Abstract
This paper reviews the principles of thrombocytic aggregation, available methods of measuring it and pitfalls in the interpretation of results obtained. A list of eight aggregometric methods provides descriptions of the evaluation of bleeding times, of optic and impedance whole blood aggregometry, of thrombelastography and flow cytometry, as well as describing measurements of urine levels of the metabolite thromboxan.
We report how results depend on the way in which the aggregation is induced. Absolute aggregation remains, as yet, immeasurable.
The effectiveness of prevention of atherosclerotic complications using anti-aggregation therapy is usually determined on the basis of studies that observe the impact of reduced thrombogenesis and emboligenesis on clinical outcome. Modifications in drug dosage are usually stipulated by such secondary and derived data.
The intensity of aggregation readiness itself - due to difficulties in assessing it - plays only a minor role in these decisions and is only slowly achieving credibility. We also summarize current views on resistance to acetylsalicylic acid, which appears in two variants: clinical resistance and laboratory resistance.
We conclude with an overview of future possibilities for monitoring aggregation.