Right Ventricular Response to Pulmonary Arterial Stiffening in a Canine Model of Acute Embolization

2012 ◽  
Author(s):  
Alessandro Bellofiore ◽  
Alejandro Roldan-Alzate ◽  
Matthieu Besse ◽  
Heidi B. Kellihan ◽  
Daniel W. Consigny ◽  
...  
Keyword(s):  
Heart Failure ◽  
Right Ventricular ◽  
Poor Prognosis ◽  
Pulmonary Arterial Pressure ◽  
Canine Model ◽  
Pulmonary Vasculature ◽  
Mean Pulmonary Arterial Pressure ◽  
Fast Progression ◽  
Ventricular Response ◽  
Pulmonary Arterial

Pulmonary arterial hypertension (PAH) is a devastating disease exhibiting fast progression [1] and poor prognosis [2]. PAH originates from an increased resistance to blood flow in the distal pulmonary vasculature and in the later stages of the disease leads to right ventricular (RV) functional impairment and subsequent heart failure, which in most cases is the direct cause of demise. In PAH, RV failure appears to be correlated to PA stiffening, which is a better predictor of mortality than the direct increases in mean pulmonary arterial pressure (mPAP) and pulmonary vasculature resistance (PVR) [3,4].

Plasma adrenomedullin level after cardiopulmonary bypass

Perfusion ◽  
1998 ◽  
Vol 13 (5) ◽  
pp. 334-337 ◽  
Author(s):  
Hiroyoshi Komai ◽  
Yasuaki Naito ◽  
Keiichi Fujiwara ◽  
Yasuzo Noguchi ◽  
Yoshiharu Nishimura
Keyword(s):  
Heart Disease ◽  
Cardiopulmonary Bypass ◽  
Pulmonary Arterial Pressure ◽  
Significant Negative Correlation ◽  
Pulmonary Vasculature ◽  
Mean Pulmonary Arterial Pressure ◽  
Level 3 ◽  
Pulmonary Arterial ◽  
The Mean ◽  
Congenital Cyanotic Heart Disease

Adrenomedullin is an intrinsic vasodilator which is metabolized mainly in the pulmonary circulation. We measured plasma levels of adrenomedullin in children with congenital cyanotic heart disease (CY group, n = 6), children with high pulmonary blood flow due to congenital heart disease (PH group, n = 8), and in adults with mitral valve disease (MV group, n = 7) before and 3 h after cardiopulmonary bypass (CPB). Before CPB, the adrenomedullin level was the highest in the MV group, possibly due to chronic heart failure. Three hours after CPB, the plasma adrenomedullin level (pg/ml) increased to 1712.7 ± 498.4 in the CY group, 167.6 ± 26.4 in the PH group, and 1404.3 ± 313.7 in the MV group, the level in the PH group being significantly lower than the rest. In the PH group, there was a statistically significant negative correlation between the mean pulmonary arterial pressure at the preoperative catheter study, and the adrenomedullin level 3 h after CPB. These results illustrate that the adrenomedullin level increased after CPB, but that the increase was less marked in the PH group, implying that where the pulmonary vasculature was damaged most, this results in increased vasoconstriction.

Inhalation of the ETAreceptor antagonist LU-135252 selectively attenuates hypoxic pulmonary vasoconstriction

2008 ◽  
Vol 294 (2) ◽  
pp. R601-R605 ◽  
Author(s):  
Bodil Petersen ◽  
Maria Deja ◽  
Roland Bartholdy ◽  
Bernd Donaubauer ◽  
Sven Laudi ◽  
...  
Keyword(s):  
Arterial Pressure ◽  
Receptor Antagonist ◽  
Experimental Model ◽  
Pulmonary Arterial Pressure ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Pulmonary Vasculature ◽  
Mean Pulmonary Arterial Pressure ◽  
Pulmonary Vasoconstriction ◽  
Pulmonary Arterial ◽  
To Receive

