Data Availability StatementThe datasets used and/or analysed during the current study are available from the corresponding author on reasonable request. stability Anethol of the dissection flap. Cardiac magnetic resonance imaging, however, confirmed the persistence of a small thrombotic formation in LV apex, thus double antithrombotic therapy with warfarin and clopidogrel was instituted. The patient remained asymptomatic during the follow-up period but was advised to suspend his job and physical activities. Conclusion Current guidelines do not discuss anticoagulant therapy in the setting of Anethol TBAD and large randomized trials are lacking. Despite it is generally considered unsafe to administer anticoagulants in patients with TBAD, we present a case in which triple antithrombotic therapy was well tolerated and did not lead to progression of the intimal flap after 6?months. Keywords: Anethol Aortic dissection, Coronary artery disease, Intraventricular thrombus, Anticoagulation Background The incidence of acute aortic dissection in the general population is estimated to be about 2.5% per 100,000 person-years . Uncomplicated patients with acute type B aortic dissection are often successfully managed conservatively with a lifelong anti-impulse therapy and serial imaging evaluation, in order to minimize aortic wall stress and to detect extension of the Anethol dissection or aneurysm formation respectively. Surgical or Anethol endovascular treatment is usually reserved for patients developing complications related to dissection. Even though current guidelines consider patent false lumen as a predictor of aortic growth and poor outcome, there is no mention about the management of antithrombotic or anticoagulant therapy in the setting of aortic dissection . This lack of data is usually further attested by a relevant interdisciplinary expert consensus on management of type B aortic dissection giving no information about anticoagulation/antiplatelet therapy in this scenario, also due to the large heterogeneity existing among Rabbit polyclonal to ISCU different studies . This substantial gap of evidence compels the physicians to deal with such critical setting without a shared or evidence-based strategy to be pursued. We report a case of acute TBAD diagnosed along with new-diagnosis of ischemic cardiomyopathy complicated by left ventricular thrombotic formation and patent foramen ovale (PFO) in the setting of multi-infarct encephalopathy. This case outlines the relevance of an individual patient-tailored therapy and further stresses the need of future studies and a consensus about the role of anticoagulant therapy in patients with acute aortic dissection. Case presentation A 51-year-old man was referred to this hospital for a follow-up cardiology visit after a right cerebellar ischemia occurred 1 month prior to presentation, from which the patient had rapidly recovered without residual deficits. He had no history of hypertension, arthritis, uveitis, mouth ulcers nor crystalline lens subluxation. He had been smoking until 2?years before presentation; his anamnesis was unfavorable for alcohol or illicit drug abuse and his family history was unremarkable. His only medication was acetylsalicylic acid. During the previous hospital stay, extensive examinations had been performed, including electrocardiogram (ECG), lipid panel, transthoracic echocardiography (TTE) and doppler ultrasonographic assessment of the supra-aortic vessels and of the lower extremities veins, all of which resulted unremarkable. A few days after hospital discharge, the patient had suffered a single episode of intense subjective vertigo, tinnitus, confusion and orthostatic imbalance, which had resolved spontaneously in about 20?min without referring to any physician. On presentation the patient was asymptomatic, eupneic and apyretic. His blood pressure was 155/90?mmHg on both arms. On physical examination a moderate pectus excavatum was noticed. Cardiac tones were valid and regular, and a third tone was heard. Radial pulses were symmetrical and valid, while the femoral and pedidial pulses were slightly attenuated. The ECG revealed a sinus rhythm at.