Publications by authors named "Carlos V Serrano"

48 Publications

Androgen deprivation therapy improves the in vitro capacity of high-density lipoprotein (HDL) to receive cholesterol and other lipids in patients with prostate carcinoma.

Lipids Health Dis 2020 Jun 10;19(1):133. Epub 2020 Jun 10.

Instituto de Coracao, Hospital das Clinicas HCFMUSP, Faculdade de Medicina, Universidade de Sao Paulo, Sao Paulo, Brazil.

Background: Androgen deprivation therapy (ADT) is widely used in the treatment of testosterone-dependent prostate carcinomas. ADT often increases plasma LDL and HDL cholesterol and triglycerides. The aim was to test whether ADT changes the transfer of lipids to HDL, an important aspect of this metabolism and HDL protective functions, and related parameters.

Methods: Sixteen volunteers with advanced prostate carcinoma submitted to pharmacological ADT or orchiectomy had plasma collected shortly before and after 6 months of ADT. In vitro transfer of lipids to HDL was performed by incubating plasma with donor emulsion containing radioactive lipids by 1 h at 37 °C. After chemical precipitation of apolipoprotein B-containing lipoprotein, the radioactivity of HDL fraction was counted.

Results: ADT reduced testosterone to nearly undetectable levels and markedly diminished PSA. ADT increased the body weight but glycemia, triglycerides, LDL and HDL cholesterol, HDL lipid composition and CETP concentration were unchanged. However, ADT increased the plasma unesterified cholesterol concentration (48 ± 12 vs 56 ± 12 mg/dL, p = 0.019) and LCAT concentration (7.15 ± 1.81 vs 8.01 ± 1.55μg/mL, p = 0.020). Transfer of unesterified (7.32 ± 1.09 vs 8.18 ± 1.52%, p < 0.05) and esterified cholesterol (6.15 ± 0.69 vs 6.94 ± 1.29%, p < 0.01) and of triglycerides (6.37 ± 0.43 vs 7.18 ± 0.91%, p < 0.001) to HDL were increased after ADT. Phospholipid transfer was unchanged.

Conclusion: Increase in transfer of unesterified and esterified cholesterol protects against cardiovascular disease, as shown previously, and increased LCAT favors cholesterol esterification and facilitates the reverse cholesterol transport. Thus, our results suggest that ADT may offer anti-atherosclerosis protection by improving HDL functional properties. This could counteract, at least partially, the eventual worse effects on plasma lipids.
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http://dx.doi.org/10.1186/s12944-020-01305-8DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7285573PMC
June 2020

Free cholesterol transfer to high-density lipoprotein (HDL) upon triglyceride lipolysis underlies the U-shape relationship between HDL-cholesterol and cardiovascular disease.

Eur J Prev Cardiol 2020 10 15;27(15):1606-1616. Epub 2019 Dec 15.

National Institute for Health and Medical Research (INSERM) UMR_S 1166, Faculty of Medicine Pitié-Salpétrière, Paris, France.

Background: Low concentrations of high-density lipoprotein cholesterol (HDL-C) represent a well-established cardiovascular risk factor. Paradoxically, extremely high HDL-C levels are equally associated with elevated cardiovascular risk, resulting in the U-shape relationship of HDL-C with cardiovascular disease. Mechanisms underlying this association are presently unknown. We hypothesised that the capacity of high-density lipoprotein (HDL) to acquire free cholesterol upon triglyceride-rich lipoprotein (TGRL) lipolysis by lipoprotein lipase underlies the non-linear relationship between HDL-C and cardiovascular risk.

Methods: To assess our hypothesis, we developed a novel assay to evaluate the capacity of HDL to acquire free cholesterol (as fluorescent TopFluor® cholesterol) from TGRL upon in vitro lipolysis by lipoprotein lipase.

Results: When the assay was applied to several populations markedly differing in plasma HDL-C levels, transfer of free cholesterol was significantly decreased in low HDL-C patients with acute myocardial infarction (-45%) and type 2 diabetes (-25%), and in subjects with extremely high HDL-C of >2.59 mmol/L (>100 mg/dL) (-20%) versus healthy normolipidaemic controls. When these data were combined and plotted against HDL-C concentrations, an inverse U-shape relationship was observed. Consistent with these findings, animal studies revealed that the capacity of HDL to acquire cholesterol upon lipolysis was reduced in low HDL-C apolipoprotein A-I knock-out mice and was negatively correlated with aortic accumulation of [H]-cholesterol after oral gavage, attesting this functional characteristic as a negative metric of postprandial atherosclerosis.

Conclusions: Free cholesterol transfer to HDL upon TGRL lipolysis may underlie the U-shape relationship between HDL-C and cardiovascular disease, linking HDL-C to triglyceride metabolism and atherosclerosis.
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http://dx.doi.org/10.1177/2047487319894114DOI Listing
October 2020

Association between Neutrophil-Lymphocyte and Platelet-Lymphocyte Ratios and Coronary Artery Calcification Score among Asymptomatic Patients: Data from a Cross-Sectional Study.

Mediators Inflamm 2019 26;2019:6513847. Epub 2019 Mar 26.

Heart Institute (InCor), Medical School, University of Sao Paulo, Brazil.

Introduction: Atherosclerosis is a low-grade inflammatory disease. Among markers of inflammation, importance has been given to the neutrophil-lymphocyte ratio (NLR) and platelet-lymphocyte ratio (PLR). The objective of this study was to examine the association between these hematological indices of inflammation and coronary atherosclerotic calcification in clinically asymptomatic patients.

Methods: This study had clinical and laboratorial data collected from consecutive asymptomatic patients that underwent computed tomography coronary artery calcium (CAC) scoring. Risk factors, NLR, and PLR were evaluated at different categories of CAC scoring. Statistical tests included chi-square, linear regression, and logistic regression. Patients ( = 247; age 60.4 ± 8.0 years and 60.7% men) were allocated into four categories according to the CAC score.