Endogenous endothelin (ET)-1 modulates hypoxic pulmonary vasoconstriction (HPV). Accordingly, intravenously applied ETAreceptor antagonists reduce HPV, but this is accompanied by systemic vasodilation. We hypothesized that inhalation of an ETAreceptor antagonist might act selectively on the pulmonary vasculature and investigated the effects of aerosolized LU-135252 in an experimental model of HPV. Sixteen piglets (weight: 25 ± 1 kg) were anesthetized and mechanically ventilated at an inspiratory oxygen fraction (FiO2) of 0.3. After 1 h of hypoxia at FiO20.15, animals were randomly assigned either to receive aerosolized LU-135252 as bolus (0.3 mg/kg for 20 min; n = 8, LU group), or to receive aerosolized saline ( n = 8, controls). In all animals, hypoxia significantly increased mean pulmonary arterial pressure (32 ± 1 vs. 23 ± 1 mmHg; P < 0.01; means ± SE) and increased arterial plasma ET-1 (0.52 ± 0.04 vs. 0.37 ± 0.05 fmol/ml; P < 0.01) compared with mild hyperoxia at FiO20.3. Inhalation of LU-135252 induced a significant and sustained decrease in mean pulmonary arterial pressure compared with controls (LU group: 27 ± 1 mmHg; controls: 32 ± 1 mmHg; values at 4 h of hypoxia; P < 0.01). In parallel, mean systemic arterial pressure and cardiac output remained stable and were not significantly different from control values. Consequently, in our experimental model of HPV, the inhaled ETAreceptor antagonist LU-135252 induced selective pulmonary vasodilation without adverse systemic hemodynamic effects.

Right ventricular adaptation in the critical phase after acute intermediate-risk pulmonary embolism

2020 ◽  
pp. 204887262092525 ◽  
Author(s):  
Mads Dam Lyhne ◽  
Jacob Gammelgaard Schultz ◽  
Anders Kramer ◽  
Christian Schmidt Mortensen ◽  
Jens Erik Nielsen-Kudsk ◽  
...  
Keyword(s):  
Pulmonary Embolism ◽  
Arterial Pressure ◽  
Right Ventricular ◽  
Acute Pulmonary Embolism ◽  
Pulmonary Arterial Pressure ◽  
Intermediate Risk ◽  
Right Ventricular Afterload ◽  
Mean Pulmonary Arterial Pressure ◽  
Ventricular Afterload ◽  
Pulmonary Arterial

Background The haemodynamic response following acute, intermediate-risk pulmonary embolism is not well described. We aimed to describe the cardiovascular changes in the initial, critical phase 0–12 hours after acute pulmonary embolism in an in-vivo porcine model. Methods Pigs were randomly allocated to pulmonary embolism ( n = 6) or sham ( n = 6). Pulmonary embolism was administered as autologous blood clots (20 × 1 cm) until doubling of mean pulmonary arterial pressure or mean pulmonary arterial pressure was greater than 34 mmHg. Sham animals received saline. Cardiopulmonary changes were evaluated for 12 hours after intervention by biventricular pressure–volume loop recordings, invasive pressure measurements, arterial and central venous blood gas analyses. Results Mean pulmonary arterial pressure increased ( P < 0.0001) and stayed elevated for 12 hours in the pulmonary embolism group compared to sham. Pulmonary vascular resistance and right ventricular arterial elastance (right ventricular afterload) were increased in the first 11 and 6 hours, respectively, after pulmonary embolism ( P < 0.01 for both) compared to sham. Right ventricular ejection fraction was reduced ( P < 0.01) for 8 hours, whereas a near-significant reduction in right ventricular stroke volume was observed ( P = 0.06) for 4 hours in the pulmonary embolism group compared to sham. Right ventricular ventriculo–arterial coupling was reduced ( P < 0.05) for 6 hours following acute pulmonary embolism despite increased right ventricular mechanical work in the pulmonary embolism group ( P < 0.01) suggesting right ventricular failure. Conclusions In a porcine model of intermediate-risk pulmonary embolism, the increased right ventricular afterload caused initial right ventricular ventriculo–arterial uncoupling and dysfunction. After approximately 6 hours, the right ventricular afterload returned to pre-pulmonary embolism values and right ventricular function improved despite a sustained high pulmonary arterial pressure. These results suggest an initial critical and vulnerable phase of acute pulmonary embolism before haemodynamic adaptation.

