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Continuous Peripheral Electrical Nerve Stimulation Improves Cardiac Function via Autonomic Nerve Regulation in MI Rats

HeartRhythm

Peripheral electrical nerve stimulation (PENS) reportedly improves cardiac function after myocardial ischemia (MI) by rebalancing the cardiac autonomic nervous system. The dynamic and continuous influence of the PENS on autonomic and cardiac functioning based on cardiac self-repair is not well understood.

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CRISPR-Cas9 base editing of pathogenic CaMKII? improves cardiac function in a humanized mouse model

Journal of Clinical Investigation - Cardiology

Ca2+/calmodulin-dependent protein kinase IIδ (CaMKIIδ) is a prominent inducer of various cardiac disorders, which is mediated by 2 oxidation-sensitive methionine residues within the regulatory domain. Here, we extended this therapeutic concept toward potential clinical translation.

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PO-05-168 CARDIOMYOCYTE STIM1 EXPRESSION REGULATES POST-ISCHEMIC CARDIAC FUNCTION BY CONTROLLING METABOLIC PROCESSES AND MITOCHONDRIAL ULTRASTRUCTURE

HeartRhythm

Loss of stromal interaction molecule 1 (STIM1) expression in smooth muscle cells protects against ischemia reperfusion (I/R) injury. Whether and how STIM1 expression in cardiomyocytes (CM) impacts cardiac remodeling in response to I/R injury is unclear.

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Transcriptome Analysis Reveals Enhancement of Cardiogenesis-Related Signaling Pathways by S-nitroso-N-pivaloyl-D-penicillamine (SNPiP): Implications for Improved Diastolic Function and Cardiac Performance

Journal of Cardiovascular Pharmacology

SNPiP-treated mice exhibited improved cardiac output and enhanced diastolic function, without an increase in heart rate. The NNA-activating effects included increased resilience to ischemia, modulation of energy metabolism preference, and activation of angiogenesis.

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ALKBH5 regulates N(6)-methyladenosine (m6A) methylation of MG53 to attenuate myocardial infarction by inhibiting apoptosis and oxidative stress

Journal of Cardiovascular Pharmacology

The ischemia/reperfusion (I/R) injury mouse model and hypoxia/reoxygenation (H/R) cell model were established. Overexpression of ALKBH5 inhibited H/R-induced cardiomyocyte apoptosis and oxidative stress in vitro, and inhibited I/R-induced collagen deposition, cardiac function, and apoptosis in vivo.

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What are treatment options for this rhythm, when all else fails?

Dr. Smith's ECG Blog

Cardiac function is poor, with akinesis of the LAD territory. There is no definite evidence of acute ischemia. (ie, Simply stated — t he patient was having recurrent PMVT without Q Tc prolongation, and without evidence of ongoing transmural ischemia. ( Some residual ischemia in the infarct border might still be present.

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What will you do for this patient transferred to you who is now asymptomatic?

Dr. Smith's ECG Blog

She requires maximal medical management per all current guidelines (including heparin and P2Y12 inhibitor per cardiology), as well as consideration for emergent cath in the case of persistent ischemia. So what will you do for this patient? They found an acute, total, thrombotic occlusion of the proximal LAD. They opened it. Patel et al.,

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