Background: Bivalirudin is a direct thrombin inhibitor (DTI) that can be an alternative to unfractionated heparin (UFH). The efficacy and safety of bivalirudin in anticoagulation therapy in extracorporeal membrane oxygenation (ECMO) remain unknown.Methods: This study followed the preferred reporting items for systematic reviews and meta-analyses (PRISMA) guidelines. A systematic literature search was performed in PubMed, EMBASE, and The Cochrane Library databases to identify all relevant original studies estimating bivalirudin’s efficacy and safety versus UFH as anticoagulation therapy in ECMO. The time limit for searching is from the search beginning to June 2021. Two researchers independently screened the literature, extracted data and evaluated the risk of bias of the included studies. The meta-analysis (CRD42020214713) was performed via the RevMan version 5.3.5 Software and STATA version 15.1 Software.Results: Ten articles with 847 patients were included for the quantitative analysis. Bivalirudin can significantly reduce the incidence of major bleeding in children (I2 = 48%, p = 0.01, odd ratio (OR) = 0.17, 95% confidence interval (CI): 0.04–0.66), patient thrombosis (I2 = 0%, p = 0.02, OR = 0.58, 95% CI: 0.37–0.93), in-circuit thrombosis/interventions (I2 = 0%, p = 0.0005, OR = 0.40, 95% CI: 0.24–0.68), and in-hospital mortality (I2 = 0%, p = 0.007, OR = 0.64, 95% CI: 0.46–0.88). Also, comparable clinical outcomes were observed in the incidence of major bleeding in adults (I2 = 48%, p = 0.65, OR = 0.87, 95% CI: 0.46–1.62), 30-day mortality (I2 = 0%, p = 0.61, OR = 0.83, 95% CI: 0.41–1.68), and ECMO duration in adults (I2 = 41%, p = 0.75, mean difference (MD) = −3.19, 95% CI: −23.01–16.63) and children (I2 = 76%, p = 0.65, MD = 40.33, 95% CI:−135.45–216.12).Conclusions: Compared with UFH, bivalirudin can be a safe and feasible alternative anticoagulant option to UFH as anticoagulation therapy in ECMO, especially for heparin resistance (HR) and heparin-induced thrombocytopenia (HIT) cases.
IntroductionOver one-half of patients with multiple myeloma (MM) die of heart failure or arrhythmia. Left ventricular ejection fraction (LVEF) is used to describe left ventricular systolic function. However, depressed LVEF means advanced stage of left ventricular dysfunction in patients with MM. Left ventricular pressure-strain-derived myocardial work (LVMW) is a novel and noninvasive method for evaluating LV function related to LV dynamic pressure load. MW is assessed by LV MW index (LVMWI), constructive work, wasted work, and LV MW efficiency (LVMWE). In this study, we aimed to investigate the value of LVMW in cardiac function assessment and clinical prognosis of MM patients with preserved LVEF.MethodsA total of 72 subjects, including 40 untreated MM patients with preserved EF (including the thick wall and normal wall groups) and 32 non-MM patients, were enrolled in this study. Laboratory data and clinical history of all the patients were collected. All the patients underwent comprehensive echocardiographic examinations and then LVMWI and LVMWE were calculated. Moreover, cardiac adverse events (CAEs) were observed in MM patients treated with bortezomib-based therapy after 6 months and the prognostic value of MW was assessed.Results(1) LV myocardial global work index (GWI), myocardial global work efficiency (GWE), and global longitudinal strain (GLS) were lower in the thick wall group of patients with MM compared with the normal wall group and controls. Cardiac segmental analysis of LVMWI in patients with MM showed an apical sparing pattern; (2) The area under the curve (AUC) of GWE for judging the disease severity based on the Revised International Staging System (R-ISS) was 0.835 (95% CI: 0.684–0.933, p < 0.05); (3) GWE, LgdFLC, and arrhythmia were independent risk factors of CAEs. The AUC of GWE for predicting CAEs in MM patients treated with bortezomib-based therapy for 6 months follow-up was 0.896 (95% CI: 0.758–0.970, p < 0.05).ConclusionMM Patients with preserved EF had subclinical LV systolic dysfunction, which was worse in the thick wall group. LVMWI was presented as “apical sparing” in patients with MM. A lower LVGWE may have a predictive value for CAEs in patients with MM after 6 months of follow-up.
