Age-related effects of smoking on culprit lesion plaque vulnerability as assessed by grayscale and virtual histology–intravascular ultrasound. Issue 6 (September 2015)

• Record Type: Journal Article
• Authors: Kang, Soo-Jin; Mintz, Gary S.; Witzenbichler, Bernhard; Metzger, D. Christopher; Rinaldi, Michael J.; Duffy, Peter L.; Weisz, Giora; Stuckey, Thomas D.; Brodie, Bruce R.; Shimizu, Takehisa; Litherland, Claire; Kirtane, Ajay J.; Stone, Gregg W.; Maehara, Akiko
• Is Part Of: Coronary artery disease. Volume 26:Issue 6(2015:Sep.)
• Publication Date: 2015-09
• Subjects: atherosclerosis -- imaging -- smoking; Coronary heart disease -- Periodicals; Coronary Disease -- Indexes; Coronary Disease -- Periodicals; 616.123005
• DOI: 10.1097/MCA.0000000000000268
• Languages: English
• ISSNs: 0954-6928

Abstract

Abstract : Background: Although smoking is a risk factor for coronary atherosclerosis, the age-related impact on lesion characteristics and plaque instability remains unclear. Patients and methods: In ADAPT-DES, 780 patients with 916 culprit lesions were evaluated by preprocedural grayscale and virtual histology–intravascular ultrasound. Results: Current smokers (smoking within 1 month) more often presented with acute coronary syndrome (67 vs. 51 vs. 51%, P <0.05) compared with former smokers (no smoking for >1 month) or nonsmokers. In patients 65 or more years of age, current smokers (vs. nonsmokers) showed larger normalized volumes of plaque and media [8.6 (7.8–9.4) vs. 7.2 (6.8–7.7) mm 3 /mm, P =0.016] and external elastic membrane [14.4 (13.2–15.5) vs. 12.8 (12.2–13.4) mm 3 /mm, P =0.05]. At the minimal lumen area site, despite a greater plaque burden, the larger external elastic membrane area [14.4 (13.1–15.7) vs. 12.0 (11.3–12.7) mm 2, P =0.003] contributed toward preserving the minimal lumen area [2.6 (2.4–2.7) vs. 2.6 (2.5–2.7) mm 2, P =0.91] in current smokers (vs. nonsmokers) 65 or more years of age. Moreover, current smokers (vs. nonsmokers) 65 or more years of age showed a greater normalized necrotic core volume [1.19 (0.96–1.46) vs. 0.75 (0.66–0.85) mm 3 /mm, P =0.0007], more thin-cap fibroatheromas (61 vs. 48%, P =0.04), and plaque ruptures (38 vs. 26%, P =0.051). Conversely, in patients younger than 65 years of age, there was no significant difference in culprit lesion morphology among current, former, and nonsmokers. Conclusion: In patients 65 or more years (not in patients<65 years), smoking increased culprit lesion plaque instability (greater plaque with more necrotic core, thin-cap fibroatheromas, positive remodeling, and plaque ruptures).