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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.