Smoking in Relation to Coronary Atherosclerotic Plaque Burden, Volume and Composition on Intravascular Ultrasound

Abstract

BackgroundThis study aimed to evaluate the relationship between cigarette smoking and coronary atherosclerotic burden, volume and composition as determined in-vivo by grayscale and virtual histology (VH) intravascular ultrasound (IVUS).Methods and ResultsBetween 2008 and 2011, (VH-)IVUS of a non-culprit coronary artery was performed in 581 patients undergoing coronary angiography. To account for differences in baseline characteristics, current smokers were matched to never smokers by age, gender and indication for catheterization, resulting in 280 patients available for further analysis. Coronary atherosclerotic plaque volume, burden, composition (fibrous, fibro-fatty, dense calcium and necrotic core) and high-risk lesions (VH-IVUS derived thin-cap fibroatheroma (TCFA), plaque burden ≥70%, minimal luminal area ≤4.0 mm2) were assessed. Cigarette smoking showed a tendency towards higher coronary plaque burden (mean±SD, 38.6±12.5% in current versus 36.4±11.0% in never smokers, p = 0.080; and odds ratio (OR) of current smoking for plaque burden above versus below the median 1.69 (1.04–2.75), p = 0.033). This effect was driven by an association in patients presenting with an acute coronary syndrome (ACS) (current smokers, plaque burden 38.3±12.8% versus never smokers, plaque burden 35.0±11.2%, p = 0.049; OR 1.88 (1.02–3.44), p = 0.042). Fibrous tissue tended to be lower in current smokers (mean±SD, 57.7±10.5% versus 60.4±12.6%, p = 0.050) and fibro-fatty tissue was higher in current smokers (median[IQR], 9.6[6.0–13.7]% versus 8.6[5.8–12.2]%, p = 0.039). However, differences in percentage necrotic core and dense calcium could not be demonstrated. Also, no differences were found with regard to high-risk lesions.ConclusionsAn association between smoking and degree of coronary atherosclerosis was present in patients undergoing coronary angiography who presented with ACS. Although smoking was associated with higher fibro-fatty percentage, no associations could be demonstrated with percentage necrotic core, nor with VH-IVUS derived TCFA lesions. Since the magnitude of the differences in both degree and composition of atherosclerosis was modest, clinical relevance of the findings may be questioned.

Coronary plaque tissue characterization in patients with premature coronary artery disease

“…In the whole plaque, the difference of plaque components between the two groups was not significant (c). The mean plaque volume in the later CAD group was greater than that in the premature CAD group, and every component was greater too (d) smoked, or quit more than 1 year ago [37,38]. After MI, continued smokers with a relative risk of 1.51 (95% CI 1.10-2.07) recurrent coronary events compared with nonsmokers, while the risk declined to equal that of nonsmokers 3 years after cessation [39].…”

Hypertension Is an Independent Predictor of Multivessel Coronary Artery Disease in Young Adults with Acute Coronary Syndrome

“…Previous studies have demonstrated that smoking is the most important risk factor associated with the severity of coronary artery disease and is significantly linked with increased risk of coronary plaque vulnerability, myocardial infarction, and cardiovascular death [ 29 , 30 ]. Previous report showed that the prevalence of smoking in younger coronary artery disease individuals (<45 years of age) ranged from 60% to 90% as compared to 24% to 56% in subjects aged 45 years and over [ 31 , 32 ].…”

Predictive value of traditional risk factors in the assessment of premature coronary artery disease

“…Smoking was both a risk factor for CAD, and a strong predictor of CAD mortality, although the risk decreased with smoking cessation 11 . Additionally, previous studies have showed that smoking is the most common risk factor associated with the complexity and severity of coronary artery disease and is significantly associated with increased risk of coronary plaque rupture, myocardial infarction, and increased cardiovascular morbidity and mortality [12][13][14] . Kannel et al 15 found in patients included in the Framingham Heart Study that smoking was associated with a three-fold increase in the relative risk for CAD in smokers age 35 to 44, compared to nonsmokers.…”