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      Pulmonary artery wave propagation and reservoir function in conscious man: impact of pulmonary vascular disease, respiration and dynamic stress tests : Wave intensity and reservoir-excess pressure analyses in the pulmonary artery

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          Abstract

          Wave travel plays an important role in cardiovascular physiology. However, many aspects of pulmonary arterial wave behaviour remain unclear. Wave intensity and reservoir-excess pressure analyses were applied in the pulmonary artery in subjects with and without pulmonary hypertension during spontaneous respiration and dynamic stress tests. Arterial wave energy decreased during expiration and Valsalva manoeuvre due to decreased ventricular preload. Wave energy also decreased during handgrip exercise due to increased heart rate. In pulmonary hypertension patients, the asymptotic pressure at which the microvascular flow ceases, the reservoir pressure related to arterial compliance and the excess pressure caused by waves increased. The reservoir and excess pressures decreased during Valsalva manoeuvre but remained unchanged during handgrip exercise. This study provides insights into the influence of pulmonary vascular disease, spontaneous respiration and dynamic stress tests on pulmonary artery wave propagation and reservoir function.

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          Most cited references49

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          Molecular pathogenesis of pulmonary arterial hypertension.

          Recent clinical and experimental studies are redefining the cellular and molecular bases of pulmonary arterial hypertension (PAH). The genetic abnormalities first identified in association with the idiopathic form of PAH--together with a vast increase in our understanding of cell signaling, cell transformation, and cell-cell interactions; gene expression; microRNA processing; and mitochondrial and ion channel function--have helped explain the abnormal response of vascular cells to injury. Experimental and clinical studies now converge on the intersection and interactions between a genetic predisposition involving the BMPR2 signaling pathway and an impaired metabolic and chronic inflammatory state in the vessel wall. These deranged processes culminate in an exuberant proliferative response that occludes the pulmonary arterial (PA) lumen and obliterates the most distal intraacinar vessels. Here, we describe emerging therapies based on preclinical studies that address these converging pathways.
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            Relationship of pulmonary arterial capacitance and mortality in idiopathic pulmonary arterial hypertension.

            The purpose of this study was to determine if pulmonary vascular capacitance predicts survival in patients with idiopathic pulmonary arterial hypertension (IPAH). The prognosis of patients with IPAH is difficult to predict, despite knowledge of clinical and hemodynamic parameters previously identified as predictors. We proposed a capacitance index of stroke volume divided by pulmonary pulse pressure (SV/PP) and prospectively gathered data on IPAH patients who underwent a right heart catheterization. SV/PP was analyzed as a predictor of mortality after adjusting for other modifiers of risk. During 4-year follow-up of 104 patients, 21 patients died. When compared with conventional markers, SV/PP was the strongest univariate predictor of mortality (hazard ratio 17.0 per ml.mm Hg(-1) decrease, 95% confidence interval 13.0 to 22.0; p < 0.0001). In successive bivariate analysis, SV/PP was the only predictor of mortality. In quartile analysis, the lowest SV/PP quartile had a 4-year mortality of 61%; the highest SV/PP had no deaths. The capacitance index (SV/PP) is a strong independent predictor of mortality in patients with IPAH.
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              Pulmonary capillary wedge pressure augments right ventricular pulsatile loading.

              Right ventricular failure from increased pulmonary vascular loading is a major cause of morbidity and mortality, yet its modulation by disease remains poorly understood. We tested the hypotheses that, unlike the systemic circulation, pulmonary vascular resistance (R(PA)) and compliance (C(PA)) are consistently and inversely related regardless of age, pulmonary hypertension, or interstitial fibrosis and that this relation may be changed by elevated pulmonary capillary wedge pressure, augmenting right ventricular pulsatile load.
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                Author and article information

                Contributors
                Journal
                The Journal of Physiology
                J Physiol
                Wiley
                00223751
                October 15 2017
                October 15 2017
                September 11 2017
                : 595
                : 20
                : 6463-6476
                Affiliations
                [1 ]Department of Biomedicine; Aarhus University; Aarhus Denmark
                [2 ]National Heart and Lung Institute; Imperial College London; London UK
                [3 ]Institute of Cardiovascular Science; University College London; London UK
                [4 ]Department of Bioengineering; Imperial College London; London UK
                Article
                10.1113/JP274385
                5638875
                28816352
                2d75f898-1a73-456b-a0ba-a5caa409070e
                © 2017

                http://doi.wiley.com/10.1002/tdm_license_1.1

                http://onlinelibrary.wiley.com/termsAndConditions#vor

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