Proximal complete occlusion of right coronary artery presenting with precordial ST-segment elevation: A case report.

BACKGROUND: It is well known that cardiologists empirically judge the culprit lesion of acute ST-segment elevation myocardial infarction (STEMI) according to the corresponding electrocardiographic leads. However, In addition to the obstruction of left anterior descending (LAD) coronary artery, rare cases with the occlusion of proximal right coronary artery (RCA) and/or isolated right ventricular (RV) branch showed the ST-segment elevation in precordial leads V1-V3 as well. CASE SUMMARY: We reported a patient complaining of acute chest pain and suffering ventricular fibrillation (VF) on admission. The electrocardiogram (ECG) showed mild ST-segment elevation in precordial leads V1-V3 and V4R. Bedside echocardiography displayed normal left ventricular ejection fraction and slight RV dilation. Proximal occlusion of nondominant RCA was confirmed by coronary angiography and urgent percutaneous coronary intervention (PCI) to RCA successfully resolved the chest pain and ST-segment elevation. CONCLUSION: Undoubtedly, coronary angiography is usually the definite measurement for the diagnosis of culprit lesion. However, bedside echocardiography, ST-segment features in left and right precordial leads, and heart rate will be the additional information for judging ST-segment elevation in precordial leads V1-V3 resulting from occlusion of RCA or LAD.

Barium chloride impaired Kir2.1 inward rectification in its stably transfected HEK 293 cell lines.

Kir2.1 channel is a typical inward rectified channel with little outward currents when the membrane depolarized. Barium blocks the inward Kir2.1 currents in a voltage-dependent manner. However, in this study we found that barium would impair the rectification and open Kir2.1 outward currents at a depolarized voltage, causing increment of outward current amplitudes by 43±7% (n=5, P<0.01) after 200s barium application. In the meanwhile, a higher barium concentration did block the outward currents by 17.5±4.3% (n=4, P<0.01) and temporarily twisted current upward tendency. The increment was likely barium specific since both calcium and Kir2.1 specific blocker, Chloroethylclonidine (CEC), did not enhance the current amplitudes. The rectification of Kir2.1 was not recovered by washing barium off, which suggested a non-competitive mechanism. Since the currents occurred at phase 1, 2 of cardiac action potential, it would likely shorten the action potential plateau and it would decrease QT duration in electrocardiography (ECG).