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1.
Menopause ; 20(1): 57-63, 2013 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-22968255

RESUMO

OBJECTIVE: Age-adjusted incidence of cardiovascular disease, including myocardial infarction, is significantly lower in premenopausal women than in men, which is thought to be caused by the cardioprotective effects of estrogen. However, there is a consistent increase in the incidence of coronary artery disease in postmenopausal women in comparison with premenopausal women. The protective benefit of hormone therapy has not been observed in postmenopausal women. It is unknown whether measures of platelet reactivity and clot strength contribute to the disproportionate incidence of cardiovascular disease between premenopausal and postmenopausal women. METHODS: Fifty healthy volunteers, including 25 premenopausal women and 25 postmenopausal women, aged between 40 and 65 years were enrolled. Total estradiol and follicle-stimulating hormone levels were measured for confirmation of menopausal state and comparison testing. Platelet reactivity was assessed using light transmission aggregometry and P-selectin, and glycoprotein IIb/IIIa receptor expression was assessed using flow cytometry. Thrombelastography was used to measure clot strength, clotting time, and fibrinogen activity. Serum cholesterol, C-reactive protein, complete blood count, and comprehensive metabolic panel were also measured. RESULTS: Platelet reactivity did not differ among menopausal states or hormone levels. Clotting time was increased in postmenopausal women (6.6 ± 2.0 vs. 7.8 ± 1.2 min, P = 0.013) and significantly correlated with estradiol levels (r = 0.68, P < 0.001). A significantly higher low-density lipoprotein cholesterol level was observed in postmenopausal women (P = 0.05). Mean C-reactive protein levels were numerically higher in the postmenopausal group. CONCLUSIONS: The thrombotic risk profile between premenopausal and postmenopausal women is similar. However, improved management of cholesterol may be of clinical benefit. Large-scale studies are required to validate these findings.


Assuntos
Plaquetas/fisiologia , Pós-Menopausa/fisiologia , Trombose/epidemiologia , Adulto , Idoso , Proteína C-Reativa/análise , Colesterol/sangue , LDL-Colesterol/sangue , Estradiol/sangue , Feminino , Hormônio Foliculoestimulante/sangue , Humanos , Integrina beta3/sangue , Pessoa de Meia-Idade , Selectina-P/sangue , Agregação Plaquetária , Glicoproteína IIb da Membrana de Plaquetas/sangue , Fatores de Risco
2.
Am J Cardiol ; 108(3 Suppl): 42B-51B, 2011 Aug 02.
Artigo em Inglês | MEDLINE | ID: mdl-21802580

RESUMO

The role of cardiovascular risk reduction in patients with diabetes mellitus is significant as several factors have been found to promote accelerated atherosclerosis in persons with diabetes including hyperglycemia-induced endothelial dysfunction, impaired fibrinolysis, increased platelet aggregation, plaque instability, dysfunctional arterial remodeling, and fibrotic and calcified coronary arteries. Recent attention has focused on identifying a cardiovascular biomarker that would propose a better noninvasive way to detect or visualize subclinical cardiovascular disease and prevent cardiovascular events. This article reviews the use of commonly used cardiovascular risk assessment tools and emerging biomarkers including coronary artery calcium scanning, metabolomics, genomics, and the role of optimal revascularization and risk reduction strategies and their impact on reducing risk in patients with cardiovascular disease and diabetes.


Assuntos
Angiopatias Diabéticas/epidemiologia , Aspirina/uso terapêutico , Aterosclerose/epidemiologia , Aterosclerose/metabolismo , Biomarcadores/análise , Cálcio/análise , Vasos Coronários/química , Angiopatias Diabéticas/diagnóstico , Angiopatias Diabéticas/metabolismo , Angiopatias Diabéticas/prevenção & controle , Progressão da Doença , Genômica , Humanos , Estilo de Vida , Metabolômica , Infarto do Miocárdio/epidemiologia , Infarto do Miocárdio/metabolismo , Isquemia Miocárdica/terapia , Revascularização Miocárdica , Inibidores da Agregação Plaquetária/uso terapêutico , Medição de Risco , Comportamento de Redução do Risco
4.
Curr Atheroscler Rep ; 13(2): 123-8, 2011 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-21287301

