Impaired systemic vascular reactivity & raised high-sensitivity C reactive protein levels in chronic obstructive pulmonary disease

BACKGROUND & OBJECTIVES Chronic obstructive pulmonary disease (COPD) is characterized by slowly progressive airflow limitaion, chronic lung inflammation and associated systemic manifestations. The objective of this preliminary study was to investigate the levels of high sensitivity C reactive protein (hs CRP) and tumour necrosis factor-α (TNF-α) as markers of systemic inflammation and assessment of systemic vascular reactivity that may play an important role in development of cardiovascular disease in COPD patients. METHODS Systemic vascular reactivity was assessed non-invasively by measuring peripheral pulse waveform changes during reactive hyperemia (RH) in 16 COPD patients and 14 controls by photoplethysmography technique (PPG). Parameters measured were pulse wave amplitude (PWA), slope and pulse transit time (PTT). Tumour necrosis factor-α (TNF-α) and hs CRP were measured as markers of inflammation. RESULTS PWA during the 1 st , 2 nd and 3 rd minutes post release of occlusion were significantly higher than the baseline means in controls, whereas in the patient group there was no significant change in the PWA during any of the observed time periods following release of occlusion, in comparison to the baseline means. Similar results were observed in slope values for patients and controls. Maximum percentage change in PWA during RH with reference to baseline was significantly lower in patients as compared to controls (26.78±20.19 vs 57.20±19.80%, p<0.001). Maximum percentage change in slope during RH with reference to baseline was significantly lower in patients as compared to controls (19.77±10.73 vs 39.25±13.49%, P<0.001). A vascular tone response as represented by PTT was also impaired in the 3 rd minute of RH as compared to baseline mean values in COPD patients only. INTERPRETATION & CONCLUSIONS Our findings showed raised hs CRP levels and impaired systemic vascular reactivity in COPD patients. Whether these may increase the risk of cardiovascular disease in COPD patients need to be confirmed in future studies with large sample size and appropriate study design.