Contemporary review on spontaneous coronary artery dissection: insights into the angiographic finding and differential diagnosis.

Spontaneous coronary artery dissection (SCAD), although in the majority of cases presents as an acute coronary syndrome (ACS), has different pathophysiology from atherosclerosis that influences specific angiography findings and enables most patients to be solved by optimal medical therapy rather than percutaneous coronary intervention (PCI). Therefore, accurate diagnosis is essential for adequate treatment of each patient as management of SCAD differs from that of ACS of atherosclerotic aetiology. So far, invasive coronary angiography remains the most important diagnostic tool in suspected SCAD. However, there are ambiguous cases that can mimic SCAD. In this review, the authors summarize current knowledge about the diagnostic algorithms, particularly angiographic features of SCAD, pitfalls of angiography, and the role of intracoronary imaging in the context of SCAD diagnosis. Finally, apart from the pathognomonic angiographic features of SCAD that are thoroughly discussed in this review, the authors focus on obscure angiography findings and findings that can mimic SCAD as well. Differential diagnosis and the timely recognition of SCAD are crucial as there are differences in the acute and long-term management of SCAD and other causes of ACS.

Early graft thrombosis due to antithrombin III deficiency following CABG.

The serine protease inhibitor antithrombin III (AT-III), an α2-globulin synthesized in the liver and endothelial cells, is the principal in vivo inhibitor of blood coagulation inactivating mainly thrombin. AT-III deficiency presents a rare hereditary or acquired disorder that most often comes to light when a patient suffers recurrent venous thrombosis and pulmonary embolism. Triggers for the onset of the thrombosis include various mechanisms such as pregnancy, delivery, surgery, trauma, and contraceptive pill use. Decreased response to heparin may be the first sign of AT-III deficiency. Since heparin is a conditio sine qua non for cardiopulmonary bypass, rapid consumption of AT-III promoted by heparin may lead to systemic thrombosis. The effect of heparin on graft patency after CABG in patients with AT-III deficiency, particularly with respect to early graft thrombosis, has not been fully investigated. The early detection and timely treatment of this disorder may impact perioperative morbidity. We present a case of simultaneous thrombosis of three venous grafts after elective coronary artery bypass surgery in a patient with AT-III deficiency.