Key result
Coronary angiography with iopromide did not significantly increase plasma concentrations of ET-1 (0.95 vs 1.36 pg/ml at baseline), histamine, or tryptase at 30 minutes post-procedure.
Why the study?
High osmolal ionic radiocontrast media cause vascular release of endothelin-1 and activate mast cells, but it was unclear if the nonionic radiocontrast medium iopromide does the same.
Does iopromide release endothelin-1 or activate cardiac mast cells during coronary angiography?
Observational (n=11)
Does iopromide release endothelin-1 or activate cardiac mast cells during coronary angiography?
Iopromide, a nonionic radiocontrast medium, does not cause significant release of endothelin-1 or activate cardiac mast cells during coronary angiography.
Answers are grounded in this paper and cite their sources.
Iopromide may avoid ET-1 release and mast cell activation risks in angiography; extends nonionic RCM observations but leaves open need for larger confirmation.
BACKGROUND: High osmolal ionic radiocontrast media (RCM) cause vascular release of endothelin-1 (ET-1) and activate mast cells. Iomeprol, a nonionic RCM, has recently been reported not to activate cardiac mast cells. This coronary angiography study was performed to extend those findings using another nonionic RCM, iopromide, and to further determine whether iopromide causes release of ET-1. METHODS: Pulmonary artery plasma ET-1, histamine and serum tryptase were determined before and 30 min following angiography with iopromide in 11 subjects. ET-1, histamine and tryptase were measured using immunoassays. RESULTS: The concentrations of ET-1 (1.36 +/- 0.66 pg/ml), histamine (2.63 +/- 1.15 nM), and beta (<1 microg/l) as well as total tryptase (8.25 +/- 4.63 microg/l) in the preangiography samples were within the normal range. Following angiography, the concentrations of ET-1 (0.95 +/- 0.80 pg/ml), histamine (3.08 +/- 1.06 nM), and beta (<1 microg/l) and total tryptase (7.00 +/- 5.56 microg/l) were not significantly different. None of the subjects demonstrated a postangiography increase in mediator concentration. CONCLUSIONS: This study demonstrates the lack of release of ET-1 by iopromide. The lack of cardiac mast cell activation by iopromide is consistent with the report that iomeprol also does not activate cardiac mast cells.
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Simon et al. (2003) conducted an observational in Coronary angiography (n=11). Iopromide vs. Preangiography baseline was evaluated on Pulmonary artery plasma ET-1, histamine and serum tryptase concentrations. Coronary angiography with iopromide did not significantly increase plasma concentrations of ET-1 (0.95 vs 1.36 pg/ml at baseline), histamine, or tryptase at 30 minutes post-procedure.
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