McEvoy, John W.

Abstract Aims To evaluate the impact of various smoking status on 10-year all-cause mortality and to examine a relative treatment benefit of coronary artery bypass grafting (CABG) vs. percutaneous coronary intervention (PCI) according to smoking habits. Methods and results The SYNTAX Extended Survival study evaluated vital status up to 10 years in 1800 patients with de novo three-vessel disease and/or left main coronary artery disease randomized to CABG or PCI in the SYNTAX trial. In the present analysis, patients were divided into three groups (current, former, or never smokers), and the primary endpoint of 10-year all-cause mortality was assessed according to smoking status. Smoking status was available in 1793 (99.6%) patients at the time of randomization, of whom 363 were current smokers, 798 were former smokers, and 632 were never smokers. The crude rates of 10-year all-cause mortality were 29.7% in current smokers, 25.3% in former smokers, and 25.9% in never smokers (Log-rank P = 0.343). After adjustment for imbalances in baseline characteristics, current smokers had a significantly higher risk of 10-year all-cause mortality than never smokers [adjusted hazard ratio (aHR): 2.29; 95% confidence interval (CI): 1.60–3.27; P < 0.001], whereas former smokers did not. PCI was associated with a higher risk of all-cause mortality than CABG among current smokers (HR: 1.60; 95% CI: 1.09–2.35; P = 0.017), but it failed to show a significant interaction between revascularization strategies and smoking status (Pinteraction = 0.910). Conclusion Current smokers had a higher adjusted risk of 10-year all-cause mortality, whereas former smokers did not. The treatment effect of CABG vs. PCI did not differ significantly according to smoking status. Clinical trial registration SYNTAX: ClinicalTrials.gov reference: NCT00114972; SYNTAX Extended Survival. ClinicalTrials.gov reference: NCT03417050.

Background: Cerebrovascular disease is often the consequence of cardiac disease. Our aim was to examine associations of biomarkers of cardiovascular disease, high sensitivity troponin T (hs-cTnT), NT-proBNP, and galectin-3, with cerebrovascular signs: lacunar infarcts, lobar and subcortical microhemorrhages, cortical infarcts, and white matter hyperintensity (WMH) volume. We also examined total cortical and Alzheimer’s Disease (AD) signature region volumes. Methods: We conducted a cross-sectional analysis of 1748 ARIC participants from the 2011-2013 exam who had biomarker measurements, completed a brain MRI, and did not have a clinical history of stroke. We used linear regression to model brain volumes, modeled as Z scores, and logistic regression for all other outcomes; biomarkers were log transformed. We repeated analyses excluding persons with coronary heart disease, atrial fibrillation, and heart failure. Results: The mean age of participants was 76, 62% were female, and 21% were Black. All biomarkers were associated with total cortical volume. Each standard deviation increase in log hs-cTnT was associated with lower total cortical volume (adjusted beta = -0.08, 95% CI: -0.12, -0.05); results for the other biomarkers were similar (Figure). All biomarkers were associated with lobar microhemorrhages. Hs-cTnT and NT-proBNP were associated with WMH volume, but galectin-3 was not. No biomarker was associated with subcortical microhemorrhages or cortical infarcts. Results were similar in persons without coronary heart disease, atrial fibrillation, or heart failure (conditions associated with cerebral thromboembolism). Conclusions: In persons free of clinical cardiovascular disease, biomarkers of cardiac stretch, strain, and fibrosis were associated cerebral small vessel disease and reduced cortical volume, but not in a specific pattern suggestive of AD pathogenesis. This suggests subclinical vascular insults affect brain structure through mixed pathogenic processes.