Potentiation by nifedipine and diltiazem of the hypotensive response after contrast angiography
DL Morris,
JA Wisneski,
EW Gertz,
M Wexman,
R Axelrod,
and
JJ Langberg
Arterial hypotension has been demonstrated after left ventriculography using currently available ionic contrast agents. This adverse hemodynamic response is significantly decreased with the newer nonionic contrast agents. Calcium channel antagonists also produce a hypotensive response. The potentially accentuated hypotensive response after bolus contrast angiography in patients receiving the calcium antagonists nifedipine and diltiazem was evaluated. Three contrast agents were compared: two ionic agents (Renografin-76 and Hypaque-76) and a nonionic agent (iopamidol). The hemodynamic response after left ventriculography was assessed in 125 patients, 65 receiving nifedipine or diltiazem and 60 not receiving these drugs. Baseline clinical characteristics were similar in all patient groups. The hypotensive response was significantly greater after left ventriculography with the ionic agents than with the nonionic agent. In those patients receiving nifedipine or diltiazem, the hypotensive response after bolus contrast angiography using the ionic agents occurred earlier after contrast injection (4.2 +/- 3.1 versus 12.9 +/- 6.0 seconds, p less than 0.0001), was more profound (maximal decrease in systolic arterial pressure, 48.5 +/- 13.9 versus 36.9 +/- 13.1 mm Hg, p less than 0.001) and was more prolonged (62.3 +/- 11.0 versus 36.4 +/- 12.0 seconds, p less than 0.0001) than in patients not receiving these drugs. A comparison of the two ionic contrast agents showed no significant difference in the hypotensive response. There was no difference in the hemodynamic response after angiography among patients receiving iopamidol alone and those receiving iopamidol and calcium antagonists. Thus, patients receiving the calcium antagonists diltiazem and nifedipine and undergoing left ventriculography with ionic contrast agents are at added risk for accentuation and prolongation of the hypotensive response.
