Hyperglycaemia, inflammation and early cardiac remodelling in non-surgically revascularized STEMI: the role of microvascular obstruction and intramyocardial haemorrhage
摘要
In ST-elevation myocardial infarction (STEMI), timely reperfusion via percutaneous coronary intervention (PCI) reduces mortality but is limited by microvascular injury (MVI), including microvascular obstruction (MVO) and intramyocardial hemorrhage (IMH), which drive adverse cardiac remodeling. This study evaluates the incidence of MVO and IMH, their combined effects, and associations with hyperglycemia, inflammation, and left ventricular (LV) dysfunction after successful non-surgical revascularization of STEMI.
Methods and resultsA single-center cohort of 60 STEMI patients (2019–2020) underwent contrast-enhanced cardiac magnetic resonance imaging (MRI) 48 ± 6 h post-infarction to assess MVI. Patients were classified into four groups: no MVI, isolated MVO, isolated IMH, and combined MVO + IMH. For some analyses, patients were also dichotomized into MVI-present versus MVI-absent groups to facilitate comparison of functional and biochemical outcomes. LV function was evaluated via echocardiography (days 7 and 90). Biomarkers were analyzed at admission and day 7. MVI occurred in 68.3% of patients: isolated MVO (16.7%), isolated IMH (15%), and combined MVO + IMH (36.7%). Combined MVO + IMH correlated with larger infarct size, prolonged ischemia, and higher admission glucose. C-reactive protein (CRP) levels on day 7 were elevated in isolated MVO (59.8 [9.1–75.9] mg/L) and MVO + IMH (32.8 [4–55.6] mg/L) versus no-MVI (4.6 [2.9–12.7] mg/L). LV ejection fraction (LVEF) was significantly lower in MVO + IMH groups (p < 0.05). Admission glucose inversely correlated with day 7 LVEF (r = -0.43, p < 0.0001).
ConclusionCombined MVO and IMH was associated with a more unfavorable remodeling pattern and subtle LV dysfunction, which may be exaggerated by hyperglycemia and inflammation. Elevated CRP links MVO to systemic inflammation, while IMH reflects mechanical capillary damage. These findings emphasize the need for early glycemic control, anti-inflammatory strategies, and imaging-guided risk stratification to mitigate microvascular injury and improve outcomes in STEMI.
Graphical AbstractAMI—Acute Myocardial Infarction; IMH—Intramyocardial Hemorrhage: MVO—Microvascular Obstruction.
Hyperglycaemia, inflammation and early cardiac remodelling in non-surgically revascularized STEMI: the role of microvascular obstruction and intramyocardial haemorrhage