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Urotensin-II levels in acute coronary syndromes
Dominique Joyal1, Thao Huynh, Nambi Aiyar
1McGill University Health Center, Montreal General Hospital, Division of Cardiology, E-5-200, 1650 avenue Cedar, Montreal, Quebec, Canada H3G 1A4.
Background:
Urotensin-II (U-II) is a vasoactive peptide with diffuse expression in human cardiomyocyte and vascular smooth muscle cells. Recent studies have reported increased plasma levels of U-II in patients with congestive heart failure.
Objective:
We sought to determine the plasma levels of U-II in patients with acute coronary syndromes (ACS), stable coronary artery disease (CAD) and healthy controls.
Methods:
We prospectively measured plasma U-II levels in 54 patients with ACS, 51 patients with stable coronary disease and 29 healthy volunteers. Monoclonal antibodies against U-II were generated and plasma U-II levels were determined by radioimmunoassay from extracted venous samples.
Results:
ACS patients had significantly lower levels than patients with stable CAD and healthy controls (2.53+/-1.62 vs. 3.45+/-2.53 vs. 3.3+/-3.9 ng/ml, p=0.008, respectively). In both ACS and stable CAD patients, we found a negative relationship between plasma U-II levels and systemic arterial pressures. The correlation coefficients for systolic and mean arterial pressure were -0.272, p=0.006 and -0.209, p=0.04, respectively.
Conclusions:
Plasma U-II levels were significantly decreased in patients with acute coronary syndromes and related negatively to systemic arterial pressures. This finding suggests a down-regulation of U-II expression in patients with acute coronary syndromes.
Condensed Abstract:
Urotensin-II (U-II) is a vasoactive peptide with diffuse staining in human cardiomyocytes and vascular smooth muscle cells. We measured plasma U-II levels in patients with acute coronary syndromes (ACS), stable coronary artery disease (CAD) and healthy controls. We observed lower U-II levels in ACS patients and a negative correlation between U-II levels and systemic arterial pressure. This finding suggests a down-regulation of U-II expression in patients with ACS.
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