[Overlap syndrome of chronic obstructive pulmonary disease and obstructive sleep apnea].

Background : Post-occlusive reactive hyperemia (RH) is impaired in Chronic Obstructive Pulmonary Disease (COPD) and Obstructive Sleep Apnea (OSA). The aim of the present study was to examine systemic vascular response and endothelial function in patients of Overlap Syndrome (OS) of COPD and OSA and also to investigate whether OS has any additional effect on endothelial dysfunction when compared to dysfunction caused by COPD alone. Methods : 31 COPD patients and 13 healthy controls participated in the study. Overnight Polysomnography was done to classify the patients into COPD only group (Apnea-Hypopnea Index <5) (n=15) and OS group (AHI >5) (n=16). Peripheral pulse waveform changes during reactive hyperemia were assessed using digital Photoplethysmography (PPG) technique in which pulse wave amplitude (PWA), Maximum slope of upstroke and Pulse Transit Time (PTT) were measured. C reactive protein was assessed as marker of inflammation by ELISA. Results : Maximum percentage changes in PWA during RH were significantly lower in the both COPD group [20.34(12.02-34.07)] (p<0.001) and Overlap Syndrome group [10.96(6.21-21.49)] (p<0.0001) as compared to Controls [49.79(46.03-65.32)], whereas amplitude responses were not significantly different in the COPD and OS group (p>0.05). Maximum percentage change in slope of upstroke showed similar responses in the three groups. CRP levels (mg/l) were raised in COPD [11.60(1.75-15.00] (p<0.001) and OS group [12.52(5.2815.70))](p<0.0001) as compared to controls [0.59(0.58-0.91)]. Maximum percentage change in amplitude negatively correlated with serum CRP levels in COPD group (r=-0.557, p=0.03) and in OS group (r=-0.552, p= 0.02). FEV1% predicted positively correlated with maximum percentage change in amplitude in OS group J Physiol Pharmacol 2016; 60(2) : 155–166 *Corresponding author : Dr. Anjana Talwar, Additional Professor, Department of Physiology, AIIMS, Ansari Nagar, Delhi, Ph.: 9811505070, Email : [email protected] (Received on April 12, 2015) 156 Khare, Talwar, Trivedi, Chandran, Guleria, Jaryal and Deepak Indian J Physiol Pharmacol 2016; 60(2) The aim of the present study was to examine systemic vascular response and endothelial function in patients of Overlap syndrome. The other aim of the study was to investigate whether patients with OS have greater endothelial dysfunction when compared to dysfunction caused by COPD alone. Another reason for evaluating COPD patients with OSA is that systemic inflammation develops in each disorder which may play an important role in underlying pathogenesis of cardiovascular diseases, like hypertension and atherosclerosis (11–13). W hi le sys tem ic in f lam m at ion & endothe l ia l dysfunction develop both in COPD & OSA (11), no study has ear l ier invest igated the endothel ial dysfunction in OS. Thus, noninvasive assessment of endothelial function in patients of overlap syndrome and its relation with inflammatory marker hs-CRP (high sensitivity C Reactive Protein) was investigated in the present study. Also, it was aimed to observe if there is any associat ion between systemic inflammation and endothelial function in patients of OS. Materials and Method Selection of participants Thirty-one diagnosed ex-smoker male stable patients of COPD were recruited in the study with mean smoking history of 16±6.67 pack years. These patients were classified into COPD (n=15) and Overlap syndrome (COPD and OSA, n=16). 13 age and gender matched non smoking healthy controls were also recruited. Patients diagnosed to have COPD, as defined by the GOLD guidelines were recruited from Medicine OPD after an informed written consent (14). Introduction Chronic obstructive pulmonary disease (COPD) and Obstructive sleep apnoea (OSA) represent two of the most prevalent chronic respiratory disorders in clinical practice. Flenley coined the term “overlap syndrome” (OS) to describe, when both these disorders coexist in a patient (1). It has been believed that, the presence of COPD could predispose to the development of OSA, since the two conditions share same etiologic factors, such as tobacco smoking. The prevalence of OSA associated with COPD has been found to vary between 1429% in COPD patients in various studies (2, 3). COPD and OSA are independent risk factors for cardiovascular events and their co-existence in Overlap Syndrome probably increases this risk. Assessment of endothelial function has been used to determine risk for cardiovascular disease in its pre-atherogenic state (4). A number of recent studies have focused on using systemic vascular function indices as surrogate markers to measure increased cardiovascular risk in patients with stable COPD, using measurements of endothelial function and or arterial wall stiffness (5, 6). A number of studies also suggest that impaired endothelial function accompanies OSA (7, 8). Patients with OS have a more prominent sleep-related oxygen desaturation than COPD patients with the same degree of bronchial obstruction and show an increased risk of developing hypercapnic respiratory failure and pulmonary hypertension when compared with patients affected by only one of the two diseases (9, 10). (r=0.579, p=0.018). No correlation of AHI was found with any of the vascular function parameter in Overlap group. Conclusion : The patients with Overlap Syndrome have systemic inflammation and impaired reactive hyperaemia response. However, no additive effect of OSA was observed on impaired RH in patients with coexisting COPD. Indian J Physiol Pharmacol 2016; 60(2) Impaired Systemic Vascular Reactivity in Overlap Syndrome 157 Stable COPD patients of 40-65 years, smoking history of at least 10 pack years or more, evidence of airflow limitation on spirometry (FEV 1 /FVC < 0.7) were included. Patients receiving long-term oxygen therapy or oral corticosteroids, hypertension, heart disease, diabetes mellitus, chronic renal diseases, collagen vascular diseases, pulmonary hypertension, history of COPD exacerbation in last four weeks were excluded. The study protocol was approved by institutional ethics committee.