Echocardiographic Speckle-Tracking–Based Strain Imaging for Rapid Cardiovascular Phenotyping in Mice
Rationale: High-sensitivity in vivo phenotyping of cardiac function is essential for evaluating genes of interest and novel therapies in small animal models of cardiovascular disease. Transthoracic echocardiography is the principal method currently used for assessing cardiac structure and function; however, standard echocardiographic techniques are relatively insensitive to early or subtle changes in cardiac performance, particularly in mice.
Objective: To develop and validate an echocardiographic strain imaging methodology for sensitive and rapid cardiac phenotyping in small animal models.
Methods and Results: Herein, we describe a modified echocardiographic technique that uses speckle-tracking–based strain analysis for the noninvasive evaluation of cardiac performance in adult mice. This method is found to be rapid, reproducible, and highly sensitive in assessing both regional and global left ventricular (LV) function. Compared with conventional echocardiographic measures of LV structure and function, peak longitudinal strain and strain rate were able to detect changes in adult mouse hearts at an earlier time point following myocardial infarction and predicted the later development of adverse LV remodeling. Moreover, speckle-tracking–based strain analysis was able to clearly identify subtle improvement in LV function that occurred early in response to standard post–myocardial infarction cardiac therapy.
Conclusions: Our results highlight the utility of speckle-tracking–based strain imaging for detecting discrete functional alterations in mouse models of cardiovascular disease in an efficient and comprehensive manner. Echocardiography speckle-tracking–based strain analysis represents a method for relatively high-throughput and sensitive cardiac phenotyping, particularly in evaluating emerging cardiac agents and therapies in mice.
- Received December 23, 2010.
- Revision received January 20, 2011.
- Accepted February 17, 2011.
- © 2011 American Heart Association, Inc.