Treatment of Severe Hypertension with Minoxidil and its Effects on Systemic and Pulmonary Haemodynamics

1976 ◽  
Vol 51 (s3) ◽  
pp. 587s-589s ◽  
Author(s):  
D. Hall ◽  
K. L. Froer ◽  
C. Loracher
Keyword(s):  
Heart Failure ◽  
Arterial Pressure ◽  
Pulmonary Arterial Pressure ◽  
Severe Hypertension ◽  
Chronic Administration ◽  
Direct Result ◽  
Small Decrease ◽  
Mean Pulmonary Arterial Pressure ◽  
Pulmonary Haemodynamics ◽  
Pulmonary Arterial

1. The chronic administration of minoxidil, 0024–0·212 mmol (5–40 mg) daily, to fifty-two severely hypertensive patients resulted in an average reduction of mean arterial pressure from 170 to 111 mmHg. 2. Haemodynamic studies in twelve of these patients indicated that the rise in pulmonary arterial pressure in patients without heart failure appears to be a direct result of a disproportionately large increase in cardiac output with respect to a relatively small decrease in pulmonary vascular resistance. Anti-hypertensive treatment of patients with congestive heart failure resulted in a decrease in mean pulmonary arterial pressure.

scholarly journals Prognostic value of the right ventricle diameter, pulmonary arterial pressure and biomarkers in patients with acute heart failure

2021 ◽  
Vol 38 (2) ◽  
pp. 116-124
Author(s):  
Dejan Petrović ◽  
Marina Deljanin-Ilić ◽  
Sanja Stojanović ◽  
Dejan Simonović ◽  
Dijana Stojanović ◽  
...  
Keyword(s):  
Heart Failure ◽  
Arterial Pressure ◽  
Right Ventricle ◽  
Right Ventricular ◽  
Acute Heart Failure ◽  
Pulmonary Arterial Pressure ◽  
Prognostic Significance ◽  
Pulmonary Arterial ◽  
One Year ◽  
The Right

The aim of the paper was to examine the echocardiographic parameters of the right ventricle (RV), its diameter and pulmonary arterial pressure (PAP); to determine their relationship to B-type natriuretic peptide (BNP), troponin and (TnI) and high-sensititity C-raective protein (hsCRP), and to evaluate their prognostic significance to one-year mortality in patients with acute heart failure (AHF). The study included a total of 225 patients (pts) (70.29 ± 9.74 years) who were admitted to Intensive care unit due to the signs and symptoms of AHF. The values of standard biochemical parameters, BNP, TnI and hsCRP were determined during the first 24 hours after admission. All patients underwent echocardiographic examination. During a one-year follow-up, 78 (34.70%) patients died. As compared with the group of survivors (n = 147), the group of non-survivors had higher values of BNP (853.10 ± 384.92 vs. 1399.68 ± 464.44 pg/mL, p < 0.001), TnI (0.59 ± 2.04 vs. 2.00 ± 8.29 ng/ml, p < 0.05), right ventricular diameter and PAP (p < 0.001). BNP was positively correlated with TnI (r = 0.311), PAP (r = 0.255) and right ventricular diameter (r = 0.304, p < 0.001 for all correlations). The cut-off value of BNP ≥ 1062.04 pg/ml, PAP ≥ 44.5 mmHg and TnI ≥ 0.04 ng/ml were associated with a higher risk of mortality. Our results have shown that BNP, PAP and TnI are strong and independent predictors of one-year mortality in hospitalized patients with acute heart failure.

