In this review article we tried to find an answer to the question, should local coronary hypothermia be a part of the early reperfusion strategy in patients with STEMI to prevent reperfusion injury, no-reflow phenomenon, and to reduce the infarct size and mortality. Hypothermia can save cardiomyocytes if achieved in a timely fashion before reperfusion. Intracoronary hypothermia can be adjunct to PCI by lessening ischemia/reperfusion injury on cardiomyocytes and reduction in infarct size. Reperfusion induced Calcium overload, generation of ROS and subsequent activation of Mitochondrial permeability transition pore (MPT) are major contributors to reperfusion injury. Hypothermia reduces calcium loading of the cell and maintains cellular energy and tissue level glucose which can scavenger ROS. Hypothermia reduces MPT activation and thus reduces infarct size. Systemic cooling trials failed to reduce infarct size, perhaps because the target temperature was not reached fast enough, and it was associated with systemic side effects. The need for rapid induction of hypothermia to <35 °C with the ethical concern of delaying reperfusion while cooling the patient and the inconsistency of endovascular cooling results lead to a belief that endovascular cooling may exceed the acceptable level of invasiveness in the context of other novels cardioprotective, regenerative and reperfusion therapies. Clinical trials showed the safety and feasibility of novel intracoronary hypothermia with rapid induction and maintenance of hypothermia using routine PCI equipment ahead of reperfusion. Two phases of cooling were applied without significant delay in the door to balloon time. Cooling of the coronary artery leads to cooling of its dependant myocardium without affecting adjacent myocardium. Heat transfer occurred by heat conduction during the occlusion phase and heat convention during the reperfusion phase. Fine-tuning of saline temperature and infusion rate helped to improve the protocol. The best duration of hypothermia before and after reperfusion is not known and needs further investigation. A balance between the undoubted cardioprotective effects of hypothermia with iatrogenic prolongation of ischemia time needs to be established. A reduction in infarct size was observed but needs to be validated with large randomized trials. Furthermore, it might be possible to augment the cardioprotective effects of intracoronary hypothermia by combination with other cardioprotective approaches such as antioxidant drugs and afterload reducing agents.
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http://dx.doi.org/10.1016/j.carrev.2020.08.004 | DOI Listing |
Purpose: We designed a study investigating the cardioprotective role of sleep apnea (SA) in patients with acute myocardial infarction (AMI), focusing on its association with infarct size and coronary collateral circulation.
Methods: We recruited adults with AMI, who underwent Level-III SA testing during hospitalization. Delayed-enhancement cardiac magnetic resonance (CMR) imaging was performed to quantify AMI size (percent-infarcted myocardium).
IBRO Neurosci Rep
June 2025
Université de la Réunion, INSERM, UMR 1188 Diabète Athérothrombose Thérapies Réunion Océan Indien (DéTROI), Saint-Pierre 97410, France.
It is well recognized that type II Diabetes (T2D) and overweight/obesity are established risk factors for stroke, worsening also their consequences. However, the underlying mechanisms by which these disorders aggravate outcomes are not yet clear limiting the therapeutic opportunities. To fill this gap, we characterized, for the first time, the effects of T2D and obesity on the brain repair mechanisms occurring 7 days after stroke, notably glial scarring.
View Article and Find Full Text PDFActa Cardiol
January 2025
Division of Cardiology, Cerrahpasa Faculty of Medicine, Istanbul University-Cerrahpasa, Istanbul, Turkey.
Objective: Current guidelines recommend the use of glycoprotein IIb/IIIa (GpIIb/IIIa) inhibitors in patients with ST-segment elevation myocardial infarction (STEMI) only as a bail-out therapy. However, drug penetration to the jeopardised area may not be achieved due to impeded blood flow and increased microvascular resistance. Aim of our study is to investigate the impact of distal intracoronary GpIIb/IIIa inhibitor agent infusion in STEMI patients.
View Article and Find Full Text PDFJ Cardiothorac Surg
January 2025
The First Hospital of Lanzhou University, Lanzhou, China.
Background: This article aims to use high-throughput sequencing to identify miRNAs associated with ferroptosis in myocardial ischemia-reperfusion injury, select a target miRNA, and investigate its role in H9C2 cells hypoxia-reoxygenation injury.
Methods: SD rats and H9C2 cells were used as subjects. ELISA kits quantified MDA, SOD, GSH, LDH, and ferritin levels.
Nat Cardiovasc Res
January 2025
Department of Pharmacy at the Second Affiliated Hospital, and Department of Pharmacology at College of Pharmacy (The Key Laboratory of Cardiovascular Research, Ministry of Education; National Key Laboratory of Frigid Zone Cardiovascular Diseases), Harbin Medical University, Harbin, China.
Targeting the cardiomyocyte cell cycle is a promising strategy for heart repair following injury. Here, we identify a cardiac-regeneration-associated PIWI-interacting RNA (CRAPIR) as a regulator of cardiomyocyte proliferation. Genetic ablation or antagomir-mediated knockdown of CRAPIR in mice impairs cardiomyocyte proliferation and reduces heart regenerative potential.
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