When receiving anticoagulant heparin (H), up to ~3% patients develop anti-platelet factor 4 (PF4)/H antibodies. These antibodies bind to PF4/H complexes followed by bridging and activating platelets, thereby forming platelet aggregation and activation. A subset of these antibodies selects their own antigens(https://www.nature.com/articles/ncomms14945), binds strongly to platelets, and activates them (https://www.ncbi.nlm.nih.gov/pubmed/30540167).
This side effect is called heparin-induced thrombocytopenia (HIT) which can result in life-threatening. It has been shown that long heparins induce more frequent HIT than short ones (https://pubs.rsc.org/en/Content/ArticleLanding/NR/2015/C5NR02132D#!divAbstract), while synthetic heparins increase binding to PF4 (https://www.ncbi.nlm.nih.gov/pubmed/31573759).