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Articles by Raul D. Santos
Total Records ( 4 ) for Raul D. Santos
  Raul D. Santos , Bela F. Asztalos , Lilton R.C. Martinez , Marcio H. Miname , Eliana Polisecki and Ernst J. Schaefer
  Our purpose is to provide a framework for diagnosing the inherited causes of marked high-density lipoprotein (HDL) deficiency (HDL cholesterol levels <10 mg/dL in the absence of severe hypertriglyceridemia or liver disease) and to provide information about coronary heart disease (CHD) risk for such cases. Published articles in the literature on severe HDL deficiencies were used as sources. If apolipoprotein (Apo) A-I is not present in plasma, then three forms of ApoA-I deficiency, all with premature CHD,and normal low-density lipoprotein (LDL) cholesterol levels have been described: ApoA-I/C-III/A-IV deficiency with fat malabsorption, ApoA-I/C-III deficiency with planar xanthomas, and ApoA-I deficiency with planar and tubero-eruptive xanthomas (pictured in this review for the first time). If ApoA-I is present in plasma at a concentration <10 mg/dL, with LDL cholesterol that is about 50% of normal and mild hypertriglyceridemia, a possible diagnosis is Tangier disease due to mutations at the adenosine triphosphate binding cassette protein A1 (ABCA1) gene locus. These patients may develop premature CHD and peripheral neuropathy, and have evidence of cholesteryl ester-laden macrophages in their liver, spleen, tonsils, and Schwann cells, as well as other tissues. The third form of severe HDL deficiency is characterized by plasma ApoA-I levels <40 mg/dL, moderate hypertriglyceridemia, and decreased LDL cholesterol, and the finding that most of the cholesterol in plasma is in the free rather than the esterified form, due to a deficiency in lecithin:cholesterol acyltransferase activity. These patients have marked corneal opacification and splenomegaly, and are at increased risk of developing renal failure, but have no clear evidence of premature CHD. Marked HDL deficiency has different etiologies and is generally associated with early CHD risk.
  Raul D. Santos , Alberto J. Lorenzatti , Carlos Fernandez Barros and Edgardo Escobar
  Traditional tools to evaluate cardiovascular disease risk may underestimate the risk of cardiovascular events. Although reduction of low-density lipoprotein cholesterol (LDL-C) is the mainstay of therapy to mitigate cardiovascular risk from atherosclerosis, noninvasive imaging techniques and biomarkers are now allowing us to identify subclinical atherosclerosis, or high-risk patients, and are providing clinical researchers with new target end points for randomized controlled clinical trials. Current surrogates include carotid intima-media thickness, coronary artery calcification, and high-sensitivity C-reactive protein levels. There is evidence that these biomarkers are useful in clinical practice to improve risk quantification in subjects considered at intermediate risk of coronary events according to clinical risk stratification. Some studies, but not all, have demonstrated achievement of surrogate end points with lipid-lowering therapy in addition to LDL-C reductions. A group of clinical lipidologists from Latin American countries convened to give a perspective on recent clinical trials in clinical lipidology, their designs, and data regarding currently used biomarkers. It was noted that the success of some surrogate end points as possible markers of clinical efficacy has relied heavily on patient selection and trial design. On the basis of current evidence, we believe that correcting elevated LDL-C levels should remain the primary target of therapy for patients with dyslipidemia. The group also agreed that the evidence from recent clinical trials supports the potential role of new biomarkers for the screening and identification of patients at high cardiovascular risk in the absence of overt hyperlipidemia.
  Scott M. Grundyemail , Hidenori Arai , Philip Barter , Thomas P. Bersot , D. John Betteridge , Rafael Carmena , Ada Cuevas , Michael H. Davidson , Jacques Genest , Y. Antero Kesaniemi , Shaukat Sadikot , Raul D. Santos , Andrey V. Susekov , Rody G. Sy , S. LaleTokgozoglu , Gerald F. Watts and Dong Zhao
  An international panel of the International Atherosclerosis Society has developed a new set of recommendations for the management of dyslipidemia. The panel identifies non-high-density lipoprotein cholesterol as the major atherogenic lipoprotein. Primary and secondary prevention are considered separately. Optimal levels for atherogenic lipoproteins are derived for the two forms of prevention. For primary prevention, the recommendations emphasize lifestyle therapies to reduce atherogenic lipoproteins; drug therapy is reserved for subjects at greater risk. Risk assessment is based on estimation of lifetime risk according to differences in baseline population risk in different nations or regions. Secondary prevention emphasizes use of cholesterol-lowering drugs to attain optimal levels of atherogenic lipoproteins.
  Gerald F. Watts , Samuel Gidding , Anthony S. Wierzbicki , Peter P. Toth , Rodrigo Alonso , W. Virgil Brown , Eric Bruckert , Joep Defesche , Khoo Kah Lin , Michael Livingston , Pedro Mata , Klaus G. Parhofer , Frederick J. Raal , Raul D. Santos , Eric J.G. Sijbrands , William G. Simpson , David R. Sullivan , Andrey V. Susekov , Brian Tomlinson , Albert Wiegman , Shizuya Yamashita and John J.P. Kastelein
  Familial hypercholesterolemia (FH) is a dominantly inherited disorder present from birth that markedly elevates plasma low-density lipoprotein cholesterol and causes premature coronary heart disease. There are at least 20 million people with FH worldwide, but the majority remains undetected, and current treatment is often suboptimal. To address this major gap in coronary prevention we present, from an international perspective, consensus-based guidance on the care of FH. The guidance was generated from seminars and workshops held at an international symposium. The recommendations focus on the detection, diagnosis, assessment, and management of FH in adults and children and set guidelines for clinical purposes. They also refer to best practice for cascade screening and risk notifying and testing families for FH, including use of genetic testing. Guidance on treatment is based on risk stratification, management of noncholesterol risk factors, and the safe and effective use of low-density lipoprotein-lowering therapies. Recommendations are given on lipoprotein apheresis. The use of emerging therapies for FH is also foreshadowed. This international guidance acknowledges evidence gaps but aims to make the best use of contemporary practice and technology to achieve the best outcomes for the care of FH. It should accordingly be used to inform clinical judgment and be adjusted for country-specific and local healthcare needs and resources.
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