RAUL DIAS DOS SANTOS FILHO
Projetos de Pesquisa
Unidades Organizacionais
Departamento de Cardio-Pneumologia, Faculdade de Medicina - Docente
Instituto do Coração, Hospital das Clínicas, Faculdade de Medicina
Instituto do Coração, Hospital das Clínicas, Faculdade de Medicina
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conferenceObject Coronary Artery Calcium Score and Risk of Cardiovascular Events in Heterozygous Familial Hypercholesterolemia Patients Undergoing Standard Lipid Lowering Therapy(2018) MINAME, Marcio; BITTENCOURT, Marcio S.; MORAES, Sergio R.; I, Romulo Alves; SILVA, Pamela R.; JANNES, Cinthia E.; PEREIRA, Alexandre C.; NASIR, Khurram; SANTOS, Raul D.- I Brazilian Guidelines On Cardiovascular Prevention(2013) SIMAO, A. F.; PRECOMA, D. B.; ANDRADE, J. P.; CORREA FILHO, H.; SARAIVA, J. F. K.; OLIVEIRA, G. M. M.; MURRO, A. L. B.; CAMPOS, A.; ALESSI, A.; AVEZUM JUNIOR, A.; ACHUTTI, A. C.; MIGUEL, A. C. M. G.; SOUSA, A. C. S.; LOTEMBERG, A. M. P.; LINS, A. P.; FALUD, A. A.; BRANDAO, A. A.; SANJULIANI, A. F.; SBISSA, A. S.; ALENCAR FILHO, A. C.; HERDY, A. H.; POLANCZYK, C. A.; LANTIERI, C. J.; MACHADO, C. A.; SCHERR, C.; STOLL, C.; AMODEO, C.; ARAUJO, C. G. S.; SARAIVA, D.; MORIGUCHI, E. H.; MESQUITA, E. T.; CESENA, F. H. Y.; FONSECA, F. A. H.; CAMPOS, G. P.; SOARES, G. P.; FEITOSA, G. S.; XAVIER, H. T.; CASTRO, I; GIULIANO, I. C. B.; V, I. Rivera; GUIMARAES, I. C. B.; ISSA, J. S.; SOUZA, J. R. M.; FARIA NETO, J. R.; CUNHA, L. B. N.; PELLANDA, L. C.; BORTOLOTTO, L. A.; BERTOLAMI, M. C.; MINAME, M. H.; GOMES, M. A. M.; TAMBASCIA, M.; MALACHIAS, M. V. B.; SILVA, M. A. M.; IZA, M. C. O.; MAGALHAES, M. E. C.; BACELLAR, M. S. C.; MILANI, M.; WAJNGARTEN, M.; GHORAYEB, N.; COELHO, O. R.; VILLELA, P. B.; V, P. C. B. Jardim; SANTOS FILHO, R. D.; STEIN, R.; CASSANI, R. S. L.; D'AVILA, R. L.; FERREIRA, R. M.; BARBOSA, R. B.; POVOA, R. M. S.; KAISER, S. E.; ISMAEL, S. C.; CARVALHO, T.; GIRALDEZ, V. Z. R.; COUTINHO, W.; SOUZA, W. K. S. B.
- Europe aspires to set the record straight on familial hypercholesterolaemia(2015) WATTS, Gerald F.; PANG, Jing; SANTOS, Raul D.
conferenceObject EVALUATION OF CARDIOVASCULAR EVENTS WITH ADMINISTRATION OF MIPOMERSEN, AN ANTISENSE APO B-100 SYNTHESIS INHIBITOR: RESULTS FROM THE PHASE 3 PROGRAM(2014) SANTOS, R.; MAHMOOD, A.; CHIN, W.; MCGOWAN, M.- Defining severe familial hypercholesterolaemia and the implications for clinical management: a consensus statement from the International Atherosclerosis Society Severe Familial Hypercholesterolemia Panel(2016) SANTOS, Raul D.; GIDDING, Samuel S.; HEGELE, Robert A.; CUCHEL, Marina A.; BARTER, Philip J.; WATTS, Gerald F.; BAUM, Seth J.; CATAPANO, Alberico L.; CHAPMAN, M. John; DEFESCHE, Joep C.; FOLCO, Emanuela; FREIBERGER, Tomas; GENEST, Jacques; HOVINGH, G. Kees; HARADA-SHIBA, Mariko; HUMPHRIES, Steve E.; JACKSON, Ann S.; MATA, Pedro; MORIARTY, Patrick M.; RAAL, Frederick J.; AL-RASADI, Khalid; RAY, Kausik K.; REINER, Zelijko; SIJBRANDS, Eric J. G.; YAMASHITA, ShizuyaFamilial hypercholesterolaemia is common in individuals who had a myocardial infarction at a young age. As many as one in 200 people could have heterozygous familial hypercholesterolaemia, and up to one in 300 000 individuals could be homozygous. The phenotypes of heterozygous and homozygous familial hypercholesterolaemia overlap considerably; the response to treatment is also heterogeneous. In this Review, we aim to define a phenotype for severe familial hypercholesterolaemia and identify people at highest risk for cardiovascular disease, based on the concentration of LDL cholesterol in blood and individuals' responsiveness to conventional lipid-lowering treatment. We assess the importance of molecular characterisation and define the role of other cardiovascular risk factors and advanced subclinical coronary atherosclerosis in risk stratification. Individuals with severe familial hypercholesterolaemia might benefit in particular from early and more aggressive cholesterol-lowering treatment (eg, with PCSK9 inhibitors). In addition to better tailored therapy, more precise characterisation of individuals with severe familial hypercholesterolaemia could improve resource use.