Results: Respective age, sex (male), NLR, and PLR distribution within groups were as follows: CAC = 0 ( = 98; 52.5 ± 13.6 years, 55%, 2.0 ± 1.0, and 121.5 ± 41.5), CAC 1-100 ( = 64; 61.3 ± 11.0 years, 60%, 2.2 ± 1.2, and 125.6 ± 45.6), CAC 101-400 ( = 37; 64.2 ± 11.6 years, 67%, 2.6 ± 1.3, and 125.4 ± 55.9), and CAC > 400 ( = 48; 69.3 ± 11.1 years, 66%, 3.3 ± 2.0, and 430.1 ± 1787.4). The association between risk factors and CAC score was assessed. Hypertension status and smoking status were similar within groups, while the presence of diabetes ( = 0.02) and older age ( ≤ 0.001) was more prevalent in the CAC > 400 group. LDL cholesterol was greater in the higher CAC score groups ( = 0.002). Multivariate logistic regression of the quartile analysis showed that age and NLR were independently associated with CAC > 100 (OR (CI), value): 2.06 (1.55-2.73, = 0.00001) and 1.82 (1.33-2.49, = 0.0002), respectively.

Conclusion: Within asymptomatic patients, NLR provides additional risk stratification, as an independent association between NLR extent and CAD extent was identified. Moreover, PLR was not an inflammation marker for CAD severity.
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http://dx.doi.org/10.1155/2019/6513847DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6458900PMC
September 2019

Distinct phospholipid and sphingolipid species are linked to altered HDL function in apolipoprotein A-I deficiency.

J Clin Lipidol 2019 May - Jun;13(3):468-480.e8. Epub 2019 Feb 25.

UMR-ICAN 1166, National Institute for Health and Medical Research (INSERM), Sorbonne University, Paris, France. Electronic address:

Background: Familial apolipoprotein A-I (apoA-I) deficiency (FAID) involving low levels of both apoA-I and high-density lipoprotein (HDL) cholesterol is associated with accelerated atherosclerosis.

Objective: The objective of this study was to define distinctive patterns in the lipidome of HDL subpopulations in FAID in relationship to antiatherogenic activities.

Methods: Five HDL subfractions were isolated by ultracentrifugation from plasma of FAID Caucasian patients (n = 5) and age-matched healthy normolipidemic Caucasian controls (n = 8), and the HDL lipidome (160 molecular species of 9 classes of phospholipids and sphingolipids) was quantitatively evaluated.

Results: Increased concentrations of numerous molecular species of lysophosphatidylcholine (up to 12-fold), ceramides (up to 3-fold), phosphatidylserine (up to 34-fold), phosphatidic acid (up to 71-fold), and phosphatidylglycerol (up to 20-fold) were detected throughout all five HDL subpopulations as compared with their counterparts from controls, whereas concentrations of phosphatidylethanolamine species were decreased (up to 5-fold). Moderately to highly abundant, within their lipid class, species of phosphatidylcholine, sphingomyelin, phosphatidylinositol, phosphatidylethanolamine, phosphatidylserine, and ceramide featuring multiple unsaturations were primarily affected by apoA-I deficiency; their HDL content, particularly that of phosphatidylcholine (34:2), was strongly correlated with HDL function, impaired in FAID. Metabolic pathway analysis revealed that sphingolipid, glycerophospholipid, and linoleic acid metabolism was significantly affected by FAID.

Conclusion: These data reveal that altered content of specific phospholipid and sphingolipid species is linked to deficient antiatherogenic properties of HDL in FAID.
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http://dx.doi.org/10.1016/j.jacl.2019.02.004DOI Listing
May 2020

Prognostic Differences between Men and Women with Acute Coronary Syndrome. Data from a Brazilian Registry.

Arq Bras Cardiol 2018 11 21;111(5):648-653. Epub 2018 Sep 21.

Unidade Clínica de Emergência - InCor - HCFMUSP, São Paulo, SP - Brazil.

Background: Gender-related differences have been reported in patients with acute coronary syndrome. The description of this comparative finding in a Brazilian registry has not yet been documented.

Objective: To compare male vs. female patients regarding the baseline characteristics, coronary findings, treatment and in-hospital and long-term prognosis.

Methods: This is a retrospective, multicenter and observational study that included 3,745 patients (2,437 males and 1,308 females) between May 2010 and May 2015. The primary in-hospital outcome was all-cause mortality. The secondary outcome consisted of combined events (cardiogenic shock, reinfarction, death, stroke and bleeding). The comparison between groups was performed using the chi-square and the t test, considering p < 0.05 as significant. In the long term, mortality and combined events were assessed using the Kaplan-Meier method, with a mean follow-up of 8.79 months.

Results: The mean age was 60.3 years for males and 64.6 for females (p < 0.0001). The most prevalent risk factor was systemic arterial hypertension in 72.9% of the women and 67.8% of the men (p = 0.001). Percutaneous coronary intervention was carried out in 44.9% of the males and 35.4% of the females (p < 0.0001), and coronary artery bypass grafting (CABG) was performed in 17% of the males and 11.8% of females (p < 0.0001), with a higher prevalence of three-vessel coronary artery disease in males (27.3% vs. 16.2%, p < 0.0001). Approximately 79.9% of the female patients received a diagnosis of acute coronary syndrome without ST-segment elevation, while in the male patients, this diagnosis was attained in 71.5% (p < 0.0001). No significant differences were observed between the groups in the short and long term, regarding both mortality and the combined events.

Conclusion: Several gender-related differences were observed in patients with acute coronary syndrome regarding the demographic characteristics, coronary artery disease pattern and implemented treatment. However, the prognostic evolution was similar between the groups.
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http://dx.doi.org/10.5935/abc.20180166DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6248255PMC
November 2018

Circulating osteogenic proteins are associated with coronary artery calcification and increase after myocardial infarction.

PLoS One 2018 23;13(8):e0202738. Epub 2018 Aug 23.

Hospital Israelita Albert Einstein, São Paulo, SP, Brazil.

Background: Coronary artery calcification (CAC) and atherosclerotic inflammation associate with increased risk of myocardial infarction (MI). Vascular calcification is regulated by osteogenic proteins (OPs). It is unknown whether an association exists between CAC and plasma OPs and if they are affected by atherothrombotic inflammation. We tested the association of osteogenic and inflammatory proteins with CAC and assessed these biomarkers after MI.

