Correlation of Pulse Wave Transit Time with Pulmonary Artery Pressure in a Porcine Model of Pulmonary Hypertension

For the non-invasive assessment of pulmonary artery pressure (PAP), surrogates like pulse wave transit time (PWTT) have been proposed. The aim of this study was to invasively validate for which kind of PAP (systolic, mean, or diastolic) PWTT is the best surrogate parameter. To assess both PWTT and PAP in six healthy pigs, two pulmonary artery Mikro-Tip™ catheters were inserted into the pulmonary vasculature at a fixed distance: one in the pulmonary artery trunk, and a second one in a distal segment of the pulmonary artery. PAP was raised using the thromboxane A2 analogue U46619 (TXA) and by hypoxic vasoconstriction. There was a negative linear correlation between PWTT and systolic PAP (r = 0.742), mean PAP (r = 0.712) and diastolic PAP (r = 0.609) under TXA. During hypoxic vasoconstriction, the correlation coefficients for systolic, mean, and diastolic PAP were consistently higher than for TXA-induced pulmonary hypertension (r = 0.809, 0.778 and 0.734, respectively). Estimation of sPAP, mPAP, and dPAP using PWTT is feasible, nevertheless slightly better correlation coefficients were detected for sPAP compared to dPAP. In this study we establish the physiological basis for future methods to obtain PAP by non-invasively measured PWTT.

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Measures of Right Ventricular Afterload Predict Exercise Pulmonary Hypertension beyond Mean Pulmonary Artery Pressure

The Journal of Heart and Lung Transplantation ◽

10.1016/j.healun.2021.01.550 ◽

2021 ◽

Vol 40 (4) ◽

pp. S189

Author(s):

S. Osman ◽

R.F. Bentley ◽

S. Mak

Keyword(s):

Pulmonary Hypertension ◽

Pulmonary Artery ◽

Right Ventricular ◽

Pulmonary Artery Pressure ◽

Artery Pressure ◽

Right Ventricular Afterload ◽

Mean Pulmonary Artery Pressure ◽

Ventricular Afterload

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The Relationship between Vitamin D Deficiency and Pulmonary Hypertension

Prague Medical Report ◽

10.14712/23362936.2014.17 ◽

2013 ◽

Vol 114 (3) ◽

pp. 154-161 ◽

Cited By ~ 15

Author(s):

Mehmet Demir ◽

U. Uyan ◽

S. Keçeoçlu ◽

C. Demir

Keyword(s):

Vitamin D ◽

Pulmonary Hypertension ◽

Pulmonary Artery ◽

Vitamin D Deficiency ◽

Pulmonary Artery Pressure ◽

Control Group ◽

Systolic Pulmonary Artery Pressure ◽

Control Groups ◽

Artery Pressure ◽

Vitamin D Levels

Vitamin D deficiency actives renin-angiotensin-aldosterone system (RAAS) which affects cardiovascular system. Activation of RAAS is associated with pulmonary hypertension (PHT). Relation between vitamin D deficiency and PHT could be therefore suggested. In  our study we compared pulmonary artery pressure between vitamin D deficiency and control groups. 115 consecutive patients (average age: 61.86 ± 5.86) who have detected very low vitamin D (vitamin D levels < 10 ng/ml) were enrolled. 117 age matched persons (average age: 61.74 ± 5.99) were selected as the control group. All groups underwent transthoracic echocardiography. Routine biochemical measurement of 25-OH vitamin D and parathormon (PTH) levels were performed. Baseline characteristics of the study groups were comparable. Systolic pulmonary artery pressure (SPAP) of patients in  the low vitamin D group was higher than the control groups. As a  result our study, a  relation between vitamin D deficiency and pulmonary artery hypertension was revealed.

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Importance of Relative Pulmonary Hypertension in Cardiac Surgery: The Mean Systemic-to-Pulmonary Artery Pressure Ratio

Journal of Cardiothoracic and Vascular Anesthesia ◽

10.1053/j.jvca.2005.11.018 ◽

2006 ◽

Vol 20 (3) ◽

pp. 331-339 ◽

Cited By ~ 55

Author(s):

Arnaud Robitaille ◽

André Y. Denault ◽

Pierre Couture ◽

Sylvain Bélisle ◽

Annik Fortier ◽

...

