Introduction: Doppler-derived pulmonary pulse transit time (pPTT) is an auspicious hemodynamic marker in chronic pulmonary diseases. The aim is to compare four distinct pPTT measurements and its relation to right cardiac and pulmonary function. Methods: Prospectively, 22 chronic obstructive pulmonary disease (COPD) patients (one patient excluded) and 32 healthy subjects underwent repeated distinct pPTT measurements, one standard echocardiography and pulmonary function testing on the same day. pPTT was defined as the interval from the R or Q-wave in the ECG to the corresponding pulse wave Doppler peak late systolic (S2) or diastolic (D) pulmonary vein flow velocity (pPTT R-S , Q-S, R-D, Q-D). Reproducibility was evaluated using Bland-Altman analysis, coefficient of variation (COV), intraclass correlation coefficient (ICC) and power calculations. Coherence to right ventricle RV tissue und pulse wave Doppler velocities (RV E´, RV S´, RV A’, RV E, RV A, RV E/E‘, RV E/A (cm/s)), tricuspid annular plane systolic excursion (TAPSE), forced expiratory volume in 1 second (FEV1), vital capacity (FVC) predicted (%) and in (l) were analyzed. Results: There was no significant difference and no bias between pPTT measures (p range: 0.1 - 0.9). COV was in COPD 1.2 - 2.3%, in healthy subjects 1.0 % - 3.1 %. ICC ranged from 0.92 (COPD) to 0.96 (healthy subjects). In COPD significant correlations were found for pPTT R-S , Q-S and R-D with RV E‘, (all >ρ: 0.49, ρ: 0.49, ρ: -0.39, Conclusions: All pPTT measures were highly reproducible and affected by diastolic RV performance. Defining Q as starting point seems clinically advantageous considering electromechanical desynchrony in patients with conduction disorders.

Aldosterone binds to the mineralocorticoid receptor (MR), a transcription factor of the nuclear receptor family, present in the kidney and in various other non-epithelial cells including the heart and the vasculature (Cannavo et al., 2018). Indeed, extra-renal pathophysiological effects of this hormone have been characterized, extending its actions to the cardiovascular (CV) system (Messaoudi et al., 2012). A growing body of clinical and pre-clinical evidence suggests that MR activation plays an important pathophysiological role in CV remodeling by promoting cardiac hypertrophy, fibrosis, arterial stiffness, as well as in inflammation and oxidative stress (Bauersachs et al., 2015). The following review article outlines the role of MR in CV disease with a focus on myocardial remodeling and heart failure (HF) including clinical trials as well as cellular and animal studies.