This is an ancillary substudy of the WARRIOR Trial (NCT03417388), a multi-site, PROBE design, that will evaluate an intensive statin/ACE-I (or ARB)/aspirin treatment strategy (IMT) vs. primary prevention risk factor therapy treatment strategy (UC) in 4,422 symptomatic (chronic angina or equivalent) women with non-obstructive CAD (<50% diameter narrowing).~In this ancillary substudy, 400 patients will be recruited from the WARRIOR trial with 200 patients from each of the treatment groups (IMT vs UC). From this cohort, 150 patients per treatment group, most compliant with WARRIOR protocol will undergo a CTA at the end of 3 years; with changes in plaque and PCAT characteristics quantified.~The main aims are as follows:~To compare changes in coronary plaque characteristics and their hemodynamic significance using CTA in WARRIOR women treated with IMT vs UC;~To compare changes in plaque inflammation-related characteristics in PCAT in WARRIOR women treated with IMT with statin in combination with angiotensin converting enzyme inhibitor (ACEI) and/or angiotensin receptor blocker (ARB) medications vs UC;~To relate plaque burden and plaque composition, CT flow reserve, and PCAT density changes to angina score (Seattle Angina Questionnaire [SAQ]) changes in IMT and UC-randomized WARRIOR women.~Data to be analyzed include CT angiography scans at baseline and Year 3 follow-up and corresponding study data and laboratory tests (e.g. hsCRP); plus, selected data from the main WARRIOR study that are relevant to the present ancillary study.
In this study, quantitative characterization of plaque using coronary computed tomographic angiography (CTA) will be used to determine if women who were treated with intensive medical therapy have a greater reduction in the amount and type of cholesterol plaque compared to women receiving usual care and if this results in beneficial changes in clinical symptoms. The study will provide an understanding of how intensive medical therapy works in providing clinical benefit in women with nonobstructive plaque.