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Original Research

Mean platelet volume as a predictor of pulmonary hypertension in patients with stable COPD

, , ORCID Icon, , &
Pages 1099-1108 | Published online: 23 May 2019
 

Abstract

Background: Pulmonary hypertension (PH) is one of the most common complications developed during the course of chronic obstructive pulmonary disease (COPD). Platelet activation plays an important role in its pathophysiology, and mean platelet volume (MPV) is considered a respectable index of platelet activation. The aim of this work is to assess the ability of MPV in predicting PH secondary to COPD as well as its severity.

Methods: A cross-sectional study was conducted on 228 stable COPD patients. CBC, echocardiography, and pulmonary function tests were performed.

Results: The prevalence of PH in stable COPD patients was high (63%), and the majority of patients had a mild degree (33%). There was no significant association between PH presence with different COPD grade, but, in very severe COPD, severe PH was significantly presented. MPV in COPD patients with PH was significantly higher than those without (9.02±1.14 vs 7.11±0.98, P<0.001). Moreover, a significant statistical rising of MPV with increased severity of PH. Multivariate regression analysis of predictors of PH demonstrated that; MPV is a real predictor of PH in such patients. The likelihood probability of PH increased up to 7-times with increasing one unit of MPV; (OR=6.7). A cut-off value of MPV >7.25 had 96% sensitivity and 76% specificity in predicting PH.

Conclusion: MPV was higher in COPD patients with PH and positively correlated with PH severity. If the data are to be confirmed, MPV may be taken into consideration in decision-making and management of COPD patients.

Ethics approval and informed consent

The research was approved from Bani-Swaif and Zagazig University Ethical Committees. Written informed consents were obtained from all participants. This study was conducted in accordance with the Declaration of Helsinki.

Author contributions

MFM, AA, and AA were responsible for study design, patient selection, and data collection. MSA and MG were responsible for performing Echocardiography for all selected patients. AMS was responsible for laboratory investigations. All authors contributed toward data analysis, drafting and revising the paper, gave final approval of the version to be published and agree to be accountable for all aspects of the work.

Disclosure

The authors report no conflicts of interest in this work.