AI Article Synopsis

  • The study investigates the role of Follistatin-like 1 (FSTL1) in human heart tissue after a heart attack, specifically its secretion in the damaged heart muscle.
  • FSTL1 levels were measured in 93 patients at various stages following an acute myocardial infarction, showing a consistent increase in FSTL1 from the aorta to the affected veins in 24% of patients.
  • The findings suggest that higher levels of FSTL1 are linked to negative changes in heart structure and function over time.

Article Abstract

Background: Although animal studies showed that Follistatin-like 1 (FSTL1) exerts cardioprotective effects against ischemic injury, little is known in humans. We examined whether FSTL1 is secreted in an infarcted myocardium and whether its production is associated with left ventricular (LV) remodeling in survivors of acute myocardial infarction.

Methods And Results: FSTL1 levels were measured by enzyme-linked immunosorbent assay in plasma collected from the aortic root and the anterior interventricular vein in 93 patients with anterior acute myocardial infarction. Measurement of FSTL1 levels and left ventriculography were repeated during the early phase (2 weeks) and the chronic phase (6 months) after MI. A persistent increment in FSTL1 levels from the aortic root to the anterior interventricular vein, reflecting FSTL1 production in the infarcted myocardium at both the early and chronic phases, was seen in 22 patients (24%). A linear regression analysis revealed that a persistent transmyocardial increment in FSTL1 levels was significantly associated with percent changes in LV end-diastolic volume index, LV end-systolic volume index, and LV ejection fraction from the early to the chronic phase (r = 0.44, 0.51, and -0.43, respectively, all P < .001).

Conclusions: The persistent production of FSTL1 in the infarcted myocardium was associated with adverse LV remodeling in survivors of acute myocardial infarction.

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Source
http://dx.doi.org/10.1016/j.cardfail.2020.05.015DOI Listing

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