Association of greenness exposure with coronary artery stenosis and biomarkers of myocardial injury in patients with myocardial infarction

Greenness has been linked to cardiovascular health; however, limited evidence is available regarding its association with coronary artery stenosis and biomarkers of myocardial injury. We aimed to assess these associations and examine their modification and mediation effects in patients with myocardial infarction (MI). This study included 2030 patients with MI. The normalized difference vegetation index (NDVI) was used to characterize greenness exposure. We used a logistic regression model to explore the relationship between coronary artery stenosis and residential greenness, and applied linear regression models to assess the association of greenness with biomarkers of myocardial injury. The bootstrap method was used to explore whether potential variables mediated the associations. To further investigate the exposure-response curve describing these relationships, we developed restricted cubic spline models. Compared to the lowest quartile of NDVI, the odds ratio (OR) (95 % confidence interval [CI]) for severe stenosis (≥75 % stenosis) was 0.68 (95 % CI: 0.47 to 0.98) for the third quartile. Participants in the highest greenness exposure quartile had lower levels of cardiac troponin I (cTnI), creatine kinase (CK), and creatine kinase isoenzyme (CKMB) than those in the lowest quartile (β = −0.22, 95 % CI: −0.40 to −0.05; β = −0.13, 95 % CI: −0.22 to −0.04; β = −0.07, 95 % CI: −0.14 to −0.003). The association between residential greenness and myocardial injury biomarkers was stronger in men and older participants. Mediation analyses revealed that the effects of greenness on coronary stenosis, cTnI, CK, and CKMB were mediated by systolic blood pressure (SBP) and diastolic blood pressure (DBP). Higher greenness exposure was associated with coronary artery stenosis and reduced levels of myocardial injury biomarkers, including cTnI, CK, and CKMB. These associations may be partially mediated by SBP and DBP levels.