Keyword(s):

Pulmonary Hypertension ◽

Cardiac Surgery ◽

Pulmonary Artery ◽

Pulmonary Artery Pressure ◽

Pressure Ratio ◽

Artery Pressure ◽

The Mean

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Effect of oxygen upon pulmonary circulation in acclimatized man at high altitude

Journal of Applied Physiology ◽

10.1152/jappl.1965.20.2.239 ◽

1965 ◽

Vol 20 (2) ◽

pp. 239-243 ◽

Cited By ~ 20

Author(s):

H. N. Hultgren ◽

J. Kelly ◽

H. Miller

Keyword(s):

Pulmonary Artery ◽

High Altitude ◽

Sea Level ◽

Pulmonary Artery Pressure ◽

Pulmonary Circulation ◽

Arterial Oxygen ◽

Artery Pressure ◽

Oxygen Breathing ◽

Hypoxic Vasoconstriction ◽

Arteriolar Resistance

The response to breathing 100% oxygen was studied in 26 acclimatized residents of the Peruvian Andes at altitudes of 12,300 and 14,200 ft. Arterial oxygen saturation increased from 86% to 96%. Mean pulmonary artery pressure decreased by 5 mm Hg and cardiac output did not change. Calculated pulmonary arteriolar resistance was lowered. Pulmonary artery pressure during oxygen breathing was not decreased to normal values observed at sea level. The data suggest the presence of two factors responsible for the increase in pulmonary arteriolar resistance at high altitude: 1) hypoxic vasoconstriction which is reversed by oxygen breathing and 2) anatomic alterations which are not affected by oxygen breathing. Oxygen breathing at high altitude also produced a slowing of the heart rate and increased the relative height of the secondary or tidal wave of the brachial arterial pressure pulse. pulmonary arteriolar resistance and 100% oxygen; arterial pulse contour–effect of 100% oxygen at high altitude; pulmonary arteriolar resistance–nature of in high altitude; hypoxic vasoconstriction at high altitude–reversal by 100% oxygen breathing; oxygen breathing–comparison of effect on pulmonary circulation at high altitude and sea level Submitted on May 8, 1964

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Pulmonary Hypertension

10.1093/med/9780199764495.003.0035 ◽

2013 ◽

Author(s):

George K Istaphanous ◽

Andreas W Loepke

Keyword(s):

Pulmonary Hypertension ◽

Pulmonary Arterial Hypertension ◽

Pulmonary Artery ◽

Arterial Hypertension ◽

Pulmonary Artery Pressure ◽

Disease Process ◽

Underlying Disease ◽

Artery Pressure ◽

Pulmonary Arterial ◽

Made In

Pediatric pulmonary arterial hypertension (PAH) is characterized by a pathologically elevated pulmonary artery pressure in children. The etiology of PAH is multifactorial, and while its prognosis is closely related to the reversibility of the underlying disease process, much progress has recently been made in its diagnosis and treatment, significantly decreasing the associated morbidity and mortality.

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Adrenomedullin activity in chronically hypoxic rat lungs

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1996.271.2.h622 ◽

1996 ◽

Vol 271 (2) ◽

pp. H622-H629 ◽

Cited By ~ 8

Author(s):

L. Zhao ◽

L. A. Brown ◽

A. A. Owji ◽

D. J. Nunez ◽

D. M. Smith ◽

...

Keyword(s):

Pulmonary Hypertension ◽

Pulmonary Artery ◽

Pulmonary Artery Pressure ◽

Mrna Levels ◽

Rat Lung ◽

Artery Pressure ◽

Isolated Perfused Lung ◽

Calcitonin Gene ◽

Perfused Lung ◽

Hypotensive Response

Adrenomedullin (AM) is a novel vasodilator with structural similarities to calcitonin gene-related peptide (CGRP). This study investigated AM activity in the rat lung during hypoxia-induced pulmonary hypertension. Both rat AM (0.2-10 nmol) and alpha-CGRP (0.2-2 nmol) produced dose-related reductions in pulmonary artery pressure in the isolated perfused lung ventilated with 2% O2. Pretreatment with alpha-CGRP, which demonstrated tachyphylaxis, or its antagonist, CGRP-(8–37), reduced the hypotensive response to AM, suggesting that part of the response to AM is mediated by CGRP receptors. 125I-labeled AM and 125I-labeled CGRP binding was significantly increased in lung membranes from 7-day hypoxic animals (AM from 1.94 +/- 0.3 to 3.36 +/- 0.4 and CGRP from 0.06 +/- 0.01 to 0.12 +/- 0.02 pmol/mg protein), with no change in dissociation constant. Moreover, the hypotensive response to both peptides was increased in the lungs of 7-day hypoxic rats. There was no significant change in lung immunoreactive AM concentrations (hypoxic 5.04 +/- 0.48 vs. control 6.28 +/- 0.76 pmol/g wet wt of tissue) or steady-state AM mRNA levels in 7-day hypoxic rats. Nonetheless, AM may be useful for the acute pharmacological manipulation of pulmonary artery pressure in hypoxia-induced pulmonary hypertension.

