Thyroid hormones play a fundamental role in cardiovascular function. They influence how the heart responds to adrenaline, how the heart uses energy and how constricted or relaxed blood vessels are. However, their effect on the strength of cardiac contraction is less understood.
To better examine the role of thyroid hormones in cardiac contractility, endocrinology clinicians at UC Davis Health examined patients with myxedema coma, the most severe form of hypothyroidism. This life‑threatening condition offers a rare opportunity to observe the heart in a state of profound thyroid hormone deprivation.
Cardiac effects of hypothyroidism and critical illness
Individuals with low thyroid hormone levels (hypothyroidism) often exhibit changes in cardiac function, including delays in the onset of contraction, prolonged contraction and relaxation times and abnormalities in blood flow during cardiac filling.
A similar pattern of cardiac dysfunction is commonly observed in septic shock, a leading cause of death in intensive care units. In this setting, low circulating triiodothyronine (T3) levels occur in up to 95% of patients, a phenomenon often referred to as non‑thyroidal illness syndrome.
At the same time, approximately 30 – 40% of patients with septic shock develop septic cardiomyopathy, characterized by impaired myocardial contractility and reduced cardiac output.
“These observations raise an important question,” explained Joaquin Lado, chief of Endocrinology, Diabetes and Metabolism at UC Davis Health. “Is it possible that untreated low thyroid hormone levels contribute to heart dysfunction?”
Traditionally, endocrinologists have been reluctant to treat low thyroid hormone levels during acute illness, viewing them as an adaptive metabolic response rather than a true hormone deficiency. However, this long‑held assumption is increasingly being challenged.
“If thyroid hormone deficiency weakens the heart,” Lado added, “why wouldn’t a prolonged deficiency worsen septic cardiomyopathy?”