References of "LANCELLOTTI, Patrizio"
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See detailLeft ventricular regional function and maximal exercise capacity in aortic stenosis.
Dulgheru, Raluca; Magne, Julien; DAVIN, Laurent ULg et al

in European Heart Journal - Cardiovascular Imaging (in press)

AIMS: The objective assessment of maximal exercise capacity (MEC) using peak oxygen consumption (VO2) measurement may be helpful in the management of asymptomatic aortic stenosis (AS) patients. However ... [more ▼]

AIMS: The objective assessment of maximal exercise capacity (MEC) using peak oxygen consumption (VO2) measurement may be helpful in the management of asymptomatic aortic stenosis (AS) patients. However, the relationship between left ventricular (LV) function and MEC has been relatively unexplored. We aimed to identify which echocardiographic parameters of LV systolic function can predict MEC in asymptomatic AS. METHODS AND RESULTS: Asymptomatic patients with moderate to severe AS (n = 44, aortic valve area <1.5 cm2, 66 ± 13 years, 75% of men) and preserved LV ejection fraction (LVEF > 50%) were prospectively referred for resting echocardiography and cardiopulmonary exercise test. LV longitudinal strain (LS) of each myocardial segment was measured by speckle tracking echocardiography (STE) from the apical (aLS) 4-, 2-, and 3-chamber views. An average value of the LS of the analysable segments was provided for each myocardial region: basal (bLS), mid (mLS), and aLS. LV circumferential and radial strains were measured from short-axis views. Peak VO2 was 20.1 ± 5.8 mL/kg/min (median 20.7 mL/kg/min; range 7.2-32.3 mL/kg/min). According to the median of peak VO2, patients with reduced MEC were significantly older (P < 0.001) and more frequently females (P = 0.05). There were significant correlations between peak VO2 and age (r = -0.44), LV end-diastolic volume (r = 0.35), LV stroke volume (r = 0.37), indexed stroke volume (r = 0.32), and E/e' ratio (r = -0.37, all P < 0.04). Parameters of AS severity and LVEF did not correlate with peak VO2 (P = NS for all). Among LV deformation parameters, bLS and mLS were significantly associated with peakVO2 (r = 0.43, P = 0.005, and r = 0.32, P = 0.04, respectively). With multivariable analysis, female gender (β = 4.9; P = 0.008) and bLS (β = 0.50; P = 0.03) were the only independent determinants (r2 = 0.423) of peak VO2. CONCLUSION: In asymptomatic AS, impaired LV myocardial longitudinal function determines reduced MEC. Basal LS was the only parameter of LV regional function independently associated with MEC. [less ▲]

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See detailImpact of Serial B-Type Natriuretic Peptide Changes for Predicting Outcome in Asymptomatic Patients With Aortic Stenosis.
Henri, Christine; DULGHERU, Raluca Elena ULg; Magne, Julien et al

in The Canadian journal of cardiology (2016)

BACKGROUND: The aim of this study was to determine the impact on the outcome of serial B-type natriuretic peptide (BNP) changes during follow-up in asymptomatic patients with >/= moderate aortic stenosis ... [more ▼]

BACKGROUND: The aim of this study was to determine the impact on the outcome of serial B-type natriuretic peptide (BNP) changes during follow-up in asymptomatic patients with >/= moderate aortic stenosis (AS) and preserved left ventricular ejection fraction. METHODS: We prospectively screened 69 patients who underwent comprehensive transthoracic echocardiography, BNP level measurement at baseline and after every 6 or 12 months. Annualized BNP changes were calculated as the difference between the last and baseline BNP measurements divided by the duration of follow-up. The primary endpoint was the occurrence of symptoms, aortic valve replacement, or cardiovascular death. RESULTS: During a follow-up of 30 +/- 19 months, 43 patients experienced a cardiac event. These patients were significantly older (73 +/- 9 vs 65 +/- 16 years; P = 0.010), had more often dyslipidemia (79% vs 42%; P = 0.038), more severe AS (peak velocity: 3.9 +/- 0.6 vs 3.5 +/- 0.6 m/s; P = 0.002), larger indexed left atrial area (10.2 +/- 2.5 vs 8.7 +/- 1.9 cm2/m2; P = 0.006), and a higher increase in annualized BNP (+90 +/- 155 vs +7 +/- 49 pg/mL/y; P = 0.010). Patients with higher annualized BNP changes (> 20 pg/mL/y) had a significantly lower cardiac event-free survival (1 year: 63 +/- 8% vs 97 +/- 3%; 3 years: 31 +/- 8% vs 68 +/- 8%; P < 0.001). Using the multivariate Cox proportional hazards model, higher annualized BNP changes were significantly associated with increased risk of cardiac events (hazard ratio: 2.73, 95% confidence interval: 1.27-5.86; P = 0.010) after adjustment for age, dyslipidemia, and echocardiographic parameters. CONCLUSIONS: In asymptomatic patients with AS and preserved left ventricular ejection fraction, the use of serial BNP changes may help to anticipate development of class I indication for aortic valve replacement. [less ▲]

