Cardiovascular System 1 out of 434
A 51-year-old man comes to the physician for 2 months of intermittent low-grade fever, malaise, and joint pain. He has a history of recurrent dental abscesses requiring drainage but has otherwise been healthy. His temperature is 38.3°C (100.9°F) and pulse is 112/min. Physical examination shows a new holosystolic murmur in the left midclavicular line that radiates to the axilla. There are linear reddish-brown lesions underneath the nail beds and tender violaceous nodules on the bilateral thenar eminences. Two sets of blood cultures grow Streptococcus mutans. A transthoracic echocardiogram shows moderate regurgitation of the mitral valve. Which of the following mechanisms is most likely directly involved in the pathogenesis of this patient's valvular condition?
Sterile platelet thrombi deposition
Nonbacterial thrombotic endocarditis (NBTE) results from sterile (i.e., noninfectious) platelet thrombi deposition on the cardiac valves. NBTE most commonly affects the mitral valve; however, it typically manifests with signs and symptoms of systemic embolization rather than mitral valve dysfunction, which is seen here. This patient presents with fever and bacteremia, which is highly suggestive of infectious endocarditis. Moreover, NBTE usually affects patients with advanced malignancy or systemic lupus erythematosus, neither of which this patient has. Leaflet calcification and fibrosisLeaflet calcification and fibrosis are pathologic changes seen in mitral stenosis (MS) due to rheumatic fever (RF). While MS does produce a murmur in the left midclavicular line, it is a diastolic murmur that follows an opening snap. Moreover, this patient has a TTE with evidence of mitral regurgitation, not stenosis. While acute RF can also manifest with joint pain, fever, and malaise, MS would not be expected until 10 to 20 years after the original illness, and blood cultures would be negative. Finally, this patient presents with subacute infective endocarditis, which individuals with MS are at an increased risk of developing, but calcification and fibrosis play no direct part in the pathogenesis of this condition. Antibody cross-reaction
Antibody cross-reaction due to molecular mimicry is the presumed pathogenic mechanism of rheumatic fever (RF). Acute RF may manifest with mitral regurgitation, joint pain, skin manifestations, and fever, all of which this patient has. However, RF also manifests with typical skin findings, such as erythema marginatum and subcutaneous nodules, which are not seen here. Moreover, this patient has no history of sore throat or group A streptococcal infection, which typically precede RF. Furthermore, blood cultures are negative in RF as it is an immunologic, non-infectious condition. Myxomatous degeneration
Myxomatous degeneration of the mitral valve is the underlying pathology of mitral valve prolapse (MVP). MVP is a risk factor for infective endocarditis, which this patient has, but it is not directly involved in the pathogenesis of the disease. It is most often an incidental finding on auscultation in asymptomatic patients. This patient presents with a new murmur on auscultation, making a pre-existing MVP unlikely. Fibrin clot formation
Fibrin clot formation is a key step in the pathogenesis of subacute infective endocarditis. First, endothelial damage occurs (in native valves this is typically due to turbulent blood flow), followed by adherence of platelets and fibrin to the damaged valve areas. These initially sterile platelet-fibrin aggregates can become infected by bacteria circulating in the blood, forming vegetations. This patient is at increased risk for streptococcal bacteremia due to recurrent dental abscesses. Microbial adherence to the platelet-fibrin nidus is mediated by interaction of bacterial cell wall components (e.g., dextrans) and the valvular endothelium. Fibrin clots encase this vegetation and subsequent destruction of the affected valves leads to valvular insufficiency, as seen here. This patient's physical examination findings of splinter hemorrhages and Osler nodes represent areas of microembolization of vegetation material.
Infective endocarditis should always be considered in a patient with a fever of unknown origin. Coagulative necrosis
Coagulative necrosis is the mechanism that causes cell death in myocardial infarction (MI). Acute mitral regurgitation, as seen in this patient, can be a complication of MI. However, further symptoms such as left-sided chest pain, dyspnea, nausea, and diaphoresis would be expected. This patient presents instead with fever, bacteremia, and skin findings that are highly suggestive of infectious endocarditis.
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