Background Primary percutaneous coronary intervention (PPCI) is the standard procedure for reperfusion for ST-segment elevation myocardial infarction (STEMI), but the occurrence of the no-reflow phenomenon remains common and is associated with adverse outcomes. Aims This study aimed to evaluate whether prolonged balloon inflation in stent deployment would lessen the occurrence of the no-reflow phenomenon in PPCI compared with conventional rapid inflation/deflation strategy. Methods Patients were randomly assigned to either the prolonged balloon inflation in stent deployment group (PBSG) or conventional deployment strategy group (CDSG) in a 1:1 ratio. A subset of patients was included in the cardiac magnetic resonance (CMR) assessment. Results Thrombolysis in MI (TIMI) flow grade 3 was found in 96.7% and 63.3% of the patients of the PBSG and CDSG, respectively (P = 0.005). The results of the PBSG and CDSG are respectively shown as follows: 0% versus 30% no-reflow or slow flow (P = 0.002); 90% versus 66.7% ST-segment resolution ≥ 50% (P = 0.028); 35.6 ± 14.5 frames versus 49.18 ± 25.2 frames on corrected TIMI frame count (P = 0.014); and 60% versus 20% myocardial blush grade 3 (P = 0.001). At 1 month, the major cardiovascular adverse event (cardiovascular mortality) rate was 3.3% in both groups; at 1 year, the rate was 3.3% and 6.7% for the PBSG and CDSG, respectively (P = 1.00). In the CMR subset of cases, the presence of microvascular obstruction (MVO) was detected in 6.7% and 50% of the patients in the PBSG and CDSG, respectively (P = 0.023). Conclusion In our pilot trial, prolonged balloon inflation during stent deployment strategy in PPCI reduces the occurrence of the no-reflow phenomenon in patients with STEMI and improved the myocardial microcirculation perfusion (ClinicalTrials.gov number: NCT03199014; registered: 26/June/2017).
BackgroundAcute myocardial infarction (AMI) can lead to sudden cardiac death after prolonged ischemia or heart failure (HF) and impaired left ventricular pump function. However, the underlying mechanism remains largely unknown. The purpose of this study was to investigate the role of mitofilin in alleviating AMI.MethodsRecombinant adenoviral vectors for mitofilin overexpression or mitofilin knockdown were constructed, respectively. A mouse AMI model was established and the effect of mitofilin on myocardial pyroptosis was examined by detecting the lactate dehydrogenase (LDH) level and inflammatory factors. Moreover, a cellular model of AMI was established by treating cardiomyocytes with hypoxia/reoxygenation (H/R). An enzyme-linked immunosorbent assay (ELISA) and a western blot analysis were used to detect the effect of mitofilin knockdown on the expression of pyroptosis-related factors. Furthermore, the regulatory role of mitofilin in PI3K/AKT pathway was evaluated by the western blot and PI3K inhibitor.ResultsMitofilin was downregulated in the heart tissue of the AMI mice and H/R induced cardiomyocytes. The overexpression of mitofilin significantly alleviated AMI and reduced pyroptosis-related factors. Meanwhile, in cardiomyocytes, mitofilin knockdown aggravated cellular damages by promoting pyroptosis. Further analysis showed that the anti-pyroptotic effect of mitofilin was dependent on the activation of the PI3K/AKT signaling pathway.ConclusionsOur study suggests that mitofilin regulates pyroptosis through the PI3K/AKT signaling pathway in cardiomyocytes to ameliorate AMI, which may serve as a therapeutic strategy for the management of AMI.
Complete revascularization vs culprit lesion-only percutaneous coronary intervention for angina-related quality of life in patients with ST-segment elevation myocardial infarction: results from the COMPLETE randomized clinical trial.
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