JOSE EDUARDO KRIEGER
Projetos de Pesquisa
Unidades Organizacionais
Departamento de Cardio-Pneumologia, Faculdade de Medicina - Docente
Instituto do Coração, Hospital das Clínicas, Faculdade de Medicina
LIM/13 - Laboratório de Genética e Cardiologia Molecular, Hospital das Clínicas, Faculdade de Medicina - Líder
Instituto do Coração, Hospital das Clínicas, Faculdade de Medicina
LIM/13 - Laboratório de Genética e Cardiologia Molecular, Hospital das Clínicas, Faculdade de Medicina - Líder
2 resultados
Resultados de Busca
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- Multi-ancestry genome-wide gene-sleep interactions identify novel loci for blood pressure(2021) WANG, Heming; NOORDAM, Raymond; CADE, Brian E.; SCHWANDER, Karen; WINKLER, Thomas W.; LEE, Jiwon; SUNG, Yun Ju; BENTLEY, Amy R.; MANNING, Alisa K.; ASCHARD, Hugues; KILPELAINEN, Tuomas O.; ILKOV, Marjan; BROWN, Michael R.; HORIMOTO, Andrea R.; RICHARD, Melissa; BARTZ, Traci M.; VOJINOVIC, Dina; LIM, Elise; NIERENBERG, Jovia L.; LIU, Yongmei; CHITRALA, Kumaraswamynaidu; RANKINEN, Tuomo; MUSANI, Solomon K.; FRANCESCHINI, Nora; RAURAMAA, Rainer; ALVER, Maris; ZEE, Phyllis C.; HARRIS, Sarah E.; MOST, Peter J. van Der; NOLTE, Ilja M.; MUNROE, Patricia B.; PALMER, Nicholette D.; KUHNEL, Brigitte; WEISS, Stefan; WEN, Wanqing; HALL, Kelly A.; LYYTIKAINEN, Leo-Pekka; CONNELL, Jeff O.; EIRIKSDOTTIR, Gudny; LAUNER, Lenore J.; VRIES, Paul S. de; ARKING, Dan E.; CHEN, Han; BOERWINKLE, Eric; KRIEGER, Jose E.; SCHREINER, Pamela J.; SIDNEY, Stephen; SHIKANY, James M.; RICE, Kenneth; CHEN, Yii-Der Ida; GHARIB, Sina A.; BIS, Joshua C.; I, Annemarie Luik; IKRAM, M. Arfan; UITTERLINDEN, Andre G.; AMIN, Najaf; XU, Hanfei; LEVY, Daniel; HE, Jiang; LOHMAN, Kurt K.; ZONDERMAN, Alan B.; RICE, Treva K.; SIMS, Mario; WILSON, Gregory; SOFER, Tamar; RICH, Stephen S.; PALMAS, Walter; YAO, Jie; GUO, Xiuqing; I, Jerome Rotter; BIERMASZ, Nienke R.; MOOK-KANAMORI, Dennis O.; MARTIN, Lisa W.; BARAC, Ana; WALLACE, Robert B.; GOTTLIEB, Daniel J.; KOMULAINEN, Pirjo; HEIKKINEN, Sami; MAGI, Reedik; MILANI, Lili; METSPALU, Andres; STARR, John M.; MILANESCHI, Yuri; WAKEN, R. J.; GAO, Chuan; WALDENBERGER, Melanie; PETERS, Annette; STRAUCH, Konstantin; MEITINGER, Thomas; ROENNEBERG, Till; VOLKER, Uwe; DORR, Marcus; SHU, Xiao-Ou; MUKHERJEE, Sutapa; HILLMAN, David R.; KAHONEN, Mika; WAGENKNECHT, Lynne E.; GIEGER, Christian; GRABE, Hans J.; ZHENG, Wei; PALMER, Lyle J.; LEHTIMAKI, Terho; GUDNASON, Vilmundur; MORRISON, Alanna C.; PEREIRA, Alexandre C.; FORNAGE, Myriam; PSATY, Bruce M.; DUIJN, Cornelia M. van; LIU, Ching-Ti; KELLY, Tanika N.; EVANS, Michele K.; BOUCHARD, Claude; FOX, Ervin R.; KOOPERBERG, Charles; ZHU, Xiaofeng; LAKKA, Timo A.; ESKO, Tonu; NORTH, Kari E.; DEARY, Ian J.; SNIEDER, Harold; PENNINX, Brenda W. J. H.; GAUDERMAN, W. James; RAO, Dabeeru C.; REDLINE, Susan; HEEMST, Diana vanLong and short sleep duration are associated with elevated blood pressure (BP), possibly through effects on molecular pathways that influence neuroendocrine and vascular systems. To gain new insights into the genetic basis of sleep-related BP variation, we performed genome-wide gene by short or long sleep duration interaction analyses on four BP traits (systolic BP, diastolic BP, mean arterial pressure, and pulse pressure) across five ancestry groups in two stages using 2 degree of