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18th World Congress on Heart Disease

 

CARDIAC TISSUE HYPOTHYROIDISM- A MAJOR PLAYER IN DIABETIC CARDIOMYOPATHY


A. Martin Gerdes, M.D., N.Y. Weltman, New York Institute of Technology, Old Westbury, NY, USA

 

Objectives and Background: Thyroid dysfunction is common in individuals with diabetes mellitus (DM) and may contribute to the associated cardiac dysfunction. However, little is known about the extent and pathophysiological consequences of low thyroid conditions on the heart in DM.

Methods and Results: DM was induced in adult rats by streptozotocin (STZ) following nicotinamide (N) pre-treatment. One month after STZ/N, rats were randomized to the following groups: STZ/N or STZ/N + 3 g/kg/day T3 orally; age-matched vehicle treated rats served as non-diabetic controls (C). After 2 months T3 treatment (3 months post DM induction), LV function was assessed by echocardiography and LV pressure transducer. Despite normal serum thyroid hormone (TH) levels, STZ/N led to reductions in myocardial tissue content of THs (T3 & T4: 39% & 17% reduction vs. C, respectively). Tissue hypothyroidism in the DM hearts correlated with increased D3 deiodinase (which converts THs to inactive metabolites) and TH transporter expression, re-expression of the fetal gene phenotype, reduced arteriolar resistance vessel density, and diminished cardiac function. Physiologic T3 replacement largely restored cardiac tissue TH levels (T3 & T4: 43% & 10% increase vs. STZ/N, respectively), improved cardiac function, reversed fetal gene expression, and preserved the arteriolar resistance vessel network without causing overt symptoms of hyperthyroidism.

Conclusion: Cardiac dysfunction in chronic DM may be associated with tissue hypothyroidism despite normal serum TH levels. Physiologic TH replacement appears to be a safe and effective adjunct therapy to prevent cardiac remodeling and dysfunction induced by experimental DM.

 

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