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A 22–year–old man, without prior cardiological history, was waiting for a concert to start many hours in summer heat. Suddenly he started to feel chest pain, dyspnea, and palpitations. Electrocardiogram (EKG), registered from first aid responders, showed a ST elevation in V1–V3 leads and ventricular repolarization alterations in inferior leads. The patient was brought to Emergency department (ED) where a new EKG resulted normalized, blood test samples showed High Sensitive Troponin T (HsTn) 35 ng/L (at plateau in three seriate measures), serum creatinine 2.0 mg/dL, total Creatine Kinase 646U/L, Ck–MB 10.6 ng/mL, Reactive C Protein (RCP) 1.2 mg/dl. The toxicological evaluation was negative. Transthoracic Echocardiography (TTE) did not show any regional ventricular kinesis alterations nor valvular defects, global systolic function was preserved. A Coronary Computed Tomography (CT) scan showed an intramyocardial bridge on Anterior Descending (DA) Coronary Artery associated to 7 mm pericardial effusion without coronary stenosis. A Cardiac Magnetic Resonance (CMR) with gadolinium was performed, which did not show (in T2 mapping sequences) oedema nor Late Gadolinium Enhancement (LGE). Considering a coexistence of Brugada syndrome pattern at EKG, an Ajmaline testing was performed, which resulted negative. Discussion: Dehydration due to any intake of water after standing many hours in summer heat could have been the trigger for a vasospasm of DA that in this patient has a partially intramyocardial course. This anatomical finding was not known until CT scan was performed. Our diagnostic hypothesis of a vasospasm on DA is supported by EKG alterations and elevation enzymes of myocardionecrosis, in absence of any coronary stenosis. Elevated creatinine values in the absence of other renal concomitant comorbidities were suggestive for acute dehydration too. Differential diagnosis took also into consideration myo–pericarditis, especially for the pericardial effusion finding revealed by CT scan: this diagnosis was not confirmed through CMR but also by the evolution of clinical conditions of our patient. We discharged the patient, asymptomatic with normalized renal function after some intravenous hydration and we prescribed a calcium channel blocker. At a follow up visit, three months after the acute event, our patient was in good clinical condition and denied occurrence of any other similar events.

Gliadins are among the most important protein fractions affecting wheat baking quality, but they are also plant allergens and a cause of celiac disease or food intolerance. Therefore, we investigated how gliadin immunoreactivity and dough rheological properties are influenced by thioredoxin, a regulatory disulfide protein that can reduce disulfide bonds, a typical motive in many allergenic proteins. Ten winter wheat genotypes of different qualities were analyzed. Reduction by thioredoxin strongly (>50%) decreased gliadin immunoreactivity as estimated by enzyme-linked immunosorbent assay with immunoglobulin E (IgE) sera from allergic patients and standard antigliadin antibodies but did not significantly affect dough rheological properties. Most parameters from the Brabender extensigraph were only slightly lower. Simultaneously, the farinograph curve exhibited a drawdown dislocation, possibly due to increased water absorption by modified flour, and dough consistency visibly improved. Results suggest that thioredoxin may be a universal natural beneficial modifier, able to significantly decrease gliadin immunoreactivity (hence its potential allergenicity) without decreasing the unique technological properties of wheat flour.