Aortic arch anomalies are rare congenital malformations with an incidence of approximately 1-3%. Right aortic arch is an anatomical variant with an incidence of <0.1% associated with various congenital heart diseases. We present a case of a 26-year-old female patient with a right aortic arch with a common origin of right carotid and left innominate artery.

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Introduction: Mechanical circulatory support (MCS) is known to potentiate hemolytic anemia. Nevertheless, patients are also at an increased risk of spontaneous bleeding due to anticoagulation or post-procedural complication. We present two cases of acute anemia due to spontaneous retroperitoneal bleeding following insertion of the Impella assist device. Case Presentation: Two male patients aged 65 and 74 presented with cardiogenic shock secondary to ischemic cardiomyopathy with a low ejection fraction of 10% and 15%). Both patients initially had an intra-aortic balloon pump (IABP) inserted. Because of progressively deteriorating hemodynamics, IABP was switched to the Impella 5.5 device through the axillary artery. Following insertion of the Impella, they developed anemia requiring multiple blood transfusions. Despite repositioning of Impella, hemoglobin continued to drop prompting further workup. CT abdomen/pelvis revealed left retroperitoneal hematoma. CT angiogram showed active bleeding from the left L3 lumbar artery in one patient and multiple foci of active arterial extravasation in the other patient. Coil embolization was performed, achieving hemostasis and stabilization of hemoglobin levels in both patients. Discussion: Hemolytic anemia associated with the use of the Impella that improves with repositioning or device removal is well known and documented. However, patients with MCS are also at increased risk of spontaneous bleeding due to procedural injury and the use of anticoagulation. We report 2 cases with retroperitoneal bleeding from the lumbar artery diagnosed a few days after the placement of Impella. The occurrence of retroperitoneal hemorrhage was possibly spontaneous due to anticoagulation along with Impella-induced hemolysis resulting in acute anemia. Neither patient had any vascular access through the left groin making post-procedural complications less likely. The concealed nature and non-specific symptoms of retroperitoneal bleed can lead to a delay in diagnosis. Early identification and control of bleeding can prevent fatal outcomes. Conclusion: Our cases highlight the importance of clinicians having a broad differential and low threshold to investigate other causes of anemia in patients with MCS.

Case Presentation: A 67-year-old female presented to the office with exertional dyspnea, atypical chest pain, palpitations, and dizziness. She had a past medical history of hypertension, hyperlipidemia, mitral valve prolapse, and moderate mitral regurgitation. Her EKG identified multiple PVCs requiring the placement of a Holter monitor, a PVC burden of 31,441 beats (15%) was captured with variable morphology. TTE showed mild global hypokinesis of the left ventricle and ejection fraction (EF) of 40%. Coronary arteries were normal on cardiac catheterization. Cardiac magnetic resonance revealed epicardial late gadolinium enhancement suggestive of fatty infiltration of the distal lateral wall of the left ventricle (LV) indicative of Arrhythmogenic left ventricular cardiomyopathy (ALVC). The basal anterolateral wall of the LV appeared thin and dyskinetic, and the right ventricle was normal in size and function. Optimal medical therapy was initiated with metoprolol, sacubitril/valsartan, dapagliflozin, and spironolactone. A dual-chamber ICD was placed for primary prevention. Over time with medical management, her PVC burden reduced, and LVEF improved to 50%. A multigene panel for cardiomyopathies identified a mutation in titin (TTN) gene variant of unknown significance. Discussion: Previously thought to affect only the right ventricle, arrhythmogenic cardiomyopathy (ACM) is a rare genetic disease characterized by fibrofatty replacement of the ventricular myocardium. ALVC refers to the predominant LV dominant phenotype of this disease. The most frequent genetic mutations occur in the genes plakophilin (PKP2), desmoplakin (DSP), and desmoglein (DSG2). However, we report a case of ALVC in the setting of titin (TTN) gene variant, which is a gene usually implicated in dilated cardiomyopathy. However, the clinical significance of the TTN gene variant identified in our patient remains unclear as more studies are needed to link it to the phenotypic findings.

Case Presentation: A 65-year-old female with a history of hypertension, hyperlipidemia, microscopic colitis, fibromyalgia, left hand dupuytren's contractures, Grave’s disease and seronegative rheumatoid arthritis presented to the outpatient office for evaluation of right sided stabbing and heavy chest pain. ECG showed sinus bradycardia without any ST segment changes. She had an Echo and exercise stress Echo prior to her office visit. Her echo showed normal left ventricular size and systolic function with no regional wall motion abnormality and thickened aortic valve with mild aortic stenosis (peak transvalvular gradient 9.9 mmHg and mean 5.9 mmHg). Her stress echo was negative for ischemia although submaximal (exercised for 6.05 minutes, achieving only 75% MPHR, and double product of 18720). It was then decided to pursue a coronary CTA given the suboptimal nature of her stress testing and intermediate pretest probability of coronary artery disease. This revealed mild-to-moderate non-obstructive CAD and thickening of her left coronary cusp. The thickening was concerning for Libman-Sacks endocarditis vs native aortic valve thrombosis (see figure). Her Antinuclear antibody (ANA) titers was 1280. She was started on therapeutic anticoagulation with a plan for repeat imaging in six months. Discussion: Coronary cusp thickening represents a variety of differentials and has comparable structural and clinical qualities. Atypical chest pain in our patient led to the incidental finding of left coronary cusp thickening. In the presence of elevated ANA and her autoimmune disorder, Libman-Sacks endocarditis vs native aortic valve thrombosis was suspected hence the initiation of anticoagulation. Both have a propensity for fatal outcomes including, but not limited to myocardial infarction, embolic events, cardiogenic shock, or death. Follow-up imaging with a resolution of thrombus would confirm the diagnosis of native aortic valve thrombus.