Methods: Circulating OPs (osteoprotegerin, RANKL, fetuin-A, Matrix Gla protein [MGP]) and inflammatory proteins (C-reactive protein, oxidized-LDL, tumoral necrosis factor-α, transforming growth factor [TGF]-β1) were compared between stable patients with CAC (CAC ≥ 100 AU, n = 100) and controls (CAC = 0 AU, n = 30). The association between biomarkers and CAC was tested by multivariate analysis. In patients with MI (n = 40), biomarkers were compared between acute phase and 1-2 months post-MI, using controls as a baseline.

Results: MGP and fetuin-A levels were higher within individuals with CAC. Higher levels of MGP and RANKL were associated with CAC (OR 3.12 [95% CI 1.20-8.11], p = 0.02; and OR 1.75 [95% CI 1.04-2.94] respectively, p = 0.035). After MI, C-reactive protein, OPG and oxidized-LDL levels increased in the acute phase, whereas MGP and TGF-β1 increased 1-2 months post-MI.

Conclusions: Higher MGP and RANKL levels associate with CAC. These findings highlight the potential role of these proteins as modulators and markers of CAC. In addition, the post-MI increase in OPG and MGP, as well as of inflammatory proteins suggest that the regulation of these OPs is affected by atherothrombotic inflammation.
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http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0202738PLOS
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6107213PMC
February 2019

Regression of Atherosclerotic Plaques of Cholesterol-Fed Rabbits by Combined Chemotherapy With Paclitaxel and Methotrexate Carried in Lipid Core Nanoparticles.

J Cardiovasc Pharmacol Ther 2018 11 20;23(6):561-569. Epub 2018 May 20.

1 Heart Institute (InCor) of the Medical School Hospital University of São Paulo, São Paulo, Brazil.

In previous studies, it was demonstrated that lipid core nanoparticles (LDE) resemble the low-density lipoprotein structure and carrying the antiproliferative agent paclitaxel (PTX) strongly reduced atherosclerosis lesions induced in rabbits by cholesterol feeding. Currently, the aim was to verify whether combining LDE-PTX treatment with methotrexate (MTX) associated with LDE (LDE-MTX) could accelerate the atherosclerosis regression attained with single LDE-PTX treatment, after withdrawing the cholesterol feeding. Thirty-eight rabbits were fed 1% cholesterol chow for 8 weeks. Six of these rabbits were then euthanized for analyses of the aorta (controls). In the remaining rabbits, cholesterol feeding was withdrawn, and those 32 animals were allocated to 3 groups submitted to different 8-week intravenous treatments, all once/week: LDE-PTX (n = 10; 4 mg/kg), LDE-PTX + LDE-MTX (n = 11; 4 mg/kg), and LDE-alone (n = 11). Rabbits were then euthanized and aortas were excised for morphometric, immunohistochemical, and gene expression analyses. After cholesterol feeding withdrawal, in comparison with LDE-alone group, both LDE-PTX and LDE-PTX + LDE-MTX treatments had the ability to increase the regression of plaque areas: -49% in LDE-PTX and -59% for LDE-PTX + LDE-MTX. However, only LDE-PTX + LDE-MTX treatment elicited reduction in the intima area, estimated in -57%. Macrophage presence in aortic lesions was reduced 48% by LDE-PTX and 43% by LDE-PTX + LDE-MTX treatment. Matrix metalloproteinase 9 was reduced by either LDE-PTX (74%) or LDE-PTX + LDE-MTX (78%). Tumor necrosis factor α gene expression was reduced 65% by LDE-PTX and 79% by LDE-PTX + LDE-MTX. In conclusion, treatment with LDE-PTX indeed accelerated plaque reduction after cholesterol feeding; LDE-PTX + LDE-MTX further increased this effect, without any observed toxicity. These results pave the way for the use of combined chemotherapy to achieve stronger effects on aggravated, highly inflamed atherosclerotic lesions.
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http://dx.doi.org/10.1177/1074248418778836DOI Listing
November 2018

Is There Any Relationship between TSH Levels and Prognosis in Acute Coronary Syndrome?

Arq Bras Cardiol 2018 Feb;110(2):113-118

Unidade Clínica de Emergência - InCor - HCFMUSP, São Paulo, SP.

Background: Some small studies have related higher levels of thyrotropin (TSH) to potentially worse prognosis in acute coronary syndromes. However, this relationship remains uncertain.

Objective: To analyze the outcomes of patients with acute coronary syndromes in relation to the value of TSH at admission.

Methods: Observational and retrospective study with 505 patients (446 in group I [TSH ≤ 4 mIU/L] and 59 in group II [TSH > 4 mIU/L]) with acute coronary syndromes between May 2010 and May 2014. We obtained data about comorbidities and the medications used at the hospital. The primary endpoint was in-hospital all-cause death. The secondary endpoint included combined events (death, non-fatal unstable angina or myocardial infarction, cardiogenic shock, bleeding and stroke). Comparisons between groups were made by one-way ANOVA and chi-square test. Multivariate analysis was determined by logistic regression. Analyses were considered significant when p < 0.05.

Results: Significant differences between groups I and II were observed regarding the use of enoxaparin (75.2% vs. 57.63%, p = 0.02) and statins (84.08% vs. 71.19%, p < 0.0001), previous stroke (5.83% vs. 15.25%, p = 0.007), combined events (14.80% vs. 27.12%, OR = 3.05, p = 0.004), cardiogenic shock (4.77% vs. 6.05%, OR = 4.77, p = 0.02) and bleeding (12.09% vs. 15.25%, OR = 3.36, p = 0.012).

Conclusions: In patients with acute coronary syndromes and TSH > 4 mIU/L at admission, worse prognosis was observed, with higher incidences of in-hospital combined events, cardiogenic shock and bleeding.
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http://dx.doi.org/10.5935/abc.20180019DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5855903PMC
February 2018

Computed tomography angiography defined vulnerable plaque in a patient with low high-density lipoprotein cholesterol and subsequent myocardial infarction.

Coron Artery Dis 2017 12;28(8):712-714

aDepartment of Cardiology, Heart Institute (InCor), School of Medicine from University of São Paulo bDepartment of Cardiology, Hospital Israelita Albert Einstein, São Paulo, Brazil.

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http://dx.doi.org/10.1097/MCA.0000000000000524DOI Listing
December 2017

Cardiovascular disease in women: are we aware?

