The Preconditioning Phenomenon

Abstract

Abstract-The possibility that an innate mechanism of myocardial protection might be inducible in the human heart has generated considerable excitement and enthusiastic research. The potential to enhance myocardial resistance to ischemic injury in patients suffering the consequences of coronary artery disease has led to studies with more direct clinical relevance. However, in common with many other areas of clinical interest based on advances in basic scientific understanding, early enthusiasm may be disproportionate to ultimate therapeutic significance. There can be little doubt that our understanding of the mechanisms underlying the pathogenesis of ischemia-reperfusion injury has been enhanced significantly by the plethora of research stimulated by interest in endogenous myocardial protection. Direct extrapolation of observations in the laboratory to the cardiology clinic or operating theater is tempting but should be avoided. The results of recent clinical experiments that suggest that preconditioning can protect against ischemia, although encouraging, should be interpreted cautiously, with particular attention to the limitations of the end points available. A reasoned evaluation of recent research should prevent unrealistic expectations and allow improved design of future trials so that this potent adaptive phenomenon can be exploited to its maximum potential. (Circ Res. 2000;87:543-550.)

Reduction of Early Reperfusion Injury With the Mitochondria-Targeting Peptide Bendavia

“…Among the cellular culprits that contribute to reperfusion injury, bursts of reactive oxygen species (ROS) occurring during early reperfusion have been known to occur since the late 1980’s 1, 2 . Transient production of ROS contributes to electromechanical dysfunction, infarction, and the coronary no-reflow phenomenon (reviewed in 3, 4 ). Despite a clear understanding of the role of ROS in reperfusion injury, there are no adjuvant treatments currently administered in routine clinical practice to protect the heart against reperfusion injury.…”

Surgical resection of multiple right atrial masses in a child with beta thalassaemia and receiving desferioxamine

“…12 Furthermore, a prospective study showed significantly fewer 30 day events in patients with onset of angina 24 hours before an ST elevation myocardial infarction. 13 This has been explained by the phenomenon of preconditioning, 14 which may explain why in our database preinfarct angina is an independent predictor for aborted myocardial infarction.…”

Ischemic Preconditioning of the Right Ventricle: A New Application for an Old Concept?

“…Since the initial observation by Murry et al [1] about 25 years ago that a series of brief episodes of ischemia and reperfusion applied before a longer coronary artery occlusion in canine hearts led to a delay in the onset of infarction and reduction in the ultimate infarct size, the concept of ischemic preconditioning has received widespread support and recognition [2,3]. The reduction of experimental myocardial infarct size by induction of prior brief episodes of ischemia has been consistently demonstrated in almost every animal studied [2,3].…”

“…The reduction of experimental myocardial infarct size by induction of prior brief episodes of ischemia has been consistently demonstrated in almost every animal studied [2,3]. Furthermore, there is abundant in vitro and clinical evidence that indicates that this phenomenon occurs in the human heart as well [2,3,4].…”

“…The aim of exploring these biochemical pathways was to develop pharmacological therapeutic strategies that could mimic or induce the preconditioning process (without inducing ischemia). Using various in vitro models these investigations have shown that the mechanisms of the preconditioning phenomenon involve adenosine as a central trigger of the process, protein kinase C as an intracellular messenger, and the ATP-dependent potassium (K ATP ) channel as a target protein [3]. The majority of animal studies that have explored ischemic preconditioning and its mechanisms focused on ischemia of the left ventricle (LV), and often induced ischemic preconditioning and MI by ligation of the left anterior descending artery.…”