Key result
In a canine model of ischemic heart failure, autologous skeletal myoblast implantation did not significantly increase ventricular tachycardia (27.3% vs 25.0%, p=ns) compared to saline control.
Why the study?
Does direct intramyocardial injection of autologous skeletal myoblasts affect rhythm stability and LVEF in a canine model of ischemic heart failure?
Does direct intramyocardial injection of autologous skeletal myoblasts affect rhythm stability and LVEF in a canine model of ischemic heart failure?
In a canine model of ischemic heart failure, autologous skeletal myoblast implantation improved LVEF without significantly increasing ventricular arrhythmias, though it affected some heart rate variability parameters.
Answers are grounded in this paper and cite their sources.
Reassures on VT risk in this canine HF model; leaves open translation to human myoblast therapy trials.
Skeletal myoblast (SM) implantation promotes recovery of myocardial function after ischemic injury. Clinical observations suggest an association of SM implantation and ventricular arrhythmias. Support for this link has been sought in animal studies, but none employing models of congestive heart failure. In a canine model of postinfarction congestive heart failure (CHF) we compared the frequency of rhythm disturbances using ambulatory electrocardiography monitoring following skeletal myoblast or saline (SAL) implantation. In 19 mongrel dogs ischemic injury and CHF were induced by intracoronary microsphere infusions. Direct intramyocardial injection of autologous skeletal myoblasts (ASM) (2.7-8.3 x 10(8) cells) or SAL controls was administered to 11 and 8 dogs, respectively. Serial echocardiography and 24-h ambulatory electrocardiography were recorded at baseline (after CHF induction) and at 4 weeks and at 8-10 weeks after injection. Comparisons between groups of left ventricular ejection fraction (LVEF) and the frequency of ventricular arrhythmias, supraventricular arrhythmias, and measures of heart rate variability (HRV) were made at each of the three time points. LVEF increased from 41 +/- 6% to 47 +/- 2% (p < 0.03) in the ASM group, and did not change (42 +/- 6% to 40 +/- 2%, p = ns) in SAL. After injection, no differences were seen in the number of dogs demonstrating ventricular tachycardia (n = 3 vs. n = 2, p = ns) or frequent PVCs (n = 3 vs. n = 3, p = ns) in the ASM versus SAL groups, respectively. Significant changes were observed in a time-domain measure of HRV, standard deviation of normal-to-normal RR interval (in ms: 4 weeks 174 +/- 95 vs. 242 +/- 19; 8 weeks 174 +/- 78 vs. 276 +/- 78, ASM vs. SAL), but not in other time domain parameters. In this canine model of ischemic CHF, ASM implantation did not result in a significant increase in ventricular arrhythmias compared to controls animals. The potential for ASM implantation to affect time-domain parameters of HRV merits further study.
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Sherman et al. (2009) studied Ischemic congestive heart failure (n=19). Autologous skeletal myoblasts (ASM) vs. Saline (SAL) was evaluated on Ventricular tachycardia (p=ns). In a canine model of ischemic heart failure, autologous skeletal myoblast implantation did not significantly increase ventricular tachycardia (27.3% vs 25.0%, p=ns) compared to saline control.
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