Rev Assoc Med Bras (1992) 2017 03;63(3):195-196

Associate Professor of Cardiology, InCor, FMUSP. Director of the Atherosclerosis Clinical Unit at the InCor, FMUSP, São Paulo, SP, Brazil.

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http://dx.doi.org/10.1590/1806-9282.63.03.195DOI Listing
March 2017

Mortality reduction with use of oral beta-blockers in patients with acute coronary syndrome.

Clinics (Sao Paulo) 2016 Nov 1;71(11):635-638. Epub 2016 Nov 1.

Faculdade de Medicina da Universidade de São Paulo, Instituto do Coração (InCor), Unidade de Emergência, São Paulo/SP, Brazil.

Objectives:: Recent studies have revealed a relationship between beta-blocker use and worse prognosis in acute coronary syndrome, mainly due to a higher incidence of cardiogenic shock. However, the relevance of this relationship in the reperfusion era is unknown. The aim of this study was to analyze the outcomes of patients with acute coronary syndrome that started oral beta-blockers within the first 24 hours of hospital admission (group I) compared to patients who did not use oral beta-blockers in this timeframe (group II).

Methods:: This was an observational, retrospective and multicentric study with 2,553 patients (2,212 in group I and 341 in group II). Data regarding demographic characteristics, coronary treatment and medication use in the hospital were obtained. The primary endpoint was in-hospital all-cause mortality. The groups were compared by ANOVA and the chi-square test. Multivariate analysis was conducted by logistic regression and results were considered significant when p<0.05.

Results:: Significant differences were observed between the groups in the use of angiotensin-converting enzyme inhibitors, enoxaparin, and statins; creatinine levels; ejection fraction; tabagism; age; and previous coronary artery bypass graft. Significant differences were also observed between the groups in mortality (2.67% vs 9.09%, OR=0.35, p=0.02) and major adverse cardiovascular events (11% vs 29.5%, OR=4.55, p=0.02).

Conclusions:: Patients with acute coronary syndrome who underwent early intervention with oral beta-blockers during the first 24 hours of hospital admission had a lower in-hospital death rate and experienced fewer major adverse cardiovascular events with no increase in cardiogenic shock or sustained ventricular arrhythmias compared to patients who did not receive oral beta-blockers within this timeframe.
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http://dx.doi.org/10.6061/clinics/2016(11)03DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5108170PMC
November 2016

Mechanical Ventilation and Clinical Outcomes in Patients with Acute Myocardial Infarction: A Retrospective Observational Study.

PLoS One 2016 15;11(3):e0151302. Epub 2016 Mar 15.

Duke University Medical Center, Duke Clinical Research Institute, Durham, North Carolina, United States of America.

Purpose: Patients with acute myocardial infarction (AMI) and respiratory impairment may be treated with either invasive or non-invasive mechanical ventilation (MV). However, there has been little testing of non-invasive MV in the setting of AMI. Our objective was to evaluate the incidence and associated clinical outcomes of patients with AMI who were treated with non-invasive or invasive MV.

Methods: This was a retrospective observational study in which consecutive patients with AMI (n = 1610) were enrolled. The association between exclusively non-invasive MV, invasive MV and outcomes was assessed by multivariable models.

Results: Mechanical ventilation was used in 293 patients (54% invasive and 46% exclusively non-invasive). In-hospital mortality rates for patients without MV, with exclusively non-invasive MV, and with invasive MV were 4.0%, 8.8%, and 39.5%, respectively (P<0.001). The median lengths of hospital stay were 6 (5.8-6.2), 13 (11.2-4.7), and 28 (18.0-37.9) days, respectively (P<0.001). Exclusively non-invasive MV was not associated with in-hospital death (adjusted HR = 0.90, 95% CI 0.40-1.99, P = 0.79). Invasive MV was strongly associated with a higher risk of in-hospital death (adjusted HR = 3.07, 95% CI 1.79-5.26, P<0.001).

Conclusions: In AMI setting, 18% of the patients required MV. Almost half of these patients were treated with exclusively non-invasive strategies with a favorable prognosis, while patients who needed to be treated invasively had a three-fold increase in the risk of death. Future prospective randomized trials are needed to compare the effectiveness of invasive and non-invasive MV for the initial approach of respiratory failure in AMI patients.
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http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0151302PLOS
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4792462PMC
August 2016

Defective functionality of small, dense HDL3 subpopulations in ST segment elevation myocardial infarction: Relevance of enrichment in lysophosphatidylcholine, phosphatidic acid and serum amyloid A.

Biochim Biophys Acta 2015 Sep 30;1851(9):1254-61. Epub 2015 May 30.

National Institute of Health and Medical Research (INSERM), UMR-ICAN 1166, University of Pierre and Marie Curie - Paris 6; Pitié-Salpétrière University Hospital, ICAN, Paris, France. Electronic address:

Background: Low plasma levels of high-density lipoprotein-cholesterol (HDL-C) are typical of acute myocardial infarction (MI) and predict risk of recurrent cardiovascular events. The potential relationships between modifications in the molecular composition and the functionality of HDL subpopulations in acute MI however remain indeterminate.

Methods And Results: ST segment elevation MI (STEMI) patients were recruited within 24h after diagnosis (n=16) and featured low HDL-C (-31%, p<0.05) and acute-phase inflammation (determined as marked elevations in C-reactive protein, serum amyloid A (SAA) and interleukin-6) as compared to age- and sex-matched controls (n=10). STEMI plasma HDL and its subpopulations (HDL2b, 2a, 3a, 3b, 3c) displayed attenuated cholesterol efflux capacity from THP-1 cells (up to -32%, p<0.01, on a unit phospholipid mass basis) vs.

Controls: Plasma HDL and small, dense HDL3b and 3c subpopulations from STEMI patients exhibited reduced anti-oxidative activity (up to -68%, p<0.05, on a unit HDL mass basis). HDL subpopulations in STEMI were enriched in two proinflammatory bioactive lipids, lysophosphatidylcholine (up to 3.0-fold, p<0.05) and phosphatidic acid (up to 8.4-fold, p<0.05), depleted in apolipoprotein A-I (up to -23%, p<0.05) and enriched in SAA (up to +10.2-fold, p<0.05); such changes were most marked in the HDL3b subfraction. In vitro HDL enrichment in both lysophosphatidylcholine and phosphatidic acid exerted deleterious effects on HDL functionality.

