Assessment of Structural and Functional Pulmonary Vascular Disease in Patients with PAH

Grignola, Juan C.; Domingo, Enric; Aguilar-Torres, Rio; Román, Antonio

doi:10.5772/25927

Cited by 2 publications

(5 citation statements)

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“…They also demonstrated that in patients with PH, the Peterson modulus of the main PA was significantly increased over that of the normal PA. 34 More recently, arterioventricular coupling and invasive techniques for its measurement, principally derived in the systemic circulation and left ventricle, [35][36][37][38][39][40][41] have been applied to the right heart and the pulmonary circulation and have reemphasized the importance of vascular stiffening in PH diseases. [42][43][44][45][46] When arterial load increases with PH severity, RV contractility cannot progress in parallel, and this leads to severe uncoupling. 45 There is a clear case for a relationship between PVS, arterioventricular coupling, and output flows from the heart, which is further discussed in the next section.…”

Section: Measurement Of Pvs In Ph: Historical Perspectivementioning

confidence: 99%

Vascular Stiffening in Pulmonary Hypertension: Cause or Consequence? (2013 Grover Conference Series)

et al. 2014

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Recent studies have indicated that systemic arterial stiffening is a precursor to hypertension and that hypertension, in turn, can perpetuate arterial stiffening. Pulmonary artery (PA) stiffening is also well documented to occur in pulmonary hypertension (PH), and there is evidence that pulmonary vascular stiffness (PVS) may be a better predictor of outcome than pulmonary vascular resistance (PVR). We have hypothesized that the decreased flow-damping function of elastic PAs in PH likely initiates and/or perpetuates dysfunction of pulmonary microvasculature. Recent studies have shown that large-vessel stiffening increases flow pulsatility in the distal pulmonary vasculature, leading to endothelial dysfunction within a proinflammatory, vasoconstricting, and profibrogenic environment. The intricate role of stiffening-stimulated high pulsatile flow in endothelial cell dysfunction includes stepwise molecular events underlying PA hypertrophy, inflammation, endothelial-mesenchymal transition, and fibrosis. In addition to contributing to microenvironmental alterations of the distal vasculature, disordered proximal-distal PA coupling likely also plays a role in increasing ventricular afterload, ultimately causing right ventricle (RV) dysfunction and death. Current therapeutic treatments do not provide a realistic approach to destiffening arteries and, thus, to potentially abrogating the effects of high pulsatile flow on the distal pulmonary vasculature or the increased work imposed by stiffening on the RV. Scrutinizing the effect of PA stiffening on high pulsatile flow-induced cellular and molecular changes, and vice versa, might lead to important new therapeutic options that abrogate PA remodeling and PH development. With a clear understanding that PA stiffening may contribute to the progression of PH to an irreversible state by contributing to chronic microvascular damage in lungs, future studies should be aimed first at defining the underlying mechanisms leading to PA stiffening and then at improved treatment approaches based on these findings.Keywords: pulmonary hypertension, arterial stiffening, wave reflection, smooth muscle cell, endothelial cell, inflammation, right ventricle, treatment. Arterial stiffening is increasingly recognized as a risk factor of cardiovascular events as well as a guide for pharmacological treatment of cardiovascular diseases. Yet its exact role in the development and progression of cardiovascular diseases such as hypertension remains elusive. A recent study, however, presented convincing data supporting the possibility of a cause-effect relationship between arterial stiffness and systemic hypertension: higher levels of arterial stiffness and central pressures preceded and were associated with an increased risk of hypertension, but hypertension did not cause arterial stiffness. 1This work demonstrated that increased vascular stiffness could be a precursor to hypertension. A key implication from these observations is that arterial stiffness, when used as a measure of cardiovascula...

