Abstract
BackgroundThe diseased human myocardium is highly susceptible to ischemia/reoxygenation (I/R)-induced injury but its response to protective interventions such as ischemic preconditioning (IPreC) is unclear. Cardiac and other pre-existing clinical conditions as well as previous or ongoing medical treatment may influence the myocardial response to I/R injury and protection. This study investigated the effect of both on myocardial susceptibility to I/R-induced injury and the protective effects of IPreC.Methods and resultsAtrial myocardium from cardiac surgery patients (n = 300) was assigned to one of three groups: aerobic control, I/R alone, and IPreC. Lactate dehydrogenase leakage, as a marker of cell injury, and cell viability were measured. The basal redox status was determined in samples from 90 patients.The response to I/R varied widely. Myocardium from patients with aortic valve disease was the most susceptible to injury whereas myocardium from dyslipidemia patients was the least susceptible. Tissue from females was better protected than tissue from males. Myocardium from patients with mitral valve disease was the least responsive to IPreC. The basal redox status was altered in the myocardium from patients with mitral and aortic valve disease.ConclusionsThe response of the myocardium to I/R and IPreC is highly variable and influenced by the underlying cardiac pathology, dyslipidemia, sex, and the basal redox status. These results should be taken into account in the design of future clinical studies on the prevention of I/R injury and protection.
Highlights
Cardiovascular diseases are the most prevalent health problem worldwide and the major cause of morbidity and mortality [1]
Ischemic injury, preconditioning and basal redox status should be taken into account in the design of future clinical studies on the prevention of I/R injury and protection
The results showed that muscle tissue with less ischemic injury either did not respond to preconditioning or was more susceptible to damage during ischemic preconditioning (IPreC)
Summary
Cardiovascular diseases are the most prevalent health problem worldwide and the major cause of morbidity and mortality [1]. According to the WHO, in 2012 ischemic heart diseases caused 17.5 million deaths. Prolonged ischemia, such as occurs during myocardial infarction, causes lactate accumulation, alterations in ion-transport mechanisms, and eventually cardiomyocyte death through apoptosis and necrosis. Over the last three decades, major efforts have been aimed at understanding the mechanisms of I/R-induced injury and developing strategies to protect the human myocardium. The diseased human myocardium is highly susceptible to ischemia/reoxygenation (I/R)induced injury but its response to protective interventions such as ischemic preconditioning (IPreC) is unclear. This study investigated the effect of both on myocardial susceptibility to I/R-induced injury and the protective effects of IPreC
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