Abstract
To the Editor: The study by Haskell et al. (March 29 issue)1 and the accompanying editorial2 convincingly argue that the “protective” effect of alcohol in coronary heart disease is not related to changes in concentrations of high-density lipoproteins. Another mechanism mediating this “protective” effect may relate to the ability of ethanol to influence platelet function. Hitherto, the ethanol concentrations required to inhibit platelet aggregation and the release of thromboxane A2 (a vasoconstrictor and stimulator of platelet aggregation) markedly were rather high and were comparable to those seen in patients with acute alcoholic intoxication.3 Using more sensitive techniques, we have.
| Original language | English |
|---|---|
| Pages (from-to) | 537-538 |
| Number of pages | 2 |
| Journal | New England Journal of Medicine |
| Volume | 311 |
| Issue number | 8 |
| DOIs | |
| State | Published - Aug 23 1984 |
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