Excessive thyroxine enhances susceptibility to apoptosis and decreases contractility of cardiomyocytes

Redox status and pro‐survival/pro‐apoptotic protein expression in the early cardiac hypertrophy induced by experimental hyperthyroidism

“…Few studies have shown that THs are involved in the induction of apoptosis. 17 Parameters evaluated in our study are not enough to define apoptotic mechanisms in the hyperthyroidism; however, the overall results suggest stimulation of proteins involved in maladaptative cardiac remodelling, which could collaborate to the heart failure development at later time points.…”

Hyperdynamic Right Heart Function in Graves’ Hyperthyroidism Measured by Echocardiography Normalises on Restoration of Euthyroidism

“…Increased heart rate via atrial pacing is known to increase intrinsic contractility by upregulating calcium entry to myocytes, but it is not clear whether hyperthyroidism per se increases contractility over and above the effects on heart rate alone [9]. Animal studies have suggested that there may be increased myocyte contractility, but the effects of this on left ventricular systole are tempered by increasing left heart fibrosis with chronic exposure to hyperthyroidism [10].…”

Cardiorespiratory Arrest Associated with Propranolol use in Thyrotoxic Heart Disease

“…Increased thyroid hormone activates the renin-angiotensin system and magnifies the sensitivity of beta-adrenergic receptors to catecholamine, which increases left ventricular contractility and heart rate. The activation of the reninangiotensin system also decreases systemic vascular resistance, and increases blood volume [5][6][7]. The chain of reaction subsequently increases myocardial oxygen consumption, cardiac output and cardiac workload [1].…”