Robert Naeije

Université Libre de Bruxelles, Bruxelles, Brussels Capital, Belgium

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Publications (469)2285.16 Total impact

  • Robert Naeije
    05/2015; 3(5). DOI:10.1016/j.jchf.2014.12.014
  • Robert Naeije
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    ABSTRACT: Right ventricular function is a major determinant of symptomatology and prognosis in severe pulmonary hypertension. The diagnosis of right heart failure rests on a clinical approach with invasive and noninvasive measurements. Magnetic resonance and echocardiographic imaging of the right ventricle is of prognostic relevance. The gold standard of right ventricular function is the ratio of end-systolic to arterial elastances determined from synchronized volume and pressure measurements. Pressure measurements can be obtained during a right heart catheterization and volume measurements by integration of Doppler pulmonary flow-velocity, magnetic resonance imaging, or, more recently, three-dimensional echocardiography. Imaging also informs about regional function and derived estimates of dyssynchrony and asynchrony. Modern imaging with 3D echocardiography and magnetic resonance aims at improved assessment of regional function and right ventriculo-arterial coupling to assist in the evaluation and prognostication of severe pulmonary hypertension.
    Current Hypertension Reports 05/2015; 17(5):546. DOI:10.1007/s11906-015-0546-0 · 3.90 Impact Factor
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    ABSTRACT: Hypoxic exposure depresses myocardial contractility in vitro, but has been associated with indices of increased cardiac performance in intact animals and in humans, possibly related to sympathetic nervous system activation. We explored left ventricular (LV) function using speckle tracking echocardiography and sympathetic tone by spectral analysis of heart rate variability (HRV) in recently acclimatized lowlanders versus adapted or maladapted highlanders at high altitude. Twenty-six recently acclimatized lowlanders, 14 healthy highlanders and 12 highlanders with chronic mountain sickness (CMS) were studied. Control measurements at sea level were also obtained in the lowlanders. Altitude exposure in the lowlanders was associated with slightly increased blood pressure, decreased LV volumes and decreased longitudinal strain with a trend to increased prevalence of post-systolic shortening (p = 0.06), whereas the low frequency/high frequency (LF/HF) ratio increased (1.62 ± 0.81 vs. 5.08 ± 4.13, p < 0.05) indicating sympathetic activation. Highlanders had a similarly raised LF/HF ratio, but no alteration in LV deformation. Highlanders with CMS had no change in LV deformation, no significant increase in LF/HF, but decreased global HRV still suggestive of increased sympathetic tone, and lower mitral E/A ratio compared to healthy highlanders. Short-term altitude exposure in lowlanders alters indices of LV systolic function and increases sympathetic nervous system tone. Life-long altitude exposure in highlanders is associated with similar sympathetic hyperactivity, but preserved parameters of LV function, whereas diastolic function may be altered in those with CMS. Altered LV systolic function in recently acclimatized lowlanders may be explained by combined effects of hypoxia and changes in loading conditions.
    The International Journal of Cardiovascular Imaging 02/2015; DOI:10.1007/s10554-015-0614-1 · 2.32 Impact Factor
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    ABSTRACT: Pulmonary hypertension is of poor prognosis in heart failure (HF), and this is related to right ventricular (RV) failure. Increased ventilatory response and exercise oscillatory ventilation (EOV) have also a negative impact. We hypothesized that severity classification of HF and risk prediction could be improved by combining functional capacity, with cardiopulmonary exercise testing (CPET) and RV-pulmonary circulation coupling, evaluated by the tricuspid annular plane systolic excursion (TAPSE)-pulmonary artery systolic pressure (PASP) relationship. 459 HF patients were assessed with Doppler echocardiography and CPET and tracked for outcome. Subjects were followed for major cardiac events [cardiac mortality, left ventricular assist device (LVAD) implantation, or heart transplantation]. Cox regression and Kaplan-Meier analyses were performed with TAPSE and PASP as individual measures and combining them in a ratio form. TAPSE/PASP was the strongest predictor whereas NYHA and EOV added predictive value. A 4-quadrant group prediction risk was created according to TAPSE (</≥16 mm) vs PASP (</≥40 mmHg) thresholds looking at CPET variables distribution within groups as follows: Group A (TAPSE> 16 mm and PASP < 40 mmHg) presented the lowest risk (HR: 0.17) and best ventilation; Group B exhibited a low risk (HR:0.88) with depressed TAPSE (< 16 mm) and normal PASP a preserved peak VO2 but high ventilation. Group C had an increased risk (HR: 1.3, TAPSE ≥ 16 mm, PASP ≥ 40 mmHg), reduced peak VO2 and high EOV prevalence. Group D had the highest risk (HR: 5.6), the worse RV-pulmonary pressure coupling (TAPSE< 16 and PASP≥ 40 mmHg), the lowest peak VO2 and the highest EOV rate. the TAPSE/PASP ratio combined with the exercise ventilation provides relevant clinical and prognostic insights in HF. A low TAPSE/PASP with EOV identifies patients at particular high risk of cardiac events.
