Why the study?
Advanced age impairs cardiac responses to cardioprotective interventions and increases the risk of post-ischaemic adverse remodelling and heart failure, but causative mechanisms remain to be elucidated.
This consensus document highlights the mechanisms by which advanced age impairs cardioprotective signaling and exacerbates ischemia/reperfusion injury, emphasizing the need for age-specific therapeutic strategies.
Clinicians should factor age into cardioprotective strategy selection; extends consensus to prioritize age-specific trials.
Advanced age is a major predisposing risk factor for the incidence of coronary syndromes and comorbid conditions which impact the heart response to cardioprotective interventions. Advanced age also significantly increases the risk of developing post-ischaemic adverse remodelling and heart failure after ischaemia/reperfusion (IR) injury. Some of the signalling pathways become defective or attenuated during ageing, whereas others with well-known detrimental consequences, such as glycoxidation or proinflammatory pathways, are exacerbated. The causative mechanisms responsible for all these changes are yet to be elucidated and are a matter of active research. Here, we review the current knowledge about the pathophysiology of cardiac ageing that eventually impacts on the increased susceptibility of cells to IR injury and can affect the efficiency of cardioprotective strategies.
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Ruiz‐Meana et al. (2020) conducted a review in Cardiac ageing and ischaemia/reperfusion injury. Advanced age was evaluated. Advanced age increases the susceptibility of cardiomyocytes to ischaemia/reperfusion injury and alters signalling pathways, which can reduce the efficacy of cardioprotective strategies.
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