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Section: Measurement Of Pvs In Ph: Historical Perspectivementioning

confidence: 99%

Vascular Stiffening in Pulmonary Hypertension: Cause or Consequence? (2013 Grover Conference Series)

et al. 2014

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“…21 The development of intravascular imaging modalities provides a realtime in vivo characterization of proximal elastic PA wall ($2-3 mm in diameter) in the PH workup. 22 We have shown in COPD and interstitial lung disease candidates for lung transplantation that patients with normal mPAP have a significant increase of EM. 9 Jorge et al reported a high thickness-diameter ratio (13 AE 1.6%) in patients with severe mitral valve disease and with a predominantly Ipc-PH phenotype.…”

Section: Discussionmentioning

confidence: 92%

“…Accordingly, Gerges et al using the pulmonary artery occlusion technique to analyze the PVR partitioning pattern in heart failure, have reported that upstream resistance is significantly lower in Cpc‐PH than in Ipc‐PH patients, consistent with the presence of pre‐capillary PVD in Cpc‐PH 21 . The development of intravascular imaging modalities provides a real‐time in vivo characterization of proximal elastic PA wall (∼2–3 mm in diameter) in the PH workup 22 . We have shown in COPD and interstitial lung disease candidates for lung transplantation that patients with normal mPAP have a significant increase of EM 9 .…”

Section: Discussionmentioning

confidence: 96%

Section: Discussionmentioning

confidence: 99%

“…Interestingly, the PA wall disease and the hemodynamic profile of Cpc-PH patients are very similar compared to historical patients with PAH. 22 Although the cellular and molecular mechanisms that drive the interactions of distal and proximal arterial remodeling in PH remains unclear, the correlation between the changes of the pulmonary hemodynamic parameters after iNO and the baseline proximal PA stiffness could illustrate the close cross-talk between the distal and proximal PAs. 27 Finally, the early proximal PA wall remodeling associated with the impairment of RV-PA coupling, together with the parallel effect of the left ventricle to RV through the interventricular septum function, could explain the absence of association of the distal pulmonary vascular remodeling with RV dysfunction in PH-LHD.…”

Section: Discussionmentioning

confidence: 99%

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Proximal pulmonary arterial wall disease in patients with persistent pulmonary hypertension after successful left‐sided valve replacement according to the hemodynamic phenotype

et al. 2018

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Regression of pulmonary hypertension (PH) is often incomplete after successful left-sided valve replacement (LSVR). Proximal pulmonary arterial (PPA) wall disease can be involved in patients with persistent-PH after LSVR, affecting the right ventricular to pulmonary arterial (RV-PA) coupling. Fifteen patients underwent successful LSVR at least one year ago presenting PH by echo (> 50 mmHg). Prosthesis-patient mismatch and left ventricular dysfunction were discarded. All patients underwent hemodynamic and intravascular ultrasound (IVUS) study. We estimated PPA stiffness (elastic modulus [EM]) and the relative area wall thickness (AWT). Acute vasoreactivity was assessed by inhaled nitric oxide (iNO) testing. RV-PA coupling was estimated by the tricuspid annular plane systolic excursion to systolic pulmonary arterial pressure ratio. Patients were classified as isolated post-capillary PH (Ipc-PH; pulmonary vascular resistance [PVR] ≤ 3 WU and/or diastolic pulmonary gradient [DPG] < 7 mmHg) and combined post- and pre-capillary PH (Cpc-PH; PVR > 3 WU and DPG ≥ 7 mmHg). Both Ipc-PH and Cpc-PH showed a significant increase of EM and AWT. Despite normal PVR and DPG, Ipc-PH had a significant decrease in pulmonary arterial capacitance and RV-PA coupling impairment. Cpc-PH had worse PA stiffness and RV-PA coupling to Ipc-PH (P < 0.05). iNO decreased RV afterload, improving the cardiac index and stroke volume only in Cpc-PH (P < 0.05). Patients with persistent PH after successful LSVR have PPA wall disease and RV-PA coupling impairment beyond the hemodynamic phenotype. Cpc-PH is responsive to iNO, having the worse PA stiffness and RV-PA coupling. The PPA remodeling could be an early event in the natural history of PH associated with left heart disease.

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Assessment of Structural and Functional Pulmonary Vascular Disease in Patients with PAH

Cited by 2 publications

References 50 publications

Vascular Stiffening in Pulmonary Hypertension: Cause or Consequence? (2013 Grover Conference Series)

Vascular Stiffening in Pulmonary Hypertension: Cause or Consequence? (2013 Grover Conference Series)

Proximal pulmonary arterial wall disease in patients with persistent pulmonary hypertension after successful left‐sided valve replacement according to the hemodynamic phenotype

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