scholarly journals A novel echocardiographic method for estimation of pulmonary artery wedge pressure and pulmonary vascular resistance

2021 ◽  
Vol 8 (2) ◽  
pp. 1216-1229
Author(s):  
Vladislav Chubuchny ◽  
Nicola Riccardo Pugliese ◽  
Claudia Taddei ◽  
Elisa Poggianti ◽  
Valentina Spini ◽  
...  
Keyword(s):  
Pulmonary Artery ◽  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Pulmonary Artery Wedge Pressure ◽  
Wedge Pressure

P4690Effects of pulmonary artery wedge pressure on right ventricular pulsatile loading in pulmonary hypertension: a reappraisal based on pulmonary arterial isobaric stiffness

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
D Chemla ◽  
E Berthelot ◽  
J Weatherald ◽  
E Lau ◽  
P Attal ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Pulmonary Artery ◽  
Stroke Volume ◽  
Right Ventricular ◽  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Pulse Pressure ◽  
Pulmonary Artery Wedge Pressure ◽  
Pulmonary Arterial ◽  
Wedge Pressure

Abstract Background Pulmonary hypertension (PH) is associated with stiffening of pulmonary arteries. Previous studies have suggested that high pulmonary artery wedge pressure (PAWP) in postcapillary PH (Pc-PH) further augments PA stiffness at a given level of pulmonary vascular resistance as compared to pulmonary arterial hypertension (PAH). However, these studies do not take into account differences in distending pressure (mean PA pressure, mPAP), which has an effect on stiffness due to non-linear stress-strain behavior of arteries. Purpose To compare total PA stiffness between Pc-PH and idiopathic PAH (iPAH) studied at similar mPAP (isobaric stiffness). Methods This was an analysis of right heart catheterization results obtained in 112 Pc-PH and 112 iPAH patients extracted from the French PAH network registry and matched for mPAP (median 38 vs 39 mmHg, P=NS), age (70.5 years each) and sex (64% female each). Total PA stiffness was calculated as the ratio of PA pulse pressure to indexed stroke volume. Results Total PA stiffness (n=224) increased with mPAP (Spearman's rho = 0.66) and decreased with PAWP (rho = - 0.17) (each P<0.01). The isobaric stiffness was lower in Pc-PH (median (IQR) = 0.91 (0.64–1.39) mmHg/mL/m2) than in iPAH (1.18 (0.83–1.62) mmHg/mL/m2, P<0.01). The patients were then stratified according to their mPAP (25–35 mmHg, n=74 (37/37); 36–43 mmHg, n=75 (34/41); and 44–66 mmHg, n=75 (41/34)). The isobaric stiffness was lower in Pc-PH than iPAH in the 1st mPAP tertile (0.62 vs 0.83 mmHg/mL/m2, P=0.06), in the 2nd mPAP tertile (0.76 vs 1.22 mmHg/mL/m2, P<0.01) and in the 3rd mPAP tertile (1.41 vs 1.77 mmHg/mL/m2, P<0.01). The pulmonary vascular resistance was lower in Pc-PH than iPAH in every mPAP tertile (each P<0.01). Finally, Pc-PH had a higher indexed stroke volume than iPAH (37 (29–48) vs 32 (27–40) mL/m2, P<0.01) while systolic PA pressure and PA pulse pressure were similar. Conclusion Unexpectedly, the isobaric pulmonary arterial stiffness was lower in Pc-PH than iPAH patients. It is proposed that PAWP attenuates the increase in RV pulsatile loading in PH when the natural high-strain-induced stiffening was accounted for. This may contribute to a less impaired right ventricular-PA coupling leading to higher indexed stroke volume in Pc-PH than iPAH despite similar PA pressure. At every mPAP level, both the lower PA stiffness and lower pulmonary vascular resistance in Pc-PH than in iPAH may contribute to explain differences in the pressure overload-induced right ventricular adaptation between the two diseased groups, a point that deserves to be confirmed by further studies. Acknowledgement/Funding University regular funds

scholarly journals Persistent Pulmonary Hypertension in Corrected Valvular Heart Disease: Hemodynamic Insights and Long‐Term Survival

2021 ◽  
Author(s):  
Javier Bermejo ◽  
Ana González‐Mansilla ◽  
Teresa Mombiela ◽  
Ana I. Fernández ◽  
Pablo Martínez‐Legazpi ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Pulmonary Hypertension ◽  
Heart Disease ◽  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Valvular Heart Disease ◽  
Pulmonary Artery Wedge Pressure ◽  
Wedge Pressure

Background The determinants and consequences of pulmonary hypertension after successfully corrected valvular heart disease remain poorly understood. We aim to clarify the hemodynamic bases and risk factors for mortality in patients with this condition. Methods and Results We analyzed long‐term follow‐up data of 222 patients with pulmonary hypertension and valvular heart disease successfully corrected at least 1 year before enrollment who had undergone comprehensive hemodynamic and imaging characterization as per the SIOVAC (Sildenafil for Improving Outcomes After Valvular Correction) clinical trial. Median (interquartile range) mean pulmonary pressure was 37 mm Hg (32–44 mm Hg) and pulmonary artery wedge pressure was 23 mm Hg (18–26 mm Hg). Most patients were classified either as having combined precapillary and postcapillary or isolated postcapillary pulmonary hypertension. After a median follow‐up of 4.5 years, 91 deaths accounted for 4.21 higher‐than‐expected mortality in the age‐matched population. Risk factors for mortality were male sex, older age, diabetes mellitus, World Health Organization functional class III and higher pulmonary vascular resistance—either measured by catheterization or approximated from ultrasound data. Higher pulmonary vascular resistance was related to diabetes mellitus and smaller residual aortic and mitral valve areas. In turn, the latter correlated with prosthetic nominal size. Six‐month changes in the composite clinical score and in the 6‐minute walk test distance were related to survival. Conclusions Persistent valvular heart disease–pulmonary hypertension is an ominous disease that is almost universally associated with elevated pulmonary artery wedge pressure. Pulmonary vascular resistance is a major determinant of mortality in this condition and is related to diabetes mellitus and the residual effective area of the corrected valve. These findings have important implications for individualizing valve correction procedures. Registration URL: https://www.clinicaltrials.gov ; Unique identifier: NCT00862043.

