Several repolarization risk markers have been used thus far, but these neglect the contributions of conduction abnormalities in the form of slowing and dispersion. A major challenge for clinicians in managing this condition is the difficulty in predicting the subset of patients who will suffer from life-threatening ventricular arrhythmic events. Evidence from computational modelling, pre-clinical and clinical studies illustrates that molecular abnormalities found in BrS lead to alterations in excitation wavelength (k), which ultimately elevates arrhythmic risk. The predominant electrophysiological mechanism underlying BrS remains disputed, commonly revolving around the three main hypotheses based on abnormal repolarization, depolarization or current-load match. Diagnosis is based on the presence of a spontaneous or drug-induced coved-type ST segment elevation. Originally believed to be predominantly associated with mutations in SCN5A encoding for the cardiac sodium channel, mutations of 18 genes other than SCN5A have been implicated in the pathogenesis of BrS to date. While the STEMI patient must be offered undelayed reperfusion therapy, the non-ischaemic ST elevation one should be kept away from the haemorrhagic risk of a useless invasive procedure.īrugada syndrome (BrS) is an inherited ion channel channelopathy predisposing to ventricular arrhyth-mias and sudden cardiac death. Yet many confounding factors are able to limit the diagnostic sensibility of ST elevation (as for example its customary absence in the conventional leads in some cases of circumflex artery occlusion, or the casual mutual cancellation of the transmural ST vectors from opposite ventricular walls), the accuracy of the electrocardiographic localisation of the occlusion site (due to coronary anatomic variants, concomitant new or old coronary lesions elsewhere, previous coronary artery bypass grafts), as well as its specificity for transmural ischaemia (by virtue of a well-known manifold of non-ischaemic causes). The early forthcoming of ST elevation during an acute transmural ischaemic episode, as well as the wide availability of the electrocardiogram, make it an invaluable diagnostic tool. Aside from the classical ST segment elevation myocardial infarction (STEMI) pattern, a handful of distinctive non-ST elevation appearances of the acute coronary occlusion also need imperative reperfusion therapy, thus qualifying themselves as STEMI equivalents. The geography of the ST segment elevations usually enables one to identify the culprit artery and to guess its likely occlusion site, as pivotal pieces of the necessary vital risk forecasting, along with somehow expected occurring arrhythmias. As the earliest indirect sign of an acute coronary occlusion arriving against non-operative collateral heart vessels, the unabating ST segment elevation accounts for the acute coronary syndrome asking for mandatory and immediate reperfusion therapy.
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