Adiponectin and ischemia-reperfusion injury in ST segment elevation myocardial infarction

Abstract

Background: Models of experimental ischemia-reperfusion (IR) in adiponectin knockout animals have shown that adiponectin mediates protection against the development of IR injury. However, the role of adiponectin in IR injury in humans is largely unknown. Methods: In a total of 234 ST segment elevation myocardial infarction (STEMI) patients, baseline circulating total adiponectin concentration was correlated with IR injury after primary percutaneous coronary intervention (pPCI) and with major adverse cardiac events (MACE, death and cardiac hospitalization) during one year of follow up. IR injury was defined by serial electrocardiography (ECG) as >30% persistent ST segment elevation despite successful restoration of vessel patency and by angiography as thrombolysis in myocardial infarction (TIMI) blush grade<2. Results: IR injury was present in 31% of patients according to ECG criteria and in 28% of patients according to angiographic criteria. The median adiponectin level was 6.8 µg/ml in patients with ECG signs of IR injury and 6.5 µg/ml in patients without ECG signs of IR (p=0.26). When the angiographic criteria of IR were used, the median adiponectin level was 6.9 µg/ml for patients with IR versus 6.3 µg/ml for patients without IR (p=0.06). MACE occurred in 27% of the patients. Median adiponectin levels were similar in patients with MACE and in those without MACE: 6.3 vs. 6.4 µg/ml (p=0.24). In a multivariate model, no significant relation between circulating adiponectin levels and IR injury or MACE was evident. Conclusion: In the current era of pPCI, IR injury still occurs in almost one third of STEMI patients. Our findings do not support a major protective role of adiponectin in the prevention or attenuation of IR injury in these patients.

Total flavones of Rhododendron simsii Planch flower protect isolated rat heart from ischaemia-reperfusion injury and its mechanism of UTR-RhoA-ROCK pathway inhibition

“…Myocardial I/R injury could result in heart dysfunction. [22] In the present study, monitoring hemodynamic parameters showed that a reduction in cardiac systolic function was indicated by the I/R-induced decreases of LVSP and +dp/dtmax in the isolated hearts. And the decreased Àdp/dtmax and the increased LVEDP suggested the I/Rproduced a decrease in cardiac diastolic function.…”

Effect of Baduanjin Sequential Therapy on the Quality of Life and Cardiac Function in Patients with AMI After PCI: A Randomized Controlled Trial

“…Relevant literature reports that nearly 60% of patients after PCI are severely deficient in exercise, and about 84% of patients after PCI have associated anxiety symptoms, while 67% have associated depressive symptoms [26,28]. Previous studies have shown that myocardial ischemia-reperfusion (IR) injury can cause ventricular cell death and is a major pathological event leading to morbidity and mortality in those with acute myocardial infarction [11,12]. Interestingly, appropriate exercise can rapidly produce a cardiac phenotype that resists IR-induced myocardial injury.…”

“…Previous studies have shown that myocardial ischemiareperfusion (IR) injury can cause ventricular cell death and is a major pathological event leading to morbidity and mortality in those with acute myocardial infarction [11,12].…”

Mitochondrial Protection by PARP Inhibition

“…PARP inhibitors were demonstrated to ameliorate all these effects in various experimental systems [172][173][174]. Acute myocardial infarction is followed by reperfusion, due to either coronary thrombolytic therapy or surgical intervention [175]. However, the return of oxygen to a respiratory chain that has suffered hypoxic damages during the preceding ischemia results in a substantial perfusion injury characterised by massive ROS and RNS production, upregulated expression of inflammatory cytokines, and PARP activation [176].…”