Pulmonary Endarterectomy: Assessment of Operability, Surgical Description, and Post-op Care

2014 ◽  
Vol 12 (4) ◽  
pp. 186-192 ◽  
Author(s):  
David Poch ◽  
Victor Pretorius
Keyword(s):  
Pulmonary Hypertension ◽  
Pulmonary Artery ◽  
Pulmonary Artery Pressure ◽  
Pulmonary Arteries ◽  
Chronic Thromboembolic Pulmonary Hypertension ◽  
Pulmonary Artery Wedge Pressure ◽  
Pulmonary Endarterectomy ◽  
Pulmonary Thromboendarterectomy ◽  
Thromboembolic Pulmonary Hypertension ◽  
Wedge Pressure

Chronic thromboembolic pulmonary hypertension (CTEPH) is defined as a mean pulmonary artery pressure ≥25 mm Hg and pulmonary artery wedge pressure ≤15 mm Hg in the presence of occlusive thrombi within the pulmonary arteries. Surgical pulmonary thromboendarterectomy (PTE) is considered the best treatment option for CTEPH.

Pulmonary Artery Wedge Pressure Respiratory Variation Increases With Sodium Nitroprusside Vasodilator Challenge

2020 ◽  
Vol 26 (12) ◽  
pp. 1096-1099
Author(s):  
Steven P. Maurides ◽  
Devin Blankinship ◽  
Kavin Panneerselvam ◽  
Gregory R. Jackson ◽  
Stefano Ghio ◽  
...  
Keyword(s):  
Pulmonary Artery ◽  
Sodium Nitroprusside ◽  
Respiratory Variation ◽  
Pulmonary Artery Wedge Pressure ◽  
Wedge Pressure

The peculiarities of pulmonary macro- and microhemodynamics changes after treatment with agonists and blockers of cholinoceptors

2021 ◽  
Vol 20 (4) ◽  
pp. 35-44
Author(s):  
Vadim I. Evlakhov ◽  
Ilya Z. Poyassov ◽  
Tatiana P. Berezina
Keyword(s):  
Pulmonary Artery ◽  
Pulmonary Vascular Resistance ◽  
Pulmonary Artery Pressure ◽  
Vascular Resistance ◽  
Venous Return ◽  
Filtration Coefficient ◽  
Artery Pressure ◽  
Capillary Filtration ◽  
Capillary Filtration Coefficient ◽  
Pulmonary Microcirculation

Background. The pulmonary arterial and venous vessels are innervated by parasympathetic cholinergic nerves. However, the studies, performed on the isolated rings of pulmonary vessels, can not give answer to the question about the role of cholinergic mechanisms in the changes of pulmonary circulation in full measure. Aim. The comparative analysis of the changes of the pulmonary macro- and microhemodynamics after acetylcholine, atropine, pentamine and nitroglycerine treatment. Materials and methods. The study was carried out on the anesthetized rabbits in the condition of intact circulation with the measurement of the pulmonary artery pressure and flow, venae cavae flows, cardiac output, and also on isolated perfused lungs in situ with stabilized pulmonary flow with measurement of the perfused pulmonary artery pressure, capillary hydrostatic pressure, capillary filtration coefficient and calculation of the pulmonary vascular resistance, pre- and postcapillary resistances. Results. In the conditions of intact circulation after acetylcholine, pentamine and nitroglycerine treatment the pulmonary artery pressure and flow decreased, the pulmonary vascular resistance did not change as a result of decreasing of pulmonary artery flow and left atrial pressure due to diminution of venous return and venae cavaе flows. On perfused isolated lungs acetylcholine caused the increasing of pulmonary artery pressure, capillary hydrostatic pressure, pulmonary vascular resistance, pre- and postcapillary resistance and capillary filtration coefficient. After M-blocker atropine treatment the indicated above parameters of pulmonary microcirculation increased, on the contrary, after N-blocker pentamine treatment they decreased. Nitroglycerine infusion caused less decreasing of the parameters of pulmonary microcirculation in comparison with effects of pentamine, but capillary filtration coefficient decreased to a greater extent. These data indicate that nitroglycerine decreases endothelial permeability of pulmonary microvessels. Conclusion. After activation or blockade of cholinergic mechanisms in the condition of intact circulation the calculated parameter of pulmonary vascular resistance is depended from the ratio of the pulmonary artery pressure and flow and left atrial pressure, which are determined by the venous return. The different character of the changes of pulmonary microcirculatory parameters after M-blocker atropine and N-blocker pentamine treatment is evidence of reciprocal relations of M- and N-cholinoceptors in the nervous regulation of the pulmonary microcirculatory bed.

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