    Chest 01/2015; DOI:10.1378/chest.14-2065 · 7.13 Impact Factor
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    ABSTRACT: Congenital diaphragmatic hernia (CDH) has a high mortality rate mainly due to lung hypoplasia and persistent pulmonary hypertension of the newborn (PPHN). Simvastatin has been shown to prevent the development of pulmonary hypertension (PH) in experimental models of PH. We, therefore, hypothesized that antenatal simvastatin would attenuate PPHN in nitrofen-induced CDH in rats. The efficacy of antenatal simvastatin was compared to antenatal sildenafil, which has already been shown to improve pathological features of PPHN in nitrofen-induced CDH. On embryonic day (E) 9.5, nitrofen or vehicle was administered to pregnant Sprague-Dawley rats. On E11, nitrofen-treated rats were randomly assigned to antenatal simvastatin (20mg/kg/day orally), antenatal sildenafil (100mg/kg/day orally) or placebo administration from E11 to E21. On E21, fetuses were delivered by cesarean section, killed and checked for left-sided CDH. Lung tissue was then harvested for further pathobiological evaluation. In nitrofen-induced CDH, simvastatin failed to reduce the incidence of nitrofen-induced CDH in the offspring and to increase the body weight, but improved the lung-to-body weight ratio and lung parenchyma structure. Antenatal simvastatin restored the pulmonary vessel density and external diameter, and reduced the pulmonary arteriolar remodeling compared to nitrofen-induced CDH. This was associated with decreased lung expression of endothelin precursor, endothelin type A and B receptors, endothelial and inducible nitric oxide synthase, together with restored lung activation of apoptotic processes mainly in the epithelium. Antenatal simvastatin presented similar effects as antenatal therapy with sildenafil on nitrofen-induced CDH. Antenatal simvastatin improves pathological features of lung hypoplasia and PPHN in experimental nitrofen-induced CDH. Copyright © 2014, American Journal of Physiology - Lung Cellular and Molecular Physiology.
    AJP Lung Cellular and Molecular Physiology 01/2015; DOI:10.1152/ajplung.00345.2014 · 4.04 Impact Factor
  • Robert Naeije, Stefano Ghio
    European Respiratory Journal 01/2015; 45(1):33-5. DOI:10.1183/09031936.00209414 · 7.13 Impact Factor
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    Robert Naeije, Michele D'Alto, Paul R Forfia
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    ABSTRACT: There has been a lot of progress in measurement techniques of the pulmonary circulation in recent years, and this has required updating of basic physiological knowledge. Pulmonary artery pressures (PAP) are normally low and dependent on left atrial pressure (LAP) and cardiac output (CO). Therefore, defining the functional state of the pulmonary circulation for the detection of pulmonary vascular disease or evaluation of disease progression requires measurements of PAP, Pla and CO. Invasive measurements have lately improved by a better definition of zero leveling and of the effects of intrathoracic pressure changes, and understanding of the inherent limitations of fluid-filled thermodilution catheters. The effects of LAP and pulmonary flow on PAP in health and disease are now integrated in the hemodynamic diagnosis of pulmonary hypertension. Development of alternative noninvasive approaches is critically dependent on their potential to quantify pulmonary vascular pressures and CO. Doppler echocardiography and magnetic resonance imaging are coming close. Both approaches are performant for flow measurements, but pressures remain indirectly assessed from flow velocities and/or structural changes. Doppler echocardiography or magnetic resonance imaging have been shown to be accurate, allowing for valid population studies, but with insufficient precision for single number-derived clinical decision making. Copyright © 2014. Published by Elsevier Inc.
