Abstract
Objective: To elucidate the molecular mechanisms leading to accelerated atherosclerosis after a myocardial infarction (MI). Approach and Results: Human studies suggest that atherosclerosis is accelerated following MI. Although, this has been recapitulated in apolipoprotein E deficient (apoE -/- ) mice, the mechanisms by which MI-accelerated atherosclerosis have not been elucidated. Here, we demonstrate that, similar to apoE -/- mice, MI accelerates atherosclerosis in high-fat diet-fed LDLr -/- mice. We fed high-fat diet (21% saturated fat, 0.15% cholesterol) to LDLr -/- mice for 1 week prior to coronary artery ligation (CAL) or sham surgery. After surgery, LDLr -/- mice were maintained on high-fat diet and sacrificed after 3 weeks. Total serum cholesterol (Sham: 1349.0 ± 50.09 and CAL: 1355 ± 20.09, p = 0.19) and triglycerides (Sham: 394.6 ± 32.4 and MI 421.1 ± 6.27, p =0.48) were comparable between sham and CAL mice. Examination of aortic sinus by oil red O-stained cross-sections revealed an increase in atherosclerotic lesion area in LDLr -/- that received an MI (CAL: 78,465 ± 15,239 microm 2 /section and sham 42,697 ± 4757 microm 2 /section, p= 0.03). Additionally, we found a statistically significant increase in the number (sham: 17,943 ± 7762, n=8 and CAL: 58,129 ± 13,444, n=6, p = 0.017) and percentages (sham: 2.2 ± 0.41, n=8, CAL: 5.32 ± 1.105, n=6, p = 0.01) of Ly6G + neutrophil infiltrate in para-aortic lymph nodes in LDLr -/- mice that received MI versus sham surgery. Analysis of cellular composition in atherosclerotic lesions is ongoing. Conclusion: Atherosclerosis is accelerated following an MI in high-fat fed LDLr -/- mice.
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