The size of myocardial infarction and peri-infarction edema are not major determinants of diastolic impairment after acute myocardial infarction

• DOI: 10.1007/s10554-024-03294-6
• Publication Date: 2024-12-05T15:03:01Z
• Authors: Martin G. Sundqvist; Dinos Verouhis; Peder Sörensson; Loghman Henareh; Jonas Persson; Nawzad Saleh; Magnus Settergren; Nils Witt; Felix Böhm; John Pernow; Per Tornvall; Martin Ugander
• Keywords: Original Paper; 03 medical and health sciences; 0302 clinical medicine; 3. Good health

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 (R2 = 0.24, p < 0.001), left atrial volume index (R2 = 0.13, p = 0.01) and the mechanistic stiffness parameter (R2 = 0.21, p < 0.001). Adding MAR improved only the e′ model (adjusted R2 increase: 0.08, p = 0.02). At 6 months follow-up, final IS was only associated with viscoelastic energy loss (R2 = 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.