    Progress in Cardiovascular Diseases 12/2014; 57(5). DOI:10.1016/j.pcad.2014.12.003 · 2.44 Impact Factor
  • Robert Naeije, Marco Guazzi
    The Journal of heart and lung transplantation: the official publication of the International Society for Heart Transplantation 12/2014; 34(3). DOI:10.1016/j.healun.2014.12.003 · 5.61 Impact Factor
  • R Naeije
    Experimental physiology 12/2014; 99(12):1593-4. DOI:10.1113/expphysiol.2014.082677 · 2.87 Impact Factor
  • Robert Naeije, Alessandra Manes
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    ABSTRACT: Pulmonary arterial hypertension (PAH) is a right heart failure syndrome. In early-stage PAH, the right ventricle tends to remain adapted to afterload with increased contractility and little or no increase in right heart chamber dimensions. However, less than optimal right ventricular (RV)-arterial coupling may already cause a decreased aerobic exercise capacity by limiting maximum cardiac output. In more advanced stages, RV systolic function cannot remain matched to afterload and dilatation of the right heart chamber progressively develops. In addition, diastolic dysfunction occurs due to myocardial fibrosis and sarcomeric stiffening. All these changes lead to limitation of RV flow output, increased right-sided filling pressures and under-filling of the left ventricle, with eventual decrease in systemic blood pressure and altered systolic ventricular interaction. These pathophysiological changes account for exertional dyspnoea and systemic venous congestion typical of PAH. Complete evaluation of RV failure requires echocardiographic or magnetic resonance imaging, and right heart catheterisation measurements. Treatment of RV failure in PAH relies on: decreasing afterload with drugs targeting pulmonary circulation; fluid management to optimise ventricular diastolic interactions; and inotropic interventions to reverse cardiogenic shock. To date, there has been no report of the efficacy of drug treatments that specifically target the right ventricle. ©ERS 2014.
    European Respiratory Review 12/2014; 23(134):476-87. DOI:10.1183/09059180.00007414
  • Gabor Kovacs, Robert Naeije, Horst Olschewski
    American Journal of Respiratory and Critical Care Medicine 11/2014; 190(10):1198-9. DOI:10.1164/rccm.201409-1608LE · 11.99 Impact Factor
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    ABSTRACT: Pulmonary hypertension (PH) secondary to left heart disease (LHD) is a largely underappreciated therapeutic target. Except for a specific focus on PH consequences in patients with advanced heart failure (HF) receiving a left ventricular assist device or candidates for heart transplant, prevention and treatment of initial subclinical forms of PH are not considered a priority in the management of this chronic disease population. Nonetheless, there is recent growing evidence supporting a clinical and prognostic role of PH in the elderly populations and in HF with preserved ejection fraction (pEF). Although the prevalence of PH in these populations still remains largely unknown, there is a large potential for effective pharmacological approaches that might impact the natural history of HFpEF by targeting earlier stages. However, pharmacological studies performed to date with traditional pulmonary vasodilators (i.e. prostanoids and endothelin receptor blockers) in cohorts with HF and left-sided PH have not been positive, primarily because of concomitant systemic hypotension and hepatic toxicity. The encouraging prelimiray data with more selective well-tolerated pulmonary vasodilators, such as phosphodiesterase type 5 inhibitors and guanylate cyclase stimulators/activators, however, suggest the need for new targets of pulmonary microvascular dysfunction and for treating PH-LHD at both early and later stages of the disease process.
    Progress in Cardiovascular Diseases 11/2014; 57(5). DOI:10.1016/j.pcad.2014.11.002 · 2.44 Impact Factor
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    ABSTRACT: Right ventricular contractile response to pharmacological stress in pulmonary arterial hypertension (PAH) has not been characterised. We evaluated right ventricular contractile reserve in adults with PAH using dobutamine stress echocardiography. 16 PAH patients and 18 age-matched controls underwent low-dose dobutamine stress echocardiography. Contractile reserve was assessed by the change (Δ; peak stress minus rest value) in tricuspid annular plane systolic excursion (TAPSE) and tricuspid annular systolic velocity (S'). A subgroup of 13 PAH patients underwent treadmill cardiopulmonary exercise testing for peak oxygen uptake (V'O2peak). At rest, TAPSE and S' were reduced in the PAH group compared with controls (1.7±0.4 versus 2.4±0.2 cm and 9.7±2.6 cm·s(-1) versus 12.5±1.2 cm·s(-1), respectively; p<0.05). Contractile reserve was markedly attenuated in PAH compared to controls (ΔTAPSE 0.1±0.2 versus 0.6±0.3 cm and ΔS' 4.6±2.8 versus 11.2±3.6 cm·s(-1); p<0.0001). In the sub-group of PAH patients with preserved right ventricular systolic function at rest, contractile reserve remained depressed compared to controls. V'O2peak was significantly correlated with ΔS' (r = 0.87, p = 0.0003) and change in stroke volume (r = 0.59, p = 0.03). Dobutamine stress can reveal sub-clinical reduction in right ventricular contractile reserve in patients with PAH. A correlation with exercise capacity suggests potential clinical value beyond resting measurements.