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See detailWhat Is the Role of Minimally Invasive Mitral Valve Surgery in High-Risk Patients? A Meta-Analysis of Observational Studies.
Moscarelli, Marco; Fattouch, Khalil; Casula, Roberto et al

in The Annals of thoracic surgery (2016)

BACKGROUND: Minimally invasive valve surgery is related to certain better postoperative outcomes. We aimed to assess the role of minimally invasive mitral valve surgery in high-risk patients. METHODS: A ... [more ▼]

BACKGROUND: Minimally invasive valve surgery is related to certain better postoperative outcomes. We aimed to assess the role of minimally invasive mitral valve surgery in high-risk patients. METHODS: A systematic literature review identified eight studies of which seven fulfilled criteria for meta-analysis. Outcomes for a total of 1,254 patients (731 were conventional standard sternotomy and 523 were minimally invasive mitral valve surgery) were submitted to meta-analysis using random effects modeling. Heterogeneity and subgroup analysis with quality scoring were assessed. The primary end point was early mortality. Secondary end points were intraoperative and postoperative outcomes and long-term follow-up. RESULTS: Minimally invasive mitral valve surgery conferred comparable early mortality to standard sternotomy (p = 0.19); it was also associated with a lower number of units of blood transfused (weighted mean difference, -1.93; 95% confidence interval [CI], -3.04 to -0.82; p = 0.0006) and atrial fibrillation rate (odds ratio, 0.49; 95% CI, 0.32 to 0.74; p = 0.0007); however, cardiopulmonary bypass time was longer (weighted mean difference, 20.88; 95% CI, -1.90 to 43.65; p = 0.07). There was no difference in terms of valve repair rate (odds ratio, 1.51; 95% CI, 0.89 to 2.54; p = 0.12), and the incidence of stroke was significantly lower in the high-quality analysis with no heterogeneity (odds ratio, 0.35; 95% CI, 0.15 to 0.82; p = 0.02; chi2, 1.67; I2, 0%; p = 0.43). CONCLUSIONS: Minimally invasive mitral valve surgery is a safe and comparable alternative to standard sternotomy in patients at high risk, with similar early mortality and repair rate and better postoperative outcomes, although a longer cardiopulmonary bypass time is required. [less ▲]

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See detailTargeting the tricuspid valve: A new therapeutic challenge.
LANCELLOTTI, Patrizio ULg; Fattouch, Khalil; DULGHERU, Raluca Elena ULg

in Archives of cardiovascular diseases (2016)

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See detail2015 ESC Guidelines for the management of infective endocarditis.
Habib, Gilbert; LANCELLOTTI, Patrizio ULg; Antunes, Manuel J. et al

in Revista espanola de cardiologia (English ed.) (2016), 69(1), 69

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See detailSTRESS (EXERCISE) ECHOCARDIOGRAPHY in asymptomatic AORTIC STENOSIS
LANCELLOTTI, Patrizio ULg; DULGHERU, Raluca Elena ULg

in ASE's comprehensive echocardiography, second edition (2016)

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See detailSTRESS ECHOCARDIOGRAPHY FOR VALVE DISEASE/: AORTIC REGURGITATION AND MITRAL STENOSIS
LANCELLOTTI, Patrizio ULg; MAGNE, Julien

in ASE's comprehensive echocardiography, second edition (2016)

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See detailRoLE OF EXERCISE STRESS TESTING
LANCELLOTTI, Patrizio ULg; MOONEN, Marie ULg; magne, Julien

in ASE's comprehensive echocardiography, second edition (2016)

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See detailL'image du mois : Le processus thrombotique sous la loupe (microscopie intravitale)
Oury, Cécile ULg; Hego, Alexandre ULg; LANCELLOTTI, Patrizio ULg

in Revue Médicale de Liège (2015), 70(11), 537-539

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See detailCLEC-2 is required for the activation of mouseplatelets by bacterial DNA mimetics
Delierneux, Céline ULg; Hego, Alexandre ULg; LECUT, Christelle ULg et al

Conference (2015, June 22)

