Coronary artery disease (CAD) is one of the leading causes of death and disability in Europe and worldwide. For patients with multi-vessel CAD, coronary artery bypass graft (CABG) surgery is a common approach for coronary revascularization, and is of proven symptomatic and prognostic benefit. Due to an aging population, higher prevalence of co-morbidities (such as diabetes mellitus, heart failure, hypertension, and renal failure), and a growing requirement for concomitant surgical procedures (such as valve and aortic surgery), higher risk patients are undergoing surgery.1–3 This has resulted in an increased risk of peri-operative myocardial injury (PMI)4 and Type 5 myocardial infarction (MI), both of which are associated with worsened clinical outcomes following CABG surgery. The aetiology and determinants of PMI and Type 5 MI are multi-factorial (see Tables ​Tables11 and ​and22 for summary). Although diagnostic criteria have been proposed for Type 5 MI (based on an elevation in cardiac biomarkers in the 48-h post-operative period and electrocardiogram/angiography/imaging evidence of MI5,13), there is currently no clear definition for prognostically significant PMI, in terms of the level of post-operative cardiac biomarker elevation, which is associated with worsened clinical outcomes following CABG surgery. 

Table 1

Causes of peri-operative myocardial injury in patients undergoing coronary artery bypass graft surgery

/pdf/esc-joint-working-groups-on-cardiovascular-surgery-and-the-1w2wekm1gb.pdf

ESC Joint Working Groups on Cardiovascular Surgery and the Cellular Biology of the Heart Position Paper: Perioperative myocardial injury and infarction in patients undergoing coronary artery bypass graft surgery.

Pulmonary arterial hypertension (PAH) is a chronic disease characterized by a progressive elevation in mean pulmonary arterial pressure. This occurs due to abnormal remodeling of small peripheral lung vasculature resulting in progressive occlusion of the artery lumen that eventually causes right heart failure and death. The most common cause of PAH is inactivating mutations in the gene encoding a bone morphogenetic protein type II receptor (BMPRII). Current therapeutic options for PAH are limited and focused mainly on reversal of pulmonary vasoconstriction and proliferation of vascular cells. Although these treatments can relieve disease symptoms, PAH remains a progressive lethal disease. Emerging data suggest that restoration of BMPRII signaling in PAH is a promising alternative that could prevent and reverse pulmonary vascular remodeling. Here we will focus on recent advances in rescuing BMPRII expression, function or signaling to prevent and reverse pulmonary vascular remodeling in PAH and its feasibility for clinical translation. Furthermore, we summarize the role of described miRNAs that directly target the BMPR2 gene in blood vessels. We discuss the therapeutic potential and the limitations of promising new approaches to restore BMPRII signaling in PAH patients. Different mutations in BMPR2 and environmental/genetic factors make PAH a heterogeneous disease and it is thus likely that the best approach will be patient-tailored therapies.

BMP type II receptor as a therapeutic target in pulmonary arterial hypertension = BMPR2 como diana terapeutica en la hipertensión arterial pulmon

The present study aimed to investigate whether magnesium isoglycyrrhizinate protects against renal ischemia‑reperfusion injury (RIRI), and to verify the underlying mechanisms. An RIRI rat model was induced by removing the right kidney, and exposing and clamping the left kidney. RIRI model rats were administered 30 mg/kg magnesium isoglycyrrhizinate for 3 days. Blood urea nitrogen (BUN) and serum creatinine levels in the blood of RIRI model rat were examined, compared with sham‑operated controls. Magnesium isoglycyrrhizinate suppressed the activities of tumor necrosis factor‑α, interleukin (IL)‑1β, IL‑6, superoxide dismutase, glutathione peroxidase, inducible nitric oxide synthase (iNOS) and caspase‑3 in RIRI model rats. Renal iNOS, matrix metalloproteinase (MMP)‑2, phosphorylated‑signal transducers and activators of transcription 3 (STAT3) and intercellular adhesion molecule‑1 (ICAM‑1) protein expression levels were suppressed by magnesium isoglycyrrhizinate treatment in RIRI model rats. These findings suggested that magnesium isoglycyrrhizinate protects RIRI via anti‑inflammatory, ‑oxidative and ‑apoptotic mechanisms in an RIRI rat model. These results implicate magnesium isoglycyrrhizinate pretreatment as a potential approach to protect against RIRI via suppression of the iNOS, ICAM‑1, MMP‑2 and STAT3 signaling pathways.

