pressure (49 ± 11), mean pulse (89 ± 15), mean pulse pressure (48 ± 10) and the number of non-dipper subjects (65) were found significantly higher in the COPD group than in the control group (10.6 ± 6, 5.4 ± 2.4, 105 ± 6 and 68 ± 7, 70 ± 10 and 78 ± 11, 42 ± 1, 75± 11, 42 ± 7 and 5, respectively); (p < 0.001, < 0.001, < 0.001 and 0.041, < 0.001 and < 0.001, < 0.001, < 0.001, < 0.001 and < 0.001, respectively). Nocturnal pulse (89 ± 17) and CRP (23.5 ± 14.8) were found to be significantly higher in COPD patients with MA than in COPD patients without MA (78 ± 8 and 8.8 ± 6.3, respectively); (p = 0.021 and < 0.001, respectively). CONCLUSIONS: The facts that CRP, a systemic inflammation marker, and mean nocturnal pulse pressure values were significantly higher in the group with MA among COPD patients, and that ambulatory blood pressure values did not differ between COPD patients with and without MA, suggest both a possible role of inflammation in MA development in COPD patients and a relationship between MA and increased heart rate.