Pulmonary Pulse Wave Transit Time is Associated with Right Ventricular–Pulmonary Artery Coupling in Pulmonary Arterial Hypertension

Abstract

Pulmonary pulse wave transit time (pPTT), defined as the time for the systolic pressure pulse wave to travel from the pulmonary valve to the pulmonary veins, has been reported to be reduced in pulmonary arterial hypertension (PAH); however, the underlying mechanism of reduced pPTT is unknown. Here, we investigate the hypothesis that abbreviated pPTT in PAH results from impaired right ventricular-pulmonary artery (RV-PA) coupling. We quantified pPTT using pulsed-wave Doppler ultrasound from 10 healthy age-and sexmatched controls and 36 patients with PAH. pPTT was reduced in patients with PAH compared with controls. Univariate analysis revealed the following significant predictors of reduced pPTT: age, right ventricular fractional area change (RV FAC), tricuspid annular plane excursion (TAPSE), pulmonary arterial pressures (PAP), diastolic pulmonary gradient, transpulmonary gradient, pulmonary vascular resistance, and RV-PA coupling (defined as RV FAC/mean PAP or TAPSE/mean PAP). Although the correlations between pPTT and invasive markers of pulmonary vascular disease were modest, RV FAC (r = 0.64, P < 0.0001), TAPSE (r = 0.67, P < 0.0001), and RV-PA coupling (RV FAC/mean PAP: r = 0.72, P < 0.0001; TAPSE/mean PAP: r = 0.74, P < 0.0001) had the strongest relationships with pPTT. On multivariable analysis, only RV FAC, TAPSE, and RV-PA coupling were independent predictors of pPTT. We conclude that shortening of pPTT in patients with PAH results from altered RV-PA coupling, probably occurring as a result of reduced pulmonary arterial compliance. Thus, pPTT allows noninvasive determination of the status of both the pulmonary vasculature and the response of the RV in patients with PAH, thereby allowing monitoring of disease progression and regression.Keywords: pulse wave velocity, right ventricular-pulmonary artery coupling, echocardiography. Pulmonary arterial hypertension (PAH) is a lethal disease, characterized by pathological pulmonary vascular remodeling, that leads to elevated pulmonary arterial pressure (PAP) and pulmonary vascular resistance (PVR), decreased pulmonary arterial compliance, and eventual right ventricular failure and death.1,2 Growing evidence suggests that pulmonary arterial compliance plays a critical role in the pathogenesis of PAH and right ventricular failure. 3 Decreased pulmonary arterial compliance causes premature reflection of waves from the distal pulmonary vasculature, leading to increased pulsatile right ventricular afterload and altered right ventricular-pulmonary artery (RV-PA) coupling. 3-5 Both loss of pulmonary arterial compliance and impaired RV-PA coupling are clinically important, because they are associated with increased mortality in patients with pulmonary hypertension. 6-11Pulse wave velocity, defined as the velocity of pressure waves traveling through the arterial system, correlates inversely with arterial compliance in the systemic circulation.12 With decreasing compliance, pulse wave velocity increases, and the time taken by the pressure wave to travel between...

Prolonged pulmonary pulse transit time is associated with symptoms in patients with significant mitral stenosis and sinus rhythm

“…Therefore, pulmonary arterial stiffness, PAP, and PCWP affect the blood flow velocity in the pulmonary artery. It has been shown that pPTT is not only shortened in PAH but also inversely correlated with PVR and DPG . In another study, pPTT was significantly shorter in PHT than without pulmonary fibrosis .…”

“…Increase in pulmonary PWV due to increased pulmonary arterial stiffness might cause shortened pPTT in patients with precapillary PHT. An inverse correlation between PVR and pPTT might be an indication of this situation . In addition, in patients with precapillary PHT, PCWP is usually in the normal range though DPG increases as a result of increased diastolic PAP.…”

Excess Protein O-GlcNAcylation Links Metabolic Derangements to Right Ventricular Dysfunction in Pulmonary Arterial Hypertension

“…PAH patients from the University of Minnesota Pulmonary Hypertension Program [ 43 ] were analyzed. PAH was defined as mean pulmonary arterial pressure (mPAP) >20 mmHg, pulmonary capillary wedge pressure <15 mmHg, and pulmonary vascular resistance (PVR) >3.0 Wood units, with other causes such as left sided heart disease, chronic lung disease, or chronic thromboembolic disease being ruled out using echocardiography, pulmonary function tests, computed tomography imaging, ventilation perfusion imaging, or invasive pulmonary angiogram [ 44 ].…”

Colchicine Depolymerizes Microtubules, Increases Junctophilin‐2, and Improves Right Ventricular Function in Experimental Pulmonary Arterial Hypertension

“…RV‐PA coupling was defined 2 ways: TAPSE divided by invasively measured mean pulmonary artery pressure (mPAP) and percentage change in RVFW thickness/mPAP as previously described 29, 30, 31, 32, 33…”

“…RV-PA coupling was defined 2 ways: TAPSE divided by invasively measured mean pulmonary artery pressure (mPAP) and percentage change in RVFW thickness/mPAP as previously described. [29][30][31][32][33] Treadmill Walk Distance Exercise capacity was tested by measuring maximal distance run on a motorized treadmill (Simplex II Instrument; Columbus Instruments, Columbus, OH). The initial treadmill speed was 10 m/min and increased 5 m/min every 5 minutes for 30 minutes or until the rat fatigued.…”