Baseline clinical and biochemical characteristics of patients and controls.

<p>The data are presented as mean ±SD, median (25^th, 75^th percentile), or numbers (%). SA =  stable angina; ACS =  acute coronary syndrome; MI =  myocardial infarction; LDL =  low density lipoprotein, HDL =  high density lipoprotein. NS =  non-significant (p≥0.05). For comparisons between groups, p-values indicating significant differences are denoted by ψ (controls vs SA), γ (controls vs NSTE-ACS) and <i>Φ</i> (SA vs NSTE-ACS), respectively.</p><p>Baseline clinical and biochemical characteristics of patients and controls.</p

Different plaque compositions as seen by CCTA.

<p>The different types of coronary plaque are shown in longitudinal views, with cross-sectional views at the level of the dotted line. A non-calcified plaque is shown on the left (A and B), with white arrowheads pointing at the non-calcified plaque component. A mixed plaque is shown in the middle (C and D), with a white arrowhead indicating the non-calcified plaque component and a black arrowhead indicating the calcified component. A large calcified plaque is shown on the right side (E and F), with black arrowhead indicating the calcifications.</p

Baseline leukocyte subsets and plasma cytokines of patients and controls.

<p>The data are presented as mean ±SD or median (25^th, 75^th percentile). SA =  stable angina; NSTE-ACS =  non-ST-elevation acute coronary syndrome; CD19+ cells, B cells; CD4+ cells, T helper cells; CD8+ cell, cytotoxic T cell; NK =  Natural killer; IL =  interleukin; CRP =  C-reactive protein. NS =  non-significant (p≥0.05). For comparisons between groups, p-values indicating significant differences are denoted by ψ (controls vs SA), γ (controls vs NSTE-ACS) and <i>Φ</i> (SA vs NSTE-ACS), respectively.</p><p>Baseline leukocyte subsets and plasma cytokines of patients and controls.</p

Independent association between symptom onset time and infarct size in patients with ST-elevation myocardial infarction undergoing primary percutaneous coronary intervention

<div><p>Recent studies have reported on circadian variation in infarct size in ST-elevation myocardial infarction (STEMI) patients. Controversy remains as to whether this finding indicates circadian dependence of myocardial tolerance to ischemia/reperfusion injury or that it can simply be explained by confounding factors such as baseline profile and ischemic time. We assessed the clinical impact and independent association between symptom onset time and infarct size, accounting for possible subgroup differences. From a multicenter registry, 6799 consecutive STEMI patients undergoing primary percutaneous coronary intervention (PCI) between 2004 and 2010 were included. Infarct size was measured using peak creatine kinase (CK). Infarct size exhibited circadian variation with largest infarct size in patients with symptom onset around 03:00 at night (estimated peak CK 1322 U/l; 95% confidence interval (CI): 1217–1436) and smallest infarct size around 11:00 in the morning (estimated peak CK 1071 U/l; 95% CI: 1001–1146; relative reduction 19%; <i>p</i> = 0.001). Circadian variation in infarct size followed an inverse pattern in patients with prior myocardial infarction (p-interaction <0.001) and prior PCI (p-interaction = 0.006), although the later did not persist in multivariable analysis. Symptom onset time remained associated with infarct size after accounting for these interactions and adjusting for baseline characteristics and ischemic time. Symptom onset time did not predict one-year mortality (<i>p</i> = 0.081). In conclusion, there is substantial circadian variation in infarct size, which cannot be fully explained by variations in baseline profile or ischemic time. Our results lend support to the hypothesis of circadian myocardial ischemic tolerance and suggest a different mechanism in patients with prior myocardial infarction.</p></div