Venoarterial extracorporeal membrane oxygenation after coronary artery bypass grafting: Results of a multicenter study.

BACKGROUND: The evidence of the benefits of using venoarterial extracorporeal membrane oxygenation (VA-ECMO) after coronary artery bypass grafting (CABG) is scarce. METHODS: We analyzed the outcomes of patients who received VA-ECMO therapy due to cardiac or respiratory failure after isolated CABG in 12 centers between 2005 and 2016. Patients treated preoperatively with ECMO were excluded from this study. RESULTS: VA-ECMO was employed in 148 patients after CABG for median of 5.0days (mean, 6.4, SD 5.6days). In-hospital mortality was 64.2%. Pooled in-hospital mortality was 65.9% without significant heterogeneity between the centers (I2 8.6%). The proportion of VA-ECMO in each center did not affect in-hospital mortality (p=0.861). No patients underwent heart transplantation and six patients received a left ventricular assist device. Logistic regression showed that creatinine clearance (p=0.004, OR 0.98, 95% CI 0.97-0.99), pulmonary disease (p=0.018, OR 4.42, 95% CI 1.29-15.15) and pre-VA-ECMO blood lactate (p=0.015, OR 1.10, 95% CI 1.02-1.18) were independent baseline predictors of in-hospital mortality. One-, 2-, and 3-year survival was 31.0%, 27.9%, and 26.1%, respectively. CONCLUSIONS: One third of patients with need for VA-ECMO after CABG survive to discharge. In view of the burden of resources associated with VA-ECMO treatment and the limited number of patients surviving to discharge, further studies are needed to identify patients who may benefit the most from this treatment.

Dietary plant stanols or sterols neither accumulate in stenotic aortic valves nor influence their structure or inflammatory status.

BACKGROUND & AIMS: Consumption of plant stanols and plant sterols decreases LDL cholesterol level and increases serum concentrations of plant stanols/sterols, but it is practically unexplored whether also their tissue concentrations increase. Thus, the aim of this study was to assess whether consuming plant stanols/sterols increases their concentrations in stenotic aortic valves and affect the valvular structure (collagen and elastin) or inflammation (macrophages and mast cells). METHODS: In a randomized, double-blind controlled intervention patients with severe aortic stenosis consumed margarine without (n = 11) or with 2 g of plant stanols (n = 12) or sterols (n = 13) until valve replacement surgery (2.6 months, on average). The effects of sitostanol and sitosterol on the expression and secretion of proinflammatory cytokines by cultured aortic valve myofibroblasts were also assessed. RESULTS: Control-related LDL-cholesterol was diminished by 16% (p < 0.05) by plant stanol and by 11% (NS) by plant sterol consumption, respectively. In the resected valves, cholesterol, plant stanol and sterol levels were similar in all groups. Consumed plant stanols or sterols had no effect on valvular structure or mast cell or macrophage numbers in valves. Incubation of cultured myofibroblasts derived from stenotic valves with sitostanol or sitosterol decreased mRNA expression of the monocyte chemotactic protein-1 (p < 0.05) and interleukin-1 beta (p < 0.05). CONCLUSIONS: In this study, plant stanol/sterol consumption did not affect cholesterol, plant stanol or sterol levels in stenotic aortic valves; neither did they influence the structure or the inflammatory status of the valves. However, these findings need to be confirmed in a larger-scale intervention. ClinicalTrials.govRegister #NCT00738933.

High-density lipoproteins (HDL) are present in stenotic aortic valves and may interfere with the mechanisms of valvular calcification.

OBJECTIVE: To determine whether differences exist in valvular high density lipoprotein (HDL) content between non-stenotic and stenotic aortic valves, and whether HDL could retard valvular calcification locally. METHODS: Stenotic aortic valves were obtained from valve replacement surgery and non-stenotic control valves from cardiac transplantations or at autopsy. The valvular localization and concentration of apolipoproteinA-I (apoA-I) were analyzed by immunohistochemistry and ELISA. The effects of HDL on the secretion of calcifying mediators and proinflammatory cytokines by cultured aortic valve myofibroblasts were assessed by ELISA and real-time PCR. RESULTS: The concentration of apoA-I was higher in control than in stenotic valves (p < 0.05). ApoA-I surrounded the calcific deposits in stenotic valves, co-localizing with apoB, apoE, and osteoprotegerin (OPG). Incubation of cultured valve myofibroblasts with HDL increased their secretion of OPG (p < 0.001). Furthermore, incubation of myofibroblasts with HDL led to decreased mRNA expression of tumor necrosis factor alpha (TNF-α) (p < 0.05). CONCLUSIONS: The amount of valvular HDL is reduced in aortic valve stenosis. HDL both induces the secretion of OPG and reduces the expression of TNF-α in vitro. Since OPG is known to inhibit and TNF-α to promote aortic valve calcification, HDL may have an anti-calcifying effect in human aortic valves.