Conclusions: In the early phase of STEMI, HDL particle subpopulations display marked, concomitant alterations in both lipidome and proteome which are implicated in impaired HDL functionality. Such modifications may act synergistically to confer novel deleterious biological activities to STEMI HDL.

Significance: Our present data highlight complex changes in the molecular composition and functionality of HDL particle subpopulations in the acute phase of STEMI, and for the first time, reveal that concomitant modifications in both the lipidome and proteome contribute to functional deficiencies in cholesterol efflux and antioxidative activities of HDL particles. These findings may provide new biomarkers and new insights in therapeutic strategy to reduce cardiovascular risk in this clinical setting where such net deficiency in HDL function, multiplied by low circulating HDL concentrations, can be expected to contribute to accelerated atherogenesis.
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http://dx.doi.org/10.1016/j.bbalip.2015.05.007DOI Listing
September 2015

Prognostic value of serial brain natriuretic Peptide measurements in patients with acute myocardial infarction.

Cardiology 2015 21;131(2):116-21. Epub 2015 Apr 21.

Hospital Israelita Albert Einstein, Faculdade de Medicina da Universidade de São Paulo, São Paulo, Brazil.

Objectives: Elevated B-type natriuretic peptide (BNP) levels following acute myocardial infarction (AMI) are associated with adverse outcomes. The role of serial BNP monitoring after AMI has been poorly investigated. We aimed to evaluate the prognostic value of in-hospital serial BNP measurements in AMI patients.

Methods: Patients with AMI (n=1,924) were retrospectively evaluated. We selected patients with at least 2 in-hospital BNP measurements. The association between in-hospital mortality and BNP measurements (earliest, highest follow-up and the variation between measurements) were tested in multivariate models.

Results: Serial BNP levels were determined in 176 patients. Compared to the rest of the population, these patients were older and had higher mortality rates. In the adjusted models, only the highest follow-up BNP remained associated with in-hospital death (odds ratio 1.06; 95% confidence interval, CI, 1.01-1.15; p=0.014). Receiver-operating characteristic curve analysis demonstrated that the highest follow-up BNP was the best predictor of in-hospital death (area under the curve=0.75; 95% CI 0.64-0.86).

Conclusions: Serial BNP monitoring was performed in a high-risk subgroup of AMI patients. The highest follow-up BNP was a better predictor of short-term death than the baseline and in-hospital variation values. In AMI patients, a later in-hospital BNP assessment may be more useful than an early measurement.
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http://dx.doi.org/10.1159/000375398DOI Listing
February 2016

Aspirin underuse, non-compliance or cessation: definition, extent, impact and potential solutions in the primary and secondary prevention of cardiovascular disease.

Int J Cardiol 2015 Mar 27;182:148-54. Epub 2014 Dec 27.

VCU Pauley Heart Center, Virginia Commonwealth University, Richmond, VA, USA.

Despite momentous breakthroughs in unraveling the pathophysiology of many chronic conditions and developing novel therapeutic agents, everyday clinical practice is still fraught with inadequate or inappropriate use of treatments with proven benefits. Aspirin is a paradigmatic example, as it is used for the primary and secondary prevention of cardiovascular disease and appears to have a beneficial impact on cancer risk. Yet, underuse, non-compliance or cessation of aspirin are not uncommon, may have an important clinical impact, and are not aggressively prevented or managed. Increasing the awareness of the extent and impact of aspirin underuse, non-compliance or cessation, and intensifying efforts at preventing them are worthy goals likely to yield significant benefits on cardiovascular morbidity and mortality worldwide, and possibly also on cancer outcomes.
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http://dx.doi.org/10.1016/j.ijcard.2014.12.091DOI Listing
March 2015

Defective functionality of HDL particles in familial apoA-I deficiency: relevance of alterations in HDL lipidome and proteome.

J Lipid Res 2014 Dec 23;55(12):2509-20. Epub 2014 Oct 23.

National Institute for Health and Medical Research (INSERM), UMR-ICAN 1166, University of Pierre and Marie Curie - Paris 6, Pitié - Salpétrière University Hospital, ICAN, Paris, France.

To evaluate functional and compositional properties of HDL in subjects from a kindred of genetic apoA-I deficiency, two homozygotes and six heterozygotes, with a nonsense mutation at APOA1 codon -2, Q[-2]X, were recruited together with age- and sex-matched healthy controls (n = 11). Homozygotes displayed undetectable plasma levels of apoA-I and reduced levels of HDL-cholesterol (HDL-C) and apoC-III (5.4% and 42.6% of controls, respectively). Heterozygotes displayed low HDL-C (21 ± 9 mg/dl), low apoA-I (79 ± 24 mg/dl), normal LDL-cholesterol (132 ± 25 mg/dl), and elevated TG (130 ± 45 mg/dl) levels. Cholesterol efflux capacity of ultracentrifugally isolated HDL subpopulations was reduced (up to -25%, P < 0.01, on a glycerophospholipid [GP] basis) in heterozygotes versus controls. Small, dense HDL3 and total HDL from heterozygotes exhibited diminished antioxidative activity (up to -48%, P < 0.001 on a total mass basis) versus controls. HDL subpopulations from both homozygotes and heterozygotes displayed altered chemical composition, with depletion in apoA-I, GP, and cholesteryl ester; enrichment in apoA-II, free cholesterol, and TG; and altered phosphosphingolipidome. The defective atheroprotective activities of HDL were correlated with altered lipid and apo composition. These data reveal that atheroprotective activities of HDL particles are impaired in homozygous and heterozygous apoA-I deficiency and are intimately related to marked alterations in protein and lipid composition.
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http://dx.doi.org/10.1194/jlr.M051631DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4242444PMC
December 2014

Intracardiac embolization of inferior vena cava filter associated with right atrium perforation and cardiac tamponade.

Rev Bras Cir Cardiovasc 2014 Apr-Jun;29(2):285-8

Insertion of inferior vena cava filters has been well established in literature, reducing occurrence of pulmonary embolism after an episode of deep venous thrombosis in patients with contraindication to anticoagulation. There are a small number of complications related to procedure and embolization is rare. In this context, we described a case of intracardiac embolization associated with cardiac tamponade.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4389464PMC
http://dx.doi.org/10.5935/1678-9741.20140060DOI Listing
July 2015

Clinically manifested myocarditis in acute rheumatic fever.