/pdf/magnesium-isoglycyrrhizinate-protects-against-renal-ischemia-g0xzop3zrd.pdf

Magnesium isoglycyrrhizinate protects against renal‑ischemia‑reperfusion injury in a rat model via anti‑inflammation, anti‑oxidation and anti‑apoptosis

Pulmonary hypertension (PH) is a condition marked by a combination of constriction and remodeling within the pulmonary vasculature. It remains a disease without a cure, as current treatments were developed with a focus on vasodilatory properties but do not reverse the remodeling component. Numerous recent advances have been made in the understanding of cellular processes that drive pathologic remodeling in each layer of the vessel wall as well as the accompanying maladaptive changes in the right ventricle. In particular, the past few years have yielded much improved insight into the pathways that contribute to altered metabolism, mitochondrial function, and reactive oxygen species signaling and how these pathways promote the proproliferative, promigratory, and antiapoptotic phenotype of the vasculature during PH. Additionally, there have been significant advances in numerous other pathways linked to PH pathogenesis, such as sex hormones and perivascular inflammation. Novel insights into cellular pathology have suggested new avenues for the development of both biomarkers and therapies that will hopefully bring us closer to the elusive goal: a therapy leading to reversal of disease.

/pdf/update-on-novel-targets-and-potential-treatment-avenues-in-27flde811x.pdf

Update on novel targets and potential treatment avenues in pulmonary hypertension

Objectives: We investigated whether the totally video-assisted thoracoscopic mitral valve surgery provides superior clinical outcomes and less inflammatory injury reaction compared with conventiona...

Retrospective Comparison of Endoscopic Versus Open Procedure for Mitral Valve Disease

Background Elafin is a potent endogenous neutrophil elastase inhibitor that protects against myocardial inflammation and injury in preclinical models of ischaemic-reperfusion injury. We investigated whether elafin could inhibit myocardial ischaemia-reperfusion injury induced during coronary artery bypass graft (CABG) surgery. Methods and results In a randomised double-blind placebo-controlled parallel group clinical trial, 87 patients undergoing CABG surgery were randomised 1:1 to intravenous elafin 200 mg or saline placebo administered after induction of anaesthesia and prior to sternotomy. Myocardial injury was measured as cardiac troponin I release over 48 h (area under the curve (AUC)) and myocardial infarction identified with MRI. Postischaemic inflammation was measured by plasma markers including AUC high-sensitive C reactive protein (hs-CRP) and myeloperoxidase (MPO). Elafin infusion was safe and resulted in >3000-fold increase in plasma elafin concentrations and >50% inhibition of elastase activity in the first 24 h. This did not reduce myocardial injury over 48 h (ratio of geometric means (elafin/placebo) of AUC troponin I 0.74 (95% CI 0.47 to 1.15, p=0.18)) although post hoc analysis of the high-sensitive assay revealed lower troponin I concentrations at 6 h in elafin-treated patients (median 2.4 vs 4.1 μg/L, p=0.035). Elafin had no effect on myocardial infarction (elafin, 7/34 vs placebo, 5/35 patients) or on markers of inflammation: mean differences for AUC hs-CRP of 499 mg/L/48 h (95% CI −207 to 1205, p=0.16), and AUC MPO of 238 ng/mL/48 h (95% CI −235 to 711, p=0.320). Conclusions There was no strong evidence that neutrophil elastase inhibition with a single-dose elafin treatment reduced myocardial injury and inflammation following CABG-induced ischaemia-reperfusion injury. Trial registration number (EudraCT 2010-019527-58, ISRCTN82061264).

https://heart.bmj.com/content/heartjnl/101/20/1639.full.pdf

Perioperative elafin for ischaemia-reperfusion injury during coronary artery bypass graft surgery: a randomised-controlled trial

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Perioperative elafin for ischaemia-reperfusion injury during coronary artery bypass graft surgery: a randomised-controlled trial