Avalia&ccedil;&atilde;o da agrega&ccedil;&atilde;o plaquet&aacute;ria e dosagem do fibrinog&ecirc;nio em pacientes com doen&ccedil;as cardiovasculares e sua correla&ccedil;&atilde;o com o uso de aspirina e fatores de risco coronariano  <span class="so-article-trans-title"> Translated title: Evaluation of platelet aggregation and level of fibrinogen in patients with cardiovascular diseases and the correlation of taking aspirin with coronary risk factors </span>

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Abstract

OBJETIVO: Avaliar a resistência à aspirina em pacientes com doenças cardiovasculares. Avaliar a dosagem do fibrinogênio sérico em pacientes usuários de aspirina, comparando-a com os que não a utilizam. Correlacionar a agregação plaquetária e o fibrinogênio sérico com parâmetros ligados ao risco cardiovascular. MÉTODO: Oitenta e dois pacientes divididos em dois grupos: grupo 1 - 41 pacientes que utilizaram aspirina na dose de 100mg/dia e grupo 2 - 41 pacientes que não utilizaram antiagregante plaquetário. Foram coletados dados epidemiológicos quanto a idade, sexo, tabagismo, etilismo, e foram realizadas dosagens de fibrinogênio sérico e agregação plaquetária. RESULTADOS: Nos grupos analisados, a idade avançada (p=0,011), o tabagismo (p=0,009) e o etilismo (p=0,007) apresentaram associação direta com o fibrinogênio sérico. Não houve correlação entre tabagismo, etilismo, fibrinogênio sérico e os valores da agregação plaquetária (p>0,05). No grupo 1, 29% dos pacientes apresentaram resistência à aspirina. Destes, os tabagistas (p=0,029) e os etilistas (p=0,033) exibiram fibrinogênio sérico mais elevado. CONCLUSÃO: A resistência à aspirina esteve presente em número elevado de pacientes. Além disso, idade avançada, tabagismo e etilismo influenciaram diretamente o fibrinogênio sérico.

Translated abstract

OBJECTIVE: To evaluate aspirin resistance in patients with cardiovascular diseases and to compare the amount of serum fibrinogen in patients taking aspirin with those who do not. To correlate the platelet aggregation and serum fibrinogen to cardiovascular risk parameters. METHODS: Eighty-two patients were divided into two groups: Group 1 - 41 patients who took 100mg aspirin daily and Group 2 - 41 patients who did not utilized platelet antiaggregates. Epidemiological data were collected including age, gender and information on smoking and alcohol intake and serum fibrinogen and platelet aggregation were mesured. RESULTS: In the groups analyzed, advanced age (p=0.011), smoking (p=0.009) and alcoholism (p=0.007) were directly associated to the serum fibrinogenen level. There were no correlations between smoking, alcoholism, serum fibrinogen and platelet aggregation values (p>0.05). In Group 1, 29% of the patients presented with aspirin resistance. Of these, smokers (p=0.029) and the alcoholics (p=0.033) had higher serum fibrinogen levels. CONCLUSION: Aspirin resistance was present in a high number of patients. Moreover, advanced age, smoking and alcoholism had a direct influence on the serum fibrinogen levels.

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We studied whether aspirin resistance, defined as failure of suppression of thromboxane generation, increases the risk of cardiovascular events in a high-risk population. Baseline urine samples were obtained from 5529 Canadian patients enrolled in the Heart Outcomes Prevention Evaluation (HOPE) Study. Using a nested case-control design, we measured urinary 11-dehydro thromboxane B2 levels, a marker of in vivo thromboxane generation, in 488 cases treated with aspirin who had myocardial infarction, stroke, or cardiovascular death during 5 years of follow-up and in 488 sex- and age-matched control subjects also receiving aspirin who did not have an event. After adjustment for baseline differences, the odds for the composite outcome of myocardial infarction, stroke, or cardiovascular death increased with each increasing quartile of 11-dehydro thromboxane B2, with patients in the upper quartile having a 1.8-times-higher risk than those in the lower quartile (OR, 1.8; 95% CI, 1.2 to 2.7; P=0.009). Those in the upper quartile had a 2-times-higher risk of myocardial infarction (OR, 2.0; 95% CI, 1.2 to 3.4; P=0.006) and a 3.5-times-higher risk of cardiovascular death (OR, 3.5; 95% CI, 1.7 to 7.4; P<0.001) than those in the lower quartile. In aspirin-treated patients, urinary concentrations of 11-dehydro thromboxane B2 predict the future risk of myocardial infarction or cardiovascular death. These findings raise the possibility that elevated urinary 11-dehydro thromboxane B2 levels identify patients who are relatively resistant to aspirin and who may benefit from additional antiplatelet therapies or treatments that more effectively block in vivo thromboxane production or activity.