Abstract
Objectives: Large ventricular aneurysm secondary to myocardial infarction (MI) results in severe heart failure (HF) and limits the effectiveness of regeneration therapy, which can be improved by surgical ventricular reconstruction (SVR). However, the conventional SVR procedures do not yield optimal long-term outcome in post-MI rodents. We hypothesized that a modified SVR procedure without aggressive purse string suture would persistently alleviate HF and improve cardiac regeneration in post-MI mice.Methods: Adult male C57 mice were subjected to MI or sham surgery. Four weeks later, mice with MI underwent SVR or 2nd open-chest operation alone. SVR was performed by plicating the aneurysm with a single diagonal linear suture from the upper left ventricle (LV) to the right side of the apex. Cardiac remodeling, heart function and myocardial regeneration were evaluated.Results: Three weeks after SVR, the scar area, LV volume, and heart weight/body weight ratio were significantly smaller, while LV ejection fraction, the maximum rising and descending rates of LV pressure, LV contractility and global myocardial strain were significantly higher in SVR group than in SVR-control group. The inhibitory effects of SVR on LV remodeling and HF persisted for at least eight-week. SVR group exhibited improved cardiac regeneration, as reflected by more Ki67-, Aurora B- and PH3-positive cardiomyocytes and a higher vessel density around the plication area of the infarcted LV.Conclusions: SVR with a single linear suture results in a significant and sustained reduction in LV volume and improvement in both LV systolic and diastolic function as well as cardiac regeneration.
Highlights
Heart failure (HF) secondary to myocardial infarction (MI) remains one of the most difficult clinical challenges worldwide despite the continuous development of new drugs and interventional therapies [1]
Current evidence suggests that prompt optimal medical therapy and revascularization after MI can reduce the incidence of HF, but a certain proportion of patients with MI inevitably develop into HF, especially patients with left ventricular aneurysm (LVA) and a larger left ventricular (LV) volume [2]
Four weeks after MI, 75% of mice survived and exhibited severe LV remodeling, as manifested by a 100% incidence of LVA, a significantly increased LV volume, a markedly reduced LV ejection fraction (LVEF), and significant upregulation of natriuretic peptide type A (Nppa) and natriuretic peptide type B (Nppb) gene expression (Figures 1C–G)
Summary
Heart failure (HF) secondary to myocardial infarction (MI) remains one of the most difficult clinical challenges worldwide despite the continuous development of new drugs and interventional therapies [1]. Medical and interventional therapies are insufficient to reverse the severe remodeling in some patients with refractory HF [5], which requires the use of more powerful techniques such as surgical correction to improve the worse prognosis. In 2004, the RESTORE team reported that SVR after coronary artery bypass grafting alleviated HF and was an effective therapy for ischemic cardiomyopathy, showing excellent fiveyear outcomes [5]. In 2009, the STICH trial showed that SVR did not result in greater benefits than coronary artery bypass grafting alone [5, 7]. The current concerns related to conventional SVR include its impacts on LV diastolic function and right ventricular function, as well as the long-term outcome [10, 11].
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