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Arsenault, Benoit

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Arsenault

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Benoit

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Université Laval. Département de médecine

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ncf10788586

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  • PublicationAccès libre
    Soluble CD14 is associated with the structural failure of bioprostheses
    (Elsevier, 2018-06-30) Dahou, Abdellaziz; Bouchareb, Rihab; Arsenault, Benoit; Mkannez, Ghada; Boulanger, Marie-Chloé; Bossé, Yohan; Pibarot, Philippe; Clavel, Marie-Annick; Nsaibia, Mohamed Jalloul; Mathieu, Patrick; Salaun, Erwan
    Introduction: Aortic valve bioprostheses, which do not mandate chronic anticoagulation, are prone to structural valve degeneration (SVD). The processes involved in SVD are likely multifactorial. We hypothesized that inflammation and macrophage activation could be involved in SVD. Methods: In 203 patients with an aortic valve bioprosthesis, we evaluated the association between the macrophage activation marker soluble CD14 (sCD14) and SVD. Results: After a mean follow-up of 8 ± 3 years, 42 (21%) patients developed SVD. Patients with SVD had higher peak (44 ± 13 mmHg vs. 25 ± 12 mmHg, p < .0001) and mean (24 ± 7 mmHg vs. 12 ± 5 mmHg, p < .0001) transprosthetic gradients. On univariable analysis, low-density lipoprotein cholesterol (LDL) and sCD14 were associated with SVD. After correction for covariates, sCD14 (OR: 1.12, 95%CI: 1.02–1.23, p = .01) remained independently associated with SVD. In turn, sCD14 was associated with the HOMA index and high-density lipoprotein (HDL) level. Patients with a metabolic syndrome (MetS) had higher level of sCD14. In a model corrected for age, sex, HOMA and HDL, the MetS remained independently associated with sCD14 levels (β = 0.65, SE = 0.30, p = .03). Conclusion: Circulating level of sCD14 is an independent predictor of SVD. In turn, patients with MetS have higher sCD14 levels.
  • PublicationRestreint
    Autotaxin interacts with lipoprotein(a) and oxidized phospholipids in predicting the risk of calcific aortic valve stenosis in patients with coronary artery disease
    (Blackwell Scientific Publication, 2020-05-30) Simard, Sébastien; Bouchareb, Rihab; Arsenault, Benoit; Boulanger, Marie-Chloé; Bossé, Yohan; Mahmut, Ablajan; Witztum, Joseph L.; Pibarot, Philippe; Clavel, Marie-Annick; Nsaibia, Mohamed Jalloul; Mathieu, Patrick; Tsimikas, Sotirios
    Background Studies have shown that lipoprotein(a) [Lp(a)], an important carrier of oxidized phospholipids, is causally related to calcific aortic valve stenosis (CAVS). Recently, we found that Lp(a) mediates the development of CAVS through autotaxin (ATX). Objective To determine the predictive value of circulating ATX mass and activity for CAVS. Methods We performed a case-control study in 300 patients with coronary artery disease (CAD). Patients with CAVS plus CAD (cases, n = 150) were age- and gender-matched (1 : 1) to patients with CAD without aortic valve disease (controls, n = 150). ATX mass and enzymatic activity and levels of Lp(a) and oxidized phospholipids on apolipoprotein B-100 (OxPL-apoB) were determined in fasting plasma samples. Results Compared to patients with CAD alone, ATX mass (P < 0.0001), ATX activity (P = 0.05), Lp(a) (P = 0.003) and OxPL-apoB (P < 0.0001) levels were elevated in those with CAVS. After adjustment, we found that ATX mass (OR 1.06, 95% CI 1.03–1.10 per 10 ng mL−1, P = 0.001) and ATX activity (OR 1.57, 95% CI 1.14–2.17 per 10 RFU min−1, P = 0.005) were independently associated with CAVS. ATX activity interacted with Lp(a) (P = 0.004) and OxPL-apoB (P = 0.001) on CAVS risk. After adjustment, compared to patients with low ATX activity (dichotomized at the median value) and low Lp(a) (<50 mg dL−1) or OxPL-apoB (<2.02 nmol L−1, median) levels (referent), patients with both higher ATX activity (≥84 RFU min−1) and Lp(a) (≥50 mg dL−1) (OR 3.46, 95% CI 1.40–8.58, P = 0.007) or OxPL-apoB (≥2.02 nmol L−1, median) (OR 5.48, 95% CI 2.45–12.27, P < 0.0001) had an elevated risk of CAVS. Conclusion Autotaxin is a novel and independent predictor of CAVS in patients with CAD.
  • PublicationAccès libre
