Activation of circulating platelets in patients with peripheral arterial disease during digital subtraction angiography and percutaneous transluminal angioplasty.
Platelet activation plays a crucial role in the pathogenesis of coronary heart disease (CHD), peripheral arterial disease (PAD) and cerebral ischaemia, the three main clinical manifestations of atherosclerosis. Circulating-activated platelets are thought to trigger ischaemic complications after angiography, angioplasty and vascular surgery. We studied activation of circulating thrombocytes in patients with PAD and evaluated the influence on platelet activation of intraarterial digital subtraction angiography (DSA) and percutaneous transluminal angioplasty (PTA) in the area of the lower extremities. Our study included 16 control subjects with PAD (clinical stage IIb according to Fontaine), 25 healthy control subjects and 34 PAD patients (clinical stage IIb according to Fontaine), 14 of whom we examined during DSA, 10 during PTA and 10 which we studied during both interventions. To characterize platelet ex vivo activation, the expression of activation-dependent platelet antigens (CD62 and CD63) was measured using flow cytometry. Platelet sensitization was analysed by an additional in vitro activation. Our results show that angioplasty in peripheral vessels causes activation and presumably slight migration or a reduction in the life span of circulating thrombocytes immediately after the PTA procedure and up to 4 h afterwards. DSA was also found to be associated with platelet activation, sensitization and presumptive minor migration or shortened life span of circulating platelets. Immediately after the intervention, PTA seems to influence platelet migration or shortened lifetime of platelets to a greater extent than DSA. We postulate that this is mainly induced by dilatation. More activated and sensitized thrombocytes circulated in patients with PAD compared to healthy control subjects. This supports our assumption that preactivated platelets are particularly involved in activation, sensitization and migration processes or affected by a reduced life span.
Buchholz
Alexander Matthias
AM
Department of Internal Medicine, Vascular Center Berlin, Academic Teaching Hospital of the Humboldt University (Charite), Berlin, Germany. alex.buchholz@t-online.de
Bruch
Leonhard
L
Schulte
Karl Ludwig
KL
D015901:Angiography, Digital Subtraction / Q000009:adverse effects*; D000800:Angioplasty, Balloon / Q000009:adverse effects*; D015703:Antigens, CD / Q000032:analysis; D001161:Arteriosclerosis / Q000097:blood; D001775:Blood Circulation; D001792:Blood Platelets / Q000166:cytology / Q000502:physiology; D016022:Case-Control Studies; D002465:Cell Movement; D005434:Flow Cytometry; D006801:Humans; D019007:P-Selectin / Q000032:analysis; D016491:Peripheral Vascular Diseases / Q000097:blood*; D015539:Platelet Activation; D010980:Platelet Membrane Glycoproteins / Q000032:analysis; D060149:Tetraspanin 30
D015703:Antigens, CD; C554586:CD63 protein, human; D019007:P-Selectin; D010980:Platelet Membrane Glycoproteins; D060149:Tetraspanin 30