RESUMO

As a result of ambiguous results from several recent trials in diabetes, scrutiny has focused on the potential effects of insulin and its role in atherosclerosis. This article reviews the premise that anti-diabetes therapy (type 2 diabetes) with insulin causes vascular impairment that leads to atherothrombosis and compromises vascular integrity, which may further potentiates cardiovascular morbidity and mortality. Underlying mechanisms are discussed, including metabolic derangements (blood pressure, lipids, body weight, and glucose) and how these factors trigger insulin-like growth factor (IGF) receptors, leading to cancer. Cellular and molecular mechanisms are discussed, as well as whether the negative results seen in recent glucose trials support this premise. As with most drug therapy, aggressive therapies designed to reach glucose control targets trigger multiple and inter-related mechanisms that, in many cases, go far beyond the pre-determined physiologic targets. From a clinical perspective, physicians should always stress lifestyle modifications, including physical exercise and diet, to their patients who show the first signs of metabolic impairment. Yet even within this context, diet and exercise should be the cornerstone of good therapy when pharmacotherapy is necessary. Given the amount of evidence seen to date with existing agents and the amount of information we do not yet know, patient-centered approaches to modifying behavior before intensive drug therapy are needed should be stressed.


Assuntos
Aterosclerose/induzido quimicamente , Doenças Cardiovasculares/induzido quimicamente , Diabetes Mellitus Tipo 2/tratamento farmacológico , Angiopatias Diabéticas/induzido quimicamente , Insulina/efeitos adversos , Idoso , Aterosclerose/epidemiologia , Aterosclerose/fisiopatologia , Glicemia/análise , Doenças Cardiovasculares/epidemiologia , Doenças Cardiovasculares/fisiopatologia , Diabetes Mellitus Tipo 2/diagnóstico , Diabetes Mellitus Tipo 2/epidemiologia , Angiopatias Diabéticas/epidemiologia , Angiopatias Diabéticas/fisiopatologia , Relação Dose-Resposta a Droga , Esquema de Medicação , Feminino , Seguimentos , Humanos , Hipoglicemiantes/efeitos adversos , Hipoglicemiantes/uso terapêutico , Insulina/uso terapêutico , Masculino , Pessoa de Meia-Idade , Neoplasias/epidemiologia , Neoplasias/etiologia , Neoplasias/fisiopatologia , Prevalência , Ensaios Clínicos Controlados Aleatórios como Assunto , Medição de Risco
5.
South Med J ; 101(12): 1203-8, 2008 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-19005437

RESUMO

BACKGROUND: Dark chocolate (DC) is one of the richest sources of flavonoids. Since DC has been demonstrated to have beneficial effects on the cardiovascular system, our study examined its effect on platelet reactivity, inflammation, and lipid levels in healthy subjects. METHODS: In 28 healthy volunteers, we analyzed the effect of one week of DC (providing 700 mg of flavonoids/day). The primary outcome was to determine the effects of DC consumption on platelet activity measured by flow cytometry (adenosine diphosphate [ADP]- and arachidonic acid [AA]-induced total and activated glycoprotein (GP) IIb/IIIa as well as P-selectin expression). In addition to this, we measured the effect of DC on high-sensitivity C-reactive protein (hsCRP), high-density lipid cholesterol (HDL) and low-density lipid cholesterol (LDL) levels. RESULTS: Following seven days of regular DC ingestion, LDL fell by 6% (120 +/- 38 vs 112 +/- 37 mg/dL, P < 0.018) and HDL rose by 9% (66 +/- 23 vs 72 +/- 26 mg/dL, P < 0.0019). ADP- and AA-induced activated GPIIb/IIIa expression was reduced by DC [27.3 +/- 27.8 vs 17.4 +/- 20.5 mean fluorescence intensity (MFI), P < 0.006; and 9.2 +/- 6.5 vs. 6.1 +/- 2.2 MFI, P < 0.005, respectively]. DC reduced hsCRP levels in women (1.8 +/- 2.1 vs. 1.4 +/- 1.7 mg/dL, P < 0.04). CONCLUSIONS: One week of DC ingestion improved lipid profiles and decreased platelet reactivity within the total group while reducing inflammation only in women. Regular dark chocolate ingestion may have cardioprotective properties. Further long-term research is warranted to evaluate the effect of flavonoids on cardiovascular health and to determine whether DC's beneficial effects are related to flavonoids or some yet unknown component. This research is based on a larger study which was presented at the American Heart Association Scientific Sessions 2007.


