Increased Pulse Pressure Causes Vascular Injury in Pulmonary and Systemic Arteries. Decreasing the Pulsatility with Banding and Vasodilators Can Stabilize Pulmonary Hypertension

2010 ◽  
Vol 01 (02) ◽  
Author(s):  
Warren G. Guntheroth
Keyword(s):  
Pulmonary Hypertension ◽  
Vascular Injury ◽  
Pulse Pressure ◽  
Systemic Arteries

Increased Pulmonary-Systemic Pulse Pressure Ratio Is Associated With Increased Mortality in Group 1 Pulmonary Hypertension

2019 ◽  
Vol 28 (7) ◽  
pp. 1059-1066 ◽  
Author(s):  
Benjamin K. Ruth ◽  
Kenneth C. Bilchick ◽  
Manu M. Mysore ◽  
Hunter Mwansa ◽  
William C. Harding ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Pulse Pressure ◽  
Pressure Ratio ◽  
Group 1

Proximal pulmonary arterial obstruction decreases the time constant of the pulmonary circulation and increases right ventricular afterload

2013 ◽  
Vol 114 (11) ◽  
pp. 1586-1592 ◽  
Author(s):  
Alberto Pagnamenta ◽  
Rebecca Vanderpool ◽  
Serge Brimioulle ◽  
Robert Naeije
Keyword(s):  
Pulmonary Hypertension ◽  
Right Ventricular ◽  
Time Constant ◽  
Pulse Pressure ◽  
Pulmonary Circulation ◽  
Characteristic Impedance ◽  
Ventricular Afterload ◽  
Hydraulic Load ◽  
Distal Obstruction ◽  
Pulmonary Arterial

The time constant of the pulmonary circulation, or product of pulmonary vascular resistance (PVR) and compliance (Ca), called the RC-time, has been reported to remain constant over a wide range of pressures, etiologies of pulmonary hypertension, and treatments. We wondered if increased wave reflection on proximal pulmonary vascular obstruction, like in operable chronic thromboembolic pulmonary hypertension, might also decrease the RC-time and thereby increase pulse pressure and right ventricular afterload. Pulmonary hypertension of variable severity was induced either by proximal obstruction (pulmonary arterial ensnarement) or distal obstruction (microembolism) eight anesthetized dogs. Pulmonary arterial pressures (Ppa) were measured with high-fidelity micromanometer-tipped catheters, and pulmonary flow with transonic technology. Pulmonary ensnarement increased mean Ppa, PVR, and characteristic impedance, decreased Ca and the RC-time (from 0.46 ± 0.07 to 0.30 ± 0.03 s), and increased the oscillatory component of hydraulic load (Wosc/Wtot) from 25 ± 2 to 29 ± 2%. Pulmonary microembolism increased mean Ppa and PVR, with no significant change in Ca and characteristic impedance, increased RC-time from 0.53 ± 0.09 to 0.74 ± 0.05 s, and decreased Wosc/Wtot from 26 ± 2 to 13 ± 2%. Pulse pressure increased more after pulmonary ensnarement than after microembolism. Concomitant measurements with fluid-filled catheters showed the same functional differences between the two types of pulmonary hypertension, with, however, an underestimation of Wosc. We conclude that pulmonary hypertension caused by proximal vs. distal obstruction is associated with a decreased RC-time and increased pulsatile component of right ventricular hydraulic load.

scholarly journals Aortic pulse pressure homeostasis emerges from physiological adaptation of systemic arteries to local mechanical stresses

2016 ◽  
Vol 311 (3) ◽  
pp. R522-R531 ◽  
Author(s):  
Phuc H. Nguyen ◽  
Egemen Tuzun ◽  
Christopher M. Quick
Keyword(s):  
Pulse Pressure ◽  
Circumferential Stress ◽  
Mechanical Stresses ◽  
Arterial System ◽  
Physiological Adaptation ◽  
Adaptive Responses ◽  
Wall Stiffness ◽  
Blood Pressures ◽  
Standard Pulse ◽  
Systemic Arteries

