Since these miRs have been associated with anxiety and depression, they could provide a mechanism whereby priming of the heart by previous stress causes an increased likelihood of TTS in the future. Conclusion: miR-16 and miR-26a sensitize the heart to TTS-like changes produced by adrenaline. Bioinformatic profiling of miR targets, followed by expression assays and functional experiments, identified reductions of CACNB1 (L-type calcium channel Cavβ subunit), RGS4 (regulator of G-protein signalling 4), and G-protein subunit Gβ (GNB1) as underlying these effects. Decreased contractility after TTS-miRs was reproduced in non-failing human apical cardiomyocytes. They also enhanced the initial positive inotropic effect of adrenaline in basal cells. In vitro miR-16 and/or miR-26a overexpression in isolated apical (but not basal), cardiomyocytes produced strong depression of contraction, with loss of adrenaline sensitivity. Ventricular basal hypercontraction and apical depression were accentuated in miR-transfected animals after induction of TTS. Untreated isolated rat cardiomyocytes were transfected with pre-/anti-miRs and functionally assessed. Methods and results: miR-16 and miR-26a were co-overexpressed in rats with AAV and TTS induced with an adrenaline bolus. We aimed to understand whether recently discovered circulating biomarkers miR-16 and miR-26a, which differentiate TTS from MI at presentation, were mechanistically involved in the pathophysiology of TTS. It is distinguished from myocardial infarction (MI) by a characteristic pattern of ventricular basal hypercontractility with hypokinesis of apical segments, and in the absence of culprit coronary occlusion.

When one component is dominant, symptoms can occur and disease entities and organ systems can suffer. Normal people should have a normal balance of braking and acceleration in their bodies. Aims: Takotsubo syndrome (TTS) is an acute heart failure, typically triggered by high adrenaline during physical or emotional stress. This involves the adrenaline portion of the body and he describes this as the accelerator of the body.

Adrenaline sensitivity syndrome