Study the association of chronic obstructive pulmonary disease with early endothelial dysfunction and its impact on cardiovascular system by estimating urinary albumin creatinine ratio.

BACKGROUND

Chronic obstructive pulmonary disease (COPD) attribute to systemic inflammation which is responsible for microalbuminuria reflecting endothelial dysfunction, could be a significant surrogate marker of potential cardiovascular morbidity.

OBJECTIVE

The aim of our study was to find out the possible association of COPD with early cardiovascular changes in the form of renal endothelial dysfunction.

SETTINGS AND DESIGN

Case-control, multi-group, cross-sectional hospital-based study was designed and conducted in the Department of Respiratory Medicine of BPS Government Medical College for Women, Khanpur Kalan, Sonipat, Haryana.

SUBJECTS AND METHODS

The study included 150 subjects, comprising of three groups with each having 50 subjects: Group 1 - acute exacerbation of COPD, Group 2 - stable COPD patients, Group 3 - asymptomatic smokers. Pulmonary function test, urine albumin creatinine ratio (UACR) and brachio-ankle pulse wave velocity were measured in all the subjects.

STATISTICAL ANALYSIS

Data were analyzed using SPSS ver 20 (IBM, USA) software. Continuous variables were compared by unpaired Student's -test while correlation was measured by Pearson correlation test, < 0.05 was considered statistically significant.

RESULTS

The mean urine albumin creatinine ratio UACR value in acute exacerbation of COPD (283.30 mg/g; standard deviation [SD] ±871.98) was found significantly higher compare to control subjects (24.17 mg/g; SD ± 32.105;) = 0.038. Besides this COPD patients with Type 2 respiratory failure having robust positive correlation in between UACR and arterial blood pH ( = 0.559; = 0.030) while it was inverse and moderate with partial pressure of arterial oxygen ( = -0.470; = 0.077).

CONCLUSIONS

Acute state of COPD with or without Type 2 respiratory failure is having a significant impact on cardiovascular system in the form of early microvascular changes.