Background: It has been proved in animal models that postconditioning (PC) could attenuate reperfusion injury. But there are not many clinical studies on the application of PC. Hypothesis: Four cycles of 1-minute balloon inflation and deflation, following initial balloon reperfusion in ST-segment elevation myocardial infarction (MI) but before stenting, might improve clinical outcomes compared with primary percutaneous coronary intervention (PCI) alone. Methods: Forty-three patients diagnosed with acute MI were randomly assigned to 2 groups: the control group (n = 20) and the PC group (n = 23). Blood samples were obtained and assayed for creatine kinase MB (CK-MB) and high-sensitive C-reactive protein. Electrocardiogram, echocardiography, and rest technetium Tc 99m-sestamibi (99mTc-MIBI) myocardial perfusion single-photon emission computed tomography (SPECT) were performed. Results:The control group presented with higher peak CK-MB as compared with the PC group (351.9 ± 153.6 vs 247.7 ± 118.3 U/L, P = 0.028) as well as the area under the curve (AUC) of CK-MB (8040 ± 3358 vs 5955 ± 2509, P = 0.04). After PCI, PC was associated with a lower level of hs-CRP in comparison with the control group (5.5 ± 4.5 vs 9.5 ± 5.2 mg/L, P = 0.019). More patients in the PC group had complete ST-segment resolution than did patients in the control group (82.6% vs 45.0%, P = 0.049). Left ventricle ejection fraction was better in the PC group than in the control group (0.57 ± 0.09 vs 0.47 ± 0.11, P = 0.002). Compared with the control group, PC greatly reduced infarct size, by 46% as measured by SPECT (13 ± 11.2% vs 24.2 ± 10.6%, P = 0.002). Conclusions: This study indicated that PC in emergent PCI was a valuable modification of primary PCI. IntroductionCoronary heart disease will become the leading cause of death worldwide by 2020. 1 Acute myocardial infarction (AMI) is a major cause of such mortality. Early and successful myocardial reperfusion with the use of thrombolytic therapy or percutaneous coronary intervention (PCI) is the most effective strategy for reducing the size of a myocardial infarct and improving the clinical outcome. But at the same time, the process of restoring blood flow to the ischemic myocardium can induce additional lethal injuries that are termed myocardial reperfusion injury. 2 Studies in animal models of AMI suggest that 50% of the final size of an MI is caused by myocardial reperfusion injury. 3 So new strategies for preventing reperfusion injury should be explored.Postconditioning (PC), defined as a cycle of brief interruptions of reperfusion applied at the onset of reperfusion after a prolonged ischemic insult, has been found to attenuate reperfusion injury in several animal experiments. 4 -7 In our study we applied this cardioprotective intervention at the time of myocardial reperfusion in 23 Chinese AMI patients receiving emergent PCI.

