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The extent and composition of coronary plaque, and its progression differ with patients' age. The interplay of patient's age with respect to risk factor control, upon atheroma progression has not been evaluated. We tested the hypothesis that risk factor control modulates the association between age and coronary atheroma progression. We performed a post hoc pooled analysis of data from 10 prospective, randomised trials involving serial coronary intravascular ultrasonography (IVUS) (n=5,823). The percent atheroma volume (PAV) was calculated as the proportion of the entire vessel wall occupied by atherosclerotic plaque. Mean overall age was 58±9 years (28% women). In a fully adjusted multivariable analysis (following adjustment of sex, body mass index, systolic blood pressure [SBP], smoking, high-density lipoprotein and low-density lipoprotein [LDL]-cholesterol, triglyceride levels, peripheral vascular disease, diabetes mellitus, trial, region, and baseline PAV), an increase in age by one standard deviation was linked with PAV progression (β-estimate 0.097; 95% confidence interval 0.048–0.15; p<0.001). In patients with good risk factor control (LDL-cholesterol <1.8 mmol/L and SBP <130 mmHg), increasing age remained associated with PAV progression (0.123; 0.014–0.23; p=0.027). Lower effect sizes for the association of age with PAV progression were observed for patients with partial control of LDL-cholesterol and SBP and were not significantly associated with PAV progression when both LDL-cholesterol and SBP were not controlled (0.099; 0.032–0.167; p=0.004 and 0.042; −0.056 to 0.14; p=0.40, respectively). Patient age is directly associated with coronary atheroma progression independently of traditional cardiovascular risk factors. In the setting of poor risk factor control, the influence of age on coronary artery disease progression is attenuated. [ABSTRACT FROM AUTHOR]

Background and aims: We tested the hypothesis that on-treatment HbA1c levels independently associate with coronary atheroma progression and major adverse cardiovascular events (MACE: death, myocardial infarction, cerebrovascular accident, coronary revascularization, or hospitalization for unstable angina) rates. Methods: We performed a post-hoc pooled analysis of data from seven prospective, randomized trials involving serial coronary intravascular ultrasonography (IVUS). The percent atheroma volume (PAV) was calculated as the proportion of the entire vessel wall occupied by atherosclerotic plaque. Using multivariable mixed modeling, we determined the association of on-treatment HbA1c with annualized change in PAV. Cox proportional hazard models were used to assess the association of HbA1c with incidence of MACE. Results: Among 3,312 patients (mean age 58.6±9years, 28.4%women) average on-treatment HbA1c was 6.2±1.1%. Overall, there was no net significant annualized change in PAV (0.12±0.19%, p = 0.52). In a fully adjusted multivariable analysis (following adjustment of age, sex, body mass index, systolic blood pressure, smoking, low- and high-density lipoprotein cholesterol, triglyceride levels, peripheral vascular disease, trial, region, and baseline PAV), higher on-treatment HbA1c levels were independently associated with annualized changes in PAV [beta-estimate (95% confidence interval): 0.13(0.08, 0.19), p