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Background Orodispersible tablet (ODT) is a different tablet formulation that disperse upon contact with the moist mucosal surfaces of the oral cavity and quickly release its components before swallowing; thus drug dissolution and absorption, as well as onset of clinical effect, can be obtained conveniently easily and quickly. Recently, Ticagrelor 90 mg ODT has become available and bioequivalence studies on healthy volunteers documented its effectiveness with consequent approval by the European Medicine Agency. It is unknown whether Ticagrelor ODT might be an effective route of drug administration in high-risk acute coronary syndrome (ACS) patients. Purpose The aim of the present study is to evaluate the superiority in platelet inhibition with 180 mg Ticagrelor loading dose (LD) administered as ODT as compared with standard (coated table) Ticagrelor formulation, among 130 ACS patients undergoing PCI. Methods Patients presenting within STEMI or very high-risk NSTEMI referred for immediate (<2 hours) angiography were randomly assigned to receive ODT or standard ticagrelor LD. Platelet reactivity was assessed by Platelet Reactivity Units (PRU) VerifyNow 1, 2, 4 and 6 hours after ticagrelor LD. The primary study endpoint was residual platelet reactivity 1 hour after Ticagrelor LD. Safety endpoints were major bleedings and other in-hospital ticagrelor administration-related adverse events across the two different regimens of Ticagrelor administration. Potential morphine-ticagrelor interaction was assessed by stratified randomization according to morphine use. An interim analysis was planned after the enrollment of 50% (n=65 patients) of the entire study population. The study was supported by an unrestricted grant from AstraZeneca. Results At the interim analysis, the 2 study group were well matched according to all the baseline characteristics (such as age, sex, diabetes mellitus, chronic renal failure, STEMI at presentation, Killip class, multivessel disease, number of stents implanted, and morphine use). Main pharmacodynamic data are depicted in Figure 1. One hour after LD, PRU (97±99 vs 115±92; p=0.40) was numerically lower, but not statistically different, in the ODT group as compared to standard ticagrelor group. The percentage of platelet inhibition was 55±44% vs 42±44% (p=0.21) in the 2 groups. No significant difference was observed between patients receiving ODT or standard ticagrelor LD regarding in-hospital adverse events or drug side-effects. The study enrollment is ongoing, and final results will be presented at the Congress. Conclusions ODT administration might represent the most convenient way of treating lying supine ACS patients in the ambulance, emergency room or on the cath lab. Moreover, in patients with difficulties in swallowing ODT represent an easy way of ticagrelor administration. Figure 1 Funding Acknowledgement Type of funding source: Private grant(s) and/or Sponsorship. Main funding source(s): AstraZeneca S.P.A.

A 44-year-old woman with obstetric antiphospholipid syndrome (APS) presented to our institution with suspected non ST-elevation myocardial infarction (NSTEMI). Shortly after coronary angiography, she developed diplopia, hypotension and chest pain with inferior ST elevation in 12-lead ECG. According to multidisciplinary evaluation, she promptly underwent systemic thrombolysis, with clinical and haemodynamic improvement. Eventually, a diagnosis of catastrophic APS was made, with multiorgan ischemic involvement confirmed by blood examinations and multimodal imaging techniques. A pluridisciplinary approach was central to define optimal medical therapy and in-hospital management that lead to clinical condition improvement at discharge.In this case, catastrophic APS was triggered or worsened by catheters insertion and invasive manoeuvres within the arterial lumen during coronary angiography. Recognizing catastrophic APS and its potential triggers, can be helpful to deliver prompt and accurate medical assistance. Moreover, in APS patients undergoing coronary angiography, preventive strategies are important to prevent possible unfavourable evolution in catastrophic APS.

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Introduction Vasovagal syncope is traditionally considered a benign condition due to parasympathetic nervous system activation. Here is a case of reflex syncopal episodes that triggered recurrent Takotsubo Syndrome (TS) with life–threatening presentation. Report of a Case A 71-year-old female presented to the Emergency Department (ED) complaining with dyspnoea and chest pain developed half an hour after a vasovagal syncope. Her past medical history was consistent with arterial hypertension, dyslipidaemia, and well-tolerated reflex syncopal episodes since she was a child. At hospital admission, a 12-leads ECG showed T-wave inversion in anterior leads while transthoracic echocardiogram (TTE) showed hypokinesia of the mid-apical segments, reduced left ventricular ejection fraction (LVEF) [40%], and severe mitral regurgitation (MR). Blood tests revealed increased hs-troponin I values [peak value: 1500 ng/L]. A coronary angiography (CA) was thus performed in the suspect of NSTEMI, showing non obstructive coronary disease. A diagnosis of TS was eventually made with ECG normalisation and resolution of echocardiographic abnormalities at 6 month follow-up. Five years later, the patients presented to the ED because of a new syncopal episode followed by severe pulmonary oedema. Since the presence of electrocardiographic T-wave inversion, apical segments akinesia and elevated hs-troponin I were consistent with NSTEMI, a CA was performed revealing (again!) normal coronary vessels. A suspect of TS relapse was thus made. Three months after discharge, ECG and echocardiogram were normal and a syncope diagnostic work–up was suggested. A 24/h ambulatory blood pressure monitoring demonstrated normal pressure values and a tilt test confirmed the well-established history of reflex syncope showing a remarkable cardioinhibitory response. A pacemaker implant was thus indicated. Discussion TS is a heart syndrome characterized by transient contractile dysfunction historically related to catecholamine activation of alpha and beta receptors. While sympathetic system involvement in the development of TS is clearly established, new evidence is emerging about the vagal role in the etiopathogenesis of the disease. Although syncopal episodes could be related to TS, because of LVOT obstruction or major arrhythmias, according to our experience, TS may be triggered by vagal hypertonus [i.e., after vasovagal syncopal episodes]. In similar situation, the implantation of a pace-maker could be considered to prevent future dangerous complications related to recurrent reflex syncope even if well tolerated by the patients. Conclusion In our experience, recurrent episodes of TS appeared triggered by reflex syncope. A condition traditionally considered benign may instead have life-threatening consequences. Moreover, the role of parasympathetic and vagal tone in the development of TS needs further investigation that may lead to the design of new strategies of clinical diagnosis and management.