Remove Cardiac Function Remove Ischemia Remove Myocardial Infarction
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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

Abstract: N(6)-methyladenosine (m6A) methylation modification is involved in the progression of myocardial infarction (MI). The ischemia/reperfusion (I/R) injury mouse model and hypoxia/reoxygenation (H/R) cell model were established. We observed that ALKBH5 and MG53 were highly expressed in MI.

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

Dr. Smith's ECG Blog

Troponin T peaked at 38,398 ng/L ( = a very large myocardial infarction, but not massive-- thanks to the pre-PCI spontaneous reperfusion, and rapid internvention!! ). Cardiac function is poor, with akinesis of the LAD territory. There is no definite evidence of acute ischemia. (ie,

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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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