Abstract 2826: Microvascular Obstruction on Cardiac MRI is Associated with an Early Peak Troponin
Background: Microvascular obstruction (MVO) post STEMI, as defined on cardiac MRI (CMR), reflects slow flow in the microvasculature. It has been postulated that MVO may result in impaired washout of troponin (Tn) and therefore a later peak.
Aim: To use CMR to explore the relationship between MVO and the pattern of TnI release after STEMI.
Methods: After successful primary angioplasty serial TnI measurements were taken at 6, 14 and 24 hours. Gadolinium (Gd) enhanced CMR was performed at 4.7±2 days and again at 191±17 days. Infarction was defined as a hyperenhanced region 10 minutes after intravenous 0.1mmol/kg Gd and MVO defined as a hypoenhanced region in the centre of this infarcted segment. A 17 segment model was used for wall motion assessment and functional recovery.
Results: 26 patients, age 57 ±11 yrs, were included in the analysis. On early scanning infarct size was 22.1±13% and MVO was 4.3± 4% of LV mass. The 81% of patients with MVO had an earlier peak TnI than those without MVO (p=0.005). Patients with severe MVO, defined as the highest quartile of MVO extent, all had the earliest peak of 6hrs. Those with MVO had higher TnI at 6hrs (p=0.002), 14hrs (p=0.027) and area under the curve (AUC) (p=0.014). TnI levels at all time points in the first 24 hours had a very strong correlation with MVO extent (r=0.80 – 0.88, p<0.001). This was stronger than between TnI and infarct size (r=0.68 – 0.78, p<0.001). Equally an early peak TnI (6hrs compared with 14hrs) was associated with a higher peak TnI level (p=0.013) and AUC (p=0.019). In the 17 patients with follow up scans infarct involution was 19.8±13% and the relationship between TnI level and infarct size did not change significantly. As MVO increased there was less functional recovery (r=−0.49, p=0.046) and increased left ventricular end diastolic volume (r=0.512, p=0.036) at 6 months. Of the 5 patients who developed dyskinetic segments 3 had severe MVO and 4 an early peak TnI.
Conclusion: MVO presence and extent is associated with an early peak in TnI after reperfused STEMI and more extensive myonecrosis as evidenced by cumulative (AUC) TnI release. These findings favour more complete myonecrosis within the MVO region, rather than impaired washout, as the predominant pathological basis for the relationship between MVO and TnI kinetics.