Interv Akut Kardiol. 2017;16(2):56-60 | DOI: 10.36290/kar.2017.010
Platelet hyperaggregability as a distinct cause of thrombosis was recognized for the first time in the late 1970s. In the 1980s, the term SPS was proposed for a thrombophilic thrombocytopathy with familiar occurrence and autosomal trait, characterized by increased platelet aggregation after low concentrations of adenosine diphosphate (ADP) and/or epinephrine (EPI). In the last 30 years, several authors – E. F. Mammen and R. L. Bick in the first place – provided clinical evidence that led to the definition of exact diagnostic criteria, with three types of aggregation patterns, and associated SPS with a variety of thrombotic events – a) arterial, including myocardial infarction and stroke, b) venous thromboembolism, and c) pregnancy complications (fetal loss and intrauterine growth retardation). SPS was initially thought to be a rare disorder but it was subsequently reportedunexpectedly often as a cause of otherwise unexplained thrombosis and pregnancy complications. However, key issues, such as the syndrome’s etiology, genetics and epidemiology, remain unclear. The first part of the review summarizes the published results of research on SPS. In addition to studies of well-known researchers, the authors include and demonstrate the syndrome’s characteristics with a retrospective analysis of their own patient cohort (> 450 symptomatic SPS cases). The second part deals with unresolved and controversial issues.
Received: April 15, 2017; Accepted: April 24, 2017; Published: May 1, 2017 Show citation