BMPR-II heterozygous mice have mild pulmonary hypertension and an impaired pulmonary vascular remodeling response to prolonged hypoxia

2004 ◽  
Vol 287 (6) ◽  
pp. L1241-L1247 ◽  
Author(s):  
Hideyuki Beppu ◽  
Fumito Ichinose ◽  
Noriko Kawai ◽  
Rosemary C. Jones ◽  
Paul B. Yu ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Arterial Pressure ◽  
Primary Pulmonary Hypertension ◽  
Pulmonary Arterial Pressure ◽  
Pulmonary Arteries ◽  
Pulmonary Vasculature ◽  
Wild Type ◽  
Mean Pulmonary Arterial Pressure ◽  
Pulmonary Arterial ◽  
Alveolar Capillary

Heterozygous mutations of the bone morphogenetic protein type II receptor ( BMPR-II) gene have been identified in patients with primary pulmonary hypertension. The mechanisms by which these mutations contribute to the pathogenesis of primary pulmonary hypertension are not fully elucidated. To assess the impact of a heterozygous mutation of the BMPR-II gene on the pulmonary vasculature, we studied mice carrying a mutant BMPR-II allele lacking exons 4 and 5 ( BMPR-II+/− mice). BMPR-II+/− mice had increased mean pulmonary arterial pressure and pulmonary vascular resistance compared with their wild-type littermates. Histological analyses revealed that the wall thickness of muscularized pulmonary arteries (<100 μm in diameter) and the number of alveolar-capillary units were greater in BMPR-II+/− than in wild-type mice. Breathing 11% oxygen for 3 wk increased mean pulmonary arterial pressure, pulmonary vascular resistance, and hemoglobin concentration to similar levels in BMPR-II+/− and wild-type mice, but the degree of muscularization of small pulmonary arteries and formation of alveolar-capillary units were reduced in BMPR-II+/− mice. Our results suggest that, in mice, mutation of one copy of the BMPR-II gene causes pulmonary hypertension but impairs the ability of the pulmonary vasculature to remodel in response to prolonged hypoxic breathing.

scholarly journals Pulmonary Hypertension in Heart Failure Patients Presenting at OAUTHC, Ile-Ife, Nigeria

2016 ◽  
Vol 10 ◽  
pp. CMC.S38447
Author(s):  
Valentine N. Amadi ◽  
Olufemi E. Ajayi ◽  
Anthony O. Akintomide ◽  
Olugbenga O. Abiodun ◽  
Olaniyi J. Bamikole ◽  
...  
Keyword(s):  
Heart Failure ◽  
Pulmonary Hypertension ◽  
Left Ventricular ◽  
Systolic Volume ◽  
Heart Failure Patients ◽  
Mean Pulmonary Arterial Pressure ◽  
Diastolic Velocity ◽  
End Systolic Volume ◽  
Pulmonary Arterial ◽  
Systolic And Diastolic Function

Background Pulmonary hypertension (PH) is common in heart failure patients. Literature on PH in heart failure is sparse in Nigeria. This study was carried out to determine the prevalence of PH in heart failure patients and ascertain the relationship between left ventricular systolic and diastolic function and the degree of PH. Methods A total of 125 heart failure patients had echocardiography done. PH was diagnosed using tricuspid regurgitation jet and pulmonary ejection jet profile. Results PH was present in 70.4% of heart failure patients. Estimated mean pulmonary arterial pressure increased with increasing severity of systolic and diastolic dysfunction and had significantly negative correlation with ejection fraction, fractional shortening, and early mitral annular tissue diastolic velocity ( E′), but positive correlation with left ventricular end-systolic volume, right ventricular dimension, transmitral E to A ratio, and E/E′ ratio. Conclusion PH is very common in heart failure and has significant relationship with left ventricular function.

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