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.

Breast dynamic contrast-enhanced examinations with fat suppression: are contrast-agent uptake curves affected by magnetic field inhomogeneity?

OBJECTIVES: To investigate the effect of magnetic field heterogeneity in breast dynamic contrast-enhanced examinations with fat saturation (DCE-FS). METHODS: The magnetic field was mapped over the breasts in ten patients. DCE-FS was undertaken at 1.5 T with fast spoiled gradient echoes and spectrally selective fat saturation. Signal intensity was calculated for T1 values 25-1,200 ms both on and off resonance, and results were verified with a test object. Clinical examinations were evaluated for the predicted effects of field heterogeneity. RESULTS: Magnetic field was found to vary by 3.6 ± 1.2 ppm over the central transaxial slice and 5.1 ± 1.5 over the whole breast volume (mean ± standard deviation). Computer simulations predict a reduction in the dynamic range if field heterogeneity leads to unintended water suppression, and distortion to CA uptake curves due to fat suppression failure (for fat containing pixels). A compromise between dynamic range and fat saturation performance is required. Both water suppression and fat suppression failure are apparent in clinical examinations. CONCLUSION: Magnetic field heterogeneity is likely to reduce the sensitivity of DCE-FS by distorting the CA uptake curves because of fat suppression failure (for fat containing pixels) and by reducing the dynamic range because of unintended water suppression. KEY POINTS: • Magnetic field heterogeneity is significant in breast magnetic resonance. • Contrast-agent uptake curves are distorted by a non-uniform magnetic field. • Radiologist must be aware of possibility of distortion to interpret uptake curves correctly. • Compromise between fat suppression and dynamic range is required.

Successful stenting of catheter-induced unprotected left main coronary artery dissection.

Catheter-induced left main coronary artery (LMCA) dissection is a dramatic, although uncommon complication of diagnostic coronary angiography and requires prompt treatment. We describe a case of iatrogenic occlusive dissection of the LMCA during coronary angiography, treated by subsequent percutaneous recanalisation.

Late stent thrombosis, endothelialisation and drug-eluting stents.

Drug-eluting stents (DES) significantly reduce the risk of restenosis after percutaneous coronary revascularisation, but an increased risk of late stent thrombosis (LST) has been put forward as a major safety concern. Meta-analysis of clinical trials, however, does not support this caveat. Even so, many interventional cardiologists think that LST is associated with DES and related to delayed endothelialisation. This hypothesis is based on autopsy studies and clinical intracoronary angioscopy. In autopsy studies, differences between endothelialisation of DES and baremetal stents (BMS) have been reported. Most preclinical studies, however, have failed to show any significant differences in endothelialisation between DES and BMS. Our own studies, using the porcine coronary artery model, also suggest that DES show no differences in re-endothelialisation. However, DES do delay vascular healing and induce endothelial dysfunction. This paper will review clinical and animal studies which consider re-endothelialisation and LST. (Neth Heart J 2009;17:177-81.).