    Impact of plasma Lp-PLA2 activity on the progression of aortic stenosis : the PROGRESSA study.
    (American College of Cardiology Foundation, 2015-01-01) Arsenault, Benoit; Mahmut, Ablajan; Larose, Éric; Bédard, Élisabeth; Capoulade, Romain; Bossé, Yohan; Pibarot, Philippe; Dumesnil, Jean G.; Després, Jean-Pierre; Tastet, Lionel; Mathieu, Patrick; Arsenault, Marie
    Objectives : The purpose of this prospective study was to examine the relationship between plasma lipoprotein–associated phospholipase A2 (Lp-PLA2) activity and the progression rate of aortic stenosis (AS). Background : We recently reported that Lp-PLA2 is highly expressed in stenotic aortic valves where it may contribute to the mineralization of valvular interstitial cells. Methods : Patients with AS were prospectively recruited in the PROGRESSA (Metabolic Determinants of the Progression of Aortic Stenosis) study. AS progression rate was assessed by annualized increase in peak aortic jet velocity (Vpeak), mean gradient (MG), and aortic valve area index (AVAi). Circulating Lp-PLA2 activity was measured and dichotomized based on the median value. Results : Of 183 patients included in this subanalysis of the PROGRESSA study, 70% were men and the mean age was 66 ± 13 years. Over the 2.5 ± 1.4 years of follow up, the AS progression rate tended to be higher in patients with high versus low Lp-PLA2 activity (annualized Vpeak = 0.17 ± 0.23 m/s vs. 0.12 ± 0.18 m/s; p = 0.14). There was a significant interaction (p < 0.05) between baseline AS severity and Lp-PLA2 activity with respect to impact on AS progression rate. In patients with mild AS (i.e., Vpeak <3 m/s; n = 123), increased Lp-PLA2 activity was associated with a significantly faster AS progression rate (Vpeak 0.16 ± 0.18 m/s vs. 0.09 ± 0.14 m/s; p = 0.01) but not in patients with moderate or severe AS (p = 0.99). After adjustment for other risk factors, increased Lp-PLA2 activity remained independently associated with faster AS progression rate (p = 0.005) in the former subset. Conclusions : There was no significant association between plasma Lp-PLA2 activity or mass and stenosis progression in the whole cohort. However, increased Lp-PLA2 activity was associated with a faster stenosis progression rate in the subset of patients with mild AS. These findings provide an impetus for the elaboration of a randomized trial targeting Lp-PLA2 activity in patients with early stages of calcific aortic valve disease.
  • PublicationRestreint
    Autotaxin Derived From Lipoprotein(a) and Valve Interstitial Cells Promotes Inflammation and Mineralization of the Aortic Valve
    (American Heart Association, etc., 2015-08-25) Dahou, Abdellaziz; Bouchareb, Rihab; Arsenault, Benoit; Trahan, Sylvain; Marette, André; Couture, Christian; Lépine, Jamie-Lee; Boulanger, Marie-Chloé; Bossé, Yohan; Mahmut, Ablajan; Pibarot, Philippe; Hadji, Fayez; Pagé, Sylvain; Scipione, Corey A.; Nsaibia, Mohamed Jalloul; Romagnuolo, Rocco; Laflamme, Marie-Hélène; Koschinsky, Marlys L.; Mathieu, Patrick
    Background—Mendelian randomization studies have highlighted that lipoprotein(a) [Lp(a)] was associated with calcific aortic valve disease (CAVD). Lp(a) transports oxidized phospholipids (OxPLs) with a high content in lysophosphatidylcholine (LPC). Autotaxin (ATX) transforms LPC into lysophosphatidic acid. We hypothesized that ATX-lysophosphatidic acid could promote inflammation/mineralization of the aortic valve. Methods and Results—We have documented the expression of ATX in control and mineralized aortic valves. By using different approaches we have also investigated the role of ATX- lysophosphatidic acid on the mineralization of isolated valves interstitial cells (VICs) and in a mouse model of CAVD. Enzyme specific ATX activity was elevated by 60% in mineralized aortic valves compared to control valves. Immunohistochemistry studies showed a high level of ATX in mineralized aortic valves, which co-localized with OxPL and apolipoprotein(a). We detected a high level of ATX activity in the Lp(a) fraction in circulation. Interaction between ATX and Lp(a) was confirmed by in situ proximity ligation assay. Moreover, we documented that VICs also expressed ATX in CAVD. We showed that ATX-lysophosphatidic acid promote the mineralization of the aortic valve through a NF-¿B/IL-6/BMP2 pathway. In LDLR-/-/ApoB100/100/IGFII mice, ATX is overexpressed and lysophosphatidic acid promotes a strong deposition of hydroxyapatite of calcium in aortic valve leaflets and accelerates the development of CAVD. Conclusions—ATX is transported in the aortic valve by Lp(a) and is also secreted by VICs. ATX-lysophosphatidic acid promotes inflammation and mineralization of the aortic valve and thus could represent novel therapeutic targets in CAVD.