    European Respiratory Journal 10/2014; 45(3). DOI:10.1183/09031936.00089914 · 7.13 Impact Factor
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    ABSTRACT: The differential diagnosis between pre- and postcapillary pulmonary hypertension (PH) is of major therapeutic relevance and thus requires optimal clinical probability assessment with echocardiography. We prospectively analyzed 152 consecutive patients referred to a PH center over a 1-year period undergoing quasi-simultaneous (within 1 hour) echocardiography and right heart catheterization. Echocardiography was performed as usually recommended for the assessment of PH and left heart conditions. PH was defined as a mean pulmonary artery pressure ≥ 25 mm Hg. Postcapillary PH was diagnosed on the basis of a pulmonary capillary wedge pressure >15 mm Hg. Ten of 152 patients (7%) had no PH, 81 of 152 (53%) had precapillary PH, and 61 of 152 (40%) had postcapillary PH. The following five echocardiographic variables were found to predict precapillary PH: right heart chamber larger than the left (P = .0018), left ventricular eccentricity index > 1.2 (P = .0039), dilated inferior vena cava without inspiratory collapse (P = .0076), E/e' ratio ≤10 (P = .00001), and the right ventricle forming the heart apex (P = .0144). Beta coefficients from multiple logistic regression were significant for dilated inferior vena cava without inspiratory collapse (P = .0464) and E/e' ratio ≤ 10 (P = .0002). The score based on β coefficients, ranging from 3 to 34 points, resulted in optimal discrimination at >5, with a positive predictive value of 67.9% and a negative predictive value of 77.5% for precapillary PH. Echocardiography enables a clinically satisfactory differential diagnosis between pre- and postcapillary PH. Copyright © 2014 American Society of Echocardiography. Published by Elsevier Inc. All rights reserved.
    Journal of the American Society of Echocardiography: official publication of the American Society of Echocardiography 10/2014; 28(1). DOI:10.1016/j.echo.2014.09.004 · 3.99 Impact Factor
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    ABSTRACT: Endothelin receptor antagonists improve pulmonary arterial hypertension (PAH). Mutations in the bone morphogenetic protein (BMP) type 2 receptor (BMPR2) predispose to PAH. Here, we sought to determine whether there might exist interactions between these 2 signaling pathways and their effect on the acquisition of the altered phenotype of pulmonary artery smooth muscle cells (PA-SMCs) observed in PAH. Expression of BMPR2, of the BMP agonist BMP4, and of the BMP antagonists gremlin1 and gremlin2 was evaluated in lungs and in PA-SMCs from 6 PAH patients and 14 controls treated with endothelin-1. Endothelin-1 pre-treated PA-SMCs were assessed for proliferation, apoptosis, and downstream signaling activation of Smad1/5/8 and p38 mitogen-activated protein kinase (p38(MAPK)) after BMP2 treatment. In PA-SMCs from PAH patients, expression of BMPR2 and BMP4 decreased, whereas expression of gremlin1 and gremlin2 increased compared with controls. Treatment of control PA-SMCs with endothelin-1 induced a dose-dependent increase in gremlin1 and gremlin2, whereas BMPR2 and BMP4 expression decreased, reaching similar levels as those observed in PAH cells. In control PA-SMCs, endothelin-1 pre-treatment reduced inhibitor of DNA binding 1 (Id1) expression and Smad1/5/8 activation induced by BMP2, whereas it enhanced p38(MAPK) activation. Moreover, BMP2 decreased serum-induced proliferation and increased the pro-apoptotic Bax/Bcl-2 ratio. These effects were attenuated by endothelin-1 pre-treatment. Endothelin-1 did not alter BMPR2 signaling in PA-SMCs from PAH patients. Endothelin-1 downregulates canonical BMPR2 signaling. This is related to decreased BMPR2 and increased anti-BMP gremlin expression associated with increased activation of p38(MAPK) and results in PA-SMC proliferation. Copyright © 2014 International Society for Heart and Lung Transplantation. Published by Elsevier Inc. All rights reserved.
