The positive lusitropic effect of thyroid hormone leads to a shortened time of cardiac muscle relaxation. This results in a modest increase in systolic blood pressure and a decrease in diastolic blood pressure. The widened pulse pressure is a combination of the increased stroke volume and the reduction in systemic vascular resistance caused by blood vessel dilation in the skin, muscles, and heart. Thyroid hormone induces an increase in heat and CO2 production in tissues, which contributes to these effects. Furthermore, thyroid hormone dilates arterioles in the peripheral circulation, further reducing systemic resistance. Activation of the renin-angiotensin-aldosterone axis increases total blood volume by enhancing renal tubular sodium reabsorption. 

The cardiac inotropic effects of T3 include both direct and indirect mechanisms. Indirect effects are mainly due to an increased responsiveness to catecholamines. Direct inotropic effects involve the regulation of multiple proteins that enhance contractility, such as increased expression of α-myosin heavy chain and inhibition of the plasma membrane Na+/Ca++ exchanger. T3 increases the activity of sarcoplasmic reticulum Ca++-ATPase (SERCA) and decreases phospholamban levels, leading to improved calcium sequestration during diastole and shortened relaxation time. Increased ryanodine Ca++ channels in the sarcoplasmic reticulum promote the release of Ca++ during systole.

Optimum cardiac performance requires thyroid hormone levels within the normal range. A deficiency of thyroid hormone in humans reduces stroke volume, left ventricular ejection fraction, cardiac output, and the efficiency of cardiac function. In contrast, excessive thyroid hormone enhances cardiac output by increasing heart rate and stroke volume. This leads to a widened pulse pressure due to increased systolic pressure and decreased diastolic pressure resulting from decreased systemic vascular resistance. Thyrotoxicosis is associated with symptoms like palpitations, atrial fibrillation, and mitral valve prolapse.

Increased oxygen usage depends on an increased supply of substrates for oxidation. T3 enhances glucose absorption from the gastrointestinal tract and increases glucose turnover. In adipose tissue, thyroid hormone stimulates the synthesis of fatty acids and enhances lipolysis by increasing the number of β-adrenergic receptors. Thyroid hormone also improves the clearance of chylomicrons, thereby augmenting lipid turnover. Protein turnover, including the release of muscle amino acids, protein degradation, and to a lesser extent, protein synthesis and urea formation, is also increased by T3. T3 potentiates the stimulatory effects of epinephrine, norepinephrine, glucagon, cortisol, and growth hormone on gluconeogenesis.
time is shortened (positive lusitropic effect). Systolic blood pressure is modestly augmented and diastolic blood pressure is decreased. The resultant widened pulse pressure reflects the combined effects of the increased stroke volume and the reduction in systemic vascular resistance secondary to blood vessel dilation in skin, muscle, and heart. These effects in turn are partly due to the increase in tissue production of heat and CO2 that thyroid hormone induces (see on Basal Metabolic Rate and Thermogenesis). In addition, however, thyroid hormone decreases systemic resistance by dilating arterioles in the peripheral circulation. Total blood volume is increased by activation of the renin-angiotensinaldosterone axis, thereby increasing renal tubular sodium reabsorption (see
The cardiac inotropic effects of T3 are both direct and indirect. The latter are due primarily to enhanced responsiveness to catecholamines (see ). Direct inotropic effects (see
Fig. 42.11 ) involve regulation of multiple proteins that enhance contractility, including increased α-myosin heavy chain expression and inhibition of the plasma membrane Na+/Ca++ exchanger. Sarcoplasmic reticulum Ca++-ATPase (SERCA) is increased by T3, whereas phospholamban is decreased. As a result, sequestration of calcium during diastole is enhanced and the relaxation time is shortened. Increased ryanodine Ca++ channels in the sarcoplasmic reticulum promote release of Ca++ from the sarcoplasmic reticulum during systole.
Thyroidhormonelevelsinthenormalrangearenecessaryforoptimumcardiacperformance.Adeficiencyofthyroidhormoneinhumansreducesstrokevolume,leftventricularejectionfraction,cardiacoutput,andtheefficiencyofcardiacfunction.Thelatterdefectisshownbythefactthatthestrokeworkindex[(strokevolume/leftventricularmass)× peaksystolicbloodpressure]isdecreasedtoagreaterextentthanmyocardialoxidativemetabolism.Theriseinsystemicvascularresistancemaycontributetothiscardiacdebility.Incontrast,excessthyroidhormoneenhancescardiacoutputbyincreasingbothheartrateandstrokevolume.Pulsepressureiswidenedbyincreasedsystolicpressureanddecreaseddiastolicpressureduetodecreasedsystemicvascularresistance.Thyrotoxicosisisassociatedwithpalpitations,atrialfibrillation,andmitralvalveprolapse(see
Increased O2 use ultimately depends on an increased supply of substrates for oxidation. T3 augments glucose absorption from the gastrointestinal tract and increases glucose turnover (glucose uptake, oxidation, and synthesis). In adipose tissue, thyroid hormone induces enzymes for the synthesis of fatty acids, including acetyl-CoA carboxylase and fatty acid synthase, and enhances lipolysis by increasing the number of β-adrenergic receptors (see the Autonomic Nervous System ). Thyroid hormone also enhances the clearance of chylomicrons. Thus lipid turnover (free fatty acid release from adipose tissue and oxidation) is augmented.
Protein turnover (release of muscle amino acids, protein degradation, and to a lesser extent protein synthesis and urea formation) is also increased. T3 potentiates the respective stimulatory effects of epinephrine, norepinephrine, glucagon, cortisol, and growth hormone on gluconeogenesis,