The period following heart failure hospitalization (HFH) is a vulnerable time with high rates of death or recurrent HFH.OBJECTIVE To evaluate clinical characteristics, outcomes, and treatment response to vericiguat according to prespecified index event subgroups and time from index HFH in the Vericiguat Global Study in Subjects With Heart Failure With Reduced Ejection Fraction (VICTORIA) trial. DESIGN, SETTING, AND PARTICIPANTSAnalysis of an international, randomized, placebo-controlled trial. All VICTORIA patients had recent (<6 months) worsening HF (ejection fraction <45%). Index event subgroups were less than 3 months after HFH (n = 3378), 3 to 6 months after HFH (n = 871), and those requiring outpatient intravenous diuretic therapy only for worsening HF (without HFH) in the previous 3 months (n = 801). Data were analyzed between May 2, 2020, and May 9, 2020.INTERVENTION Vericiguat titrated to 10 mg daily vs placebo. MAIN OUTCOMES AND MEASURESThe primary outcome was time to a composite of HFH or cardiovascular death; secondary outcomes were time to HFH, cardiovascular death, a composite of all-cause mortality or HFH, all-cause death, and total HFH. RESULTS Among 5050 patients in the VICTORIA trial, mean age was 67 years, 24% were women, 64% were White, 22% were Asian, and 5% were Black. Baseline characteristics were balanced between treatment arms within each subgroup. Over a median follow-up of 10.8 months, the primary event rates were 40.9, 29.6, and 23.4 events per 100 patient-years in the HFH at less than 3 months, HFH 3 to 6 months, and outpatient worsening subgroups, respectively. Compared with the outpatient worsening subgroup, the multivariable-adjusted relative risk of the primary outcome was higher in HFH less than 3 months (adjusted hazard ratio, 1.48; 95% CI, 1.27-1.73), with a time-dependent gradient of risk demonstrating that patients closest to their index HFH had the highest risk. Vericiguat was associated with reduced risk of the primary outcome overall and in all subgroups, without evidence of treatment heterogeneity. Similar results were evident for all-cause death and HFH. Addtionally, a continuous association between time from HFH and vericiguat treatment showed a trend toward greater benefit with longer duration since HFH. Safety events (symptomatic hypotension and syncope) were infrequent in all subgroups, with no difference between treatment arms.CONCLUSIONS AND RELEVANCE Among patients with worsening chronic HF, those in closest proximity to their index HFH had the highest risk of cardiovascular death or HFH, irrespective of age or clinical risk factors. The benefit of vericiguat did not differ significantly across the spectrum of risk in worsening HF.

The glutathione (GSH) system is considered to be one of the most powerful endogenous antioxidant systems in the cardiovascular system due to its key contribution to detoxifying xenobiotics and scavenging overreactive oxygen species (ROS). Numerous investigations have suggested that disruption of the GSH system is a critical element in the pathogenesis of myocardial injury. Meanwhile, a newly proposed type of cell death, ferroptosis, has been demonstrated to be closely related to the GSH system, which affects the process and outcome of myocardial injury. Moreover, in facing various pathological challenges, the mammalian heart, which possesses high levels of mitochondria and weak antioxidant capacity, is susceptible to oxidant production and oxidative damage. Therefore, targeted enhancement of the GSH system along with prevention of ferroptosis in the myocardium is a promising therapeutic strategy. In this review, we first systematically describe the physiological functions and anabolism of the GSH system, as well as its effects on cardiac injury. Then, we discuss the relationship between the GSH system and ferroptosis in myocardial injury. Moreover, a comprehensive summary of the activation strategies of the GSH system is presented, where we mainly identify several promising herbal monomers, which may provide valuable guidelines for the exploration of new therapeutic approaches.

Patients with acute myocardial infarction (AMI) complicated by heart failure with preserved ejection fraction (HFpEF) are likely to have more adverse cardiovascular events and higher mortality. The purpose of this study was to examine the predictors and outcomes in AMI patients complicated by HFpEF.We examined the demographics, clinical data, and clinical outcomes in 405 consecutive subjects who firstly presented with AMI after undergoing emergency percutaneous coronary intervention from January 2013 to June 2016.Three hundred twenty patients and eighty-five patients were classified into the nonheart failure (non-HF) group and HFpEF group, respectively. Patients with HFpEF had higher prevalence of prior hypertension, had higher levels of biomarkers, and had a larger left atrial diameter with a nondilated left ventricle were more likely to develop multivessel disease-vessels and had infarction-related artery located in left anterior descending artery than patients without HF. Moreover, patients with HFpEF had a higher probability of developing the in-hospital incident cardiovascular complications and death than non-HF patients.Two routine biomarkers, levels of hypersensitive C-reactive protein and N-terminal-pro brain natriuretic peptide, and number of diseased-vessels were independent predictors for in-hospital HFpEF incidence in AMI patients with preserved LVEF. AMI patients with HFpEF had a higher probability of in-hospital cardiovascular outcomes and mortality.

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