Background: Short nuclease-resistant phosphorothioate synthetic CpG motif-bearing oligonucleotides (CpG ODNs) mimicking bacterial DNA display potent immunostimulatory activity and are therefore being used ... [more ▼]

Background: Short nuclease-resistant phosphorothioate synthetic CpG motif-bearing oligonucleotides (CpG ODNs) mimicking bacterial DNA display potent immunostimulatory activity and are therefore being used in clinical trials as vaccine adjuvants. Cellular uptake and activation depends on the interaction of CpG ODNs with the C-type lectin receptor DEC-205 and subsequent stimulation of the Toll-like receptor 9 (TLR9) and myeloid differentiation primary response 88 (MyD88) signaling cascade. Platelets express TLR9, MyD88, and the C-type lectin-like receptor 2 (CLEC-2). However, the impacts of CpG ODNs on platelet function have been elusive. Aims: To evaluate whether CpG ODNs affect platelet activation and thrombus formation via CLEC-2 and TLR9. Methods: We incubated washed platelets or whole blood from TLR9-, MyD88- or CLEC-2- deficient mice with CpG ODNs. We performed platelet aggregometry, flow cytometric binding and platelet activation assays as well as signal transduction analyses. Thrombus formation and fibrin generation were also analyzed by intravital microscopy in mouse microcirculation upon intravenous injection of CpG ODNs. Results: We show that CpG ODNs bind on platelet surface and are internalized. They activate platelets and induce their aggregation. TLR9- or MyD88-deficient platelets aggregated normally in response to CpG ODN. Interestingly, platelets deficient for the C-type lectin receptor CLEC-2 were unable to capture and internalize CpG ODN. CLEC-2 deficiencyabolished CpG ODN-induced platelet activation and aggregation. CpG ODN stimulated CLEC-2 dependent tyrosine kinase pathway and Syk phosphorylation. In vivo, intravenously injected CpG ODN interacted with platelets adhered to laser injured arteriolar endothelia and promoted fibrin generation and thrombus growth. Conclusion: CLEC-2 mediates CpG ODN uptake and subsequent platelet activation, independently of TLR9, which may serve an important role in the interplay between platelets and immunity. [less ▲]

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See detailCLEC-2 is required for the activation of mouse platelets by bacterial DNA mimetics
Delierneux, Céline ULg; Hego, Alexandre ULg; LECUT, Christelle ULg et al

Conference (2015, June 22)

Aims: To evaluate whether CpG ODNs affect platelet activation and thrombus formation via CLEC-2 and TLR9. Methods: We incubated washed platelets or whole blood from TLR9-, MyD88- or CLEC-2- deficient mice ... [more ▼]

Aims: To evaluate whether CpG ODNs affect platelet activation and thrombus formation via CLEC-2 and TLR9. Methods: We incubated washed platelets or whole blood from TLR9-, MyD88- or CLEC-2- deficient mice with CpG ODNs. We performed platelet aggregometry, flow cytometric binding and platelet activation assays as well as signal transduction analyses. Thrombus formation and fibrin generation were also analyzed by intravital microscopy in mouse microcirculation upon intravenous injection of CpG ODNs. Results: We show that CpG ODNs bind on platelet surface and are internalized. They activate platelets and induce their aggregation. TLR9- or MyD88-deficient platelets aggregated normally in response to CpG ODN. Interestingly, platelets deficient for the C-type lectin receptor CLEC-2 were unable to capture and internalize CpG ODN. CLEC-2 deficiency abolished CpG ODN-induced platelet activation and aggregation. CpG ODN stimulated CLEC-2 dependent tyrosine kinase pathway and Syk phosphorylation. In vivo, intravenously injected CpG ODN interacted with platelets adhered to laser injured arteriolar endothelia and promoted fibrin generation and thrombus growth. Conclusion: CLEC-2 mediates CpG ODN uptake and subsequent platelet activation, independently of TLR9, which may serve an important role in the interplay between platelets and immunity. [less ▲]

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See detailHigh-dose oral intake of serotonin induces valvular heart disease in rabbits.
Lancellotti, Patrizio ULg; NCHIMI LONGANG, Alain ULg; Hego, Alexandre ULg et al

in International Journal of Cardiology (2015), 197

Carcinoid tumors are rare neuroendocrine malignancies, often originating from enterochromaffin cells in the gastrointestinal tract. They can secrete serotonin (5-hydroxytryptamine, 5-HT), which is largely ... [more ▼]

