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Flurpiridaz F 18: First Approval.

Am J Cardiovasc Drugs

January 2025

Springer Nature, Private Bag 65901, Mairangi Bay, Auckland, 0754, New Zealand.

Flurpiridaz F 18 (FLYRCADO™) is an intravenous (IV) radioactive diagnostic drug being developed by GE Healthcare and Lantheus Medical Imaging for use in positron emission tomography (PET) myocardial perfusion imaging (MPI) to detect coronary artery disease (CAD). In September 2024, flurpiridaz F 18 was approved in the USA for PET MPI under rest or stress (pharmacologic or exercise) in adult patients with known or suspected CAD to evaluate for myocardial ischemia and infarction. This article summarizes the milestones in the development of flurpiridaz F 18 leading to this first approval for use in PET MPI in adult patients to evaluate for myocardial ischemia and infarction.

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Aim: To define the association between severe coronary artery disease and widespread atherosclerosis in younger individuals.

Methods: Individuals aged 1-50 years with sudden cardiac death (SCD) from 2019-23, autopsy-proven to be due to coronary artery disease, were identified using the state-wide EndUCD registry. Presence of extra-coronary atherosclerosis greater than modified American Heart Association class III was assessed in 5 arterial beds (intra-cerebral vessels, aorta, carotid, renal and femoral arteries).

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Myocardial infarction can lead to the loss of billions of cardiomyocytes, and while cell-based therapies are an option, immature nature of in vitro-generated human induced pluripotent stem cell (iPSC)-derived cardiomyocytes (iCMs) is a roadblock to their development. Existing iPSC differentiation protocols don't go beyond producing fetal iCMs. Recently, adult extracellular matrix (ECM) was shown to retain tissue memory and have some success driving tissue-specific differentiation in unspecified cells in various organ systems.

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Background: Myocardial ischemia-reperfusion (I/R) injury refers to cell damage that occurs as a consequence of the restoration of blood circulation following reperfusion therapy for cardiovascular diseases, and it is a primary cause of myocardial infarction. The search for nove therapeutic targets in the context of I/R injury is currently a highly active area of research. p70 ribosomal S6 kinase (S6K1) plays an important role in I/R induced necrosis, although the specific mechanisms remain unclear.

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Background: Myocardial ischemia-reperfusion (I/R) injury and coronary microcirculation dysfunction (CMD) are observed in patients with myocardial infarction after vascular recanalization. The antianginal drug trimetazidine has been demonstrated to exert a protective effect in myocardial ischemia-reperfusion injury.

Objectives: This study aimed to investigate the role of trimetazidine in endothelial cell dysfunction caused by myocardial I/R injury and thus improve coronary microcirculation.

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