Assuntos
Proteína C-Reativa/metabolismo , Cacau , HDL-Colesterol/sangue , LDL-Colesterol/sangue , Flavonoides/administração & dosagem , Ativação Plaquetária/efeitos dos fármacos , Agregação Plaquetária/efeitos dos fármacos , Adulto , Cacau/química , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Complexo Glicoproteico GPIIb-IIIa de Plaquetas/efeitos dos fármacos , Estudos Prospectivos , Fatores Sexuais
6.
Diabetes ; 56(12): 3014-9, 2007 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-17848625

RESUMO

OBJECTIVE: Diabetic patients may have a higher prevalence of platelet aspirin resistance than nondiabetic patients. Our goal was to analyze platelet aspirin responsiveness to various aspirin doses in diabetic and nondiabetic patients. RESEARCH DESIGN AND METHODS: We examined the effect of aspirin (81, 162, and 325 mg/day for 4 weeks each) on platelet aspirin responsiveness in 120 stable outpatients (30 diabetic patients and 90 nondiabetic patients) with coronary artery disease (CAD) using light transmittance aggregometry (LTA), VerifyNow, platelet function analyzer (PFA)-100, and levels of urinary 11-dehydro-thromboxane B(2) (11-dh-TxB(2)). RESULTS: In the total group, a low prevalence (0-2%) of aspirin resistance was observed with all aspirin doses as determined by arachidonic acid-induced LTA. Aspirin resistance was higher at the 81-mg dose in diabetic versus nondiabetic patients using collagen-induced LTA (27 vs. 4%, P = 0.001), VerifyNow (13 vs. 3%, P = 0.05), and urinary 11-dh-TxB(2) (37 vs. 17%, P = 0.03). Diabetic patients treated with 81 mg exhibited higher platelet function measured by VerifyNow, collagen- and ADP-induced LTA, and 11-dh-TxB(2) levels (P

Assuntos
Aspirina/uso terapêutico , Plaquetas/fisiologia , Doença das Coronárias/sangue , Angiopatias Diabéticas/sangue , Inibidores da Agregação Plaquetária/uso terapêutico , Idoso , Plaquetas/efeitos dos fármacos , Doença das Coronárias/tratamento farmacológico , Estudos Cross-Over , Angiopatias Diabéticas/tratamento farmacológico , Método Duplo-Cego , Resistência a Medicamentos , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Agregação Plaquetária/efeitos dos fármacos , Valores de Referência , Tromboxano B2/urina
7.
Rev. méd. hered ; 8(1): 11-8, mar. 1997. tab
Artigo em Espanhol | LILACS, LIPECS | ID: lil-224917

RESUMO

El presente trabajo tuvo como objetivo, conocer la prevalencia de la deficiencia de la G-6-PDH, en la población masculina mestiza, aparentemente sana que acude a los Bancos de sangre de los hospitales nacionales Cayetano Heredia (HNCH) y Arzobispo Loayza (HNAL). Material y métodos: Se examinó 140 muestras de hemodonadores entre junio y julio, 60 (42.85 por ciento) correspondieron al HNCH y 80 (57.15 por ciento) al HNCH. Se aplicó un cuestionario a todos los donantes indagando por: raza en los ancestros y antecedentes patológicos compatibles con episodios de hemódialisis enzimopática. En todas las muestras se empleó el método cualitativo de Brewer (tamizaje) y posteriormente fueron sometidos a la prueba cuantitativa SIGMA. Resultados: Con el método de Brewer resultaron 9 casos positivos (6.42 por ciento) de los cuales sólo uno resultó positivo con el método confirmatorio, lo cual da una prevalencia de 0.71 por ciento. La totalidad de los participantes fueron de raza mestiza, carecían de antecedentes importantes, las edades estuvieron comprendidas entre los 18 a 58 años y el hematocrito entre 40 y 48 por ciento. Conclusiones: Se confirma que la prevalencia de esta deficiencia, en nuestra población es bastante baja.


Assuntos
Humanos , Masculino , Doadores de Sangue , Glucosefosfato Desidrogenase , Deficiência de Glucosefosfato Desidrogenase
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