Carcinoid tumors are rare neuroendocrine malignancies, often originating from enterochromaffin cells in the gastrointestinal tract. They can secrete serotonin (5-hydroxytryptamine, 5-HT), which is largely inactivated by the liver. Carcinoid heart disease occurs when tumor cells metastasize to the liver, as the vasoactive substances produced are able to reach the systemic circulation via the hepatic vein, causing deposition of fibrous tissue on the endocardial surfaces of the heart. It is predominantly manifested by right-sided valvular heart disease (VHD). Scavenging enzymes in the pulmonary endothelium may explain why left-sided cardiac involvement is unusual. The severity of cardiac damage is correlated with the plasmatic levels of serotonin, but the lowspecificity of serotonin for cardiac damage suggests that serotonin may be necessary but not sufficient to induce cardiac lesions. Therefore, other factors combined with serotonin might be required to induce VHD. However, recent animal studies confirmed the development of carcinoid-like valvular deposits in rats after 3 months of daily subcutaneous/intraperitoneal serotonin injections to avoid the liver first-pass clearance.Whether oral administration of serotonin can also induce VHD is unknown. We hypothesized that long-term oral serotonin overload in rabbits can lead to VHD, mimicking serotonin-induced lesions of carcinoid heart disease. We demonstrate, for the first time that high dose long-term oral administration of serotonin can lead to VHD in rabbits. [less ▲]

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See detailPrise en charge de l'IM dystrophique: nouveaux indices pronostiques
henri, Christine; LANCELLOTTI, Patrizio ULg

in Réalités Cardiologiques (2015)

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See detailSTENOSE AORTIQUE SEVERE ASYMPTOMATIQUE A FRACTION D'EJECTION VENTRICULAIRE GAUCHE PRESERVEE. EVALUATION A L'EFFORT: QUELS RESULTATS ET QUELLES DECISIONS?
BENSAHI, I; ELFHAL, A; MAGNE, Julien et al

in Annales de Cardiologie et d'Angeiologie (2015), 64(2), 100-108

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See detailDUSP3 Phosphatase Deficiency or Inhibition Limit Platelet Activation and Arterial Thrombosis
Musumeci, Lucia ULg; Kuijpers, Marijke; Gilio, Karen et al

in Circulation (2015), 131(7), 656-68

Background A limitation of current antiplatelet therapies is their inability to separate thrombotic events from bleeding occurrences. Better understanding of the molecular mechanisms leading to platelet ... [more ▼]

Background A limitation of current antiplatelet therapies is their inability to separate thrombotic events from bleeding occurrences. Better understanding of the molecular mechanisms leading to platelet activation is of importance for the development of improved therapies. Recently, protein tyrosine phosphatases (PTPs) have emerged as critical regulators of platelet function. Methods and Results This is the first report implicating the dual-specificity phosphatase 3 (DUSP3) in platelet signaling and thrombosis. This phosphatase is highly expressed in human and mouse platelets. Platelets from DUSP3-deficient mice displayed a selective impairment of aggregation and granule secretion mediated through the collagen receptor glycoprotein VI (GPVI) and the C-type lectin-like receptor 2 (CLEC-2). DUSP3-deficient mice were more resistant to collagen- and epinephrine-induced thromboembolism, compared to wild-type mice, and showed severely impaired thrombus formation upon ferric chloride-induced carotid artery injury. Intriguingly, bleeding times were not altered in DUSP3-deficient mice. At the molecular level, DUSP3 deficiency impaired Syk tyrosine phosphorylation, subsequently reducing phosphorylation of PLCγ2 and calcium fluxes. To investigate DUSP3 function in human platelets, a novel small-molecule inhibitor of DUSP3 was developed. This compound specifically inhibited collagen and CLEC-2-induced human platelet aggregation, thereby phenocopying the effect of DUSP3 deficiency in murine cells. Conclusions DUSP3 plays a selective and essential role in collagen- and CLEC-2-mediated platelet activation and thrombus formation in vivo. Inhibition of DUSP3 may prove therapeutic for arterial thrombosis. This is the first time a PTP, implicated in platelet signaling, has been targeted with a small-molecule drug. [less ▲]

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See detailLa cardiomyopathie du cirrhotique : un bref aperçu
MARCHETTA, Stella ULg; DELWAIDE, Jean ULg; LANCELLOTTI, Patrizio ULg

in Revue Médicale de Liège (2015), 2

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See detailBacterial DNA mimetics activate platelets and promote thrombosis via CLEC-2
Delierneux, Céline; Hego, Alexandre; Lecut, Christelle et al

Poster (2015, January 27)

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See detailExercice stress echocardiography in secondary mitral regurgitation : impact of pulmonary hypertension
MAGNE, Julien; PIERARD, Luc ULg; LANCELLOTTI, Patrizio ULg

in Archives of Cardiovascular Diseases (2015, January), 7

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