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20th World Congress on Heart Disease

 

CARDIOPROTECTIVE EFFECTS OF THERAPEUTIC T3 TREATMENT IN MYOCARDIAL INFARCTION AND ISCHEMIA REPERFUSION



A. Martin Gerdes, Ph.D, Department of Biomedical Sciences, New York Institute of Technology-College of Osteopathic Medicine, Old Westbury, USA

 

Background: Myocardial Infarction (MI) leads to cardiac tissue hypothyroidism, a condition that by itself can lead to heart failure (HF). Potential improvements in LV remodeling and function with a therapeutic T3 dose after MI and ischemia/reperfusion (IR) are not clear.

Objectives: We hypothesize that a safe, low-dose T3 treatment/monitoring regimen will lead to significant cardioprotection in rats following MI and 60 minute IR.

Methods: MI was produced in adult rats by LAD ligation. T3 (4-5 g/kg/day) in drinking water was started after MI and continued for 2 months (Mo). Vehicle (V) was used in MI controls (n=16-20/group). The same 2 month treatment protocol was used for rats with IR.

Results: Infarct size was similar in MI and MI+T3 groups. D3 mRNA expression increased in MI+V (2.7-fold) and was reversed in MI+T3 (0.49-fold). MI+T3 improved ejection fraction by 51% at 1 Mo and by 47% at 2 Mo post-MI as assessed by magnetic resonance imaging (MRI). Mean MRI wall thickness was increased at both latter time-points. Histologically, non-infarct area and wall thickness increased significantly (30% and 18% respectively). Non-infarct length was also increased. Remarkably, following MI, the incidence of atrial tachyarrhythmias that persisted following discontinuation of experimental atrial tachypacing was significantly diminished by 63% with T3. T3 did not affect heart rate. The T3 dose led to feedback inhibition of Thyroid-Stimulating Hormone (TSH) but no significant change in serum T3. T3 treatment for 2 months after IR also led to an increase in viable myocardium and improvement in LF function.

Conclusion: Results demonstrate a safe and effective post-MI and IR T3 treatment strategy that dramatically improves LV function, atrial arrhythmogenesis, non-infarct tissue remodeling, and myocyte survival with no adverse effects. This study describes an effective, translatable, treatment/monitoring protocol for T3 treatment of MI and IR.

 

 

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