In patients with acute myocardial infarction (AMI), the guideline-recommended treatment is mechanical revascularization by percutaneous coronary intervention (PCI), which is effective at reducing mortality. However, a substantial proportion of patients with AMI develop chronic cardiac failure owing to poor restoration of microvascular function and myocardial perfusion, despite restoration of epicardial vessel patency. This occurrence is called the 'no-reflow' phenomenon. Although pathological and clinical observations initially seemed to support the hypothesis that no-reflow was the result of microvascular obstruction, irreversible microvascular injury and subsequent intramyocardial haemorrhage are now also thought to be important factors in this process. Intramyocardial haemorrhage shares several pathophysiological features with the haemorrhagic transformation that occurs after ischaemic stroke. Understanding of the role of intramyocardial haemorrhage in the no-reflow phenomenon and myocardial injury is crucial to the development of new therapeutic strategies to treat AMI. In this Review, we provide a comprehensive overview of the pathogenesis and clinical relevance of intramyocardial haemorrhage, and discuss diagnostic options and future therapeutic strategies.
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http://dx.doi.org/10.1038/nrcardio.2014.188 | DOI Listing |
Leg Med (Tokyo)
January 2025
Department of Medical and Surgical Sciences, Unit of Legal Medicine, University of Bologna 40126 Bologna, Italy.
In this case report, the role of a myocardial bridge of the left anterior descending artery (LAD) and recent use of cannabis in a sudden death of a drug user is discussed, also considering the relevance of histopathological pulmonary findings. A 37-year-old man with a history of drug abuse was found dead in his house. External and autoptic examination were performed, as well as histologic and toxicologic analyses of tissues, organs and body fluids samples.
View Article and Find Full Text PDFJ Mol Cell Cardiol Plus
December 2024
Department of Pathology, Amsterdam University Medical Center (AUMC), location AMC and VUmc, Amsterdam, the Netherlands.
Background And Objectives: Structural and functional changes in the intramyocardial microcirculation increase the risk of myocardial infarction (MI). This study investigated intramyocardial perivascular fibrosis and pro-fibrotic cellular transitions in deceased acute and subacute MI patients to explore their involvement in the pathogenesis of MI.
Methods: Left ventricular tissue (LV) was obtained from the infarction area of autopsied patients with acute-phase MI (3-6 h; = 24), subacute-phase MI (5-14 days; = 12), and noninfarcted controls ( = 14).
JACC Cardiovasc Imaging
January 2025
Department of Radiology and Imaging Sciences and Krannert Cardiovascular Research Center, Indiana University School of Medicine, Indianapolis, Indiana, USA. Electronic address:
Background: Hemorrhagic myocardial infarction (hMI) can rapidly diminish the benefits of reperfusion therapy and direct the heart toward chronic heart failure. T2∗ cardiac magnetic resonance (CMR) is the reference standard for detecting hMI. However, the lack of clarity around the earliest time point for detection, time-dependent changes in hemorrhage volume, and the optimal methods for detection can limit the development of strategies to manage hMI.
View Article and Find Full Text PDFJACC Cardiovasc Imaging
January 2025
Department of Cardiovascular Medicine, Stanford University, Stanford, California, USA; Department of Radiology, Stanford University, Stanford, California, USA. Electronic address:
Am J Physiol Heart Circ Physiol
February 2025
Cardiovascular Research Center, Rhode Island Hospital, Providence, Rhode Island, United States.
The promise of injection of extracellular matrix (ECM) from animal hearts as a treatment of myocardial ischemia has been limited by immune reactions and harsh ECM-damaging extraction procedures. We developed a novel method to produce lab-grown human three-dimensional (3-D) acellular ECM particles from human mesenchymal stem cells (MSCs) to mitigate product variability, immunogenicity, and preserve ECM architecture. We hypothesized that intramyocardial injection (I/M) of this novel ECM (dia ∼ 200 microns) would improve cardiac function in a postmyocardial infarction (MI) murine model.
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