T-wave inversions in inferior ST-elevation myocardial infarction - A case of "inferior Wellens sign".

BACKGROUND: Although T-wave inversions are nonspecific, in the appropriate clinical setting, the pattern of negative biphasic T-waves or T-wave inversion in V2-V3 can indicate critical stenosis of the left anterior descending coronary artery (i.e. "anterior Wellens sign"). Recently tall T-waves in V2-V3 have been reported in association with posterior reperfusion (i.e."posterior Wellens sign"). Less commonly, negative biphasic T-waves or T-wave inversions in the inferior leads have been reported in association with critical stenosis of the right coronary artery (RCA) or left circumflex artery (LCx). We present a case where T wave inversions (i.e. "inferior Wellens sign") and a tall T-wave in V2-V3 (i.e. "posterior Wellens sign") preceded the development of an inferior-posterior ST-elevation myocardial infarction (STEMI). CASE REPORT: A 37-year-old man presented to the Emergency Department for one day of chest pain. On arrival, his pain had resolved, and his 1st ECG showed inverted/biphasic T-waves in lead III and aVF and a tall T wave in V2-V3. Three- and one-half hours after arrival, his chest pain returned and his ECG showed an inferior-posterior STEMI. WHY SHOULD AN EMERGENCY PHYSICIAN BE AWARE OF THIS?: New, focal T-wave inversions in an anatomic distribution may be an early warning sign of impending myocardial infarction. Careful attention to the T-waves during asymptomatic periods may assist in identifying patients that may have critical stenosis of an underlying coronary artery. In this case, T-wave inversions in the inferior leads, along with a tall T-wave in V2-V3, were seen prior to the development of an inferior-posterior STEMI.

Keratin 16 regulates innate immunity in response to epidermal barrier breach.

Mutations in the type I keratin 16 (Krt16) and its partner type II keratin 6 (Krt6a, Krt6b) cause pachyonychia congenita (PC), a disorder typified by dystrophic nails, painful hyperkeratotic calluses in glabrous skin, and lesions involving other epithelial appendages. The pathophysiology of these symptoms and its relationship to settings in which Krt16 and Krt6 are induced in response to epidermal barrier stress are poorly understood. We report that hyperkeratotic calluses arising in the glabrous skin of individuals with PC and Krt16 null mice share a gene expression signature enriched in genes involved in inflammation and innate immunity, in particular damage-associated molecular patterns. Transcriptional hyper-activation of damage-associated molecular pattern genes occurs following de novo chemical or mechanical irritation to ear skin and in spontaneously arising skin lesions in Krt16 null mice. Genome-wide expression analysis of normal mouse tail skin and benign proliferative lesions reveals a tight, context-dependent coregulation of Krt16 and Krt6 with genes involved in skin barrier maintenance and innate immunity. Our results uncover a role for Krt16 in regulating epithelial inflammation that is relevant to genodermatoses, psoriasis, and cancer and suggest a avenue for the therapeutic management of PC and related disorders.