Cellular cardiomyoplasty in large myocardial infarction: Can the beneficial effect be enhanced by ACE‐inhibitor therapy?

Abstract

Background: Cellular cardiomyoplasty with bone marrow derived stromal (MSC) and mononuclear (BMNC) cells has been shown to improve performance of infarcted hearts. We performed a comparative study with MSC and BMNC and tested the hypothesis that captopril treatment could enhance the beneficial effect of cell therapy in large myocardial infarctions. Methods: Male syngeneic Wistar rats underwent experimental infarction and were randomized to receive 1-3 × 10 6 MSC, 10 8 BMNC or vehicle (BSS group). Two additional groups were treated with captopril and received 1-3 × 10 6 MSC (Cap.MSC) or vehicle (Cap). Results: The ejection fraction (EF%) of MSC and BMNC-treated rats was higher than in the BSS rats, eight weeks after transplantation (33.0± 4.0, 34.0 ± 2.0 and 20.0 ± 2.0% respectively, P b 0.01). Both captopril-treated groups improved EF% similarly. But only captopril plus MSC treatment almost restored cardiac function to control levels, 8 weeks after injection (60.50 ± 5.40% vs. 41.00 ± 4.50% in Cap.MSC and Cap respectively, P b 0.05). Many DAPI-labelled cells were found in the scar tissue of the left ventricle only in the Cap.MSC group. Conclusions: Cell transplantation with both MSC and BMNC produced a similar stabilisation of heart function, but the success of the cell engraftment and the recovery of cardiac performance were dependent on concomitant treatment with captopril.

Granulocyte-colony Stimulating Factor Treatment of Chronic Myocardial Infarction

“…We demonstrated that bone marrow stromal cells alone ameliorate cardiac performance in healed infarcted rat hearts [1] and bone marrow monuclear cells when associated with classical pharmacological approaches as angiotensin converting enzyme inhibitors restored the functional competence of rat hearts with large infarcts [2]. However, intracardiac cell injection constitutes an invasive surgical intervention.…”

β-Blocker inhibits myocardial infarction-induced brown adipose tissue D2 activation and maintains a low thyroid hormone state in rats

“…Another potential mechanism to explain serum T3 normalization lies in D3 activity. If high cardiac D3 activity is associated with low serum thyroid hormones in the early phase of HF (38), T3 normalization observed in the late phase could be secondary to D3 inactivation.…”

Inhibition of Brain Renin–angiotensin System Improves Diastolic Cardiac Function Following Myocardial Infarction in Rats

“…Left ventricular (LV) MI was induced following the procedure described by Johns and Olson 18 and modified in our laboratory 1,5,6 . Briefly, male Wistar rats (200–250 g) were anaesthetized with ketamine (50 mg/kg, i.p.…”

“…These beneficial effects are also evident on electrocardiographic examination 5 . In addition, using the same experimental model, we demonstrated that the beneficial effects of stem cell therapy could be enhanced by ACEI pretreatment, probably due to decreases in infarct size that ultimately improve diastolic function 6 …”