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Cavernous transformation of the portal vein secondary to tumor thrombosis of hepatocellular carcinoma: spiral CT visualization of the collateral vessels (2000)

Song, Bin ; Min, Pengqui ; Oudkerk, M. ; [et al.]

Springer

Abdominal imaging 25 (2000), S. 385-393

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ISSN: 1432-0509

Keywords: Key words: Portal venous system—Cavernous transformation—Collateral circulation—Computed tomography, spiral.

Source: Springer Online Journal Archives 1860-2000

Topics: Medicine

Notes: Abstract Background: We investigated the constituting collateral vessels in cavernous transformation of the portal vein (CTPV) caused by tumor thrombosis of hepatocellular carcinoma (HCC) by using contrast-enhanced spiral computed tomographic (CT) examination. Methods: Fifty-four histopathologically proven HCC patients with tumor thrombosis-induced CTPV were retrospectively included and assigned to cirrhosis negative (n= 31) and positive (n= 23) groups. Another 15 cirrhotic patients with portal hypertension but no HCC and CTPV were used for comparison. Standardized dual-phase contrast-enhanced spiral CT was performed for all patients. CT appearances of the collateral vessels of CTPV were observed, and their visualization rates were analyzed. Results: Biliary (cystic and paracholedochal veins) and gastric (left and right gastric veins) branches of the portal vein were the most frequently visualized collateral vessels of CTPV. There was a marked difference in CT visualization rates for biliary branches between patients with and without CTPV (83–94% vs. 0). No difference existed in visualization rates for gastric branches across the three groups (77–87% for left gastric, 58–61% for right gastric vein). Conclusions: Biliary and gastric branches of the portal vein are the major collateral vessels of CTPV. The intergroup differences in CT visualization rates may provide clues to the roles that they might play in the hemodynamic adaptation process of CTPV.

Type of Medium: Electronic Resource

URL: http://dx.doi.org/10.1107/s002610000057

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Multiethnic Exome-Wide Association Study of Subclinical Atherosclerosis [Original Articles] (2016)

Natarajan, P., Bis, J. C., Bielak, L. F., Cox, A. J., Dorr, M., Feitosa, M. F., Franceschini, N., Guo, X., Hwang, S.-J., Isaacs, A., Jhun, M. A., Kavousi, M., Li-Gao, R., Lyytikainen, L.-P., Marioni, R. E., Schminke, U., Stitziel, N. O., Tada, H., van Setten, J., Smith, A. V., Vojinovic, D., Yanek, L. R., Yao, J., Yerges-Armstrong, L. M., Amin, N., Baber, U., Borecki, I. B., Carr, J. J., Chen, Y.-D. I., Cupples, L. A., de Jong, P. A., de Koning, H., de Vos, B. D., Demirkan, A., Fuster, V., Franco, O. H., Goodarzi, M. O., Harris, T. B., Heckbert, S. R., Heiss, G., Hoffmann, U., Hofman, A., Išgum, I., Jukema, J. W., Kahonen, M., Kardia, S. L. R., Kral, B. G., Launer, L. J., Massaro, J., Mehran, R., Mitchell, B. D., Mosley, T. H., de Mutsert, R., Newman, A. B., Nguyen, K.-d., North, K. E., OConnell, J. R., Oudkerk, M., Pankow, J. S., Peloso, G. M., Post, W., Province, M. A., Raffield, L. M., Raitakari, O. T., Reilly, D. F., Rivadeneira, F., Rosendaal, F., Sartori, S., Taylor, K. D., Teumer, A., Trompet, S., Turner, S. T., Uitterlinden, A. G., Vaidya, D., van der Lugt, A., Volker, U., Wardlaw, J. M., Wassel, C. L., Weiss, S., Wojczynski, M. K., Becker, D. M., Becker, L. C., Boerwinkle, E., Bowden, D. W., Deary, I. J., Dehghan, A., Felix, S. B., Gudnason, V., Lehtimaki, T., Mathias, R., Mook-Kanamori, D. O., Psaty, B. M., Rader, D. J., Rotter, J. I., Wilson, J. G., van Duijn, C. M., Volzke, H., Kathiresan, S., Peyser, P. A., ODonnell, C. J., CHARGE Consortium

American Heart Association (AHA)

In: Circulation: Cardiovascular Genetics

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Publication Date: 2016-12-21

Description: Background— The burden of subclinical atherosclerosis in asymptomatic individuals is heritable and associated with elevated risk of developing clinical coronary heart disease. We sought to identify genetic variants in protein-coding regions associated with subclinical atherosclerosis and the risk of subsequent coronary heart disease. Methods and Results— We studied a total of 25 109 European ancestry and African ancestry participants with coronary artery calcification (CAC) measured by cardiac computed tomography and 52 869 participants with common carotid intima–media thickness measured by ultrasonography within the CHARGE Consortium (Cohorts for Heart and Aging Research in Genomic Epidemiology). Participants were genotyped for 247 870 DNA sequence variants (231 539 in exons) across the genome. A meta-analysis of exome-wide association studies was performed across cohorts for CAC and carotid intima–media thickness. APOB p.Arg3527Gln was associated with 4-fold excess CAC ( P =3 x 10 – 10 ). The APOE 2 allele (p.Arg176Cys) was associated with both 22.3% reduced CAC ( P =1 x 10 – 12 ) and 1.4% reduced carotid intima–media thickness ( P =4 x 10 – 14 ) in carriers compared with noncarriers. In secondary analyses conditioning on low-density lipoprotein cholesterol concentration, the 2 protective association with CAC, although attenuated, remained strongly significant. Additionally, the presence of 2 was associated with reduced risk for coronary heart disease (odds ratio 0.77; P =1 x 10 – 11 ). Conclusions— Exome-wide association meta-analysis demonstrates that protein-coding variants in APOB and APOE associate with subclinical atherosclerosis. APOE 2 represents the first significant association for multiple subclinical atherosclerosis traits across multiple ethnicities, as well as clinical coronary heart disease.

Keywords: Cardiovascular Disease, Primary Prevention, Genetic, Association Studies, Genetics, Computerized Tomography (CT)

Print ISSN: 1942-325X

Electronic ISSN: 1942-3268

Topics: Medicine

Published by American Heart Association (AHA)

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