Tricuspid regurgitation following mitral valve replacement: an echocardiographic study.

The development of late tricuspid regurgitation following mitral valve replacement is accompanied by a severe reduction in exercise capacity and a poor functional outcome. In this study, we compared the clinical and echocardiographic characteristics of two matched groups with (n = 13) and without (n = 13) clinically significant tricuspid regurgitation. The preoperative pulmonary artery pressures and symptom durations were similar, but tricuspid regurgitation at palpation was detected only in patients who later developed severe tricuspid regurgitation (5/13 vs. 0/13; p < 0.02). None of the patients had echocardiographic evidence of rheumatic tricuspid valve disease at the time of the study, but the tricuspid annular diameter (3.7 +/- 0.5 cm vs. 3.2 +/- 0.4 cm; p < 0.05) and right ventricular diameter (4.9 +/- 0.4 cm vs. 4.0 +/- 0.8 cm; p < 0.01) were greater in patients who had developed severe late tricuspid regurgitation. Echocardiographic parameters of left ventricular function and Doppler estimated pulmonary artery systolic pressures were similar in the two groups, and no evidence of prosthetic dysfunction or aortic valve disease was found. These results imply that late tricuspid regurgitation following mitral valve replacement develops as a result of dilation of the tricuspid annulus associated with right ventricular decompensation. The persistence of uncorrected tricuspid incompetence would seem to be an important contributory factor, and its accurate detection and correction at the time of initial surgery may prove to be the most effective means of preventing the development of this important complication of mitral valve replacement.

Heterogeneity of auxin-accumulating membrane vesicles from Cucurbita and Zea: a possible reflection of cell polarity.

When microsomes from hypocotyls of Cucurbita pepo L. or coleoptiles of Zea mays L. were centrifuged on dextran-sucrose gradients a heterogeneity of auxin-accumulating vesicles was observed. Vesicles from the top part of the gradient showed saturable, specific accumulation of indole-3-acetic acid with only a small stimulation by phytotropins, and with very few binding sites for 1-N-naphthylphthalamic acid. In the vesicles from the lower part of the gradient, net accumulation of indole-3-acetic acid could be strongly increased by addition of phytotropins; binding of 1-N-naphthylphthalamic acid was high in this region. After two-phase partitioning, both kinds of vesicles were found in the upper-phase membrane fraction considered to be purified plasma membrane. The hypothesis is discussed that vesicles can be separated from the apical and basal parts of the cell's plasmalemma.

The site of leakage of intrafollicular thyroglobulin into the blood stream in simple human goiter.

Serum thyroglobulin is increased in many thyroid diseases, including simple goiter. We followed thyroglobulin levels in 19 patients with diffuse and nodular euthyroid goiters by serial measurements of 80 samples over 2 yr. The large intraindividual variations suggested episodic release of thyroglobulin in this thyroid disease. To test the hypothesis that the phenomenon was due to sporadic release of colloid from diseased follicles, we studied 98 multinodular goiters by conventional histological techniques. Sixty-four surgical samples were auto-radiographed. Focal necrosis of single follicles as well as large necrotic areas, involving multiple follicles together with interstitial stroma, were found in 42% of the goiter specimens. The earliest stage of necrosis was focal death of epithelial cells, often followed by hemorrhages. Through the epithelial gaps, colloid leaked out into the interstitial space. In later stages, granulation tissue containing numerous macrophages invaded damaged follicles. Fibrous scars remained as ultimate witness of repair processes. In one chance observation, acute release of highly labeled thyroglobulin from follicular lumina into the interfollicular interstitium was autoradiographically documented. We conclude that the varying concentrations of thyroglobulin in serum of patients with simple goiter may result from episodic necrosis of follicles, permitting leakage of colloid into the interfollicular space.