{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,5]],"date-time":"2026-10-05T12:31:31Z","timestamp":1791203491095,"version":"4.2.0"},"reference-count":0,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"3","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Circulation"],"published-print":{"date-parts":[[1994,3]]},"abstract":"<jats:sec>\n            <jats:title>BACKGROUND<\/jats:title>\n            <jats:p>3-Hydroxy-3-methylglutaryl coenzyme A reductase inhibitors are widely prescribed for hyperlipidemia, yet their effect on the evolution of coronary atherosclerosis has not been defined.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>METHODS AND RESULTS<\/jats:title>\n            <jats:p>To address this issue, 331 patients with diffuse but not necessarily severe coronary atherosclerosis documented on a recent arteriogram and with fasting serum cholesterol between 220 and 300 mg\/dL were enrolled in a randomized, double-blind, placebo-controlled trial. All patients received intensive dietary counseling. Lovastatin or placebo was begun at 20 mg\/d and was titrated to 40 and 80 mg during the first 16 weeks to attain a fasting low-density lipoprotein (LDL) cholesterol &lt; or = 130 mg\/dL. The mean lovastatin dose was 36 mg\/d. Coronary arteriography was repeated after 2 years. In 299 patients (90%), 3858 coronary segments containing 2309 stenoses were measured blindly on pairs of films with an automated computerized quantitative system. Total and LDL cholesterol decreased by 21 +\/- 11% and 29 +\/- 11%, respectively, in the lovastatin-treated group but changed by &lt; 2% in placebo patients. The primary end point, coronary change score, defined as the per-patient mean of the minimum lumen diameter changes (follow-up minus baseline angiogram) for all lesions measured, excluding those &lt; 25% on both films, worsened by 0.09 +\/- 0.16 mm in the placebo group and by 0.05 +\/- 0.13 mm in the lovastatin group (P = .01). Progression (a worsening in minimum diameter of one or more stenoses by &gt; or = 0.4 mm) with no regression at other sites occurred in 48 of 146 lovastatin and 76 of 153 placebo patients (33% versus 50%, P = .003). New coronary lesions developed in 23 lovastatin and 49 placebo patients (P = .001). The beneficial effect of treatment was most pronounced in the more numerous, milder lesions and in patients whose baseline total or LDL cholesterol levels were above the group median.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>CONCLUSIONS<\/jats:title>\n            <jats:p>Lovastatin slows the progression of coronary atherosclerosis and inhibits the development of new coronary lesions.<\/jats:p>\n          <\/jats:sec>","DOI":"10.1161\/01.cir.89.3.959","type":"journal-article","created":{"date-parts":[[2012,6,12]],"date-time":"2012-06-12T00:34:42Z","timestamp":1339461282000},"page":"959-968","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":357,"title":["Effects of monotherapy with an HMG-CoA reductase inhibitor on the progression of coronary atherosclerosis as assessed by serial quantitative arteriography. The Canadian Coronary Atherosclerosis Intervention Trial."],"prefix":"10.1161","volume":"89","author":[{"given":"D","family":"Waters","sequence":"first","affiliation":[{"name":"Division of Cardiology, Hartford Hospital, Conn 06115."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"L","family":"Higginson","sequence":"additional","affiliation":[{"name":"Division of Cardiology, Hartford Hospital, Conn 06115."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"P","family":"Gladstone","sequence":"additional","affiliation":[{"name":"Division of Cardiology, Hartford Hospital, Conn 06115."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"B","family":"Kimball","sequence":"additional","affiliation":[{"name":"Division of Cardiology, Hartford Hospital, Conn 06115."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"M","family":"Le May","sequence":"additional","affiliation":[{"name":"Division of Cardiology, Hartford Hospital, Conn 06115."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"S J","family":"Boccuzzi","sequence":"additional","affiliation":[{"name":"Division of Cardiology, Hartford Hospital, Conn 06115."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"J","family":"Lesp\u00e9rance","sequence":"additional","affiliation":[{"name":"Division of Cardiology, Hartford Hospital, Conn 06115."}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"276","container-title":["Circulation"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/www.ahajournals.org\/doi\/pdf\/10.1161\/01.CIR.89.3.959","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2024,5,12]],"date-time":"2024-05-12T15:34:33Z","timestamp":1715528073000},"score":1,"resource":{"primary":{"URL":"https:\/\/www.ahajournals.org\/doi\/10.1161\/01.CIR.89.3.959"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[1994,3]]},"references-count":0,"journal-issue":{"issue":"3","published-print":{"date-parts":[[1994,3]]}},"alternative-id":["10.1161\/01.CIR.89.3.959"],"URL":"https:\/\/doi.org\/10.1161\/01.cir.89.3.959","relation":{},"ISSN":["0009-7322","1524-4539"],"issn-type":[{"value":"0009-7322","type":"print"},{"value":"1524-4539","type":"electronic"}],"subject":[],"published":{"date-parts":[[1994,3]]},"assertion":[{"value":"1994-03-01","order":2,"name":"published","label":"Published","group":{"name":"publication_history","label":"Publication History"}}]}}