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ORIGINAL ARTICLE
Year : 2020  |  Volume : 30  |  Issue : 2  |  Page : 75-81

Effect of obesity on pulmonary vascular hemodynamics


Department of Cardiology, Konya Education and Research Hospital, Konya, Turkey

Correspondence Address:
Murat Ziyrek
Konya Education and Research Hospital, Hac. Saban District Yeni Meram St. Meram, Konya
Turkey
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/jcecho.jcecho_70_19

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Context: Obesity-related pulmonary arterial hypertension (PAH) is associated with hypoxia and metabolic abnormalities. Although right heart catheterization is the gold standard method for the diagnosis of PAH, Doppler echocardiography is more common. On the other hand, there is no definite echocardiographic parameter for PAH diagnosis. Novel echocardiographic parameter, pulmonary pulse transit time (pPTT), is assumed to be a surrogate marker for the assessment of PAH. Aims: The aim was to evaluate whether pPTT might be valuable for evaluating pulmonary vascular hemodynamics in obese patients. Settings and Design: A cross-sectional observational study. Methods: A total of 130 consecutive obese patients and 50 controls were included. Obese patients were divided into three groups according to body mass index (BMI): 25 < BMI <30 kg/m2 formed Group 1, 30 < BMI <35 kg/m2 formed Group 2, and 35 2 formed Group 3. All patients underwent a standard echocardiography including pPTT measurement. pPTT was defined as the interval between R-wave in the electrocardiography and the corresponding peak late systolic pulmonary vein flow velocity measured by pulse wave-Doppler in the pulmonary vein. Statistical Analysis Used: Intergroup differences were analyzed with analysis of variance or Kruskal–Wallis test. Pearson's or Spearman's correlation analysis was used for correlation, multivariate logistic regression analysis, and regression. Results: Statistically significant reduction in pPTT was detected as early as in the first group (361.24 ± 25.54 vs. 391.26 ± 15.07; P = 0.015) and continued throughout Groups 2 and 3 (299.92 ± 35.10 vs. 391.26 ± 15.07;P < 0.0001, and 245.46 ± 11.25 vs. 391.26 ± 15.07;P < 0.0001, respectively). There was a strong negative correlation between pPTT and BMI (r = −0.848, P = 0.001). On linear regression analysis, BMI was found to be an independent risk factor for pPTT (confidence interval: −9.164–6.379, β = −0.525, P = 0.0001). Conclusion: The results of this study suggest that obesity leads to an increase in PAH, and pPTT allows noninvasive determination of the pulmonary hemodynamics in obese patients. pPTT might be a useful parameter in terms of predicting pulmonary hemodynamics and vascular alterations in obese patients. Further studies are warranted to evaluate the association between obesity and PAH.


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