- Imaging biomarkers to track subclinical atherosclerosis in heterozygous familial hypercholesterolemia(2013) MINAME, Marcio H.; SANTOS, Raul D.Heterozygous familial hypercholesterolennia (FH) is characterized by high LDL cholesterol levels and premature coronary heart disease onset. Nonetheless, the course of coronary disease events in heterozygous FH subjects is variable. The presence and severity of subclinical atherosclerosis predicts cardiovascular event onset and may help reclassify the risk of clinical events in the general population. In this review, we discuss the possible use of subclinical coronary, carotid and aortic atherosclerosis testing in heterozygous FH subjects for cardiovascular risk stratification and treatment. Many FH subjects present an increased and precocious burden of subclinical vascular disease in comparison to normolipidemic subjects. These subjects may be at higher risk of cardiovascular events and might deserve more aggressive lipid-lowering treatment. Nevertheless, routine screening of imaging biomarkers for FH subjects in clinical practice remains to be determined in prospective trials.
conferenceObject PREDICTORS OF CORONARY ARTERY CALCIFICATION INCIDENCE IN SEVERE HYPERCHOLESTEROLEMIA(2023) MARTE, Ana; MINAME, Marcio Hiroshi; PARDI, Estevao Magalhaes; GANEM, Lucas; MIZUTA, Marjorie Hayashida; ROCHA, Viviane Zorzanelli; PEREIRA, Alexandre Costa; KRIEGER, Jose Eduardo; SANTOS, Raul- NHLBI Working Group Recommendations to Reduce Lipoprotein(a)-Mediated Risk of Cardiovascular Disease and Aortic Stenosis(2018) TSIMIKAS, Sotirios; FAZIO, Sergio; FERDINAND, Keith C.; GINSBERG, Henry N.; KOSCHINSKY, Marlys L.; MARCOVINA, Santica M.; MORIARTY, Patrick M.; RADER, Daniel J.; REMALEY, Alan T.; REYES-SOFFER, Gissette; SANTOS, Raul D.; THANASSOULIS, George; WITZTUM, Joseph L.; DANTHI, Simhan; OLIVE, Michelle; LIU, LijuanPathophysiological, epidemiological, and genetic studies provide strong evidence that lipoprotein(a) [Lp(a)] is a causal mediator of cardiovascular disease (CVD) and calcific aortic valve disease (CAVD). Specific therapies to address Lp(a)-mediated CVD and CAVD are in clinical development. Due to knowledge gaps, the National Heart, Lung, and Blood Institute organized a working group that identified challenges in fully understanding the role of Lp(a) in CVD/CAVD. These included the lack of research funding, inadequate experimental models, lack of globally standardized Lp(a) assays, and inadequate understanding of the mechanisms underlying current drug therapies on Lp(a) levels. Specific recommendations were provided to facilitate basic, mechanistic, preclinical, and clinical research on Lp(a); foster collaborative research and resource sharing; leverage expertise of different groups and centers with complementary skills; and use existing National Heart, Lung, and Blood Institute resources. Concerted efforts to understand Lp(a) pathophysiology, together with diagnostic and therapeutic advances, are required to reduce Lp(a)-mediated risk of CVD and CAVD. (c) 2018 by the American College of Cardiology Foundation.
- Favorable effects of ezetimibe alone or in association with simvastatin on the removal from plasma of chylomicrons in coronary heart disease subjects(2014) MANGILI, Otavio Celeste; GAGLIARDI, Ana C. Moron; MANGILI, Leonardo Celeste; MESQUITA, Carlos H.; CESAR, Luiz A. Machado; TANAKA, Akira; SCHAEFER, Ernst J.; MARANHAO, Raul C.; SANTOS, Raul D.Objective: Reductions on the clearance from plasma of chylomicrons are associated with atherosclerosis. Statins improve the removal from plasma of chylomicrons in a dose dependent manner. There is controversy whether ezetimibe modifies the plasma clearance of chylomicrons. Effects of ezetimibe alone or in combination with simvastatin were compared with low and high dose of the latter, upon the kinetics of a chylomicron-like emulsion in coronary heart disease (CHD) patients. Methods: 25 CHD patients were randomized for treatment with ezetimibe 10 mg (group 1) or simvastatin 20 mg (group 2) with progression to ezetimibe + simvastatin 10/20 mg or simvastatin 80 mg, respectively. Kinetic studies were performed at baseline and after each treatment period of 6 weeks. The fractional catabolic rates (FCR) of the emulsion labeled with C-14-CE and H-3-TG, that represent respectively chylomicron remnant and triglyceride removal, were calculated. Comparisons were made by ANOVA. Results: The (CE)-C-14-FCR in group 1 were 0.005 +/- 0.004, 0.011 +/- 0.008 and 0.018 +/- 0.005 min(-1) and in group 2 were 0.004 +/- 0.003, 0.011 +/- 0.008 and 0.019 +/- 0.007 min(-1) respectively at baseline, after 6 and 12 weeks (p < 0.05 vs. baseline, and 6 vs. 12 weeks). The H-3-TG-FCR in group 1 were 0.017 +/- 0.011, 0.024 +/- 0.011 and 0.042 +/- 0.013 min(-1) and in group 2 were 0.016 +/- 0.009, 0.022 +/- 0.009 and 0.037 +/- 0.012 min(-1) at baseline, after 6 and 12 weeks (p < 0.05 vs. baseline, and 6 vs. 12 weeks). There were no differences between groups in time. Conclusion: Both treatments increased similarly the removal from plasma of chylomicron and remnants in CHD patients.