Current Trends in Cardiology

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Mini Review - Current Trends in Cardiology (2023) Volume 7, Issue 12

Ischaemic preconditioning and heart failure after myocardial infarction

Bart Geest*

Department of Medicine, University of Heidelberg, Mannheim, Germany.

*Corresponding Author:
Bart Geest
Department of Medicine
University of Heidelberg, Mannheim

Received:28-Nov-2023,Manuscript No. AACC-23-128818; Editor assigned:01-Dec-2023,PreQC No. AACC-23-128818(PQ); Reviewed:15-Dec-2023,QC No. AACC-23-128818; Revised:20-Dec-2023, Manuscript No. AACC-23-128818(R); Published:27-Dec-2023,DOI:10.35841/aacc-7.12.227

Citation:Geest B. Ischaemic preconditioning and heart failure after myocardial infarction. Curr Trend Cardiol. 2023;7(12):227.

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Heart failure following a myocardial infarction (MI), commonly known as a heart attack, remains a major global health concern. While advancements in acute MI management have improved survival rates, many individuals still experience significant cardiac damage and develop heart failure in the aftermath of the event. Ischaemic preconditioning a phenomenon initially observed in the late 1980s, has emerged as a promising strategy to mitigate the detrimental effects of MI and reduce the risk of subsequent heart failure. This article explores the concept of ischaemic preconditioning and its potential applications in preventing heart failure after myocardial infarction.Ischaemic preconditioning is a phenomenon in which brief, controlled episodes of ischemia (reduced blood supply) and reperfusion (restoration of blood supply) are applied to an organ or tissue before a more extended period of ischemia. Initially discovered in the heart, IPC has since been observed in various other organs, including the brain, kidneys, and liver. Its primary purpose is to protect tissues from the harmful consequences of prolonged ischemia, which can occur during events such as a heart attack.[1,2].

The underlying mechanisms of IPC are multifaceted. One key aspect involves the activation of endogenous protective pathways that increase the heart's tolerance to subsequent ischemia-reperfusion injury. This involves the release of signaling molecules, such as adenosine and bradykinin, which activate intracellular pathways that promote cell survival. Additionally, IPC triggers the opening of mitochondrial ATP-sensitive potassium channels and the inhibition of mitochondrial permeability transition pores, both of which help maintain cellular energy production and prevent cell death during ischemia-reperfusion.When applied specifically to myocardial infarction, IPC is achieved by inducing brief episodes of ischemia in the heart muscle before the onset of a more extended period of ischemia during a heart attack. This pre-exposure to ischemia primes the heart tissue to better withstand the subsequent, more severe ischemic insult. Some of the key mechanisms by which IPC protects the heart during a heart attack [3,4].

Reduced Cell Death: IPC reduces myocardial cell death by inhibiting apoptosis (programmed cell death) and necrosis (uncontrolled cell death) pathways, thereby preserving a more substantial portion of the heart tissue. Enhanced Blood Flow: IPC helps to improve blood flow in the coronary arteries, even during a heart attack, by dilating blood vessels and reducing vascular resistance. This increased perfusion can reduce the extent of heart damage.Anti-Inflammatory Effects: IPC can attenuate the inflammatory response that occurs during myocardial infarction, limiting damage to the heart tissue and reducing the risk of heart failure.While the concept of ischaemic preconditioning has shown great promise in experimental settings, its translation into clinical practice remains a topic of ongoing research. Several strategies have been explored to harness the protective effects of IPC in patients at risk of heart attacks.Remote Ischaemic Conditioning: Instead of directly preconditioning the heart, remote ischaemic conditioning involves inducing brief episodes of ischemia and reperfusion in an accessible limb (e.g., arm or leg). This approach triggers systemic protective responses that can benefit the heart. Clinical trials have demonstrated potential benefits in reducing heart muscle damage during MI and improving outcomes.[5,6].


Pharmacological Preconditioning: Researchers are investigating the use of drugs that mimic the protective effects of IPC. These pharmacological agents can be administered before or during a heart attack to limit damage to the heart tissue. Preconditioning in Cardiac Surgery: IPC can also be applied during cardiac surgery, where the heart may undergo temporary ischemia. By preconditioning the heart before such procedures, surgeons can minimize the risk of postoperative heart damage and improve patient outcomes.While the potential of ischaemic preconditioning in preventing heart failure after myocardial infarction is promising, several challenges remain.Timing and Dosing: Determining the optimal timing and duration of IPC or remote ischaemic conditioning remains a subject of ongoing research. The ideal dosing regimen may vary among individuals and clinical scenarios.[7,8].



Individual Variability: The response to IPC may vary among patients due to differences in genetics, comorbidities, and other factors. Tailoring preconditioning strategies to individual patients may be necessary.Clinical Implementation: Widespread adoption of IPC in clinical practice requires further research, including large-scale clinical trials to establish its safety and efficacy.[


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