Faculty Bibliography

BACKGROUND:Gross angioinvasion with intraluminal tumor thrombus is rarely seen in thyroid cancer, with few cases reported in the literature. METHODS:We report an insular carcinoma of the thyroid displaying this aggressive local invasion and angioinvasion of the internal jugular chain. Complete surgical removal of the intraluminal disease, regional metastasis, and primary tumor was carried out. RESULTS:Adjuvant external beam radiation therapy and iodine-131 were administered, and the patient died with pulmonary metastases 30 months after surgery. No locoregional recurrence was noted at last follow-up. CONCLUSIONS:Treatment of insular carcinoma of the thyroid with invasion of the internal jugular vein is amenable to surgical resection. Postoperative radioactive iodine and external beam radiotherapy can achieve locoregional disease control and prolonged survival.

BACKGROUND:Unlike myxomatous degeneration in Marfan syndrome, which has been reported to result from a mutation in the gene that codes for the extracellular structural protein fibrillin, no specific molecular abnormality has been documented to be the underlying cause of myxomatous degeneration in mitral valve prolapse syndrome (MVPS). The present study examined the distribution of fibrillin and other extracellular matrix proteins in patients with isolated MVPS. METHODS:Mitral valve leaflets from 7 MVPS patients and 5 rheumatic heart disease (RHD) patients were characterized immunohistochemically for fibrillin, elastin, collagen I, and collagen III distribution, and compared with five normal mitral valves. RESULTS:In normal mitral valve leaflets immunostaining for fibrillin, elastin, collagen I, and collagen III revealed a fibrillary and laminar pattern in the atrialis and the spongiosa. In addition, both the collagens were present in the ventricularis, and the coarse bundles in the fibrosa exhibited alternating bandlike collagen I immunoreactivity. The staining patterns of fibrillin, elastin, and collagens I and III revealed distinctly different distribution in MVPS relative to the normal and RHD leaflets. MVPS leaflets in areas of myxoid degeneration displayed a more diffuse, weaker, and nonlaminar pattern of staining for fibrillin. Similar, but less severe abnormality of elastin, collagen I, and collagen III was also observed. Unlike diffuse abnormality in MVPS, the disruption of extracellular proteins in RHD only occurred at the site of the inflammatory damage, but the overall architecture was preserved. CONCLUSIONS:The results of the current study suggest a primary role for abnormal fibrillin and other matrix proteins in producing myxoid degeneration of mitral valve leaflets in MVPS.

BACKGROUND:Apoptosis is common in advanced human atheroma and contributes to plaque instability. Because annexin V has a high affinity for exposed phosphatidylserine on apoptotic cells, radiolabeled annexin V may be used for noninvasive detection of apoptosis in atherosclerotic lesions. METHODS AND RESULTS/RESULTS:Atherosclerotic plaques were produced in 5 rabbits by deendothelialization of the infradiaphragmatic aorta followed by 12 weeks of cholesterol diet; 5 controls were studied without manipulation. Animals were injected with human recombinant annexin V labeled with technetium-99m before imaging. Aortas were explanted for ex vivo imaging, macroautoradiography, and histological characterization of plaque. Radiolabeled annexin V cleared rapidly from the circulation (T1/2, alpha 9 and beta 46 minutes). There was intense uptake of radiolabel within lesions by 2 hours; no uptake was seen in controls. The results were confirmed in the ex vivo imaging of the explanted aorta. Quantitative annexin uptake was 9.3-fold higher in lesion versus nonlesion areas; the lesion-to-blood ratio was 3.0+/-0.37. Annexin uptake paralleled lesion severity and macrophage burden; no correlation was observed with smooth muscle cells. DNA fragmentation staining of apoptotic nuclei was increased in advanced lesions with evolving necrotic cores, predominantly in macrophages; the uptake of radiolabel correlated with the apoptotic index. CONCLUSIONS:Because annexin V clears rapidly from blood and targets apoptotic macrophage population, it should constitute an attractive imaging agent for the noninvasive detection of unstable atherosclerotic plaques.

PURPOSE OF REVIEW/OBJECTIVE:Myocardial contrast echocardiography (MCE) has evolved into an important clinical tool for imaging coronary microcirculation. It can be used to delineate the spectrum of perfusion derangements that characterize acute myocardial infarction. RECENT FINDINGS/RESULTS:Presently, MCE uses microcirculatory perfusion as the basis to distinguish myocardial necrosis and viability in the post-infarct stage. Its future role may expand to image cellular integrity, inflammation, and angiogenesis, all of which contribute to the pathophysiology of the myocardial infarction. SUMMARY/CONCLUSIONS:This review provides an update of the current role and future clinical applications of MCE in acute myocardial infarction.