Abstract
Background and objectivesStructural and functional changes in the intramyocardial microcirculation increase the risk of myocardial infarction (MI). This study investigated intramyocardial perivascular fibrosis and pro-fibrotic cellular transitions in deceased acute and subacute MI patients to explore their involvement in the pathogenesis of MI. MethodsLeft ventricular tissue (LV) was obtained from the infarction area of autopsied patients with acute-phase MI (3–6 h; n = 24), subacute-phase MI (5–14 days; n = 12), and noninfarcted controls (n = 14). Perivascular fibrosis and fibroblast activation protein (FAP) expression were quantified using (immuno)histochemistry. Fibroblast-like transitioning of vascular smooth muscle cells (VSMC) and endothelial cells (EC) was quantified using immunofluorescent microscopy. ResultsPerivascular fibrosis was elevated in acute-phase (77.69 %) and subacute-phase (72.19 %: border zone 95.18 %: infarct core) MI patients (p < 0.0001) compared to controls (61.03 %). FAP expression was higher in both acute-phase (1.46 %) and subacute-phase (18.01 %: border zone 5.67 %: infarct core) compared to controls (0.46 %) (p < 0.05). VSMC fibroblast-like cellular transition (SMA + S100A4+ vessels fraction) was higher in acute-phase (31.96 %) and subacute-phase (21.90 %: border zone; 37.25 %: infarct core) MI compared to controls (8.95 %) (p < 0.05). Similarly, EC fibroblast-like cellular transition (CD31 + S100A4+ area fraction) was increased in acute-phase MI (10.14 %) and subacute-phase MI (8.31 %: border zone 10.15 %: infarct core) compared to controls (2.67 %) (p < 0.05). ConclusionIncreased perivascular fibrosis, fibroblast activation and vascular cellular transition in intramyocardial blood vessels of MI patients may contribute to MI development. Further increases of FAP expression and perivascular fibrosis, particularly in subacute-phase infarct cores, suggest MI itself exacerbates fibroblast activation and perivascular fibrosis, theoretically increasing reinfarction risk.
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