Pathophysiology of myocardial remodeling in survivors of ST-elevation myocardial infarction revealed by native T1 mapping: inflammation, remote myocardium and prognostic significance

Background: The pathophysiology and prognostic significance of remote myocardium in the natural history of STEMI is uncertain. Cardiac magnetic resonance (CMR) provides a non-invasive assessment of myocardial pathology that is spatially and temporally coordinated. Native T1 quantified by CMR (T1 relaxation time, milliseconds) is a fundamental tissue property determined by water content and cellularity. We aimed to investigate the clinical significance of remote myocardium in survivors of acute ST-elevation myocardial infarction (STEMI) using native T1 mapping. Methods: We performed a prospective single center cohort study in reperfused STEMI patients who underwent CMR 2 days and 6 months post-MI and long term follow-up (18 months minimum). Native T1 CMR (MOLLI investigational prototype sequence: 3 (3) 3 (3) 5) was measured in regions-of-interest in remote and injured myocardium. Infarction was depicted on late gadolinium contrast enhancement imaging. Adverse remodeling was defined as an increase in left ventricular end-diastolic volume ≥ 20% at 6 months. Major adverse cardiac events (MACE) were defined as cardiac death or hospitalization for non-fatal MI or heart failure. Results are mean±SD unless specified. Results: 300 STEMI patients (mean age 59 years, 74% male) gave informed consent (14 July 2011 - 21 November 2012). Of these, 288 STEMI patients had evaluable native T1 CMR and follow-up data (median duration 845 days). Infarct size was 18±14% of left ventricular mass. Two days post-STEMI, native T1 in remote myocardium was lower than native T1 in the infarct zone (961±25 ms vs. 1097±52 ms; p<0.01). In multivariable linear regression, remote zone native T1 was independently associated with incomplete ST-segment resolution (9.42 (2.37 to 16.47); p=0.009), the log of the initial CRP concentration (regression coefficient 3.01 (95% CI 0.016 to 5.55); p=0.038) and the peak monocyte count within 2 days of admission (10.20 (0.74, 19.67); p=0.035). At 6 months, left ventricular end-diastolic volume increased by 5 (25) ml (n=262 patients with evaluable data) overall, and adverse remodeling occurred in 30 (12%) patients. Remote zone native T1 was a multivariable predictor of the change in left ventricular end-diastolic volume from baseline (0.13 (0.01, 0.24); p=0.035). 39 (13.5%) patients experienced a MACE including 20 (6.9%) patients with a post-discharge MACE. Remote zone native T1 was an independent predictor of post-discharge MACE (hazard ratio 1.016, 95% CI 1.000, 1.032; p=0.048) including after adjustment for changes in LVEF (p=0.032), LV end-diastolic volume (p=0.053), and monocyte count (p=0.036). Conclusions: Remote zone tissue characteristics early post-MI are temporally linked with reperfusion injury and inflammation and independently predict left ventricular remodeling and MACE in STEMI survivors

Prognostic significance of infarct core pathology in ST-elevation myocardial infarction survivors revealed by non-contrast T1 mapping cardiac magnetic resonance

Background: Myocardial longitudinal relaxation time (T1, ms) is a fundamental magnetic property of tissue that is related to water content and mobility. The pathophysiological and prognostic importance of native myocardial T1 values in acute ST-elevation myocardial infarction (STEMI) patients is unknown. We aimed to assess the clinical significance of infarct core native T1. Methods: We performed a prospective single center cohort study in reperfused STEMI patients who underwent CMR 2 days and 6 months post-MI. Native T1 CMR (MOLLI investigational prototype sequence: 3 (3) 3 (3) 5) was measured in myocardial regions-of-interest. The infarct territory and microvascular obstruction (MVO) were depicted with late gadolinium enhancement CMR. Adverse remodeling was defined as an increase in LV end-diastolic volume (LVEDV) ≥ 20% at 6 months. All-cause death or heart failure hospitalization was a pre-specified outcome that was assessed during follow-up. Results: 300 STEMI patients (mean±SD age 59±12 years, 74% male, 114 with anterior STEMI) gave informed consent and had CMR (14 July 2011 - 22 November 2012). Of these, 288 STEMI patients had evaluable T1 maps. Infarct size was 18 ±14% of LV mass. One hundred and forty five (50%) of 288 patients had late MVO, whereas 160 (56%) patients had infarct core pathology revealed by native T1. Native T1 within the infarct core (996.9±57.3; p<0.01) was higher than in the remote zone (961±25 ms; p<0.01) but lower than in the area-at-risk (1097 ±52 ms). In multivariable linear regression, native T1 in the infarct core was negatively associated with age, initial systolic blood pressure, TIMI coronary flow grade at initial angiography, Killip class at presentation and neutrophil count (all p<0.05), independent of LVEF, LVEDV or infarct size. At 6 months, LVEDV increased by 5 (25) ml (n=262 patients with evaluable data). Adverse remodeling occurred in 30 (12%) patients and 23 (76.7%) of these patients MVO at baseline. T1 in the infarct core was a multivariable predictor of adverse remodeling (-0.01 (-0.02, -0.00); p=0.048). 288 (100%) patients were followed-up for a median of 845 days. Thirty (10.4%) patients died or experienced a heart failure event and 13 (4.5%) of these patients experienced the event post-discharge. Infarct core native T1 predicted all-cause death or heart failure post-discharge (hazard ratio 0.969, 95% CI 0.953, 0.985; p<0.001) including after adjustment for LVEF (p<0.001) and LVEDV at baseline (p<0.001), and was comparable with MVO

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Available from TIB Hannover: RN2805(1319) / FIZ - Fachinformationszzentrum Karlsruhe / TIB - Technische InformationsbibliothekSIGLEDEGerman