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Changes in venous return parameters associated with univentricular Fontan circulations

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.2000.279.5.h2335 ◽

2000 ◽

Vol 279 (5) ◽

pp. H2335-H2343 ◽

Cited By ~ 35

Author(s):

Loïc Macé ◽

Patrice Dervanian ◽

Armand Bourriez ◽

Guy M. Mazmanian ◽

Virginie Lambert ◽

...

Keyword(s):

Pulmonary Artery ◽

Pulmonary Artery Pressure ◽

Venous Return ◽

Correlation Coefficients ◽

Volume Loading ◽

Systemic Blood ◽

Systemic Blood Flow ◽

Artery Pressure ◽

Straight Lines ◽

Proportional Decrease

To clarify the physiology of venous return (Qvr) in Fontan circulations, venous return conductance ( Gvr) and mean circulatory filling pressure (Pmcf) were determined in pentobarbital sodium-anesthetized pigs. Relationships between Qvrand right (biventricular, n = 8) or left (Fontan, n = 8) filling pressures are described by straight lines with significant correlation coefficients. Estimated Pmcfvalues were correlated with observed Pmcfvalues in either circulations ( P ≤ 0.02). Gvrwas smaller in Fontan than in biventricular circulations (4.51 ± 0.36 vs. 7.83 ± 0.69 ml · min−1· kg−1· mmHg−1, P = 0.002) and inversely correlated with pulmonary vascular resistances in Fontan circulations ( P = 0.01). Estimated Pmcf(20.5 ± 1.4 vs. 11.1 ± 0.9 mmHg, P = 0.001) and observed Pmcf(21.8 ± 1.3 vs. 10.6 ± 0.8 mmHg, P < 0.001) were higher in Fontan versus biventricular circulations, respectively. Pulmonary artery pressure in Fontan circulations was correlated with either Pmcf( P ≤ 0.04). We conclude that in Fontan circulations 1) pulmonary vascular resistances induce a proportional decrease in Gvr; and 2) volume loading, while increasing Pmcf(similar to pulmonary artery pressure), allows the gradient for Qvrto increase and maintains systemic blood flow at a biventricular level.

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Sarcoidosis-Associated Pulmonary Hypertension

Seminars in Respiratory and Critical Care Medicine ◽

10.1055/s-0040-1713615 ◽

2020 ◽

Vol 41 (05) ◽

pp. 659-672

Author(s):

Marloes P. Huitema ◽

Harold Mathijssen ◽

Johannes J. Mager ◽

Repke J. Snijder ◽

Jan C. Grutters ◽

...

Keyword(s):

Pulmonary Hypertension ◽

Pulmonary Artery ◽

Pulmonary Artery Pressure ◽

Lung Transplant ◽

Pulmonary Function Tests ◽

High Morbidity ◽

Artery Pressure ◽

Extrinsic Compression ◽

Tertiary Center ◽

Parenchymal Disease

AbstractPulmonary hypertension (PH) is a well-known complication of sarcoidosis, defined by a mean pulmonary artery pressure of ≥25 mm Hg. Since both PH and sarcoidosis are rare diseases, data on sarcoidosis-associated PH (SAPH) is retrieved mostly from small retrospective studies. Estimated prevalence of SAPH ranges from 3% in patients referred to a tertiary center up to 79% in patients awaiting lung transplant. Most patients with SAPH show advanced parenchymal disease as the underlying mechanism. However, some patients have disproportional elevated pulmonary artery pressure, and PH can occur in sarcoidosis patients without parenchymal disease. Other mechanisms such as vascular disease, pulmonary embolisms, postcapillary PH, extrinsic compression, and other sarcoidosis-related comorbidities might contribute to SAPH. The diagnosis of PH in sarcoidosis is challenging since symptoms and signs overlap. Suspicion can be raised based on symptoms or tests, such as pulmonary function tests, laboratory findings, electrocardiography, or chest CT. PH screening mainly relies on transthoracic echocardiography. Right heart catheterization should be considered on a case-by-case basis in patients with clinical suspicion of PH, taking into account clinical consequences. Treatment options are considered on patient level in a PH expert center, and might include oxygen therapy, immunosuppressive, or PH-specific therapy. However, qualitative evidence is scarce. Furthermore, in a subset of patients, interventional therapy or eventually lung transplant can be considered. SAPH is associated with high morbidity. Mortality is higher in sarcoidosis patients with PH compared with those without PH, and increases in patients with more advanced stages of sarcoidosis and/or PH.

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