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The molecular mechanism underlying acute right heart failure (RHF) is poorly understood. We used pulmonary artery banding (PAB) to induce acute RHF characterized by a rapid rise of right ventricular pressure, and then a decrease in right ventricular pressure along with a decrease in blood pressure right after banding. We found higher brain natriuretic peptide (BNP) and beta-myosin heavy chain (βMHC) levels and lower alpha-myosin heavy chain (αMHC) levels in RHF rats than sham-operated rats. Hemodynamic indexes in rats with acute RHF were slightly improved by trimedazidine TMZ, a key inhibitor of fatty acid (FA) oxidation. TMZ also reversed downregulation of peroxisome proliferator-activated receptor gamma coactivator 1-beta (PGC-1β) and peroxisome proliferator-activated receptor alpha (PPARα) by PAB and up-regulates peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α), peroxisome proliferator-activated receptor delta (PPARδ) and pyruvate dehydrogenase kinase isoform 4 (PDK4). In addition, TMZ reversed upregulation of phosphorylated Akt by PAB and increased phosphorylated proline-rich Akt-substrate 40 (PRAS40). Autophagy and apoptosis were not modified by PAB or TMZ. An acute RHF model was established in rats through 70% constriction of the pulmonary artery. TMZ treatment alleviated PAB-induced acute RHF by activating PRAS40 and upregulatingPGC-1α, PGC-1β, PPARα, PPARδ, and PDK4.

Background ST‐segment elevation (STE) in lead aVR is a useful tool in recognizing patients with left main or left anterior descending coronary obstruction during acute coronary syndrome (ACS). The prognostic implication of STE in lead aVR on outcomes has not been established. Methods We performed a systematic search for clinical studies about STE in lead aVR in four databases including PubMed, EMBASE, Cochrane Library, and Web of Science. Primary outcome was in‐hospital mortality. Secondary outcomes included in‐hospital (re)infarction, in‐hospital heart failure, and 90‐day mortality. Results We included 7 studies with a total of 7,700 patients. The all‐cause in‐hospital mortality of patients with STE in lead aVR during ACS was significantly higher than that of patients without STE (OR: 4.37, 95% CI 1.63 to 11.68, p = .003). Patients with greater STE (>0.1 mV) in lead aVR had a higher in‐hospital mortality when compared to lower STE (0.05–0.1 mV) (OR: 2.00, 95% CI 1.11–3.60, p = .02), However, STE in aVR was not independently associated with in‐hospital mortality in ACS patients (OR: 2.72, 95% CI 0.85–8.63, p = .09). The incidence of in‐hospital myocardial (re)infarction (OR: 2.77, 95% CI 1.30–5.94, p = .009), in‐hospital heart failure (OR: 2.62, 95% CI 1.06–6.50, p = .04), and 90‐day mortality (OR: 10.19, 95% CI 5.27–19.71, p < .00001) was also noted to be higher in patients STE in lead aVR. Conclusions This contemporary meta‐analysis shows STE in lead aVR is a poor prognostic marker in patients with ACS with higher in‐hospital mortality, reinfarction, heart failure and 90‐day mortality. Greater magnitude of STE portends worse prognosis. Further studies are needed to establish an independent predictive role of STE in aVR for these adverse outcomes.

<b><i>Introduction:</i></b> This study is to analyze the neuroprotective effects of long-term metformin (Met) preconditioning on rats with ischemic brain injuries and the related mechanisms. <b><i>Methods:</i></b> Twenty-five Sprague-Dawley rats were randomly divided into 5 groups: sham group, middle cerebral artery occlusion (MCAO) group, normal saline + MCAO group, pre- Met + MCAO group, and 3-MA + Met + MCAO group. Pathological changes of brain were observed by hematoxylin-eosin staining. Neurobehavior scores were calculated. Infarct area was assessed by 2,3,5-triphenyltetrazolium chloride staining. Apoptosis of neurons was detected by TdT-mediated dUTP Nick-End Labeling (TUNEL). Western blot tested the expression of LC3 (microtubule-associated protein 1 light chain 3), Beclin-1, adenosine 5′-monophosphate ([AMP]-activated protein kinase [AMPK]), and p-AMPK in hippocampal CA1 region. <b><i>Results:</i></b> Compared with the sham group, the MCAO group induced severe pathological changes in the brain. The neurobehavior scores and infarct area in the brain were increased in the MCAO group than in the sham group. The apoptosis level in the MCAO group was also higher than in the sham group. However, after pretreatment with Met, the pathological changes in the brain were attenuated. Compared with the MCAO group, the pre-Met + MCAO group also had decreased neurobehavior scores and infarct area in the brain. Additionally, the apoptosis level in the pre-Met + MCAO group was lower than in the MCAO group. Moreover, the MCAO group had increased levels of LC3 and Beclin-1 than in the sham group. In the pre-Met + MCAO group, their levels were decreased than in the MCAO group. The p-AMPK level in the pre-Met + MCAO group was also increased than in the MCAO group, suggesting activation of p-AMPK by Met. <b><i>Conclusion:</i></b> Long-term Met pretreatment has neuroprotective effect on ischemic brain injury, which may be related to the regulation of autophagy-related protein expression and apoptosis.