LAUSR

Heart disease remains the leading cause of death globally. Heart failure (HF) is a clinical syndrome that results from impairment of the ability of the ventricle to fill with or eject blood. Over the past two decades, accumulated evidence has revealed the contribution of thyroid hormones to cardiovascular (CV) events, exerting their action through genomic and non-genomic pathways within the cardiomyocytes. The pivotal role of thyroid hormones in maintaining cardiac homeostasis has been observed in previous investigations which suggest that the CV system is adversely impacted by fluctuations in thyroid hormone levels, such as those that occur in hypothyroidism, hyperthyroidism, and low triiodothyronine syndrome (LT 3 S). Thyroid dysfunction has direct effects on myocardial contractility, systolic and diastolic blood pressure, heart mass, heart rate, ejection fraction, and heart output, which may ultimately lead to HF. Recent clinical data have shown that thyroid hormone replacement therapy for hypothyroid patients appears to provide the potential for reducing CV events. Therefore, this review aims to address the impact of thyroid hormone dysfunction on pathophysiological mechanisms contributing to the development and progression of HF.