The cardiac growth process (hypertrophy) is a crucial phenomenon conserved across a wide array of species and it is critically involved in maintenance of cardiac homeostasis. This process enables organism adaptation to changes of systemic demand and occurs due to a plethora of responses, depending on the type of signal or stimuli received. The growth of cardiac muscle cells in response to environmental conditions depends on the type, strength and duration of stimuli, and results in adaptive physiologic response or non-adaptive pathologic response. Thyroid hormones (TH) have a direct effect on the heart and induce a cardiac hypertrophy phenotype, which may evolve to heart failure. In this review, we summarize the literature on TH function in heart presenting results from experimental studies. We discuss the mechanistic aspects of TH associated with cardiac myocyte hypertrophy, increased cardiac myocyte contractility and electrical remodeling as well as the signaling pathways associated. In addition to classical crosstalk with the Sympathetic Nervous System (SNS), emerging work points to the new endocrine interaction between TH and Renin-Angiotensin System (RAS) is also explored. Given the inflammatory potential of the angiotensin II peptide, this new interaction may open the door for new therapeutic approaches that target key mechanisms responsible for TH-induced cardiac hypertrophy.