Faculty Bibliography

BACKGROUND:Despite the expanded application of thoracic endovascular aortic repair (TEVAR) in patients with significant cardiac comorbidities, the effect of decreased left ventricular ejection fraction (EF) on outcomes remains unknown. The aim of this study was to compare outcomes in patients with normal and abnormal EFs undergoing TEVAR for type-B aortic dissection (TBAD). METHODS:The Vascular Quality Initiative database was reviewed from 2012 to 2020. Patients were categorized into severely reduced (EF ≤ 30%), reduced (EF 30-50%) and normal EF (EF>50%). Baseline characteristics, procedural details and 18-month outcomes were compared. Multivariable logistic regression identified factors associated with mortality, major adverse cardiac events (MACEs), and aortic-related reintervention. RESULTS:Of 1,993 patients, 38 (2%) and 208 (10%) patients had severely reduced ejection fraction (SREF) and reduced ejection fraction (REF). Patients with abnormal EF were more likely to have cardiac comorbidities and be prescribed angiotensin-converting enzyme inhibitors and anticoagulants. Perioperatively, patients with SREF were more likely to experience mortality (13.2% vs. 6.7% vs. 4.4%, P = 0.018), MACE (26.3% vs. 11.5% vs. 8%, P < 0.001), hemodialysis (13.5% vs. 5% vs. 2.9%, P = 0.001) and aortic related reintervention (21.1% vs. 13% vs. 10%, P = 0.041), compared to REF and normal ejection fraction (NEF) patients. However, these associations were not present on multivariable analysis. At 18 months, mortality was significantly higher in patients with SREF, which was confirmed on multivariable analysis, but depressed EF was not associated with increased aortic reintervention compared to NEF. CONCLUSIONS:SREF was not independently associated with perioperative mortality or MACE compared to NEF. REF had similar risk of morbidity and mortality compared to NEF in both the perioperative and early postoperative periods. TEVAR-related complications were similar among the cohorts. As such, TEVAR may be offered to appropriately selected patients regardless of EF.

BACKGROUND:Male sex, elevated troponin levels, and elevated D-dimer levels are associated with more complicated COVID-19 illness and greater mortality; however, while there are known sex differences in the prognostic value of troponin and D-dimer in other disease states, it is unknown whether they exist in the setting of COVID-19. OBJECTIVE:We assessed whether sex modified the relationship between troponin, D-dimer, and severe COVID-19 illness (defined as mechanical ventilation, ICU admission or transfer, discharge to hospice, or death). METHODS:We conducted a retrospective cohort study of patients hospitalized with COVID-19 at a large, academic health system. We used multivariable regression to assess associations between sex, troponin, D-dimer, and severe COVID-19 illness, adjusting for demographic, clinical, and laboratory covariates. To test whether sex modified the relationship between severe COVID-19 illness and troponin or D-dimer, models with interaction terms were utilized. RESULTS:Among 4,574 patients hospitalized with COVID-19, male sex was associated with higher levels of troponin and greater odds of severe COVID-19 illness, but lower levels of initial D-dimer when compared with female sex. While sex did not modify the relationship between troponin level and severe COVID-19 illness, peak D-dimer level was more strongly associated with severe COVID-19 illness in male patients compared to female patients (males: OR=2.91, 95%CI=2.63-2.34, p<0.001; females: OR=2.31, 95%CI=2.04-2.63, p<0.001; p-interaction=0.005). CONCLUSION/CONCLUSIONS:Sex did not modify the association between troponin level and severe COVID-19 illness, but did modify the association between peak D-dimer and severe COVID-19 illness, suggesting greater prognostic value for D-dimer in males with COVID-19.

We report what appears to be the first case of biopsy-proven nonvalvular endocarditis with biventricular apical infected thrombi. A 47-year-old man presented with hypoxic respiratory failure from a multilobar pneumonia due to methicillin-resistant Staphylococcus aureus (MRSA). Transthoracic echocardiography and cardiac magnetic resonance imaging revealed biventricular apical masses suggestive of nonvalvular endocarditis with infected thrombi. Given concern for ongoing septic embolization to the lungs and brain despite appropriate antimicrobial therapy, the masses were surgically resected. Culture and histopathology confirmed MRSA-positive infected thrombi. In this case report, we highlight the differential diagnosis of apical masses and the role of multimodality imaging.

Coronary artery disease (CAD) is a known potential complication of thoracic radiation treatment that typically affects the proximal segments of the coronary arteries, requiring coronary artery bypass grafting (CABG). We present a case of acute coronary syndrome occurring in a 57-year-old man with prior thoracic radiation therapy following resection of a chest wall chondrosarcoma. Coronary angiogram demonstrated significant areas of stenosis in the left main coronary artery (LMCA) and ostial left anterior descending (LAD) coronary artery. The patient was also found to have atretic bilateral internal mammary arteries as a consequence of his radiation therapy, rendering them unsuitable as grafts. Percutaneous coronary intervention (PCI) was thus performed with a successful outcome. To our knowledge, this is the first case of radiation-induced CAD of the LMCA with atretic internal mammary arteries treated successfully with PCI.

Primary cardiac tumors are a rare set of benign and malignant neoplasms found in the heart or pericardium. We describe a patient presenting with nonspecific symptoms and ultimately diagnosed with primary cardiac non-Hodgkin's lymphoma (PCL). Our patient had extensive tumor in the right ventricle, which extended into the right atrium and right ventricular outflow tract. The tumor also encased the right coronary artery, which manifested as ischemic changes on EKG and cardiac MRI. The patient was treated with chemotherapy and achieved complete remission, with dramatic and full resolution of the mass on repeat echocardiography in nine weeks. More studies are needed to understand the optimal management and prognosis of patients with PCL.

Pulmonary fibrosis is characterized by an inflammatory response that includes macrophages, neutrophils, lymphocytes, and mast cells. The purpose of this study was to evaluate whether mast cells play a role in initiating pulmonary fibrosis. Pulmonary fibrosis was induced with bleomycin in mast-cell-deficient WBB6F1-W/W(v) (MCD) mice and their congenic controls (WBB6F1-(+)/(+)). Mast cell deficiency protected against bleomycin-induced pulmonary fibrosis, but protection was reversed with the re-introduction of mast cells to the lungs of MCD mice. Two mast cell mediators were identified as fibrogenic: histamine and renin, via angiotensin (ANG II). Both human and rat lung fibroblasts express the histamine H1 and ANG II AT1 receptor subtypes and when activated, they promote proliferation, transforming growth factor β1 secretion, and collagen synthesis. Mast cells appear to be critical to pulmonary fibrosis. Therapeutic blockade of mast cell degranulation and/or histamine and ANG II receptors should attenuate pulmonary fibrosis.