Key result
Obesity was independently associated with a significant reduction in pulmonary pulse transit time (β = -0.525), indicating early pulmonary hemodynamic dysfunction that worsened with increasing body mass index.
Why the study?
There is no definite echocardiographic parameter for PAH diagnosis, and the utility of pulmonary pulse transit time for evaluating pulmonary vascular hemodynamics in obese patients was unknown.
Does pulmonary pulse transit time (pPTT) correlate with BMI and serve as a marker for pulmonary vascular hemodynamics in obese patients?
Cross-Sectional (n=180)
Single-blind
No
Does pulmonary pulse transit time (pPTT) correlate with BMI and serve as a marker for pulmonary vascular hemodynamics in obese patients?
Pulmonary pulse transit time (pPTT) measured by echocardiography is significantly reduced in obesity and correlates inversely with BMI, suggesting its potential as a noninvasive marker for altered pulmonary hemodynamics.
Answers are grounded in this paper and cite their sources.
Obesity-linked pPTT shortening may signal PAH risk; leaves open validation against catheterization and outcome impact.
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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Zıyrek et al. (2020) conducted a cross-sectional in Obesity and Pulmonary Arterial Hypertension (n=180). Obesity vs. Healthy volunteers (BMI 20-25 kg/m2) was evaluated on Pulmonary pulse transit time (pPTT) (β = -0.525, 95% CI -9.164 to -6.379, p=0.0001). Obesity was independently associated with a significant reduction in pulmonary pulse transit time (β = -0.525), indicating early pulmonary hemodynamic dysfunction that worsened with increasing body mass index.
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