  • PublicationRestreint
    Circulating Lp-PLA2 is associated with high valvuloarterial impedance and low arterial compliance in patients with aortic valve bioprostheses
    (Elsevier, 2016-04-01) Dahou, Abdellaziz; Bouchareb, Rihab; Arsenault, Benoit; Larose, Éric; Mahjoub, Haïfa; Boulanger, Marie-Chloé; Capoulade, Romain; Bossé, Yohan; Mahmut, Ablajan; Pibarot, Philippe; Mathieu, Patrick
    Background: We previously reported that plasma Lp-PLA2 was associated with aortic valve disease progression and degeneration of bioprostheses. Low systemic arterial compliance and high valvuloarterial impedance (Zva) are predictors of poor survival in patients with aortic valve disease. However, the prevalence of high Zva after AVR is largely unknown and whether Lp-PLA2 could predict Zva has not been documented. We investigated the relationships between plasma lipoprotein-associated phospholipase A2 (Lp-PLA2) mass and activity and valvuloarterial impedance (Zva), an index of global LV hemodynamic load, in patients that underwent aortic valve replacement (AVR). Methods: A total of 195 patients with aortic bioprostheses underwent echocardiographic assessment of the prosthetic aortic valve function 8 ± 3.4 years after AVR. Lp-PLA2 mass and activity were measured. Results: In this group of patients, the mean Zvawas elevated (5.73±1.21mmHg·ml-1·m2). In univariate analyses, Lp-PLA2 mass (p=0.003) and Lp-PLA2 activity (p=0.046) were associated with Zva. After adjustment for covariates including age, gender, clinical risk factors, anti-hypertensive medications, body mass index and prosthesis size, Lp-PLA2 mass was associatedwith high Zva (=4.5mmHg·ml-1·m2) (OR: 1.29, 95%CI: 1.10–1.53; p= 0.005) and was inversely related with the systemic arterial compliance (ß =-0.01, SEM=0.003; p=0.003). Conclusions: An increased Zva, an index of excessive hemodynamic load, was highly prevalent 8-year post-AVR and was independently related to circulating Lp-PLA2.
  • PublicationRestreint
    Lipoprotein lipase in aortic valve stenosis is associated with lipid retention and remodelling
    (Blackwell Scientific Publications, 2013-06-01) Arsenault, Benoit; Trahan, Sylvain; Fournier, Dominique; Couture, Christian; Boulanger, Marie-Chloé; Mahmut, Ablajan; Pibarot, Philippe; Pagé, Sylvain; Després, Jean-Pierre; Mathieu, Patrick
    Background: Calcific aortic valve disease (CAVD) is a chronic disorder characterized by a fibrocalcific remodelling. It is suspected that lipid retention within the aortic valve may be one important mechanism participating to aortic valve remodelling. Lipoprotein lipase (LPL) is implicated in lipid metabolism and may play a role in lipid retention within the aortic valve. Methods: In 57 patients, CAVD were analysed for the expression of LPL by q-PCR and immunohistochemistry. Expression of oxidized-LDL (ox-LDL) and decorin was also documented. In addition, a complete blood profile, including the size of LDL and high-density lipoprotein (HDL) particles, were performed to find associations between the blood lipid profile and expression of ox-LDL and LPL within CAVD. Results: Immunohistochemistry studies revealed that LPL was expressed in stenotic aortic valves as a diffuse staining and also in dense cellular areas where macrophages were abundant. Expression of LPL co-localized with decorin and ox-LDL. In turn, valves with higher amount of ox-LDL had elevated number of LPL transcripts. In addition, we documented that the small, dense HDL phenotype was associated with an elevated amount of ox-LDL and LPL transcripts within CAVD. Furthermore, expression of LPL was associated with several indices of fibrocalcific remodelling of the aortic valve. Conclusion: Expression of LPL within CAVD is related to the amount of ox-LDL, which is, in turn, associated with the small, dense HDL phenotype. Lipid retention associated with smaller HDL particles may participate in the expression of LPL, whereby a fibrocalcific remodelling of the aortic valve is promoted.