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Left cardiac sympathetic denervation (LCSD) is an effective method to prevent post-infarction ventricular arrhythmia and sudden cardiac death. This study was to test the hypothesis that LCSD with tetanus toxin C fragment (TTC)-conjugated nanoparticles could attenuate cardiac dysfunction and ventricular arrhythmia in a canine post-infarction heart failure model.
Twenty dogs underwent embolization of the left anterior descending artery followed by right ventricular pacing (240 bpm) for 3 weeks to produce heart failure. Sixteen surviving animals were assigned to the LCSD group (n=8) and control group (n=8). In LCSD group, TTC-conjugated nanoparticles carrying N-isopropylacrylamide monomer were injected into canine upper limb vein, then external magnetic field will be fixed on the left stellate ganglion corresponding surface location to guide nano-composites move to this area to achieve LCSD. Animals were monitored for 8 weeks.
After 8 weeks follow-up, comparing to the control group, LCSD with nano-composites significantly (1) reduced left atrial and left ventricular dilatation and improved left ventricular function (left ventricular ejection fraction: 36±6% vs. 25±4%, p<0.05); (2) decreased ventricular arrhythmia inducibility (arrhythmia score: 2.1±0.9 vs. 4.2±0.8, p<0.05); (3) alleviated cardiac fibrosis and decreased plasma level of N-terminal pro-B-type-natriuretic peptide; (4) reduced left stellate ganglion neural activity (frequency: 12±7 vs. 183±42 impulses/s; and amplitude: 0.12±0.08 vs. 0.45±0.15 mV, p<0.05 for both).
LCSD with nano-composites significantly improved cardiac function and reduced ventricular arrhythmia inducibility in canine heart failure.