Article,

Intracavitary contrast intensity after transpulmonary transmission of a second-generation contrast agent at normal and reduced myocardial contractility

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J Am Soc Echocardiogr, 13 (11): 1030-7 (November 2000)Greim, C A Broscheit, J A Lorenz, K W Thiel, H Roewer, N United states Journal of the American Society of Echocardiography : official publication of the American Society of Echocardiography J Am Soc Echocardiogr. 2000 Nov;13(11):1030-7..

Abstract

In this closed-chest preparation in 10 anesthetized pigs, we determined the effects of left ventricular (LV) contractility changes on the echocardiographic contrast intensity variation of a second-generation contrast agent within the LV cavity. The peak positive rate of change in LV pressure (dP/dt(max)), as an index of the isovolumetric phase, was gradually reduced by administration of halothane and propranolol, and the velocity of circumferential fiber shortening (Vcfs) was referenced as an index for the LV ejection phase. Contrast intensity-time curves of the LV cavity were obtained after transpulmonary transmission of the contrast agent. An off-line densitometric method was performed to determine peak maximum and minimum intensities (I(max), I(min)) and their difference (I(amp)). Compared with baseline values, at reductions in dP/dt(max) of 50% and 75%, the contrast intensity parameters I(max), I(min), and I(amp) were decreased by 23% +/- 6% and 44% +/- 5%, 24% +/- 5% and 44% +/- 3%, and 31% +/- 6% and 45% +/- 3%, respectively (P <.05). Significant correlations were observed between I(amp) and dp/dt(max) (r = 0.82, P <.003, n = 30) and their changes (r = 0.59, P <.03, n = 20), but correlations between contrast indexes and Vcfs were only moderate. The sensitivity of I(amp) to indicate changes in dP/dt(max) and Vcfs was 0.95 and 0.83, respectively. The cyclic variation of LV intracavitary contrast intensity reflects the isovolumetric contraction phase better than the ejection phase. The results suggest that measurements of cyclic intensity changes may contribute to the assessment of myocardial contractility changes. Underlying biophysical mechanisms and load dependency of this phenomenon require further investigation.

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