Heart rhythm · 2022
Regional heterogeneity in determinants of atrial matrix remodeling and association with atrial fibrillation vulnerability postmyocardial infarction.
СтатьяПоддержка правительства СШАПоддержка NIH: внешняя программаНазвание и аннотация: Перевод в очереди
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Stacy Mitchel R, Lin Ben A, Thorn Stephanie L, Lobb David C, Maxfield Mark W, Novack Craig, Zellars Kia N, Freeburg Lisa, Akar Joseph G, Sinusas Albert J, Spinale Francis G
Аннотация
BACKGROUND: Left ventricular (LV) remodeling following a myocardial infarction (MI) is associated with new-onset atrial fibrillation (AF). LV remodeling post-MI is characterized by regional changes in matrix metalloproteinases (MMPs) and tissue inhibitors of metalloproteinases (TIMPs), causing extracellular matrix (ECM) remodeling.
OBJECTIVE: The purpose of this study was to test the hypothesis that a shift in regional atrial MMP activity, MMP/TIMP expression, and ECM remodeling occurs post-MI, which cause increased vulnerability to AF.
METHODS: MI was induced in pigs (weight 25 kg; coronary ligation; n = 9). At approximately 14 days post-MI, an atrial electrical stimulation protocol was performed, after which an MMP radiotracer was infused, MMP/TIMP mRNA profiling performed, and ECM collagen assessed by histochemistry. An additional 7 non-MI pigs served as controls.
RESULTS: AF could be induced in 89% (8/9) of the post-MI pigs but none of the controls. MMP activity (MMP radiotracer uptake) increased by approximately 2-fold in most atrial regions post-MI, whereas fibrillar collagen content was unchanged or actually reduced in right atrial regions and increased in left atrial regions. MMP/TIMP profiles revealed a heterogeneous pattern from the left atrial appendage to right atrial regions.
CONCLUSION: AF vulnerability early post-MI was associated with a heterogeneous pattern of atrial ECM remodeling, detectable by noninvasive molecular imaging. Detection of early atrial MMP activation post-MI may help define the myocardial substrate underlying AF.
OBJECTIVE: The purpose of this study was to test the hypothesis that a shift in regional atrial MMP activity, MMP/TIMP expression, and ECM remodeling occurs post-MI, which cause increased vulnerability to AF.
METHODS: MI was induced in pigs (weight 25 kg; coronary ligation; n = 9). At approximately 14 days post-MI, an atrial electrical stimulation protocol was performed, after which an MMP radiotracer was infused, MMP/TIMP mRNA profiling performed, and ECM collagen assessed by histochemistry. An additional 7 non-MI pigs served as controls.
RESULTS: AF could be induced in 89% (8/9) of the post-MI pigs but none of the controls. MMP activity (MMP radiotracer uptake) increased by approximately 2-fold in most atrial regions post-MI, whereas fibrillar collagen content was unchanged or actually reduced in right atrial regions and increased in left atrial regions. MMP/TIMP profiles revealed a heterogeneous pattern from the left atrial appendage to right atrial regions.
CONCLUSION: AF vulnerability early post-MI was associated with a heterogeneous pattern of atrial ECM remodeling, detectable by noninvasive molecular imaging. Detection of early atrial MMP activation post-MI may help define the myocardial substrate underlying AF.