En mann i 50-årene med brystsmerter og synkope.

BACKGROUND: A man in his fifties with hypertension and no other previous health problems was admitted to the hospital after frequent episodes of retrosternal squeezing chest pain, and an episode of syncope. A recent computer tomography coronary angiography demonstrated normal coronary arteries with no atherosclerosis. CASE PRESENTATION: During admission, the patient developed several episodes of chest pain lasting five to fifteen minutes followed by non-sustained ventricular tachycardia, and initially no ST elevation in the electrocardiogram (ECG). He had normal findings on ECG and magnetic resonance imaging of the heart. During hospitalisation, ST elevations in the ECG were observed in relation to chest pain. Due to ST elevation, invasive coronary angiography was performed, revealing a suspected culprit lesion in the left anterior descending artery, treated with percutaneous coronary intervention (PCI). Despite PCI, he had persistent episodes of chest pain with ST elevation and non-sustained ventricular tachycardia. Vasospastic angina was suspected. INTERPRETATION: The clinical presentation is classical for vasospastic angina. After treatment with calcium channel blocker together with long-acting nitrate, there were no new episodes of chest pain or non-sustained ventricular tachycardia. Because of non-sustained ventricular tachycardia with haemodynamic instability and syncope, an implantable cardioverter-defibrillator was implanted.

Deletion of aquaporin-4 increases extracellular K(+) concentration during synaptic stimulation in mouse hippocampus.

The coupling between the water channel aquaporin-4 (AQP4) and K(+) transport has attracted much interest. In this study, we assessed the effect of Aqp4 deletion on activity-induced [K(+)]o changes in acute slices from hippocampus and corpus callosum of adult mice. We show that Aqp4 deletion has a layer-specific effect on [K(+)]o that precisely mirrors the known effect on extracellular volume dynamics. In CA1, the peak [K(+)]o in stratum radiatum during 20 Hz stimulation of Schaffer collateral/commissural fibers was significantly higher in Aqp4 (-/-) mice than in wild types, whereas no differences were observed throughout the [K(+)]o recovery phase. In stratum pyramidale and corpus callosum, neither peak [K(+)]o nor post-stimulus [K(+)]o recovery was affected by Aqp4 deletion. Our data suggest that AQP4 modulates [K(+)]o during synaptic stimulation through its effect on extracellular space volume.