Related Experiment Video
Updated: Sep 4, 2026

Technique of Minimally Invasive Transverse Aortic Constriction in Mice for Induction of Left Ventricular Hypertrophy
Published on: September 25, 2017
Change of c-Myc expression and cardiac hypertrophy in patients with aortic valve replacement
S Taketani1, Y Sawa, H Ichikawa
1Department of Surgery Course of Interventional Medicine E1, and Allied Health Sciences, Osaka University Graduate School of Medicine, Japan.
Insights
Preoperative c-Myc protein expression in patients with aortic regurgitation (AR) indicates the potential for reversing left ventricular (LV) dysfunction and hypertrophy after aortic valve replacement (AVR). This finding is crucial for predicting recovery outcomes.
Area of Science:
- Cardiovascular Medicine
- Molecular Cardiology
- Cardiac Surgery
Background:
- Chronic aortic regurgitation (AR) leads to left ventricular (LV) dysfunction that may not resolve after aortic valve replacement (AVR).
- The protooncogene c-myc has been implicated in the development of cardiac hypertrophy and LV dysfunction in AR patients.
- The role of c-myc in the reversibility of cardiac changes post-AVR remains unclear.
Purpose of the Study:
- To investigate the association between preoperative c-myc expression and the reversibility of cardiac hypertrophy and LV dysfunction following AVR in patients with chronic AR.
Main Methods:
- Twenty patients with isolated chronic AR undergoing AVR were assessed.
- Left ventricular function, including ejection fraction (EF), end-diastolic volume index (EDVI), and end-systolic volume index (ESVI), was measured pre- and post-AVR.
- Myocardial c-myc protein expression was quantified preoperatively and post-AVR, alongside measurements of cell diameter (CD) and end-systolic stress (ESS).
Main Results:
- Post-AVR, LV volumes (ESVI, EDVI) improved, but LV mass index (LVMI) did not normalize in all patients.
- Preoperative c-myc protein was detected in 16/20 patients; only 2 patients showed expression post-AVR.
- Preoperative c-myc expression correlated significantly with postoperative cell diameter, ESVI, and ESS/ESVI, and was higher in patients with normalized cardiac parameters.
Conclusions:
- Preoperative c-myc protein expression serves as a potential biomarker for predicting the reversibility of myocardial cellular hypertrophy and LV dysfunction after AVR in AR patients.
Background:
Long-term volume overload to the left ventricle (LV) due to aortic regurgitation (AR) tends to cause severe impairment in LV function that cannot be reversed even with aortic valve replacement (AVR). Recently, we reported that the protooncogene c-myc is related to the onset of the cardiac hypertrophy and LV dysfunction in patients with chronic AR. However, it is still unclear whether c-myc is related to reversibility of the cardiac hypertrophy or LV dysfunction after AVR.
Methods And Results:
Twenty patients with isolated chronic AR who underwent AVR were included in this study. LV function was calculated before and after AVR. After AVR, end-systolic volume index (ESVI) and enddiastolic volume index (EDVI) were improved, but not mass index (LVMI). However, normalization of ESVI and EDVI was observed only in 12 and 9 patients, respectively. Preoperatively, c-Myc protein was expressed in the myocardium of 16 out of 20 patients with an average point count of 35+/-30%. After AVR, c-Myc protein was observed only in 2 patients. Preoperative ejection fraction (EF), ESVI, and postoperative end-systolic stress (ESS)/ESVI had significant correlation to postoperative cell diameter (CD). Percent c-Myc protein expression before the operation was significantly correlated to postoperative CD, ESVI, and ESS/ESVI. Average c-Myc expression was higher in patients who showed normalization of CD and ESS/ESVI after AVR than the patients who did not.
Conclusions:
These data suggest that preoperative expression of c-Myc can be indicative of the reversibility of myocardial cellular hypertrophy and LV dysfunction.
More Related Videos
Related Concept Videos
Mitral Valve Prolapse I: Introduction
Aortic Regurgitation II: Clinical Features and Diagnostic Tests
Myocarditis I: Introduction
Cardiomyopathy III: Hypertrophic Cardiomyopathy
Cellular Adaptation II: Hypertrophy

