Sudden cardiac death after myocardial infarction

Chatterjee, Neal A.; Levy, Wayne C.

doi:10.1002/ejhf.1744

Cited by 13 publications

(8 citation statements)

References 21 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Induction of arrhythmias after myocardial infarction is associated with an increased risk of sudden death (Zaman and Kovoor, 2014;Chatterjee and Levy, 2020). Following MI, the risk for ventricular tachyarrhythmia and sudden cardiac death in patients is increased (Hegyi et al, 2018;Li et al, 2020;Liu et al, 2021).…”

Section: Discussionmentioning

confidence: 99%

Sodium–Glucose cotransporter 2 inhibitor empagliflozin decreases ventricular arrhythmia susceptibility by alleviating electrophysiological remodeling post-myocardial-infarction in mice

et al. 2022

View full text Add to dashboard Cite

Background: Recent clinical trials indicate that sodium–glucose cotransporter 2 (SGLT2) inhibitors improve cardiovascular outcomes in myocardial infarction (MI) patients, but the underlying mechanisms remain unknown. As arrhythmia often occurs during myocardial infarction, it is the main cause of death.Objective: The purpose of this study was to investigate the influence of empagliflozin (EMPA), an SGLT2 inhibitor, on cardiac electrophysiological remodeling and arrhythmia susceptibility of myocardial infarction mice.Methods: ECG was obtained from mice 1 week after MI to determine the QT interval. In an electrophysiological study and optical mapping was performed to evaluate the function of EMPA and underlying mechanisms of post-myocardial-infarction in mice.Results: EMPA treatment significantly reduced the QT interval of MI mice (MI + EMPA 50.24 ms vs. MI 64.68 ms). The membrane potential and intracellular Ca [Cai] were mapped from 13 MI hearts and five normal hearts using an optical mapping technique. A dynamic pacing protocol was used to determine action potential duration and [Cai] at baseline and after EMPA (10 umol/L) infusion. EMPA perfusion did not change the APD80 and CaT80 in normal ventricles while shortening them in an infarct zone, bordering zone, and remote zone of MI hearts at 200 ms, 150 ms, 120 ms, and 100 ms pacing cycle length. The conduction velocity of infarcted ventricles was 0.278 m/s and 0.533 m/s in normal ventricles at baseline (p < 0.05). After EMPA administration, the conduction velocity of infarcted ventricles increased to 0.363 m/s, whereas no significant changes were observed in normal ventricles. The action potential rise time, CaT rise time, and CaT tau time were improved after EMPA perfusion in infarcted ventricles, whereas no significant changes were observed in normal ventricles. EMPA decreases early afterdepolarizations premature ventricular beats, and ventricular fibrillation (VF) in infarcted ventricles. The number of phase singularities (baseline versus EMPA, 6.26 versus 3.25), dominant frequency (20.52 versus 10.675 Hz), and ventricular fibrillation duration (1.072 versus 0.361 s) during ventricular fibrillation in infarcted ventricles were all significantly decreased by EMPA.Conclusion: Treatment with EMPA improved post-MI electrophysiological remodeling and decreased substrate for VF of MI mice. The inhibitors of SGLT2 may be a new class of agents for the prevention of ventricle arrhythmia after chronic MI.

show abstract

Section: Discussionmentioning

confidence: 99%

Sodium–Glucose cotransporter 2 inhibitor empagliflozin decreases ventricular arrhythmia susceptibility by alleviating electrophysiological remodeling post-myocardial-infarction in mice

et al. 2022

View full text Add to dashboard Cite

show abstract

“…We congratulate the authors for their thoughtful consideration of competing risk in this study, 3 and would highlight that given the co‐association of the SCD risk factors identified with non‐SCD mortality, we would not anticipate that those identified at highest risk of SCD in this study would necessarily be more likely to benefit from ICD therapy. As we have proposed previously, 18 for any given absolute risk of SCD, the proportional risk of SCD serves as a ‘rheostat’ for ICD survival benefit ( Figure ) 19,20 . Indeed, when assessed in prior randomized ICD trials, increasing absolute SCD rates were associated with attenuated survival benefit as these patients had an even greater absolute risk of non‐SCD mortality, thereby lowering their proportional risk of SCD ( Figure ) 16,17 .…”

Section: Figurementioning

confidence: 86%

Looking forward and backward for sudden death risk: competing risk is everywhere

Chatterjee

Levy

2021

European J of Heart Fail

Self Cite

View full text Add to dashboard Cite

“…MI is a crucial clinical challenge and explaining in detail its molecular events would help to highlight our strategies for reducing the death rate in patients with cardiovascular diseases ( Chatterjee & Levy, 2020 ; Pollard, 2000 ). Thus, exploring the molecular regulator of cardiomyocytes activity will introduce a new insight into MI treatment.…”

Section: Discussionmentioning

confidence: 99%

Circ_0030235 knockdown protects H9c2 cells against OGD/R-induced injury via regulation of miR-526b

Zhang

Liu

Ding

et al. 2021

PeerJ

View full text Add to dashboard Cite

Backgrounds Acute myocardial infarction (MI) is the common clinical manifestation of coronary heart disease. Circular RNAs (circRNAs) act key roles in cardiomyocytes growth and angiogenesis. However, their functions in MI are not entirely clear. This research intended to investigate the role and underlying mechanisms of circ_0030235 in H9c2 cells. Methods H9c2 cells were conducted to oxygen glucose deprivation/reperfusion (OGD/R) inducement to establish the MI model. Circ_0030235 and miR-526b expression was tested and altered by qRT-PCR and transfection. Cell viability, apoptosis and reactive oxygen species (ROS) injury were tested by CCK-8 assay, TUNEL assay kit, and ROS Detection Assay Kit, respectively. Assessment of cell injury-related factors was performed by employing ELISA, Mitochondrial Viability Staining and the JC-1-Mitochondrial Membrane Potential Assay Kit. The relationship between circ_0030235 and miR-526b was analyzed by dual luciferase reporter assay. The expression of key proteins was analyzed by western blot. Results Circ_0030235 was highly expressed in OGD/R-induced H9c2 cells. OGD/R inducement cell viability, while accelerated apoptosis. Besides, the level ROS, cell injury-related factors, mitochondrial membrane potential were notably elevated by OGD/R inducement, while mitochondrial viability was remarkably declined. Whereas, these impacts were all noticeably remitted by circ_0030235 knockdown. miR-526b was a target of circ_0030235. Circ_0030235 knockdown-induced impacts were all notably abrogated by miR-526b inhibition, including the activating impacts on PI3K/AKT and MEK/ERK pathways. Conclusions This research implied that circ_0030235 knockdown might remit OGD/R-induced impacts via activation of PI3K/AKT and MEK/ERK pathways and regulation of miR-526b.

show abstract

Sudden cardiac death after myocardial infarction

Abstract: This article refers to 'Predictors of sudden cardiac death in high-risk patients following a myocardial infarction' by K.F. Docherty et al., published in this issue on pages 848-855.

Cited by 13 publications

References 21 publications

Sodium–Glucose cotransporter 2 inhibitor empagliflozin decreases ventricular arrhythmia susceptibility by alleviating electrophysiological remodeling post-myocardial-infarction in mice

Sodium–Glucose cotransporter 2 inhibitor empagliflozin decreases ventricular arrhythmia susceptibility by alleviating electrophysiological remodeling post-myocardial-infarction in mice

Looking forward and backward for sudden death risk: competing risk is everywhere

Circ_0030235 knockdown protects H9c2 cells against OGD/R-induced injury via regulation of miR-526b

Contact Info

Product

Resources

About