Arq Bras Cardiol 2014 Feb;102(2):e17-20

Unidade Clinica de Emergencia, Instituto do Coracao, HCFM, USP, Sao Paulo, SP, Brasil.

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3987339PMC
http://dx.doi.org/10.5935/abc.20140017DOI Listing
February 2014

Clinical manifestations and pulmonary histopathological analysis related to different diseases in patients with fatal pulmonary thromboembolism: an autopsy study.

Open Access Emerg Med 2014 10;6:15-21. Epub 2014 Mar 10.

Department of Pathology, University of São Paulo Medical School, São Paulo, Brazil.

Background: To correlate underlying diseases, in autopsies of patients with pulmonary thromboembolism (PTE) to histological findings and manifestations reviewed in the medical records.

Methods: The autopsy records between 2001 and 2008 of 291 patients whose cause of death was PTE were reviewed. The following data were obtained: age, sex, clinical "in vivo" manifestations, postmortem pathological patterns, and main associated underlying diseases, cancers, and surgeries performed in the last hospitalization. The pulmonary histopathological changes were categorized as diffuse alveolar damage, pulmonary edema, alveolar hemorrhage, and lymphoid interstitial pneumonia. Odds ratios of positive relations were obtained by logistic regression and were considered significant when P<0.05.

Results: The median age was 64 years old. About 64% of patients presented cardiovascular illness associated with PTE. The most prevalent pulmonary finding was pulmonary edema. Only 13% of cases had clinical suspicion of PTE. Acute respiratory failure was positively related to pulmonary edema, alveolar hemorrhage, and diffuse alveolar damage as well as hemodynamic instability to alveolar hemorrhage and diffuse alveolar damage.

Conclusion: We found important relations between clinical data and histological findings of patients with fatal PTE. A greater understanding of the pulmonary physiopathological mechanisms involved with each disease associated to PTE could improve its diagnosis and treatment.
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http://dx.doi.org/10.2147/OAEM.S52891DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4753983PMC
May 2016

Increasing doses of simvastatin versus combined ezetimibe/simvastatin: effect on circulating endothelial progenitor cells.

J Cardiovasc Pharmacol Ther 2013 Sep 5;18(5):447-52. Epub 2013 Jun 5.

Hospital Israelita Albert Einstein, Av Albert Einstein, Paulo-SP, Brazil.

Background: Patients with coronary artery disease (CAD) should be treated with statins to attain very low cholesterol levels, in order to reduce cardiovascular adverse events. More than 70% of these patients do not reach the appropriate cholesterol goal despite moderate statin doses. However, it is not known whether therapeutic uptitration with different lipid-lowering strategies has a similar "pleiotropic" effect on atherosclerotic endothelial dysfunction evaluated by measurement of endothelial progenitor cells (EPCs).

Objective: We sought to compare, in patients with stable CAD and with a low-density lipoprotein cholesterol (LDL-C) >70 mg/dL on treatment with simvastatin 20 mg, the effects on EPCs by increasing simvastatin to 80 mg versus adding ezetimibe 10 mg.

Methods: Patients (n = 68, 63 ± 9 years, 39% men) were randomly allocated to receive ezetimibe 10/simvastatin 20 mg or simvastatin 80 mg for 6 weeks. Circulating EPCs were measured by flow cytometry before and after the treatment.

Results: Both strategies presented similar effects on metabolic parameters. The LDLs were equally reduced by ezetimibe 10/simvastatin 20 mg and simvastatin 80 mg (28.9% ± 13% vs 21.1% ± 33%; P = .46, respectively). The levels of EPCs were unaffected by ezetimibe 10/simvastatin 20 mg (median [25th, 75th]: pre- vs posttreatment, 7.0 [2.3; 13.3] vs 3.1 [0.1; 13.2] EPCs/10(4) mononuclear cells; P = .43) or simvastatin 80 mg (pre- vs posttreatment, 6.1 [2.9; 15.2] vs 4.0 [1.4; 10.7] EPCs/10(4) mononuclear cells; P = .5), and there were no differences between the groups on treatment effects (P = .9).

Conclusions: Among stable patients with CAD and with an LDL-C >70 mg/dL on simvastatin 20 mg, increasing simvastatin dose to 80 mg or adding ezetimibe 10 mg promoted similar further cholesterol reduction but did not have incremental effects on circulating EPCs. These data suggest that the effects of simvastatin moderate doses on EPCs are not increased by intensive lipid-lowering strategies (clinicaltrials.gov: NCT00474123).
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http://dx.doi.org/10.1177/1074248413489771DOI Listing
September 2013

Preprocedural statin therapy, inflammation, and myocardial injury in low-risk stable coronary artery disease patients submitted to coronary stent implantation.

Catheter Cardiovasc Interv 2016 Feb 27;87(2):222-9. Epub 2015 Nov 27.

Acute Coronary Care Division Heart Institute (InCor), Medical School, University of São Paulo.

Objective: Evaluate if statin therapy prior to elective coronary stent implantation (CSI) reduces the plasma levels of markers of inflammation and of myocardial necrosis in low-risk stable coronary artery disease patients (CAD).

Background: The elevation of markers of inflammation and of myocardial necrosis after percutaneous coronary intervention may interfere with clinical outcome. Among acute coronary syndrome patients, statins improve clinical outcomes when used before CSI-mostly due to reduction of CSI-related myocardial infarction. However, little is known concerning preprocedural statin therapy on the reduction of these markers in stable patients at low-risk.

Methods: In this prospective, observational study, 100 patients (n = 50 on statin therapy vs. n = 50 not on statin) with stable coronary artery disease underwent elective CSI. Inflammatory (C-reactive protein [CRP], interleukin [IL]-6, tumor necrosis factor-α and matrix metalloproteinase-9) and myocardial necrosis markers (troponin I and CK-MB) were determined before and 24 hr after CSI.

Results: All patients presented a significant increase of CRP and IL-6 after CSI. However, this increase was attenuated in patients on statin therapy prior to CSI than those without statin therapy: 75% vs. 150% (P < 0.001) and 192% vs. 300% (P < 0.01). The other pro-inflammatory markers were similar for both sets of patients. Troponin I and CK-MB did not change after CSI regardless of previous statin therapy or not.