Aortic pulse pressure arises from the interaction of the heart, the systemic arterial system, and peripheral microcirculations. The complex interaction between hemodynamics and arterial remodeling precludes the ability to experimentally ascribe changes in aortic pulse pressure to particular adaptive responses. Therefore, the purpose of the present work was to use a human systemic arterial system model to test the hypothesis that pulse pressure homeostasis can emerge from physiological adaptation of systemic arteries to local mechanical stresses. First, we assumed a systemic arterial system that had a realistic topology consisting of 121 arterial segments. Then the relationships of pulsatile blood pressures and flows in arterial segments were characterized by standard pulse transmission equations. Finally, each arterial segment was assumed to remodel to local stresses following three simple rules: 1) increases in endothelial shear stress increases radius, 2) increases in wall circumferential stress increases wall thickness, and 3) increases in wall circumferential stress decreases wall stiffness. Simulation of adaptation by iteratively calculating pulsatile hemodynamics, mechanical stresses, and vascular remodeling led to a general behavior in response to mechanical perturbations: initial increases in pulse pressure led to increased arterial compliances, and decreases in pulse pressure led to decreased compliances. Consequently, vascular adaptation returned pulse pressures back toward baseline conditions. This behavior manifested when modeling physiological adaptive responses to changes in cardiac output, changes in peripheral resistances, and changes in local arterial radii. The present work, thus, revealed that pulse pressure homeostasis emerges from physiological adaptation of systemic arteries to local mechanical stresses.

scholarly journals Pulmonary artery pulse pressure and wave reflection in chronic pulmonary thromboembolism and primary pulmonary hypertension

2001 ◽  
Vol 37 (4) ◽  
pp. 1085-1092 ◽  
Author(s):  
Vincent Castelain ◽  
Philippe Hervé ◽  
Yves Lecarpentier ◽  
Pierre Duroux ◽  
Gerald Simonneau ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Pulmonary Artery ◽  
Pulse Pressure ◽  
Wave Reflection ◽  
Primary Pulmonary Hypertension ◽  
Pulmonary Thromboembolism

P4677Balloon pulmonary angioplasty improves pulmonary arterial compliance in patients with inoperable chronic thromboembolic pulmonary hypertension

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
S Umemoto ◽  
K Abe ◽  
K Horimoto ◽  
K Hosokawa ◽  
H Tsutsui
Keyword(s):  
Pulmonary Hypertension ◽  
Stroke Volume ◽  
Pulse Pressure ◽  
Arterial Compliance ◽  
Chronic Thromboembolic Pulmonary Hypertension ◽  
Heart Catheterization ◽  
Thromboembolic Pulmonary Hypertension ◽  
Pulmonary Arterial ◽  
The Impact

Abstract Background Right ventricular (RV) pressure overload is directly related to the increase in mortality in pulmonary hypertension. Pulmonary arterial compliance (CPA; stroke volume/pulmonary pulse pressure) was reported to be an independent determinant of RV systolic afterload in patients with pulmonary arterial hypertension (PAH). Recently, balloon pulmonary angioplasty (BPA) has been reported to reduce mean pulmonary artery pressure (mPAP) and pulmonary vascular resistance (RPA) in patients with inoperable chronic thromboembolic pulmonary hypertension (CTEPH). However, the effects of BPA on CPA remain unclear. Purpose The aim of this study was to investigate the impact of BPA on CPA in patients with inoperable CTEPH. Methods We retrospectively analyzed 78 patients (388 BPA sessions) with inoperable CTEPH who underwent BPA in our hospital from September 2012 to June 2018. Total number of BPA sessions was 5.0±1.8 (range 1–10). The pressure values were obtained from right heart catheterization at baseline (n=78), just after the final BPA (n=78) and follow-up (n=19) periods. The intervals from baseline to the final BPA and the final BPA to follow-up were 593±498 days and 397±276 days, respectively. Results Mean age was 60.5±12.6 years old, and 64 (82%) were female. All patients were symptomatic (WHO functional class II/III/IV 16/55/7). Patients who had pulmonary vasodilators decreased from 70 (90%) at baseline to 23 (28%) at the final BPA and 2 (15%) at follow-up. BPA reduced mPAP and RPA significantly from baseline to the final BPA and follow-up periods. BPA also improved CPA with significant reduction of pulse pressure despite no significant changes in stroke volume between baseline and follow-up (Table). CPA between the final BPA and follow-up was equivalent (p=0.95). Conclusions BPA improved CPA just after the final BPA in inoperable CTEPH patients. In addition, CPA was preserved during the follow-up after the final BPA sessions. These data suggest that BPA consistently unloads RV systolic afterload in those patients.

scholarly journals Decreased pulmonary arterial proportional pulse pressure is associated with increased mortality in group 1 pulmonary hypertension

2017 ◽  
Vol 40 (11) ◽  
pp. 988-992
Author(s):  
Hunter Mwansa ◽  
Kenneth C. Bilchick ◽  
Alex M. Parker ◽  
William Harding ◽  
Benjamin Ruth ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Pulse Pressure ◽  
Pulmonary Arterial ◽  
Group 1

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

Sign in / Sign up

Export Citation Format

Share Document