{"id":"97fcb0ae4fe4","type":"article","url":"https://hartvaat.nl/2020/08/18/carotis-intima-media-dikte-als-surrogaatmarker-meta-analyse-van-119-trials/","title":"Carotis intima-media dikte als surrogaatmarker: meta-analyse van 119 trials","title_en":"Carotid Intima-Media Thickness Progression as Surrogate Marker for Cardiovascular Risk: Meta-Analysis of 119 Clinical Trials Involving 100 667 Patients.","category":"preventie","category_label":"Preventie","professions":["cardioloog","internist"],"tags":[],"journal":"Circulation","doi":"10.1161/CIRCULATIONAHA.120.046361","source_url":"https://doi.org/10.1161/CIRCULATIONAHA.120.046361","authors":["Peter Willeit","Lena Tschiderer","Elias Allara","Kathrin Reuber","Lisa Seekircher","Lu Gao","Ximing Liao","Eva Lonn","Hertzel C Gerstein","Salim Yusuf","Frank P Brouwers","Folkert W Asselbergs","Wiek van Gilst","Sigmund A Anderssen","Diederick E Grobbee","John J P Kastelein","Frank L J Visseren","George Ntaios","Apostolos I Hatzitolios","Christos Savopoulos","Pythia T Nieuwkerk","Erik Stroes","Matthew Walters","Peter Higgins","Jesse Dawson","Paolo Gresele","Giuseppe Guglielmini","Rino Migliacci","Marat Ezhov","Maya Safarova","Tatyana Balakhonova","Eiichi Sato","Mayuko Amaha","Tsukasa Nakamura","Kostas Kapellas","Lisa M Jamieson","Michael Skilton","James A Blumenthal","Alan Hinderliter","Andrew Sherwood","Patrick J Smith","Michiel A van Agtmael","Peter Reiss","Marit G A van Vonderen","Stefan Kiechl","Gerhard Klingenschmid","Matthias Sitzer","Coen D A Stehouwer","Heiko Uthoff","Zhi-Yong Zou","Ana R Cunha","Mario F Neves","Miles D Witham","Hyun-Woong Park","Moo-Sik Lee","Jang-Ho Bae","Enrique Bernal","Kristian Wachtell","Sverre E Kjeldsen","Michael H Olsen","David Preiss","Naveed Sattar","Edith Beishuizen","Menno V Huisman","Mark A Espeland","Caroline Schmidt","Stefan Agewall","Ercan Ok","Gülay Aşçi","Eric de Groot","Muriel P C Grooteman","Peter J Blankestijn","Michiel L Bots","Michael J Sweeting","Simon G Thompson","Matthias W Lorenz"],"significance":7,"published":"2020-08-18","source_date":"2020-08-18","image":"","kennis":["https://hartvaat.nl/kennis/cardiometabool/inflammatie-en-atherosclerose/"],"congress":"","summary_en":"This meta-analysis of 119 clinical trials found no consistent association between drug effects on carotid intima-media thickness progression and cardiovascular outcomes, questioning the utility of cIMT as a surrogate endpoint for cardiovascular trials.","created":"2026-07-03T10:28:43Z","updated":"2026-07-03T13:27:52Z","licence":"Citeer vrij, met bronvermelding en een link naar hartvaat.nl (de url van het record). Samenvattingen zijn redactioneel werk van HartVaat; de oorspronkelijke publicaties blijven van hun uitgevers (doi). Geen medisch advies.","body_markdown":"Meta-analyse van 119 klinische trials die de bruikbaarheid van carotis intima-media dikteprogresse als surrogaatmarker voor CV-risico evalueerde.","abstract_original":"BACKGROUND: To quantify the association between effects of interventions on carotid intima-media thickness (cIMT) progression and their effects on cardiovascular disease (CVD) risk. METHODS: We systematically collated data from randomized, controlled trials. cIMT was assessed as the mean value at the common-carotid-artery; if unavailable, the maximum value at the common-carotid-artery or other cIMT measures were used. The primary outcome was a combined CVD end point defined as myocardial infarction, stroke, revascularization procedures, or fatal CVD. We estimated intervention effects on cIMT progression and incident CVD for each trial, before relating the 2 using a Bayesian meta-regression approach. RESULTS: We analyzed data of 119 randomized, controlled trials involving 100 667 patients (mean age 62 years, 42% female). Over an average follow-up of 3.7 years, 12 038 patients developed the combined CVD end point. Across all interventions, each 10 μm/y reduction of cIMT progression resulted in a relative risk for CVD of 0.91 (95% Credible Interval, 0.87-0.94), with an additional relative risk for CVD of 0.92 (0.87-0.97) being achieved independent of cIMT progression. Taken together, we estimated that interventions reducing cIMT progression by 10, 20, 30, or 40 μm/y would yield relative risks of 0.84 (0.75-0.93), 0.76 (0.67-0.85), 0.69 (0.59-0.79), or 0.63 (0.52-0.74), respectively. Results were similar when grouping trials by type of intervention, time of conduct, time to ultrasound follow-up, availability of individual-participant data, primary versus secondary prevention trials, type of cIMT measurement, and proportion of female patients. CONCLUSIONS: The extent of intervention effects on cIMT progression predicted the degree of CVD risk reduction. This provides a missing link supporting the usefulness of cIMT progression as a surrogate marker for CVD risk in clinical trials."}