Faculty Bibliography

Currently, there is no approved guideline regarding management of patients with polycythemia vera (PCV) undergoing percutaneous coronary intervention (PCI) given the low prevalence. Standard maintenance therapy may be inadequate in cases where patients' response to standard treatment show heterogeneity. Approximately 5-10% of patients undergoing PCI are reported to have an additional indication for triple antiplatelet therapy consisting of aspirin, an adenosine diphosphate (ADP)-receptor antagonist and oral anticoagulant. However, considering the higher bleeding risk that arises with triple antiplatelet therapy, physicians act reluctantly in prescribing the regimen. Here, we present a case of subacute stent thrombosis in a patient with PCV prompting the consideration of triple antiplatelet therapy given increased thrombotic risk.

It is vital to recognize correctly, chest pain of cardiac etiology. Most commonly, it is because of blood supply-demand inequity in the myocardium. However, the phenomenon of myocardial bridging as a cause of cardiac chest pain has come to attention reasonably recently. Herein, a coronary artery with a normal epicardial orientation develops a transient myocardial course. If the cardiac muscle burden is substantial, the respective artery gets compressed during each cycle of systole, thereby impeding blood flow in the artery. Hence, myocardial bridging has been attributed to as a rare cause of angina. In this case report, the authors discuss a patient in whom myocardial bridging turned out to be an elusive cause of angina. We wish to underscore the importance of being clinically mindful of myocardial bridging when assessing a patient with angina.

BACKGROUND Femoral neuropathy as a result of retroperitoneal hemorrhage most commonly occurs following pelvic and lower extremity trauma, but has been described to develop as a less frequent complication of anticoagulation. CASE REPORT We present the case of a 64-year-old white woman who was being treated for pulmonary embolism and deep venous thrombosis with enoxaparin. In the course of her treatment, she was noted to be hypotensive, with a sudden drop in hematocrit. She had been previously ambulatory, but noted an inability to move her bilateral lower extremities. A diagnosis of bilateral femoral neuropathy as a result of psoas hematomas caused by enoxaparin was made. Anticoagulation was discontinued and she was treated conservatively, with an excellent outcome. At the time of discharge to a rehabilitation center, she had regained most of the motor strength in her lower extremities. CONCLUSIONS We believe this is the first reported case of bilateral femoral nerve neuropathy following use of enoxaparin. A full neurological examination should always be performed when there is sudden loss of function. The constellation of bilateral groin pain, loss of lower extremity mobility, and decreased hematocrit raised the suspicion of massive blood loss into the cavity/compartment. Thus, a high index of suspicion should be maintained by clinicians when presented with such symptoms and signs, as there can be significant morbidity and mortality when prompt diagnosis is not made.

A 23-year-old African American woman with a past medical history of systemic lupus erythematous (SLE), secondary hypertension, and end stage renal disease (ESRD) on hemodialysis for eight years was stable until she developed symptomatic severe mitral regurgitation with preserved ejection fraction. She underwent a bioprosthetic mitral valve replacement (MVR) at outside hospital. However, within a year of her surgery, she presented to our hospital with NYHA class IV symptoms. She was treated for heart failure but in view of her persistent symptoms and low EF was considered for heart and kidney transplant. This was a challenge in view of her history of lupus. We presumed that her stenosis of bioprosthetic valve was secondary to lupus and renal disease. We hypothesized that her low ejection fraction was secondary to mitral stenosis and potentially reversible. We performed a dobutamine stress echocardiogram, which revealed an improved ejection fraction to more than 50% and confirmed preserved inotropic contractile reserve of her myocardium. Based on this finding, she underwent a metallic mitral valve and tricuspid valve replacement. Following surgery, her symptoms completely resolved. This case highlights the pathophysiology of lupus causing stenosis of prosthetic valves and low ejection cardiomyopathy.