ABSTRACT
Amyloidosis is characterized by depositing insoluble fibrillar proteins that misfold into beta-pleated sheets. This phenomenon occurs on a systemic or local level and may interfere with the function of various organs, including the heart, kidneys, and liver. Among those presenting with amyloidosis, hepatic, gastrointestinal, renal, cardiac, vitreous, and immunological involvement may occur. These manifestations are linked to several clinical presentations, varying from abdominal pain and hepatomegaly to restrictive cardiomyopathy and chronic renal failure. The two most common types of amyloid proteins are amyloid light chain (AL) and serum amyloid A (AA) proteins. AL produced by immunoglobulin light chains kappa and lambda (κ, λ) circulate systemically and accumulate in organs. At the same time, serum AA proteins are acute-phase reactants seen in infectious, chronic inflammatory states. In an immune-mediated infection such as COVID-19, serum AA levels may be a predictive factor of disease severity and a valuable biomarker to monitor the clinical course of COVID-19 patients. This report highlights a case in which infection with COVID-19 provoked an effective immune response that may have contributed to the accelerated progression of systemic amyloidosis with hepatic involvement. The study further investigates the involvement of AL and AA proteins in COVID-19 infections, including their role in synergistically exacerbating an already grueling clinical course.
ABSTRACT
Coronavirus disease 2019 (COVID-19) is known to primarily have respiratory tract involvement, but thromboembolic complications can occur as well, leading to increased overall mortality seen in these patients. We present a case of a patient infected with COVID-19 who then developed two simultaneous thrombotic events. Our patient is a 57-year-old male who presented to the emergency department with sudden onset dysarthria and left lower extremity weakness. Medical records indicated he recently tested positive for COVID-19 infection 10 days ago. Magnetic resonance imaging (MRI) of the brain revealed an acute right cerebellar infarction as well as acute bilateral thalamic infarcts. Later in the hospital course, computed tomography angiography (CTA) of the chest revealed a right lower lobe segmental pulmonary artery embolism. Patients with COVID-19 have been seen to develop a wide spectrum of thromboembolic manifestations, most commonly being venous thromboembolism. Arterial thrombosis and microvascular disease can be detected as well. Early diagnosis and treatment of clotting disease is essential and may decrease overall mortality in COVID-19-infected patients.
ABSTRACT
Infective endocarditis (IE), commonly caused by Staphylococcus aureus, can affect multiple cardiac structures and lead to significant morbidity and mortality. We present a case of IE with extensive mitral valve involvement causing perforation and hemodynamic compromise. A 66-year-old Caucasian female presented to the emergency department for progressive altered mental status and lethargy. The patient and family denied history of intravenous drug use (IVDU) on interview. Physical exam revealed tachypnea, tachycardia, lethargy, and fluctuance in the right antecubital fossa draining serous fluid. Initial studies revealed a urinary tract infection, patchy bilateral opacities on chest x-ray, hypoxic respiratory failure, elevated lactate and cardiac markers, leukocytosis, and positive urine toxicology for opioid and benzodiazepine. She was intubated and admitted to the ICU, and later developed acute respiratory distress syndrome with requirement for vasopressors. Antibiotics were started, and blood cultures ultimately grew methicillin-sensitive S. aureus. Coronavirus disease 2019 (COVID-19) results were negative. Cardiology was consulted for elevated cardiac markers that were due to myocardial injury in the setting of septic shock. A transthoracic echocardiogram showed a large mobile mass on the anterior mitral leaflet. Further evaluation with transesophageal echocardiogram revealed a large, mobile, and centrally necrotic vegetation on the medial portion of the mitral annulus extending to both the anterior and posterior leaflets. Doppler of the valve showed holosystolic retrograde ejection into the left atrium confirming a perforation. The patient was transferred urgently to a cardiothoracic surgery capable center for operative intervention on the mitral valve. IE is most commonly caused by S. aureus and seen in highest rates among patients with a prosthetic valve, congenital heart disease, and intracardiac device. However, roughly 50% of IE occurs in patients without any valvular disease. Other risk factors include IVDU, valvular disease, and prior history of endocarditis. Clinical diagnosis of IE is made using the Duke's criteria, with echocardiogram and bacteremia playing a major role. The initial management involves empiric antibiotics until a pathogen is identified. Surgical consult is also suggested, and indications for surgery include heart failure due to valve dysfunction, uncontrolled infection, prevention of embolism, and hemodynamic compromise. Prompt recognition and intervention is crucial in the prevention of mortality in patients with IE leading to mitral perforation and hemodynamic compromise.