Key result
Infarct size predicts impaired relaxation while microvascular obstruction drives elevated E/e′ after STEMI.
Why the study?
Whether the functional components of LV diastole—active relaxation, chamber compliance, and filling pressure response—reflect distinct patterns of myocardial injury early after STEMI remained unclear.
Observational (n=258)
Multimodality imaging with CMR and echocardiography early after STEMI reveals that distinct components of diastolic dysfunction—impaired relaxation versus elevated filling pressures and reduced compliance—arise from different patterns of infarct-zone microvascular and remote myocardial injury.
Distinct post-STEMI diastolic impairments link to specific CMR injury patterns; hypothesis-generating for multimodality imaging before clinical adoption.
Background Left ventricular (LV) diastole comprises active relaxation, chamber compliance, and filling pressure response. Whether these functional components reflect distinct patterns of myocardial injury early after ST-elevation myocardial infarction (STEMI) remains unclear. Methods We studied 258 STEMI patients (mean age 59.4 ± 11.1 years; 22.5% women) undergoing discharge cardiac magnetic resonance (CMR) and comprehensive echocardiography. Markers of relaxation (e′), filling pressure (E/e′), chamber compliance (deceleration time of the E-wave, DT), and left atrial reservoir strain (PALS) were analyzed. CMR-derived infarct size, remote native T1 (NT1), microvascular obstruction (MVO), myocardial edema (T2), and LVEF were entered into multivariable linear regression models adjusted for age. Results Impaired relaxation (e′) was independently associated with age (β = −0.391, p < 0.001), LVEF (β = 0.226, p = 0.003), infarct size (β = −0.216, p = 0.005), and remote myocardial injury (NT1) (β = −0.125, p = 0.029) (model R² = 0.311), indicating that early slowing of relaxation is associated not only with infarct-related myocyte loss but also with diffuse myocardial involvement beyond the infarct zone. Elevated LV filling pressure (E/e′) was independently associated with MVO (β = 0.271, p < 0.001), age (β = 0.277, p < 0.001), and remote NT1 (β = 0.131, p = 0.036) (R² = 0.142), suggesting that increased filling pressures early after STEMI are linked to infarct-zone microvascular injury on a background of global myocardial involvement. Chamber compliance (DT) was inversely associated with MVO burden (β = −0.183, p = 0.009) and infarct-related myocardial edema (T2) (β = −0.145, p = 0.026), while being positively associated with age (β = 0.167, p = 0.010), indicating reduced LV distensibility in the presence of acute microvascular and interstitial injury. PALS was independently associated only with LVEF (β = 0.290, p < 0.001) and age (β = −0.311, p < 0.001) (R² = 0.175), without association with CMR-derived tissue injury markers, supporting ventricular–atrial mechanical coupling rather than intrinsic atrial injury. Conclusions Early LV diastolic dysfunction after STEMI arises from distinct patterns of myocardial injury. Impaired relaxation is associated with infarct extent and remote myocardial involvement, whereas elevated filling pressures and reduced compliance are more closely linked to infarct-zone microvascular obstruction and myocardial edema. Multimodality imaging enables early differentiation of these mechanisms and may help identify patients with haemodynamic compromise not explained by infarct size alone. Figure 1 legend. Infarct-zone microvascular obstruction and edema translate into reduced compliance (DT) and elevated filling pressure (E/e′), whereas infarct extent and remote myocardial injury relate to impaired relaxation (e′). PALS reflects LVEF-driven ventricular–atrial coupling rather than tissue injury.
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Vratonjic et al. (2026) conducted an observational in ST-elevation myocardial infarction (STEMI) (n=258). CMR-derived myocardial injury markers (infarct size, remote native T1, microvascular obstruction, myocardial edema) was evaluated on Echocardiographic markers of LV diastolic function: relaxation (e′), filling pressure (E/e′), chamber compliance (DT), and left atrial reservoir strain (PALS) (β = -0.216 (infarct size on e′); β = 0.271 (MVO on E/e′), p=0.005 (infarct size on e′); <0.001 (MVO on E/e′)). Infarct size and remote T1 independently predicted impaired relaxation (e′; β=-0.216, p=0.005), while microvascular obstruction drove elevated E/e′ (β=0.271, p<0.001) after STEMI.
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