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1.  Cylinder Mania in Valvulopathy Back to the Future 
Arquivos Brasileiros de Cardiologia  2014;103(3):e41-e44.
PMCID: PMC4193077  PMID: 25317945
Heart Valve Diseases; Stethoscopes / utilization; Heart Auscultation / trends
2.  Bioethics Cardioteam Useful for Bedside Crisis Management 
Arquivos Brasileiros de Cardiologia  2014;103(2):e26-e28.
PMCID: PMC4150672  PMID: 25211318
Bioethics; Health Management; Point of Care Systems / organization & administration
3.  Valvular Heart Team 
Arquivos Brasileiros de Cardiologia  2014;103(1):e15-e17.
PMCID: PMC4126767  PMID: 25120089
Aortic Valve Stenosis; Cardiac Catheterization; Heart Valve Prosthesis Implantation / methods; Bioprosthesis; Bioethics
4.  Patients' use of the Internet 
PMCID: PMC4028942  PMID: 24838603
Access to Information; Bioethics; Internet / utilization
5.  Paternalism, Autonomy and Ontology 
Arquivos Brasileiros de Cardiologia  2013;101(4):e83-e85.
PMCID: PMC4062380  PMID: 24217437
Cardiomyopathies; Heart Valve Diseases; Rheumatic Heart Disease; Paternalism
6.  Feminization of Medicine 
PMCID: PMC4032310  PMID: 24061755
Feminization; Physicians, Women / statistics & numerical data, Education, Medical; Age and Sex Distribution
7.  Prophylaxis of Infective Endocarditis: A Different Brazilian Reality? 
Arquivos brasileiros de cardiologia  2013;101(2):e37-e38.
PMCID: PMC3998147  PMID: 24030084
Endocarditis / mortality; Antibiotic Prophylaxis; Rheumatic Fever
8.  Poll - Jehovah's Witness Patient Among Baixada Santista and ABC Paulista Cardiologists 
PMCID: PMC3998179  PMID: 23917510
Environmental Statistics; Jehovah's Witnesses; Bioethics
9.  Protein Quality Control Disruption by PKCβII in Heart Failure; Rescue by the Selective PKCβII Inhibitor, βIIV5-3 
PLoS ONE  2012;7(3):e33175.
Myocardial remodeling and heart failure (HF) are common sequelae of many forms of cardiovascular disease and a leading cause of mortality worldwide. Accumulation of damaged cardiac proteins in heart failure has been described. However, how protein quality control (PQC) is regulated and its contribution to HF development are not known. Here, we describe a novel role for activated protein kinase C isoform βII (PKCβII) in disrupting PQC. We show that active PKCβII directly phosphorylated the proteasome and inhibited proteasomal activity in vitro and in cultured neonatal cardiomyocytes. Importantly, inhibition of PKCβII, using a selective PKCβII peptide inhibitor (βIIV5-3), improved proteasomal activity and conferred protection in cultured neonatal cardiomyocytes. We also show that sustained inhibition of PKCβII increased proteasomal activity, decreased accumulation of damaged and misfolded proteins and increased animal survival in two rat models of HF. Interestingly, βIIV5-3-mediated protection was blunted by sustained proteasomal inhibition in HF. Finally, increased cardiac PKCβII activity and accumulation of misfolded proteins associated with decreased proteasomal function were found also in remodeled and failing human hearts, indicating a potential clinical relevance of our findings. Together, our data highlights PKCβII as a novel inhibitor of proteasomal function. PQC disruption by increased PKCβII activity in vivo appears to contribute to the pathophysiology of heart failure, suggesting that PKCβII inhibition may benefit patients with heart failure. (218 words)
PMCID: PMC3316563  PMID: 22479367
10.  Association of Mannose-Binding Lectin Gene Polymorphism but Not of Mannose-Binding Serine Protease 2 with Chronic Severe Aortic Regurgitation of Rheumatic Etiology▿  
N-Acetylglucosamine (GlcNAc) is the major immunoepitope of group A streptococcal cell wall carbohydrates. Antistreptococcal antibodies cross-reactive with anti-GlcNAc and laminin are present in sera of patients with rheumatic fever. The cross-reactivity of these antibodies with human heart valvular endothelium and the underlying basement membrane has been suggested to be a possible cause of immune-mediated valve lesion. Mannose-binding lectin (MBL) encoded by the MBL2 gene, a soluble pathogen recognition receptor, has high affinity for GlcNAc. We postulated that mutations in exon 1 of the MBL2 gene associated with a deficient serum level of MBL may contribute to chronic severe aortic regurgitation (AR) of rheumatic etiology. We studied 90 patients with severe chronic AR of rheumatic etiology and 281 healthy controls (HC) for the variants of the MBL2 gene at codons 52, 54, and 57 by using a PCR-restriction fragment length polymorphism-based method. We observed a significant difference in the prevalence of defective MBL2 alleles between patients with chronic severe AR and HC. Sixteen percent of patients with chronic severe AR were homozygotes or compound heterozygotes for defective MBL alleles in contrast to 5% for HC (P = 0.0022; odds ratio, 3.5 [95% confidence interval, 1.6 to 7.7]). No association was detected with the variant of the MASP2 gene. Our study suggests that MBL deficiency may contribute to the development of chronic severe AR of rheumatic etiology.
PMCID: PMC2446618  PMID: 18400978
11.  Rheumatic heart disease: 15 years of clinical and immunological follow-up 
Vascular Health and Risk Management  2007;3(6):1007-1017.
Rheumatic fever (RF) is a sequel of group A streptococcal throat infection and occurs in untreated susceptible children. Rheumatic heart disease (RHD), the major sequel of RF, occurs in 30%–45% of RF patients. RF is still considered endemic in some regions of Brazil and is responsible for approximately 90% of early childhood valvular surgery in the country. In this study, we present a 15-year clinical follow-up of 25 children who underwent surgical valvular repair. Histopathological and immunological features of heart tissue lesions of RHD patients were also evaluated. The patients presented severe forms of RHD with congestive symptoms at a very young age. Many of them had surgery at the acute phase of RF. Histological analysis showed the presence of dense valvular inflammatory infiltrates and Aschoff nodules in the myocardium of 21% of acute RHD patients. Infiltrating T-cells were mainly CD4+ in heart tissue biopsies of patients with rheumatic activity. In addition, CD4+ and CD8+ infiltrating T-cell clones recognized streptococcal M peptides and cardiac tissue proteins. These findings may open the possibilities of new ways of immunotherapy. In addition, we demonstrated that the surgical procedure during acute phase of the disease improved the quality of life of young RHD patients.
PMCID: PMC2350126  PMID: 18200819
rheumatic heart disease; Streptococcus pyogenes; heart failure; inflammatory infiltrate; T lymphocytes; molecular mimicry

Results 1-11 (11)