Effect of intracoronary injections of sonicated microbubbles on left ventricular contractility

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Abstract

Despite the recent interest in contrast-enhanced echocardiography as a means of defining myocardial perfusion, the effects of echo contrast agents on left ventricular (LV) contractility in humans remains poorly defined. This is particularly relevant because intracoronary injection of contrast agents used for angiographic visualization of coronary arteries produces significant alterations in LV hemodynamics. The relation of LV end-systolic wall stress (δes) to rate-corrected velocity of fiber shortening (Vcfc), a load-independent index of contractility, was studied in 7 patients undergoing elective coronary arteriography. Two-dimensional and targeted M-mode echocardiographic and central aortic pressure tracings were recorded during injections of standard volumes of angiographic (7 to 9 ml of nonsonicated Renografin-76) and echocardiographic (1.5 to 2.0 ml of sonicated Renografin-76) contrast agents into the left main coronary artery. The order in which agents were injected was randomly determined. Myocardial contractility was assessed under control conditions and 5 and 15 seconds after injection. Alterations in contractility relative to control were measured as the change in Vcfc after elimination of afterload (αes) as a confounding variable. An injection of Renografin-76 adequate for angiographic imaging of coronary artery anatomy resulted in a significant depression of LV contractility (p <0.001) in conjunction with a tendency toward increased afterload (p = 0.12); recovery occurred by 15 seconds after injection. The smaller amounts of sonicated Renografin-76 required to give adequate contrast enhancement of the myocardium did not alter LV contractile state or afterload. Thus, sonicated Renografin-76 is a safe echocardiographic contrast agent without adverse effects on LV contractility and the volume of contrast material injected rather than the presence of microbubbles appears to be the major determinant of altered myocardial mechanics.

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This work was supported in part by grants from the Goldblatt Research Foundation and the Amoco Foundation, Chicago, Illinois.

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