Conclusions: Pretreatment with statin attenuates procedural inflammation, denoted by markedly lower increases of CRP and IL-6 levels, in elective CSI within low-risk stable CAD patients. Periprocedural myocardial injury was irrelevant and was not affected by preprocedural statin therapy in this population.
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http://dx.doi.org/10.1002/ccd.24937DOI Listing
February 2016

Clinical characteristics and long-term outcome of patients with acute coronary syndromes and Takayasu arteritis.

Rev Port Cardiol 2013 Apr 20;32(4):297-302. Epub 2013 Mar 20.

Unidade Clínica de Emergência, Instituto do Coração, Faculdade de Medicina, Universidade de São Paulo, São Paulo, Brazil.

Introduction: Monitoring of disease activity and the best therapeutic approach are a challenge in Takayasu arteritis (TA). When associated with acute coronary syndromes (ACS), the best interventional treatment has not been established. The objective of this study was to describe the baseline characteristics, clinical manifestations, treatment and long-term outcome of patients with TA and ACS.

Methods: We retrospectively analyzed eight patients between 2004 and 2010. The following data were obtained: age, gender, clinical and electrocardiographic manifestations, Killip class, risk factors for ACS, markers of myocardial necrosis (CK-MB and troponin), creatinine clearance, left ventricular ejection fraction, inflammatory markers (C-reactive protein and erythrocyte sedimentation rate [ESR]), medication during hospital stay, angiographic findings, treatment (medical, percutaneous or surgical) and long-term outcome. Statistical data were expressed as percentages and absolute values.

Results: All eight patients were women, median age 49 years. Typical chest pain was present in 37.5%. Elevated ESR was observed in 85.7%. Three patients underwent coronary artery bypass grafting, three underwent percutaneous coronary angioplasty (two with bare-metal stents and one with a drug-eluting stent) and two were treated medically. In-hospital mortality was 25%. There were no deaths during a mean follow-up of 30 months.

Conclusions: In our study, patients who were discharged home had good outcomes in long-term follow-up with medical, percutaneous or surgical treatment. ESR appears to be associated with ACS in TA.
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http://dx.doi.org/10.1016/j.repc.2012.06.020DOI Listing
April 2013

Postmortem diagnosis of acute myocardial infarction in patients with acute respiratory failure: demographics, etiologic and pulmonary histologic analysis.

Clinics (Sao Paulo) 2012 ;67(3):213-7

Universidade de São Paulo, São Paulo, SP, Brazil.

Objectives: Acute respiratory failure is present in 5% of patients with acute myocardial infarction and is responsible for 20% to 30% of the fatal post-acute myocardial infarction. The role of inflammation associated with pulmonary edema as a cause of acute respiratory failure post-acute myocardial infarction remains to be determined. We aimed to describe the demographics, etiologic data and histological pulmonary findings obtained through autopsies of patients who died during the period from 1990 to 2008 due to acute respiratory failure with no diagnosis of acute myocardial infarction during life.

Methods: This study considers 4,223 autopsies of patients who died of acute respiratory failure that was not preceded by any particular diagnosis while they were alive. The diagnosis of acute myocardial infarction was given in 218 (4.63%) patients. The age, sex and major associated diseases were recorded for each patient. Pulmonary histopathology was categorized as follows: diffuse alveolar damage, pulmonary edema, alveolar hemorrhage and lymphoplasmacytic interstitial pneumonia. The odds ratio of acute myocardial infarction associated with specific histopathology was determined by logistic regression.

Results: In total, 147 men were included in the study. The mean age at the time of death was 64 years. Pulmonary histopathology revealed pulmonary edema as well as the presence of diffuse alveolar damage in 72.9% of patients. Bacterial bronchopneumonia was present in 11.9% of patients, systemic arterial hypertension in 10.1% and dilated cardiomyopathy in 6.9%. A multivariate analysis demonstrated a significant positive association between acute myocardial infarction with diffuse alveolar damage and pulmonary edema.

Conclusions: For the first time, we demonstrated that in autopsies of patients with acute respiratory failure as the cause of death, 5% were diagnosed with acute myocardial infarction. Pulmonary histology revealed a significant inflammatory response, which has not previously been reported.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3297028PMC
http://dx.doi.org/10.6061/clinics/2012(03)02DOI Listing
December 2012

[Rheumatoid arthritis and cardiovascular disease: what is known about this relationship and what can currently be done for affected patients?].

Rev Port Cardiol 2012 Mar;31(3):225-32

Instituto do Coraçã do do Hospital das Clínicas, Faculdade de Medicina, Universidade de São Paulo, São Paulo, Brasil.

There is increasing interest in autoimmune diseases, especially their relationship with cardiovascular disease. Rheumatoid arthritis in particular has been considered an independent risk factor for coronary artery disease in recent years. Various studies have aimed to clarify important aspects of risk stratification and treatment options in patients with rheumatoid arthritis, and specific therapies are being studied that promise to reduce their long-term cardiovascular risk. We performed a wide-ranging review of the literature to highlight the importance of atherosclerotic and inflammatory mechanisms in coronary artery disease. We also suggest strategies for risk stratification and treatment of cardiovascular disease in patients with rheumatoid arthritis.
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http://dx.doi.org/10.1016/j.repc.2012.01.005DOI Listing
March 2012

Association between depression and development of coronary artery disease: pathophysiologic and diagnostic implications.

Vasc Health Risk Manag 2011 16;7:159-64. Epub 2011 Mar 16.

Heart Institute (InCor HCFMUSP), Avenida Enéas de Carvalho Aguiar, 44 Building II, 2nd Floor, Room 12, São Paulo, SP 05403-901, Brazil.

