Carlos A. Roldan

Iatrogenic aortic dissection (IAD) is an extremely rare complication of coronary angiography, most often occurring during percutaneous coronary intervention (PCI) and typically resulting from retrograde extension of a coronary artery dissection. The coexistence of IAD with acute coronary syndrome (ACS) presents significant management challenges, with no established guidelines to guide therapy. Management decisions are influenced by several factors, including whether angiography is performed in the setting of stable angina versus ACS, the extent of ischemic myocardium at risk, the patient’s hemodynamic stability, and the extent of aortic involvement - particularly whether the dissection is confined to the aortic root or extends into the ascending aorta by less than or greater than 4 cm. Treatment strategies may include PCI alone for the coronary dissection or urgent surgical repair of the aorta with coronary artery bypass grafting (CABG). The role of off-pump CABG in this context remains poorly defined. We describe a unique case of a patient with severe mid-left anterior descending (LAD) artery disease presenting with a non-ST elevation myocardial infarction (NSTEMI), who developed a type II IAD during diagnostic coronary angiography without associated coronary artery dissection. Prompt recognition, careful imaging with transesophageal echocardiography (TEE) and computed tomography angiography (CTA), and immediate medical stabilization prevented progression of the dissection. This allowed for a successful and uncomplicated off-pump left internal mammary artery (LIMA) CABG to the LAD, resulting in excellent short- and long-term clinical outcomes.

Background: Libman-Sacks endocarditis in patients with systemic lupus erythematosus (SLE) is commonly complicated with embolic cerebrovascular disease (CVD) or valve dysfunction for which high-risk valve surgery is frequently performed. However, the role of medical therapy alone for Libman-Sacks endocarditis and associated acute CVD remains undefined. Objective: To determine in this cross-sectional and longitudinal study if conventional anti-inflammatory and anti-thrombotic therapy may be an effective therapy in SLE patients with Libman-Sacks endocarditis and associated acute CVD. Methods and materials: 17 SLE patients with Libman-Sacks endocarditis detected by two-and-three-dimensional transesophageal echocardiography (TEE) and complicated with acute CVD [stroke/TIA, focal brain injury on MRI, or cognitive dysfunction] were treated with conventional anti-inflammatory and anti-thrombotic therapy for a median of 6 months and then underwent repeat TEE, transcranial Doppler, brain MRI, and neurocognitive testing for re-assessment of Libman-Sacks endocarditis and CVD. Results: Valve vegetations decreased in number, diameter, and area (all p ≤0.01); associated valve regurgitation significantly improved (p = 0.04), and valve thickening did not progress (p = 0.56). In 13 (76%) patients, valve vegetations or valve regurgitation resolved or improved in number and size or by ≥1 degree, respectively, as compared to 4 (24%) patients in whom vegetations or valve regurgitation persisted unchanged or increased in size or by ≥1 degree (p = 0.03). Also, cerebromicroembolism, lobar and global gray and white matter cerebral perfusion, ischemic brain lesion load, and neurocognitive dysfunction resolved or significantly improved (all p ≤0.04). Conclusion: These preliminary data suggest that combined conventional anti-inflammatory and antithrombotic therapy may be an effective treatment for Libman-Sacks endocarditis and its associated CVD and may obviate the need for high-risk valve surgery.

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.

In the section of Results of the original published version of the above article the bold text emphasis under the following section should have been delete