Subject(s)
Coronary Artery Disease , Depression , Anxiety , Coronary Artery Bypass , Depressive Disorder , HumansABSTRACT
OBJECTIVE: To explore the relationship between inflammation, oxidative stress and poor myocardial perfusion in patients with acute ST-segment elevation myocardial infarction (STEMI) after primary percutaneous coronary intervention (PCI). BACKGROUND: Risk factors and mechanisms of poor reperfusion in patients with STEMI after primary PCI remain unclear. METHODS: A total of 143 patients who underwent primary PCI after STEMI were divided into good and poor perfusion groups according to sum-ST-segment resolution (sumSTR) and TIMI myocardial perfusion grade (TMP) results. Aortic sinus arterial blood was collected after primary PCI. The platelet-leukocyte aggregation (PLA), platelet-neutrophil aggregation (PNA), platelet-monocyte aggregation (PMA) and platelet-lymphocyte aggregation (PLyA) were measured by flow cytometry. The malondialdehyde (MDA) and superoxide dismutase (SOD) levels were measured by chemical colorimetry. RESULTS: The leukocyte count, neutrophil ratio and high-sensitivity C-reactive protein were significantly higher in the poor perfusion group than the good perfusion group (p < 0.05). Multiple linear regression analysis showed that neutrophil ratio was an independent risk factor of sumSTR in STEMI patients after primary PCI (p < 0.01). The poor myocardial perfusion group had higher levels of PLA, PNA, PMA and MDA (p < 0.05). There were no differences in PLyA and SOD levels between the good and poor myocardial perfusion groups (p > 0.05). CONCLUSION: Inflammation and oxidative stress were related to poor myocardial perfusion in patients with STEMI after primary PCI.
Subject(s)
Blood Platelets/physiology , Coronary Circulation/physiology , Leukocytes/physiology , Percutaneous Coronary Intervention , Platelet Aggregation/physiology , ST Elevation Myocardial Infarction/blood , Coronary Angiography , Electrocardiography , Female , Humans , Leukocyte Count , Male , Middle Aged , Postoperative Period , Risk Factors , ST Elevation Myocardial Infarction/diagnosis , ST Elevation Myocardial Infarction/surgerySubject(s)
Hyperuricemia/epidemiology , Hyperuricemia/surgery , Percutaneous Coronary Intervention/adverse effects , Postoperative Complications/epidemiology , Follow-Up Studies , Humans , Hyperuricemia/diagnosis , Percutaneous Coronary Intervention/trends , Postoperative Complications/diagnosis , Treatment OutcomeABSTRACT
The aim of the present study was to investigate whether postconditioning with simvastatin attenuated myocardial ischemia reperfusion injury by inhibiting the expression of high mobility group box 1 (HMGB1) in rat myocardium following acute myocardial ischemia. In total, 30 male Sprague-Dawley rats were divided into sham operation (sham; n=10), acute myocardial infarction (AMI; n=10) and simvastatin (sim; n=10) groups. The AMI and sim groups were subjected to ischemia for 30 min, followed by reperfusion for 180 min. The rats in the sim group were administered 20 mg/kg simvastatin intravenously 5 min prior to reperfusion. Subsequently, the infarct size, serum cardiac troponin (c-TnI), tumor necrosis factor (TNF)-α and myocardial malondialdehyde (MDA) levels and superoxide dismutase (SOD) activity were measured. Western blot analysis was used to detect the protein expression of HMGB1. Postconditioning with simvastatin was shown to decrease the infarct size and HMGB1 expression levels in the myocardium following AMI (P<0.05). In addition, postconditioning with simvastatin not only decreased the serum levels of c-TnI and TNF-α (P<0.05), but also inhibited the increase in MDA levels and the reduction in SOD activity (P<0.05). Therefore, postconditioning with simvastatin was shown to attenuate myocardial injury. The underlying mechanism may be associated with the downregulation of HMGB1 expression in the ischemic myocardium.