Protection of the abnormal heart

Abstract

Myocardial ischemia and reperfusion injury have been extensively investigated in the laboratory mainly in healthy tissues. However, in clinical settings, ischemic heart disease coexists with certain illnesses, which could potentially influence the response of the myocardium to ischemia and reperfusion. Recent research has revealed that the abnormal heart may not be always vulnerable to ischemic injury. Furthermore, the effect of powerful means of protection, such as ischemic preconditioning, may not be in operation under certain pathological conditions. With this evidence in mind, the present review will focus on the response of the abnormal heart to ischemia and reperfusion, the possible underlying mechanisms, and potential cardioprotective strategies.

Effects of ischemic preconditioning on ischemia/reperfusion-induced arrhythmias by upregulatation of connexin 43 expression

“…It is known that arrhythmia occurrence increases with the susceptibility of hypertrophied myocardium to ischemia-reperfusion injury during open heart surgeries [9,14,15]. Pathological changes in cell structure and metabolism of hypertrophied myocardium decrease its tolerance to ischemia-reperfusion injury.…”

Anaesthesia and myocardial ischaemia/reperfusion injury

“…Whereas in hypertrophic myocardium, preconditioning seems to be preserved, in the failing heart, this powerful endogenous cardioprotection is not present (reviewed in Pantos and colleagues). 73 In the aged heart, preconditioning is also abolished, 1 but can be restored by exercise and food restriction. 2 The first studies of ischaemic preconditioning were performed using a protocol of multiple short-term ischaemia episodes interspersed by reperfusion.…”

New insights into the role of thyroid hormone in cardiac remodeling: time to reconsider?

“…The physiological relevance of this response and the potential underlying mechanisms are not fully understood. It may be viewed as maladaptive response regarding cardiac function but also may be an adaptive process regarding cardioprotection and tissue regeneration [2,3]. The latter hypothesis is recently strongly supported by experimental evidence coming from zebra fish models of heart regeneration and showing that the source of cardiomyocytes is rather the de-differentiated mature cells than the progenitor cells [4].…”