Myocardial contrast echocardiography without significant hemodynamic effects or reactive hyperemia: a major advantage in the imaging of regional myocardial perfusion.
All agents used for myocardial contrast echocardiography to date produce adverse hemodynamic effects and alter coronary blood flow. It was hypothesized that because 5% human albumin, when sonicated for use as a contrast agent, is neither hyperosmolar nor a calcium chelator, it would not have significant effects on coronary blood flow, left ventricular function or systemic hemodynamics. Albumin microbubbles of two distinct sizes (mean size 2.9 and 5.8 micron) were produced and compared with nonsonicated albumin, nonsonicated Renografin, sonicated Renografin and hand-agitated Renografin for their effects on hemodynamics, coronary blood flow and regional left ventricular systolic thickening in 15 open chest anesthetized dogs. None of the albumin solutions significantly altered left atrial, left ventricular systolic and end-diastolic and mean aortic pressures. These agents did not cause a coronary hyperemic response or alter left ventricular systolic thickening, but slightly lowered the peak positive left ventricular maximal rate of rise in pressure (dP/dt) (-4.1 +/- 5.4%, p less than 0.01). In contrast, all the Renografin solutions caused significant changes in all these variables (p less than 0.02). In six dogs. albumin solutions did not alter these variables even in the presence of critical coronary stenosis. The contrast opacification produced by 5.8 micron albumin microbubbles was equivalent to that produced by sonicated Renografin. Compared with an equivalent amount of saline and nonsonicated albumin solutions, 10 ml of sonicated albumin did not produce any evidence of infarction, embolization or hemorrhage in the myocardium, brain or kidneys of rabbits.(ABSTRACT TRUNCATED AT 250 WORDS)[1]References
- Myocardial contrast echocardiography without significant hemodynamic effects or reactive hyperemia: a major advantage in the imaging of regional myocardial perfusion. Keller, M.W., Glasheen, W., Teja, K., Gear, A., Kaul, S. J. Am. Coll. Cardiol. (1988) [Pubmed]
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