Treatment with DCB was associated with a similar risk of TLR and a lower risk of definite TLT compared with nDES. In selected cases, DCB appears as a good alternative to nDES for the treatment of de novo coronary lesions.

SummarySeventy-three (58 men and 15 women) survivors of myocardial infarction below 45 years of age and 73 healthy matched controls were investigated regarding in vitro platelet aggregability to ADP and collagen, platelet sensitivity to prostacyclin and plasma levels of beta-thromboglobulin, platelet factor 4 and fibrinogen. The patients, studied 3-6 months after the acute event, had a reduced platelet sensitivity to prostacyclin. They did not differ from the controls regarding the other platelet function tests. Females had higher platelet reactivity than men. Smoking, obesity or beta- blocker treatment did not influence platelet function. The patients had higher fibrinogen levels than the controls. Gender did not influence, while smoking and obesity increased plasma fibrinogen. Patients on beta-blockade had lower fibrinogen levels than patients without this therapy. The high fibrinogen level and the low platelet sensitivity to prostacyclin might indicate an increased thrombotic liability in young myocardial infarction patients.

One-hundred-and-ninety-three men with unstable coronary artery disease (CAD) (i.e. unstable angina or a non-Q wave myocardial infarction) were randomized in a double-blind fashion to acetylsalicylic acid (ASA) 75 mg daily (n = 100) or placebo (n = 93) within 72 h of admission to the Coronary Care Unit. Platelet function was evaluated as ex vivo aggregation toward collagen and ADP before and after 5 days, 1, 12, 18 and 24 months of treatment. ASA decreased aggregation by collagen 1 mg l-1 from 81.3 +/- 1.7% before to 34.0 +/- 1.7% after 1 month (P less than 0.001), while no change was observed in the placebo group. Aggregation by ADP 1 microM after 1 month was 42.1 +/- 1.1% and 51.0 +/- 2.0% in the ASA and placebo groups respectively (P less than 0.001). The platelet inhibition by ASA was maintained during 24 months. All ASA patients had reduced aggregation during treatment. A cumulative dose of 300 mg (4 doses of 75 mg) was not enough for maximal inhibition at the second aggregation test. Thus, ASA 75 mg daily causes platelet inhibition in all patients without attenuation during long-term treatment. If low dose ASA is started in unstable coronary artery disease a loading dose exceeding 300 mg is suggested.

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