Author + information
- Received July 14, 1994
- Revision received February 16, 1995
- Accepted February 27, 1995
- Published online July 1, 1995.
- ↵*Address for correspondence: Dr. Daniele Rovai, CNR, Clinical Physiology Institute, Via Savi 8, 56100 Pisa, Italy.
Despite the useful information provided by myocardial contrast echocardiography, the meaning of myocardial contrast intensity remains elusive. This review is meant to define the contribution of physical and biologic factors in producing myocardial contrast and to elucidate the relative roles of coronary blood flow and intramyocardial blood volume in determining contrast effect. The main physical factors influencing the contrast echo effect include the properties of microbubbles as scattering elements (mainly their radius, compressibility, stability and concentration), electronic signal processing, instrument setting and contrast-induced signal attenuation. The effect of these factors can be limited by an appropriate experimental or clinical setup. Biologic factors are less easily controllable, and changes in coronary blood flow and alterations in myocardial blood volume appear to be the main determinants of myocardial contrast intensity. Moreover, these factors influence contrast intensity in opposite directions. Both the area under the time-intensity curve and the mean transit time of myocardial contrast are inversely related to coronary blood flow but directly related to myocardial vascularity and blood volume. Therefore, an increase in coronary flow not accompanied by an increase in myocardial vascularity and volume is accompanied by a decrease in the area under the curve and mean transit time of contrast. Conversely, an increase in coronary flow mediated by augmented myocardial vascularity and volume will produce an increase in the area under the curve and mean transit time. A better understanding of the physical and biologic determinants of contrast echo intensity will be fundamental in the clinical application of new agents and technologies.
This review was supported in part by the National Research Council of Italy, Rome, Italy; the University of California San Diego, San Diego, California; and Nycomed AS, Oslo, Norway.
- Received July 14, 1994.
- Revision received February 16, 1995.
- Accepted February 27, 1995.
- The American College of Cardiology