Aneurysm of the mitral valve occurs most commonly in association with infective endocarditis of the aortic valve. The probable mechanism of its formation is destruction of the aortic valve which results in a regurgitant jet that strikes the anterior leaflet of the mitral valve, creating a secondary site of infection leading to the development of an aneurysm. Perforation of these aneurysms may occur, resulting in mitral regurgitation and pulmonary edema from a ventricle already volume overloaded from aortic regurgitation. This report describes the clinical and echocardiographic-pathologic findings in five patients with pathologically proven aneurysm of the mitral valve. There are no clinical features that appear specific for this abnormality. The two-dimensional echocardiographic feature that is helpful in the diagnosis is a bulge of the mitral valve leaflet toward the left atrium that persists throughout the cardiac cycle. Preoperative diagnosis is important because a mitral valve aneurysm may produce serious complications and is frequently overlooked during surgery. Repair of the aneurysm may be feasible; otherwise, valve replacement becomes necessary. Careful two-dimensional echocardiographic examination should be done in patients with left-sided infective endocarditis to detect an aneurysm of the mitral valve.
A new TSH immunoenzymometric assay was found to be capable of discriminating between the serum TSH values of normal subjects [2.28 +/- 1.02 (+/-SD); range, 0.6-6.5 microU/ml] and those of clinically euthyroid, antithyroid drug-treated (n = 22) or clinically thyrotoxic (n = 34) patients. While a wide spectrum of basal TSH values was found in the antithyroid drug group [ranging from undetectable (less than 0.05 microU/ml: 57%) to 17.9 microU/ml], all clinically thyrotoxic patients had undetectable values. In 33 patients receiving chronic oral T4 therapy for treatment of goiter (n = 15) or thyroid cancer (n = 18), 48% (6 of 33) had undetectable basal TSH levels and no TSH response to TRH stimulation. Detectable TSH levels were found in 42% (14 of 33), and TRH responsiveness was found in 52% (17 of 33). The TSH response to TRH stimulation was less than 2.0 microU/ml in 7 patients. Serum free T4 index, free T3 index, and free T4 levels and oral T4 dosage were inferior predictors of TRH responsiveness compared to the basal TSH value. No patient receiving more than 0.2 mg T4 daily or having a free T4 index above 18, a free T3 index above 205 or a free T4 level above 3.0 ng/dl had a TSH response to TRH. Seventy-six percent (16 of 21) of the patients, when reevaluated 1-6 weeks after increased oral T4 dosage, had a significant reduction in their serum thyroglobulin level. This was true of both patients with initially detectable (11 of 14) as well as undetectable (5 of 7) basal serum TSH levels. These findings support the concept that subnormal and, for that matter, as yet undetectable levels of circulating TSH may exert stimulatory effects on thyroid tissue.
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