Key result
Cardiosphere-derived cell secretome reduces VT inducibility ~43% vs control in post-MI swine.
Why the study?
Ventricular tachycardia causing sudden cardiac death is common after myocardial infarction, prompting evaluation of intracoronary cardiosphere-derived cell secretome effects on inducibility and cardiac function.
Does intracoronary cardiosphere-derived cell secretome reduce VT inducibility and improve cardiac function in a swine model of myocardial infarction?
Does intracoronary cardiosphere-derived cell secretome reduce VT inducibility and improve cardiac function in a swine model of myocardial infarction?
Intracoronary administration of S-CDCs safely reduces VT inducibility and infarct size in a preclinical chronic MI model, highlighting its potential as a cell-free regenerative therapy.
Answers are grounded in this paper and cite their sources.
Hypothesis-generating for intracoronary cell secretome in reducing post-MI VT inducibility; prospective human trials needed before clinical adoption.
Background/Objectives: Ventricular tachycardia (VT) resulting in sudden cardiac death is common following a myocardial infarction (MI). Our objective was to evaluate the effects of an intracoronary (IC) administration of cardiosphere-derived cell secretome (S-CDCs) on VT inducibility and cardiac function in a swine model of MI. Methods: Fourteen pigs underwent endovascular MI model creation. At 4 weeks, saline (CON; 5 mL; n = 7) or S-CDCs (S-CDCs; 9.16 mg protein in 5 mL saline; n = 7) was blindly administered via the IC route. VT inducibility and magnetic resonance imaging (MRI) studies were performed both pre- and 4 months post-IC therapy, calculating left ventricular ejection fraction (LVEF), infarct size as a percentage of left ventricle (% MI), and left ventricular indexed end-diastolic and end-systolic volumes (LVEDVi, LVESVi). Results: While VT was inducible in 100% of the animals before IC therapy, at 4 months, the inducibility rate was lower in the S-CDCs group compared to the CON group (57% versus 100%, p = 0.05). Likewise, in the S-CDCs group, % MI was significantly lower than in the CON group (12 ± 3% versus 16 ± 3%, p = 0.03). LVEF (S-CDCs: 35 ± 10% versus CON: 29 ± 10%, p = NS), LVEDVi and LVESVi (S-CDCs: 83 ± 18 mL/m2 and 56 ± 20 mL/m2 versus CON: 88 ± 29 mL/m2 and 64 ± 20 mL/m2, p = NS) did not change. Conclusions: IC therapy with S-CDCs appears to reduce the development of post-MI VT. Furthermore, it suggests a beneficial effect on infarct size, reducing % MI in this experimental swine model.
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Báez-Díaz et al. (2025) studied Myocardial infarction (swine model) (n=14). Cardiosphere-derived cell secretome (S-CDCs) vs. Saline (5 mL) was evaluated on VT inducibility rate at 4 months (p=0.05). Intracoronary administration of cardiosphere-derived cell secretome reduced the ventricular tachycardia inducibility rate to 57% compared to 100% in the control group (p=0.05) in a swine MI model.
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