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A 66-year-old gentleman with no prior cardiac history presented with dyspnea on exertion and chest pain for 1 month. His workup included a transthoracic echocardiogram, which demonstrated findings suggestive of cor triatriatum (C-TAT) with uncertain degree of hemodynamic obstruction. In addition, mild left ventricular systolic dysfunction and segmental wall motion abnormalities suggestive of coronary artery disease were noted. The patient then underwent transesophageal echocardiography (TEE) to define better the structural characteristics and hemodynamic significance of the C-TAT, left and right heart catheterization to assess pressure gradients between the upper and lower left atrial chambers by simultaneous measurement of pulmonary capillary wedge and left ventricular end-diastolic pressures, and coronary angiography. Multiplane 2-dimensional TEE demonstrated an atrial membrane extending from the inferior portion of the interatrial septum to the superior aspect of the lateral atrial wall. This membrane exhibited a medial large oval opening with bidirectional flow and a ≤2 mm Hg gradient. Three-dimensional TEE imaging re-demonstrated this obliquely oriented membrane; however, of most importance, it revealed that the membrane divided the atria into a medial funnel and C-shaped cavity with a large distal oval shape opening and an even larger lateral atrial cavity. These findings were inconsistent with a true C-TAT and rather demonstrated what we defined as a pseudo-C-TAT membrane. Simultaneous right and left heart catheterization confirmed a minimal gradient of 3 to 5 mm Hg and coronary angiography demonstrated severe 3-vessel coronary disease as the primary cause of the patient’s clinical syndrome.

This article presents the case of a 53-year-old man who presented with acute right superficial femoral and popliteal arterial thrombosis for which he underwent an emergent uncomplicated thrombectomy. He denied preceding cardiovascular or neurologic symptomatology and had no history of coronary or peripheral arterial disease, trauma, hypercoagulability, or malignancy. However, he reported having several days of intense emotional stress prior to presentation. His cardiac exam was normal, his electrocardiogram showed normal sinus rhythm and nonspecific ST-T wave abnormalities, and his troponin levels were normal. Transthoracic echocardiography (TTE) revealed a large (2.4 × 2 cm) apical left ventricle (LV) thrombus, LV apical akinesis, and LV ejection fraction of 40% to 45%. Coronary angiography revealed only luminal irregularities. A repeat TTE performed 3 days after initiating unfractionated heparin revealed complete resolution of the LV thrombus. The patient had an uneventful clinical course and was discharged home in stable condition on oral anticoagulants. The lower incidence of LV thrombus in takotsubo cardiomyopathy (TC) of 1.3% in comparison to 4% to 8% in acute myocardial infarction due to coronary artery disease in the current era of early reperfusion may be explained by the lower extent of ischemic myocardial necrosis associated with TC. This case suggests that the lower extent of myocardial necrosis in TC may also lead to faster resolution of LV thrombus. Therefore, earlier follow-up with TTE (within 2 weeks) and shorter duration of anticoagulation (

The patient is a 70-year-old male with no other atherogenic risk factors who presented with an acute coronary syndrome (ACS) of unstable angina subsequently complicated by a non-ST elevation myocardial infarction (NSTEMI). The patient’s presentation posed 3 unique features: (1) cardiac catheterization demonstrated nonobstructive 3-vessel multi-aneurysmal coronary artery disease with sluggish antegrade coronary flow; (2) a nonobstructive aneurysmal dissection flap based on contrast staining of the mid left anterior descending artery, which may have led to in situ nonocclusive thrombosis and distal microvascular embolization; and (3) successful conservative medical therapy of coronary artery aneurysmal disease (CAAD) complicated with ACS. CAAD has an incidence of 1.5% to 4.9% in adults. The most common etiology of CAAD is atherosclerotic coronary artery disease. There are no guidelines for the management of CAAD complicated by ACS, and controversies exist as to whether conservative, catheter-based, or surgical management should be pursued.