freedom (df) joint test followed by 1df test of interaction effects. Primary multi-ancestry analysis in 62,969 individuals in stage 1 identified three novel gene by sleep interactions that were replicated in an additional 59,296 individuals in stage 2 (stage 1 + 2 P-joint < 5 x 10(-8)), including rs7955964 (FIGNL2/ANKRD33) that increases BP among long sleepers, and rs73493041 (SNORA26/C9orf170) and rs10406644 (KCTD15/LSM14A) that increase BP among short sleepers (P-int < 5 x 10(-8)). Secondary ancestry-specific analysis identified another novel gene by long sleep interaction at rs111887471 (TRPC3/KIAA1109) in individuals of African ancestry (P-int = 2 x 10(-6)). Combined stage 1 and 2 analyses additionally identified significant gene by long sleep interactions at 10 loci including MKLN1 and RGL3/ELAVL3 previously associated with BP, and significant gene by short sleep interactions at 10 loci including C2orf43 previously associated with BP (P-int < 10(-3)). 2df test also identified novel loci for BP after modeling sleep that has known functions in sleep-wake regulation, nervous and cardiometabolic systems. This study indicates that sleep and primary mechanisms regulating BP may interact to elevate BP level, suggesting novel insights into sleep-related BP regulation.
- Familial hypercholesterolemia and cardiovascular disease in older individuals(2021) COUTINHO, Elaine R.; MINAME, Marcio H.; ROCHA, Viviane Z.; BITTENCOURT, Marcio S.; JANNES, Cinthia E.; TADA, Mauricio T.; LIMA, Isabella R.; SALGADO FILHO, Wilson; CHACRA, Ana P.; PEREIRA, Alexandre C.; KRIEGER, Jose E.; SANTOS, Raul D.Background and aims: Familial hypercholestemlemia (FH) is characterized by high LDL-cholesterol (LDL-C) and early atherosclerotic cardiovascular disease (ASCVD). With a lipid lowering therapy (LLT), most individuals with FH may have a longer ASCVD-free survival. However, there is scant data about older individuals with FH. Methods: We compared characteristics of genetically defined FH older individuals with age-matched non-FH counterparts. Results: From 4111 genotyped individuals, 462 older than 60 years were included (198 positive and 264 negative for FH variants). There were no differences regarding median age [%25; 75%] 66.0 (62.0; 71.0) and 66.0 (62.2; 71.0) years, p = 0.68 for FH and non-FH, respectively. In both groups, there was a higher frequency of females, however, there were more males in the FH group 37.4% vs. 24.2%, p = 0.002. No differences were seen between FH and non-FH in LLT use: 88.5% vs. 91.5%, p = 0.29. Despite a longer LLT duration in FH patients (with 11.0 (7.0; 20.0) vs. 7.0 (3.0; 13.0) years, p < 0.001), treatment was started late in both groups: at 54.0 (47.0; 61.0) and 59.0 (52.0; 64.0) years, p < 0.001, in FH and non-FH, respectively. FH had greater frequencies of previous and early ASCVD (40.9% vs. 27.3%, p = 0.002, and 22.2% vs. 9.0%, p < 0.001). In FH, male sex [HR (95%C01 2.67 (1.50-4.73), p = 0.001, and LLT onset age 0.96 (0.93-0.99), p = 0.009, were independently associated with ASCVD. Conclusions: Among hypercholesterolemic older individuals participating in a cascade screening program, the genetic diagnosis of FH was associated with higher ASCVD rates, emphasizing the relevance of a monogenic defect as the cause of long-lasting hypercholesterolemia and ASCVD risk, particularly in men.