    The Journal of Heart and Lung Transplantation 09/2014; 34(3). DOI:10.1016/j.healun.2014.09.011 · 5.61 Impact Factor
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    ABSTRACT: In early stage uncomplicated systemic hypertension (HT), increased pulmonary vascular resistance (PVR) has been reported at rest, but more rarely during exercise. Recently, limits of normal for stress echocardiography in the evaluation of the pulmonary circulation have been better defined. We therefore used this approach to assess the pulmonary circulation in early HT. One hundred thirteen patients with mild to moderate untreated, uncomplicated HT (blood pressure, 152 ± 19/89 ± 11 mm Hg, heart rate, 70 ± 13 beats per minute) and 345 age- and sex-matched healthy control subjects underwent resting Doppler echocardiography with estimation of mean pulmonary arterial pressure (mPAP), left atrial pressure (LAP), and cardiac output (CO). Measurements were repeated at exercise stress test in 25 patients from each group. At rest, hypertensive patients had normal right and left ventricular structure and function, higher systemic vascular resistance, mPAP (16 ± 5 vs 14 ± 5 mm Hg; P < 0.0001), and PVR (1.3 ± 1.1 vs 1.0 ± 1.2 Wood units; P = 0.006) than control participants, but similar LAP. During exercise, hypertensive patients showed a lower maximum workload and CO and higher peak mPAP than control subjects, but a similar increase in LAP. PVR determined according to multipoint mPAP-CO relationships was also higher in hypertensive patients than in control subjects (2.5 ± 1.1 vs 1.5 ± 0.7 mm Hg/L/min; P < 0.05), with no changes in pulmonary resistive vessel distensibility coefficient α (0.012 ± 0.007 vs 0.012 ± 0.010% change in diameter for each mm Hg increase in mPAP). Resting and exercise PVR are increased in uncomplicated HT, without this being related to increased pulmonary venous pressure or resistive vessel stiffness, suggesting an early increase in pulmonary vascular tone. Copyright © 2015 Canadian Cardiovascular Society. Published by Elsevier Inc. All rights reserved.
    The Canadian journal of cardiology 09/2014; 31(4). DOI:10.1016/j.cjca.2014.09.022 · 3.94 Impact Factor
  • Laurence Dewachter, Robert Naeije
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    ABSTRACT: Introduction: Parenteral prostacyclins are considered the gold standard treatment of severe pulmonary arterial hypertension (PAH). However, the technical and clinical burden of their continuous parenteral administration has led to the development of long-acting oral analogs.Areas covered: Following suggestive uncontrolled studies, an initial 3-month randomized placebo-controlled trial of the oral prostacyclin analog beraprost sodium (BPS) was completed, demonstrating significant improvement in the primary endpoint, which was the six-minute walk test. However, a subgroup analysis revealed that only idiopathic PAH patients benefited from the drug, secondary end points were negative and dosing was limited by side effects. A second 1-year randomized trial with a primary end point combining clinical stability and exercise capacity was negative. A secondary analysis revealed significant improvement after BPS intake at 6 months. Recent open-label studies with a modified release BPS formulation (BPS-MR) suggested long-term improvement in exercise capacity and clinical state in PAH patients. Randomized controlled trials with BPS-MR are underway but have been slowed by regulatory requirements of single optical isomer reformulation of BPS-MR (BPS-414d-MR).Expert opinion: BPS is efficacious in PAH but has failed until now in randomized controlled trials mainly because of side effects limiting dosing. Successive reformulations will hopefully produce better tolerated, purer and longer-acting preparations.
    09/2014; DOI:10.1517/21678707.2014.961422
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    ABSTRACT: Objective Prognosis in pulmonary hypertension (PH) is largely determined by RV function. However, uncertainty remains about what metrics of RV function might be most clinically relevant. The purpose of this study was to assess the clinical relevance of metrics of RV functional adaptation to increased afterload. Methods Patients referred for PH underwent right heart catheterisation and RV volumetric assessment within 48 h. A RV maximum pressure (Pmax) was calculated from the RV pressure curve. The adequacy of RV systolic functional adaptation to increased afterload was estimated either by a stroke volume (SV)/end-systolic volume (ESV) ratio, a Pmax/mean pulmonary artery pressure (mPAP) ratio, or by EF (RVEF). Diastolic function of the RV was estimated by a diastolic elastance coefficient beta. Survival analysis was via Cox proportional HR, and Kaplan-Meier with the primary outcome of time to death or lung transplant. Results Patients (n=50; age 58 +/- 13 yrs) covered a range of mPAP (13-79 mm Hg) with an average RVEF of 39 +/- 17% and ESV of 143 +/- 89 mL. Average estimates of the ratio of end-systolic ventricular to arterial elastance were 0.79 +/- 0.67 (SV/ESV) and 2.3 +/- 0.65 (Pmax/mPAP-1). Transplantation-free survival was predicted by right atrial pressure, mPAP, pulmonary vascular resistance, beta, SV, ESV, SV/ESV and RVEF, but after controlling for right atrial pressure, mPAP, and SV, SV/ESV was the only independent predictor. Conclusions The adequacy of RV functional adaptation to afterload predicts survival in patients referred for PH. Whether this can simply be evaluated using RV volumetric imaging will require additional confirmation.
