[Acute myocardial infarction in patients recovering from COVID-19 pneumonia].

Coronary involvement in COVID-19 infection usually presents as type 2 acute myocardial infarction (AMI), due to increased 02 consumption and reduction of oxygen supply, and less frequently as type 1 (STEMI). In that cases, thrombogenicity of the infection may contribute to acute coronary occlusion. We present 2 cases of middle-aged men, with few or none cardiovascular risk factors, who were in hospital during 10 days because pneumonia due to COVID-19 with good evolution.

Efficacy of a Novel Mitochondrial-Derived Peptide in a Porcine Model of Myocardial Ischemia/Reperfusion Injury.

With the complexities that surround myocardial ischemia/reperfusion (MI/R) injury, therapies adjunctive to reperfusion that elicit beneficial pleiotropic effects and do not overlap with standard of care are necessary. This study found that the mitochondrial-derived peptide S14G-humanin (HNG) (2 mg/kg), an analogue of humanin, reduced infarct size in a large animal model of MI/R. However, when ischemic time was increased, the infarct-sparing effects were abolished with the same dose of HNG.

Renal Denervation Prevents Heart Failure Progression Via Inhibition of the Renin-Angiotensin System.

Background: Previously, we have shown that radiofrequency (RF) renal denervation (RDN) reduces myocardial infarct size in a rat model of acute myocardial infarction (MI) and improves left ventricular (LV) function and vascular reactivity in the setting of heart failure following MI.

Objectives: The authors investigated the therapeutic efficacy of RF-RDN in a clinically relevant normotensive swine model of heart failure with reduced ejection fraction (HFrEF).

Methods: Yucatan miniswine underwent 75 min of left anterior descending coronary artery balloon occlusion to induce MI followed by reperfusion (R) for 18 weeks.

A novel fibroblast activation inhibitor attenuates left ventricular remodeling and preserves cardiac function in heart failure.

Cardiac fibroblasts are critical mediators of fibrotic remodeling in the failing heart and transform into myofibroblasts in the presence of profibrotic factors such as transforming growth factor-β. Myocardial fibrosis worsens cardiac function, accelerating the progression to decompensated heart failure (HF). We investigated the effects of a novel inhibitor (NM922; NovoMedix, San Diego, CA) of the conversion of normal fibroblasts to the myofibroblast phenotype in the setting of pressure overload-induced HF.