RESUMO
In 386 men aged 40-49 years the number of platelets was related to differences in smoking habits. "Platelet adhesiveness" (retention) was estimated by a glass bead filter method in 376 of these men. The estimation of "adhesiveness" was performed in native blood without anticoagulants at least 12 hr after the last cigarette smoked. A small but statistically highly significant increase in platelet count, in number of "adhesive platelets" and percentage of "adhesive platelets" was found in smokers as compared with non-smokers, the highest values being found in the heaviest smokers and vice versa. Such smoking-related changes in platelet count and reactiveness might unfavourably influence the tendency towards coronary thrombosis, and might in part explain the deleterious effects of smoking on coronary heart disease morbidity and mortality.
Assuntos
Plaquetas , Adesividade Plaquetária , Fumar/fisiopatologia , Adulto , Contagem de Células Sanguíneas , Doença Crônica , Feminino , Humanos , Pessoa de Meia-IdadeRESUMO
The view based on epidemiological and laboratory data that blood group A subjects (=A) have clinically significant higher thrombotic potential than blood group 0 subjects (=O), is supported by the present finding of a significantly higher platelet retention in A than 0. The completely normal AB0 distribution found among 71 cases of proven latent CHD, and the disproportionate excess of 0 vs. A in a consecutive series of 191 coronary artery bypass candidates apparently conflict with epidemiological data indicating a higher risk of achieving CHD in A than 0. The conflict may be solved by suggesting a) that the "thrombotic proneness" in A compared with 0 causes a poorer prognosis in CHD among the former, leaving a disproportionate excess of 0 among longterm CHD survivors, and b) that AB0-related factors have had an insignificant, independent impact on the evolution of preclinical coronary artery disease in our 71 men with latent CHD.
Assuntos
Sistema ABO de Grupos Sanguíneos/genética , Doença das Coronárias/sangue , Adulto , Angiografia , Artérias/cirurgia , Plaquetas , Humanos , Lipídeos/fisiologia , Masculino , Pessoa de Meia-IdadeAssuntos
Doenças Cardiovasculares/epidemiologia , Fator de von Willebrand/metabolismo , Antígenos/análise , Arteriosclerose/epidemiologia , Transtornos Cerebrovasculares/epidemiologia , Colesterol/sangue , Doença das Coronárias/epidemiologia , Humanos , Masculino , Pessoa de Meia-Idade , Estudos Prospectivos , Risco , Fator de von Willebrand/imunologiaRESUMO
Hypothyroidism is associated with severe coronary atherosclerosis. In spite of this the reported incidence of angina pectoris and myocardial infarction in untreated hypothyroidism is small. Since many authors consider the formation of a thrombus in coronary arteries to be the final event of the process which leads to myocardial infarction, changes in the platelet function may explain the paradoxical rarity of myocardial infarction in untreated hypothyroidism. To evaluate this hypothesis, platelet adhesiveness has been estimated before and after treatment in 9 hypothyroid and 16 thyrotoxic patients. In thyrotoxicosis the platelet adhesiveness was significantly increased, but decreased to normal after treatment. In hypothyroidism platelet adhesiveness was abnormally low but increased to normal value after thyroid hormone replacement. This may be an important factor in precipitating myocardial infarction in patients with hypothyroidism and coronary artery atherosclerosis.
Assuntos
Hipertireoidismo/sangue , Hipotireoidismo/sangue , Adesividade Plaquetária , Doença das Coronárias/sangue , Humanos , Hipertireoidismo/terapia , Hipotireoidismo/tratamento farmacológico , Hipotireoidismo/terapia , Infarto do Miocárdio/sangue , Infarto do Miocárdio/induzido quimicamente , Hormônios Tireóideos/efeitos adversos , Hormônios Tireóideos/uso terapêuticoRESUMO
Among 2014 apparently healthy men aged 40-59 years platelet function was studied with Hellem's retention method in 488 men. In 55 of these 488 men coronary heart disease (CHD) was strongly suspected and coronary angiography confirmed the diagnosis in 34 of 51 angiographied men. Platelet responsiveness was significantly lower among those who had angina pectoris than among their CHD-suspect counterparts without angina, regardless of coronary angiographic findings. Since angiopositive men without angina and 408 "normals" had similar retention values, it seems as if presenting symptoms, but not the development of CHD are linked to platelet function. During a near maximal bicycle exercise test significantly higher peak exercise blood pressure was found among men with very low retention values than among men with retention values in the middle and upper range. This could not be explained by differences in maximal heart rate or work performance. This indicates that blood pressure regulation during exercise may in part be linked to platelet function related mechanisms.