Oxidative stress and paraoxonase 1 activity predict contrast-induced nephropathy in patients with ST-segment elevation myocardial infarction undergoing primary percutaneous coronary intervention.

Reactive oxygen species have been implicated in the pathogenesis of contrast-induced nephropathy (CIN). We investigated the relationship between CIN with paraoxonase 1 (PON-1) activity and oxidative stress markers (total antioxidant status [TAS], total oxidant status [TOS], and oxidative stress index [OSI]) in patients with anterior ST-segment elevation myocardial infarction (STEMI) undergoing primary percutaneous coronary intervention; 289 consecutive patients with STEMI were prospectively included. The patients were divided into 2 groups: CIN (n = 69) and non-CIN (n = 220). Activity of PON-1 and TAS levels were significantly lower and OSI and TOS levels were significantly higher in patients with CIN compared to the non-CIN group (P < .05, for all). On multivariate logistic regression analysis, PON-1 activity and OSI as well as the amount of contrast medium and diabetes were independent predictors for CIN in patients with anterior STEMI. Activity of PON-1 and oxidative stress may play a role in the pathogenesis of CIN.

Paraoxonase-1 activity and oxidative stress in patients with anterior ST elevation myocardial infarction undergoing primary percutaneous coronary intervention with and without no-reflow.

BACKGROUND: Reperfusion and ischemic injuries are pathogenetic mechanisms of no-reflow. Oxidative stress plays a critical role during ischemia as well as during the reperfusion phase following ST elevation myocardial infarction (STEMI). We sought to investigate the relationship between no-reflow with paraoxonase-1 (PON-1) activity and oxidative stress markers (total antioxidant capacity (TAC), total oxidant status (TOS), oxidative stress index (OSI), lipid hydro-peroxide (LOOH)) in patients with anterior STEMI undergoing primary percutaneous coronary intervention (PCI). METHODS: In this study, 319 consecutive anterior STEMI patients undergoing primary PCI were prospectively included (mean age 56.5 ± 12.5 years). The patients were divided into two groups as normal flow (n = 231) and no-reflow (n = 88) groups. Serum PON-1 activity was measured spectrophotometrically. TAC and TOS levels were determined by using an automated measurement method. LOOH levels were measured by ferrous oxidation with xylenol orange assay. RESULTS: PON-1 activity and TAC levels were significantly lower and TOS, OSI and LOOH levels were significantly higher in patients with no-reflow compared to normal flow group (p < 0.05, for all). On multivariate logistic regression analysis, PON-1 activity (ß = 0.976, 95% CI = 0.962-0.990, p = 0.001) and OSI (ß = 1.094, 95% CI = 1.042-1.148, p < 0.001) as well as diabetes, infarction time, thrombus score and initial SYNTAX score were independently associated with no-reflow. CONCLUSION: In patients with no-reflow compared with normal flow, oxidants are increased, while serum PON-1 activity and antioxidants are decreased. This result shows that increased oxidative stress has a role in the pathogenesis of no-reflow.

[Correlation between electrocardiogram, myocardial biomarkers and left ventricular dysfunction in acute anterior ST segment elevation myocardial infarction].

OBJECTIVE: To analyze the correlation between ST segment elevation, Q wave and peak biomarkers with left ventricular dysfunction in patients with acute anterior ST elevation myocardial infarction (STEMI). METHODS: A total of 138 consecutive inpatients with acute anterior STEMI, left anterior descending branch as the convict vessel, from January 2009 to January 2012 in our hospital were enrolled in this study. They were divided into reperfusion (n = 92) and non-reperfusion group(n = 46). Clinical data, electrocardiogram, peak biomarkers, type B natriuretic peptide (BNP) were collected by physicians and the patients were followed up three months. RESULTS: The sum of the ST segments elevation, Q waves and Q wave leads in anterior STEMI were positive correlation with the Killip grades, myocardium biomarkers, BNP and left ventricle end diastolic diameters (LVEDD) [γ, 0.52-0.75, P < 0.01], while negative correlation with left ventricle ejection fraction (LVEF) [γ, -0.63--0.95, P < 0.01]. The sum of R wave altitude was negative correlation with myocardium biomarkers, BNP and LVEDD in three months after the onset of STEMI [γ, -0.48--0.79, P < 0.01], while positive correlation with LVEF [γ, 0.73-0.82, P < 0.01]. BNP, one of the best markers of left heart dysfunction, was found to be strongly negative correlation with LVEF in acute stage and three months after the onset of STEMI [γ , -0.92, -0.80, P < 0.01]. CONCLUSION: There are close correlations between electrocardiogram, myocardial biomarkers and left ventricular dysfunction in acute anterior ST segment elevation myocardial infarction, which may be strong predictors for the short-term prognosis.