AI Article Synopsis

  • The study examines how the size of a heart attack (myocardial infarction size or IS) affects inflammation in the heart (myocardial edema) and heart function (diastolic dysfunction) shortly after the attack and in the six months following it.
  • Researchers used advanced imaging techniques (cardiovascular magnetic resonance and echocardiography) to analyze 74 patients within a week and six months after their first heart attack.
  • Findings indicate that while some initial diastolic heart function parameters showed a slight relationship with IS shortly after the attack, these correlations were limited; after six months, increased IS correlated mainly with decreased energy loss in the heart, suggesting other factors influence the development of diastolic dysfunction.

Article Abstract

To study the relationship between myocardial infarction size (IS), myocardial edema, and diastolic dysfunction after acute myocardial infarction (MI) both in the acute phase, and in the development of diastolic dysfunction in the follow-up setting. A further purpose is to study diastolic function using a mechanistic model as well as conventional parameters. Patients underwent cardiovascular magnetic resonance (CMR) imaging and echocardiography including mechanistic analysis using the parameterized diastolic filling method within 4-7 days (acute) and 6 months after a first acute anterior MI (n = 74). Linear regression modeling of echocardiographic diastolic parameters using CMR IS with and without inclusion of the myocardium at risk (MAR) and model comparisons with likelihood ratio tests were performed. Diastolic parameters at 6 months follow-up were modelled using final IS. For most parameters there was no association with acute IS, except for deceleration time (R = 0.24, p < 0.001), left atrial volume index (R = 0.13, p = 0.01) and the mechanistic stiffness parameter (R = 0.21, p < 0.001). Adding MAR improved only the e' model (adjusted R increase: 0.08, p = 0.02). At 6 months follow-up, final IS was only associated with viscoelastic energy loss (R = 0.22, p = 0.001). In acute MI, both IS and MAR are related to diastolic function but only to a limited extent. At 6 months after infarction, increasing IS is related to less viscoelastic energy loss, albeit also to a limited extent. The relationship between IS and diastolic dysfunction seems to be mediated by mechanisms beyond simply the spatial extent of ischemia or infarction.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11742324PMC
http://dx.doi.org/10.1007/s10554-024-03294-6DOI Listing

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