Parikh, Sahil A.

AbstractThe Society for Cardiovascular Angiography and Interventions (SCAI) Think Tank is a collaborative venture that brings together interventional cardiologists, administrative partners, and select members of the cardiovascular industry community annually for high‐level field‐wide discussions. The 2021 Think Tank was organized into four parallel sessions reflective of the field of interventional cardiology: (a) coronary intervention, (b) endovascular medicine, (c) structural heart disease, and (d) congenital heart disease. Each session was moderated by a senior content expert and co‐moderated by a member of SCAI's Emerging Leader Mentorship program. This document presents the proceedings to the wider cardiovascular community in order to enhance participation in this discussion, create additional dialog from a broader base, and thereby aid SCAI, the industry community and external stakeholders in developing specific action items to move these areas forward.

A 33-year-old male with systemic lupus erythematosus (SLE) presented with acute abdominal pain and was found to have lupus mesenteric vasculitis on imaging and during exploratory laparotomy. Post laparotomy he continued to have persistent nausea and dyspepsia and an electrocardiogram showed evidence of an inferior ST elevation myocardial infarction (STEMI). Emergency cardiac catheterization showed evidence of thrombotic right coronary artery occlusion. His coronaries were otherwise normal with no evidence of underlying coronary artery disease. Extensive workup with trans-esophageal echo, serologies for antiphospholipid antibody syndrome (APS) and bubble study was negative. This effectively ruled out Libman–Sacks endocarditis, APS-induced arterial thrombus and paradoxical emboli as potential causes of his STEMI. By exclusion of other causes, the etiology of his STEMI was felt to be secondary to in-situ coronary artery thrombosis in the setting of active SLE. To the best of our knowledge, this is the first report of a patient with SLE presenting with both lupus mesenteric vasculitis and in-situ coronary arterial thrombosis in the absence of APS.

AbstractAlthough current antiplatelet therapies provide potent antithrombotic effects, their efficacy is limited by a heightened risk of bleeding and failure to affect vascular remodeling after injury. New lines of research suggest that thrombosis and hemorrhage may be uncoupled at the interface of pathways controlling thrombosis and inflammation. Here, as one remarkable example, studies using a novel and highly selective pharmacologic inhibitor of the spleen tyrosine kinase Syk [PRT060318; 2-((1R,2S)-2-aminocyclohexylamino)-4-(m-tolylamino)pyrimidine-5-carboxamide] coupled with genetic experiments, demonstrate that Syk inhibition ameliorates both the acute and chronic responses to vascular injury without affecting hemostasis. Specifically, lack of Syk (murine radiation chimeras) attenuated shear-induced thrombus formation ex vivo, and PRT060318 strongly inhibited arterial thrombosis in vivo in multiple animal species while having minimal impact on bleeding. Furthermore, leukocyte-platelet–dependent responses to vascular injury, including inflammatory cell recruitment and neointima formation, were markedly inhibited by PRT060318. Thus, Syk controls acute and long-term responses to arterial vascular injury. The therapeutic potential of Syk may be exemplary of a new class of antiatherothrombotic agents that target the interface between thrombosis and inflammation.