| Summary: | ABSTRACT: Introduction: Despite achieving normal epicardial coronary artery flow after primary percutaneous coronary intervention (P-PCI), a significant proportion of patients with acute ST elevation myocardial infarction has a poorer outcome because of microvascular coronary damage and/or dysfunction. Endothelial dysfunction may play a role in this microvascular coronary damage after STEMI, and its evaluation by peripheral arterial tonometry may be useful to predict the extent of microvascular coronary damage and the extent of myocardial infarction. Objectives: To evaluate the relation of early peripheral endothelial dysfunction, as measured by the reactive hyperemia index (RHI, obtained by peripheral arterial tonometry) and the index of microcirculatory resistance (IMR) immediately after P-PCI and to access the relation between RHI and IMR values and: 1) the extent of myocardial infarct evaluated by contrast enhanced cardiac magnetic resonance (ceCMR) and troponin release; 2) the extent of microvascular obstruction (MVO), evaluated by ceCMR and by other available indirect indicators; 3) late (3 months) left ventricular remodelling, measured by echocardiography. Methods: Observational, prospective cohort study. Patients with a first STEMI successfully treated with P-PCI, hemodynamically stable and without contra-indications for adenosine administration were included. After successful P-PCI, IMR was determined, using a pressure-wire. RHI was evaluated acutely and after 24 hours, using EndoPAT; endothelial dysfunction was defined as RHI<1.67, and RHI was also analysed by tertiles. Corrected TIMI frame count (cTFC) and TIMI myocardial perfusion grade (TMBG) were evaluated at the end of the procedure. Blood tests for cardiac biomarkers were collected on admission and on scheduled intervals during the first 48 hours. ECGs were recorded before and immediately after P-PCI and at 90 and 180 minutes, for ST resolution evaluation. Left ventricular global and regional function were evaluated by echocardiography at baseline and at 3 months. ceCMR was performed on the 7-8th day post-MI. Results: 60 patients were included (48 males, mean age 59.6±12.7 years). In the first acute RHI values were higher than expected (mean 2.15±0.58) suggesting important technical pitfalls; no relation was found between this acute RHI and any of the infarct extent or microvascular obstruction indicators. Mean RHI values measured at 24 hours were 1.87±0.60. Patients with an RHI<1.67 on this second evaluation tended to have higher IMR (median 40.5 IQR 54.4 vs. median 22.0 IQR 26.0, p=0.09), worse ST resolution, worse angiographic (cTFC and TMPG) results and had more MVO in the ceCMR (54.1% vs. 11.1%, p=0.03). They also had significantly larger infarcts as evaluated by peal TnI (p=0.024) and AUC TnI (p=0.012) and a tendency to have larger infarcts in the ceCMR. Left ventricular ejection fraction (LVEF) was lower and wall motion score index (WMSI) was higher in the first Echocardiogram in these patients. IMR median values were 24 (IQR 33). IMR strongly correlated with MVO on the ceCMR (r=0.91, p<0.0001; ROC curve 0.723, CI95% 0.500-0.896, p=0.018). Patients with IMR>24 had significantly worse ST resolution and angiographic indicators of microvascular dysfunction. IMR also correlated with infarct mass (r=0.70, p<0.001) and salvage mass (r=0.35, p=0.014) in the ceCMR. Patients with IMR>24 had significantly higher peak (p=0.013) and AUC (p=0.003) TnI. LVEF improved significantly only in patients with IMR<24 (p=0.01). IMR independent predictors were age, glucose and HbA1c. Conclusions: RHI measured in the acute phase of STEMI after P-PCI seems to be unfeasible. RHI measured 24h after the P-PCI is feasible and predicts infarct size and MVO, confirming endothelial dysfunction as an important mechanism in microvascular dysfunction in STEM patients. IMR is strongly correlated with MVO and predicts both infarct size and LV remodelling.
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