Endothelial dysfunction evaluated by peripheral arterial tonometry is related with peak TnI values in patients with...

The role of endothelial-dependent function in patients with acute ST elevation myocardial infarction (STEMI) is not clear. Endothelial dysfunction may contribute to the pathophysiological processes occurring after STEMI and influence the extension of myocardial necrosis. Endothelial-dependent dysfunction evaluated by peripheral arterial tonometry (PAT) has already showed to be correlated with microvascular coronary endothelial dysfunction. Our purpose was to evaluate the impact of endothelial dysfunction on peak Troponin I (TnI) values, as a surrogate for the extension of myocardial infarction, in patients with STEMI treated with primary angioplasty (P-PCI).

58 patients with STEMI treated with P-PCI (mean age 59.0 ± 14.0 years, 46 males) were included. Endothelial function was assessed by reactive hyperaemia index (RHI) determined by PAT. Patients were divided in two groups according to the previously reported RHI threshold for high risk (1.67). The extension of myocardial necrosis was evaluated by peak TnI levels.

RHI median value was 1.78 (IQR0.74);25 patients had endothelial dysfunction (RHI b 1.67). The two groups had no significant differences in age, gender, main risk factors and pain-to-balloon time. Patients with an RHI b 1.67 had significant larger infarcts: TnI 73.5 ng/mL (IQR 114.42 ng/mL) versus TnI 33.2 ng/mL (IQR 65.2 ng/mL); p = 0.028. On multivariate analysis, the presence of an RHI b 1.67 kept significant impact on TnI peak values (p=0.02).

The presence of endothelial-dependent dysfunction, assessed by PAT, is related with higher peak TnI values in STEMI patients treated with P-PCI. These results strength the possibility that endothelial-dependent dysfunction may be a marker of poor prognosis and eventually a therapeutic target in patients with STEMI.