Zwolle risk score predicts contrast-induced acute kidney injury in STEMI patients undergoing PCI.

OBJECTIVE: Contrast-induced acute kidney injury (CI-AKI) is a common complication in patients with acute ST-elevation myocardial infarction (STEMI) undergoing primary percutaneous coronary intervention (PCI). The Mehran risk score was defined originally in elective PCI and may be predictive of CI-AKI. The aim of the present study was to investigate whether the Zwolle score predicts CI-AKI in patients with acute STEMI undergoing primary PCI. PATIENTS AND METHODS: We analyzed the data of 314 consecutive patients (mean age 56.3 ± 11.4 years) with acute STEMI undergoing primary PCI. The study population was divided into two groups according to CI-AKI development. The Mehran score, Zwolle score, baseline characteristics, and in-hospital outcomes were recorded. RESULTS: Patients with CI-AKI had higher Mehran and Zwolle scores. In a receiver operating characteristic (ROC) curve analysis, high area under the curve (AUC) values were determined for Zwolle and Mehran scores (0.85 and 0.79, respectively) for CI-AKI development. A Zwolle score greater than 2 predicted CI-AKI with a sensitivity of 76.3 % and a specificity of 75.4 %. A Mehran score greater than 5 predicted CI-AKI with a sensitivity of 71.1 % and a specificity of 73.6 %. CONCLUSION: Zwolle score predicts CI-AKI slightly better than the Mehran score in patients with STEMI undergoing primary PCI. This simple score can be used at the catheterization laboratory for risk stratification for the development of CI-AKI.

Does pantoprazole protect against reperfusion injury following myocardial ischemia in rats?

BACKGROUND: Myocardial ischemia is inadequate perfusion due to reduced blood flow. Sudden onset of reperfusion could result with damage to the myocytes that have not been affected during ischemia called ischemia reperfusion (I/R) injury. Extracellular accumulation of H+ ions resulting in tissue acidosis is one of the underlying mechanisms. Inhibition of myocardial H+/K+-ATPase, namely proton pump, may lead to intracellular acidification via decreasing the extracellular H+ transport. AIM: The aim of this study is to investigate the effects of a proton pump inhibitor pantoprazole in intact rat I/R models. MATERIALS AND METHODS: A total of 30 adult male Wistar albino rats weighing 200-300 g were studied. Rats were allocated into four groups: sham (n=6), ischemia (n=8), control (n=8), and pantoprazole (n=8). Left anterior descending coronary artery was occluded for 30 minutes and then reperfused for two hours. Pantoprazole was administered via jugular vein at the dose of 9 mg/kg starting from 30 minutes before ischemia, to the first 30 minutes of reperfusion. Haemodynamic parameters were recorded and serum CK-MB levels were measured. After reperfusion, heart was removed for the measurement of myocardial infarct size. Myocardial infarct area was measured using triphenyltetrazolium chloride (TTC) staining technique. Myocardial infarction size were expressed as the percentage of the total left ventricular weight. RESULTS: Compared with other groups, plasma concentrations of CK-MB at the end of ischemia and reperfusion and myocardial infarct size were significantly lower in pantoprazole group (p < 0.008). CONCLUSIONS: Pantoprazole preconditioning induces delayed cardioprotection in intact rat I/R model, which may be triggered via H+/K+-ATPase ion channels.

Relation of interatrial duration and p wave terminal force as a novel indicator of severe mitral regurgitation.

OBJECTIVES: Interatrial duration is defined as prolonged p wave on electrocardiogram. p waves with a negative terminal phase recorded in V1 enclosing an area of one small square on the electrocardiogram is significantly and strongly correlated with interatrial duration. The aim of study was to investigate whether interatrial duration with p terminal force can be used as reflection of echocardiographic severity of mitral regurgitation. MATERIALS AND METHODS: Sixty two consecutive patients with mitral regurgitation. were prospectively studied. Age/gender matched 57 subjects who had normal mitral structure and did not have mitral regurgitation. Patients with mitral regurgitation referred to a single cardiac center for echocardiography and who met the entry criteria documented moderate or severe mitral regurgitation with sinus were included. The interatrial duration was defined on the routine 12-lead electrocardiogram (50 mm/s, 10 mm/mV) using the greatest duration of p waves from D2, D3, AVF and V1. RESULTS: There was a positive correlation between interatrial duration (>/= 110 ms) and effective regurgitant orifice (r = 0.3, p < 0.001). However, left atrial diameter and brain natriuretic peptide were significantly higher in cases with mitral regurgitation. There was also strong correlation between interatrial duration (>/= 110 ms) and p terminal force and left atrial diameter. ROC analysis revealed that interatrial duration of > 110 msec. could predict of severe mitral regurgitation with 88% sensitivity and 100% specificity. CONCLUSIONS: Severe mitral regurgitation, left atrial diameter was correlated with p terminal force and interatrial duration. Significant interatrial duration (>/= 110 ms) and p terminal force might be considered as novel indicators of severe mitral regurgitation.