    Heart (British Cardiac Society) 09/2014; 101(1). DOI:10.1136/heartjnl-2014-306142 · 6.02 Impact Factor
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    ABSTRACT: Pulmonary hypertension is characterized by cellular and structural changes in the vascular wall of pulmonary arteries. We hypothesized that lysophosphatidic acid (LPA), a bioactive lipid, is implicated in this vascular remodeling in a rat model of hypoxic pulmonary hypertension. Exposure of Wistar rats to 10% O2 for 3 weeks induced an increase in the mean serum levels of LPA, to 40.9 (log-detransformed standard deviations: 23.4-71.7) μM versus 21.6 (11.0-42.3) μM in a matched control animal group (P = 0.037). We also observed perivascular LPA immunohistochemical staining in lungs of hypoxic rats colocalized with the secreted lysophospholipase D autotaxin (ATX). Moreover, ATX colocalized with mast cell tryptase, suggesting implication of these cells in perivascular LPA production. Hypoxic rat lungs expressed more ATX transcripts (2.4-fold) and more transcripts of proteins implicated in cell migration: β2 integrin (1.74-fold), intracellular adhesion molecule 1 (ICAM-1; 1.84-fold), and αM integrin (2.70-fold). Serum from the hypoxic group of animals had significantly higher chemoattractant properties toward rat primary lung fibroblasts, and this increase in cell migration could be prevented by the LPA receptor 1 and 3 antagonists. LPA also increased adhesive properties of human pulmonary artery endothelial cells as well as those of human peripheral blood mononuclear cells, via the activation of LPA receptor 1 or 3 followed by the stimulation of gene expression of ICAM-1, β-1, E-selectin, and vascular cell adhesion molecule integrins. In conclusion, chronic hypoxia increases circulating and tissue levels of LPA, which might induce fibroblast migration and recruitment of mononuclear cells in pulmonary vasculature, both of which contribute to pulmonary vascular remodeling.
    09/2014; 4(3):471-481. DOI:10.1086/677362
  • Echocardiography 09/2014; 32. DOI:10.1111/echo.12563 · 1.25 Impact Factor

Publication Stats

11k Citations
2,285.16 Total Impact Points

Institutions

  • 2002–2015
    • Université Libre de Bruxelles
      • • Faculty of Medicine
      • • Laboratory of Physiology and Physiopathology (PHYSIO)
      Bruxelles, Brussels Capital, Belgium
    • Hôpital Antoine-Béclère – Hôpitaux universitaires Paris-Sud
      Clamart, Île-de-France, France
    • University of Bologna
      • Institute of Cardiology
      Bolonia, Emilia-Romagna, Italy
  • 1976–2015
    • University Hospital Brussels
      • Department of Pneumology
      Bruxelles, Brussels Capital, Belgium
  • 1984–2014
    • Vrije Universiteit Brussel
      • • Physiology (FYSP)
      • • Department of Intensive Care Medicine
      • • Department of Internal Medicine
      Bruxelles, Brussels Capital Region, Belgium
  • 2010
    • Universitair Ziekenhuis Leuven
      • Department of Cardiology
      Louvain, Flanders, Belgium
  • 2009
    • University of Wisconsin, Madison
      • Department of Biomedical Engineering
      Madison, MS, United States
  • 2005–2008
    • Erasmushogeschool Brussel
      Bruxelles, Brussels Capital, Belgium
  • 2006
    • French Institute of Health and Medical Research
      Lutetia Parisorum, Île-de-France, France
    • University-Hospital Brugmann UVC
      Bruxelles, Brussels Capital Region, Belgium
  • 2004
    • University of California, San Diego
      San Diego, California, United States
  • 1988
    • Erasmus Universiteit Rotterdam
      • Department of Intensive Care
      Rotterdam, South Holland, Netherlands
  • 1979–1984
    • Centre Hospitalier Universitaire Saint-Pierre
      Bruxelles, Brussels Capital Region, Belgium