Depression and coronary artery disease (CAD) are both extremely prevalent diseases. In addition, compromised quality of life and life expectancy are characteristics of both situations. There are several conditions that aggravate depression and facilitate the development of CAD, as well as provoke a worse prognosis in patients with already established CAD: inferior adherence to medical orientations (medications and life style modifications), greater platelet activation and aggregation, endothelial dysfunction, and impaired autonomic dysfunction (lowered heart rate variability). Recent literature has shown that depression alone is becoming an independent risk factor for cardiac events both in primary and secondary prevention. As the diagnosis of depression in patients with heart disease is difficult, due to similarities of symptoms, the health professional should perform a careful evaluation to differentiate the clinical signs of depression from those related with general heart diseases. After a myocardial infarction, depression is an independent risk factor for mortality. Successful therapy of depression has been shown to improve patients' quality of life and cardiovascular outcome. However, multicentric clinical trials are needed to support this inference. A practical liaison between qualified professionals is necessary for the better management of depressed patients with excess risk in developing CAD. Accordingly, pathophysiological and clinical implications between depression and CAD are discussed in this article.
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http://dx.doi.org/10.2147/VHRM.S10783DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3072738PMC
August 2011

Skeletonized coronary arteries: pathophysiological and clinical aspects of vascular calcification.

Vasc Health Risk Manag 2011 9;7:143-51. Epub 2011 Mar 9.

Heart Institute, Av Enéas de C Aguiar, 44 Building II, 2nd Floor, Room 12, São Paulo, SP 05403-000, Brazil.

The role of calcification in coronary artery disease is gaining importance, both in research studies and in clinical application. Calcified plaque has long been considered to be the most important atherosclerotic plaque within the arterial tree and frequently presents a challenge for percutaneous intervention. Current investigations have shown that plaque calcification has a dynamic course that is closely related to the magnitude of vascular inflammation. Numerous inflammatory factors synthesized during the early stages of atherosclerosis induce the expression and activation of osteoblast-like cells localized in the arterial wall that produce calcium. There is no doubt that the role of these factors in calcification associated with coronary artery disease could be a crucial strategic point in prevention and treatment. A number of diagnostic imaging methods have been developed in recent years, but their performance needs to be improved. In this context, we undertook an update on coronary calcification, focusing on physiopathology, clinical implications, and imaging techniques.
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http://dx.doi.org/10.2147/VHRM.S16328DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3072737PMC
August 2011

Pleiotropic effects of ezetimibe/simvastatin vs. high dose simvastatin.

Int J Cardiol 2012 Jul 21;158(3):400-4. Epub 2011 Feb 21.

Heart Institute, University of Sao Paulo, Av. Enéas de C. Aguiar, 44, Building II, 2nd Floor, Room 12, Sao Paulo, SP 05403-901, Brazil.

Background: In the setting of stable coronary artery disease (CAD), it is not known if the pleiotropic effects of cholesterol reduction differ between combined ezetimibe/simvastatin and high-dose simvastatin alone.

Objective: We sought to compare the anti-inflammatory and antiplatelet effects of ezetimibe 10mg/simvastatin 20mg (E10/S20) with simvastatin 80 mg (S80).

Methods And Results: CAD patients (n=83, 63 ± 9 years, 57% men) receiving S20, were randomly allocated to receive E10/S20 or S80, for 6 weeks. Lipids, inflammatory markers (C-reactive protein, interleukin-6, monocyte chemoattractant protein-1, soluble CD40 ligand and oxidized LDL), and platelet aggregation (platelet function analyzer [PFA]-100) changes were determined. Baseline lipids, inflammatory markers and PFA-100 were similar between groups. After treatment, E10/S20 and S80 patients presented, respectively: (1) similar reduction in LDL-C (29 ± 13% vs. 28 ± 30%, p=0.46), apo-B (18 ± 17% vs. 22 ± 15%, p=0.22) and oxidized LDL (15 ± 33% vs. 18 ± 47%, p=0.30); (2) no changes in inflammatory markers; and, (3) a higher increase of the PFA-100 with E10/S20 than with S80 (27 ± 43% vs. 8 ± 33%, p=0.02).

Conclusions: These data suggest that among stable CAD patients treated with S20, (1) both E10/S20 and S80 were equally effective in further reducing LDL-C; (2) neither treatment had any further significant anti-inflammatory effects; and (3) E10/S20 was more effective than S80 in inhibiting platelet aggregation. Thus, despite similar lipid lowering and doses 4× less of simvastatin, E10/S20 induced a greater platelet inhibitory effect than S80.
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http://dx.doi.org/10.1016/j.ijcard.2011.01.062DOI Listing
July 2012

Preoperative B-type natriuretic peptide, and not the inflammation status, predicts an adverse outcome for patients undergoing heart surgery.

Interact Cardiovasc Thorac Surg 2011 May 5;12(5):778-83. Epub 2011 Feb 5.

Heart Institute (InCor), Medical School, University of Säo Paulo, Säo Paulo, Brazil.

Objectives: B-type natriuretic peptide (BNP) and inflammatory markers are implicated in the pathophysiology of both ischemic cardiomyopathy and complications after cardiac surgery with cardiopulmonary bypass (CPB). The purpose of this study was to assess preoperative and postoperative levels of BNP, interleukin-6 (IL-6), interleukin-8 (IL-8), P-selectin, intercellular adhesion molecule (ICAM), C-reactive protein (CRP) in patients undergoing cardiac surgery with CPB and investigate their variation and ability to correlate with immediate outcome.

Methods: Plasma levels of these markers were measured preoperatively, 6 and 24 h after CBP in 62 patients. Main endpoints were requirements for intra-aortic balloon pump, intensive care unit (ICU) stay longer than five days, ventilator dependence >24 h, requirement for dobutamine, hospital stay >10 days, clinical complications (infection, myocardial infarction, renal failure, stroke and ventricular arrhythmias) and in-hospital mortality.

Results: Preoperative BNP levels correlate with longer ICU stay (P = 0.003), longer ventilator use (P = 0.018) and duration of dobutamine use (P < 0.001). The receiver-operating characteristic curve demonstrated BNP levels >190 pg/ml as predictor of ICU >5 days and BNP levels >20.5 pg/ml correlated with dobutamine use, with areas under the curve of 0.712 and 0.842, respectively. Preoperative levels of ICAM-1 were associated with in-hospital mortality (P = 0.042). In the postoperative period, was found association between CRP, IL-6 and P-selectin with ventilation duration (P = 0.013, P = 0.006, P < 0.001, respectively) and P-selectin with ICU stay (P = 0.009).

Conclusions: BNP correlates with clinical endpoints more than inflammatory markers and can be used as a predictor of early outcome after heart surgery.
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http://dx.doi.org/10.1510/icvts.2010.255257DOI Listing
May 2011