Oxidative Stress and Spontaneous Reperfusion of Infarct-Related Artery in Patients With ST-Segment Elevation Myocardial Infarction

Abstract

In the pathogenesis of atherosclerosis, oxidative stress plays a major role in plaque instability, rupture, and erosion, which subsequently leads to thrombus formation and causes total infarct-related artery (IRA) occlusion. We investigated the relationship between spontaneous reperfusion (SR) of IRA and oxidative stress in patients with anterior ST-segment elevation myocardial infarction (STEMI) undergoing primary percutaneous coronary intervention. A total of 341 consecutive patients with anterior STEMI were prospectively included in the present study. Patients were divided into 2 groups according to their thrombolysis in myocardial infarction (TIMI) flow grade: SR group (66 patients, TIMI flow 3) and non-SR group (275 patients, TIMI flow 0-2). On multivariate logistic regression analysis, oxidative stress index (β = 0.868, 95% confidence interval [CI] = 0.806-0.934, P < .001), neutrophil to lymphocyte ratio, uric acid, mean platelet volume, Killip 2 to 4 class, and initial SYNTAX score were independently associated with SR. Oxidative stress as well as inflammation may play a pivotal role in the pathogenesis of SR in patients with STEMI.

The Mean Platelet Volume in the Prognosis of Coronary Artery Disease Severity and Risk Stratification of Acute Coronary Syndromes

“…MPV and the severity of CAD have been positively correlated in some studies, either in an emergency setting, such as in patients undergoing primary PCI (41-43) or in patients suffering from stable CAD (41-46). In the majority of studies, the SYNTAX score was used as a measurement of the severity of CAD (22).…”

Oxidative stress and its association with ST resolution and clinical outcome measures in patients with ST-segment elevation myocardial infarction (STEMI) undergoing primary percutaneous coronary intervention

“…Moreover, antioxidant protects the cellular and sub-cellular membranes against the oxidative stress injury. It was indicated that the increased activity of total antioxidant capacity reduces the damages produced by the enhancement of lipid peroxidation, which may act by counteracting the harmful products [ 16 , 17 ].…”

Isoquercetin ameliorates myocardial infarction through anti-inflammation and anti-apoptosis factor and regulating TLR4-NF-κB signal pathway

“…However, overdose of ROS could cause the cell apoptosis or necrosis. It is universally accepted that the myocardial infarction will cause the oxidative stress and lead to the pathologic myocardial remodeling and myocardial enlargement (10).…”