Effects of 3-aminobenzamide on ventricular function in infarct heart assessed by quantitative tissue velocity imaging
Man Wang1, Bing Hu, Yue-Li Zhang
1Department of Ultrasound in Medicine, Shanghai Sixth People Hospital Affiliated to Shanghai Jiao Tong University, Shanghai, China.
Background:
Coronary artery disease is a common cardiovascular disease that often causes myocardial infarction (MI), which, after a certain period, can develop into congestive heart failure, resulting in high mortality and mortality rates. Overactivation of the nuclear enzyme poly(ADP-ribose) polymerase (PARP) has recently been considered a final common effector in myocardial ischemia/reperfusion injury. The aim of this study was to have a comprehensive understanding of the beneficial effects of 3-aminobenzamide (3-AB) on postinfarct myocardial injuries by inhibiting PARP.
Methods:
A rat model of acute MI was established. Quantitative tissue velocity imaging technology in conjunction with conventional two-dimensional echocardiography and traditional pathological examinations was used to evaluate cardiac function.
Results:
We observed detrimental alterations of cardiac morphology and function in MI hearts which were otherwise absent in sham-operated control rats. We found that 3-AB (30 mg/kg, i.p.) significantly restored MI-induced depression of the peak longitudinal systolic velocity in the left-ventricular anterior and lateral walls, and of the peak centripetal systolic velocity in the anterior septum, indicating that it improved the systolic function of the left ventricle. Administration of 3-AB significantly ameliorated MI-induced myocardial injuries as revealed by two-dimensional echocardiography, showing the improvement of multiple parameters including left-ventricular end-systolic diameter, left-ventricular end-diastolic diameter, end-diastolic volume, fractional shortening, left-ventricular ejection fraction, left-ventricular anterior wall end-diastolic thickness, and spherical index, indicating that it improved the overall cardiac structure and function. Additionally, 3-AB significantly reduced infarct size, MI-induced increase in left-ventricular mass, pathological score, and PARP overactivation. However, at the dosage tested in the present study, the improvement is in general moderate.
Conclusion:
Inhibition of PARP may be an alternative approach for improving cardiac function in the setting of MI, and quantitative tissue velocity imaging, combined with two-dimensional echocardiography, provides a more comprehensive, quantitative, rapid, noninvasive evaluation of global and regional cardiac function in rats.
