| First Author | Nyrop M | Year | 1989 |
| Journal | Ugeskr Laeger | Volume | 151 |
| Issue | 39 | Pages | 2504-7 |
| PubMed ID | 2678654 | Mgi Jnum | J:161690 |
| Mgi Id | MGI:4460868 | Citation | Nyrop M (1989) [Platelet function, hypertension and ischemic heart disease]. Ugeskr Laeger 151(39):2504-7 |
| abstractText | Treatment of mild to moderate hypertension does not result in any obvious reduction in the frequency of coronary heart disease (CDH) whereas the frequency of cerebrovascular disease is reduced. Platelet activation assumes a central role in the development of arteriosclerosis which is presumed to be the basis of coronary heart disease. Platelet activation may occur at sites of damaged endothelium (eg in the arteriosclerotic plaque) and by means of influencing specific thrombocyte receptors. The receptors may also be activated in vitro, which may be utilized experimentally. By means of stratification of material from the literature, it appears possible that patients with high mean arterial blood pressures (MAP) (over approximately 120 mmHg) have an increased tendency to platelet aggregation for ADP and adrenalin. This hyper-aggregability appears to be related to the blood pressure as it is normalized when MAP is reduced by treatment to values around 120 mmHg. If MAP is under 120 mmHg already, no further decrease in the tendency to platelet aggregation occurs. Some investigations suggest an effect on ischaemic heart disease on treatment of the most hypersensitive patients. The observations quoted in the present article are in agreement with the theory that thrombocyte aggregation may be of significance for development of CDH. |
