IntroductionA rare electrocardiographic finding of hyperkalemia is ST segment elevation or the so called 'pseudoinfarction' pattern. It has been suggested that hyperkalemia causes the 'pseudoinfarction' pattern not only through its direct myocardial effects, but also through other mechanisms, such as anoxia, acidosis, and coronary artery spasm.Case presentationA 33-year-old Caucasian woman with insulin-treated diabetes presented with continuous epigastric pain of four hours duration. Her coronary heart disease risk factors apart from diabetes included hypercholesterolemia and smoking. Her initial electrocardiogram revealed ST segment elevation in the anteroseptal leads consistent with anterior myocardial infarction. Blood tests revealed hyperglycemia, hyperkalemia, metabolic acidosis and urine ketones, while a bed-side cardiac echocardiogram showed no segmental wall motion abnormality. We provisionally diagnosed diabetic ketoacidosis that was possibly precipitated by acute myocardial infarction, as there were findings in favor of (epigastric pain, electrocardiogram pattern, presence of 3 coronary heart disease risk factors) and against (young age, normal echocardiogram) the diagnosis of acute myocardial infarction. We performed cardiac angiography in order to exclude an anterior acute myocardial infarction, which could lead to myocardial damage and possible severe complications should there be a delay in treatment. Angiography revealed normal coronary arteries. During the procedure, ST segment elevation in the anteroseptal leads was still present in our patient's electrocardiogram results.ConclusionST segment elevation is a rare manifestation of hyperkalemia. In our patient, coronary spasm did not contribute to such an electrocardiography finding.

Fib, CRP, IL-6, and CP levels alter in patients with severe unstable angina. However, only CP levels were related to 12-month follow-up prognosis.

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Renal sympathetic innervation plays an important role in blood pressure regulation. Gradual activation of renal sympathetic efferent nerves enhances renin release, promotes sodium and water re-absorption, and reduces renal blood flow and glomerular filtration rate. On the other hand, activation of renal afferent sympathetic nerves induced by renal injury results in central sympathetic activation. This reciprocal relationship between the kidneys and the brain is involved in the pathogenesis of hypertension and other disease conditions characterized by sympathetic overactivity. Renal sympathetic nerve ablation has been recently introduced for the treatment of resistant hypertension. This review aims to provide the pathophysiological basis of renal nerve ablation for the attenuation of sympathetic overactivity.

Reported is a technique that was used to treat a distal left anterior descending (LAD) perforation in a patient undergoing percutaneous coronary intervention (PCI) for distal LAD total occlusion. The perforation was successfully treated by re-occluding the LAD with implantation of a polytetrafluoroethylene (PTFE)-covered stent in a diagonal branch extending to the LAD (side branch graft stenting technique) delivered using the dual catheter technique. This approach is proposed as an alternative bail-out technique that can be used in cases where other treatment options for coronary perforation are either unavailable or potentially not successful, especially during PCI for total occlusions, where the disadvantage of main vessel occlusion is already present.