{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,27]],"date-time":"2025-10-27T04:58:03Z","timestamp":1761541083678},"reference-count":0,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"2","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Circulation"],"published-print":{"date-parts":[[1991,8]]},"abstract":"<jats:sec>\n            <jats:title>BACKGROUND<\/jats:title>\n            <jats:p>Platelet-thrombus formation is a complication of arterial wall deep injury by balloon angioplasty that may lead to acute arterial occlusion and may contribute to restenosis.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>METHODS AND RESULTS<\/jats:title>\n            <jats:p>Because common platelet-inhibitor drugs with a heparin bolus (100 units\/kg) may be effective in inhibiting platelet-thrombus formation after arterial angioplasty, these were compared with a bolus of heparin alone (control), the specific thrombin inhibitor hirudin (1.0 mg\/kg), and saline (hirudin control) in normal pigs after angioplasty of the common carotid arteries. In the presence of deep arterial wall injury (injury exposing the media), indium-111-labeled platelet deposition (x 10(6)\/cm2) was 68.8 +\/- 12.3 and 48.1 +\/- 16.9 in the control animals. This was significantly reduced by pretreatment with low-dose aspirin (1 mg\/kg\/day), by high-dose aspirin (20 mg\/kg\/day) plus dipyridamole, and especially by thrombin inhibition with hirudin. Treatment regimens with aspirin alone (20 mg\/kg\/day), dipyridamole alone, or sulfinpyrazone were ineffective. Likewise, the incidence of mural thrombosis was 75% and 80% in deeply injured arteries of controls and was significantly reduced to 46% with aspirin plus dipyridamole, 25% with low-dose aspirin, and 0% with hirudin. The incidence of mural thrombosis was unchanged with high-dose aspirin (69%), dipyridamole (90%), or sulfinpyrazone (92%). This mural thrombosis could not be identified by angiography. In the presence of mild injury (deendothelialization), platelet deposition was low (less than 10 x 10(6)\/cm2, a single layer) and was not changed by any therapy, including hirudin.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>CONCLUSIONS<\/jats:title>\n            <jats:p>These therapies do not affect platelet adhesion to deeply or mildly injured artery. These data suggest a greater role for thrombin inhibition than with thromboxane or cyclooxygenase inhibition in the pathogenesis of platelet-rich mural thrombosis after deep injury during angioplasty. Antithrombotic therapy for arterial thrombosis by thrombin inhibition appears promising.<\/jats:p>\n          <\/jats:sec>","DOI":"10.1161\/01.cir.84.2.814","type":"journal-article","created":{"date-parts":[[2012,6,12]],"date-time":"2012-06-12T00:01:09Z","timestamp":1339459269000},"page":"814-820","update-policy":"http:\/\/dx.doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":45,"title":["Antithrombotic therapy for deep arterial injury by angioplasty. Efficacy of common platelet inhibition compared with thrombin inhibition in pigs."],"prefix":"10.1161","volume":"84","author":[{"given":"J Y","family":"Lam","sequence":"first","affiliation":[{"name":"Division of Cardiovascular Disease and Internal Medicine, Mayo Clinic, Rochester, MN 55905."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"J H","family":"Chesebro","sequence":"additional","affiliation":[{"name":"Division of Cardiovascular Disease and Internal Medicine, Mayo Clinic, Rochester, MN 55905."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"P M","family":"Steele","sequence":"additional","affiliation":[{"name":"Division of Cardiovascular Disease and Internal Medicine, Mayo Clinic, Rochester, MN 55905."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"M","family":"Heras","sequence":"additional","affiliation":[{"name":"Division of Cardiovascular Disease and Internal Medicine, Mayo Clinic, Rochester, MN 55905."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"M W","family":"Webster","sequence":"additional","affiliation":[{"name":"Division of Cardiovascular Disease and Internal Medicine, Mayo Clinic, Rochester, MN 55905."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"L","family":"Badimon","sequence":"additional","affiliation":[{"name":"Division of Cardiovascular Disease and Internal Medicine, Mayo Clinic, Rochester, MN 55905."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"V","family":"Fuster","sequence":"additional","affiliation":[{"name":"Division of Cardiovascular Disease and Internal Medicine, Mayo Clinic, Rochester, MN 55905."}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"276","container-title":["Circulation"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/www.ahajournals.org\/doi\/pdf\/10.1161\/01.CIR.84.2.814","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2024,5,12]],"date-time":"2024-05-12T15:51:46Z","timestamp":1715529106000},"score":1,"resource":{"primary":{"URL":"https:\/\/www.ahajournals.org\/doi\/10.1161\/01.CIR.84.2.814"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[1991,8]]},"references-count":0,"journal-issue":{"issue":"2","published-print":{"date-parts":[[1991,8]]}},"alternative-id":["10.1161\/01.CIR.84.2.814"],"URL":"https:\/\/doi.org\/10.1161\/01.cir.84.2.814","relation":{},"ISSN":["0009-7322","1524-4539"],"issn-type":[{"value":"0009-7322","type":"print"},{"value":"1524-4539","type":"electronic"}],"subject":[],"published":{"date-parts":[[1991,8]]},"assertion":[{"value":"1991-08-01","order":2,"name":"published","label":"Published","group":{"name":"publication_history","label":"Publication History"}}]}}