Cardiovascular Effects of Hyperthyroidism
Thyroid hormones affect the respiratory system, skeletal muscles, and cardiac muscle. Hyperthyroid patients have impaired cardiopulmonary function which is usually reversible after thyroid hormone function is normalized.
The normal cardiac response to hyperthyroidism:
Sinus tachycardia is the most common problem in patients with both overt and subclinical hyperthyroidism. This is what causes the sensation of palpitations. 24 hour holter monitoring shows that in young patients there is a constantly increased heart rate during the day with decreased heart rate variability.
The cardiac effects of hyperthyroidism commonly cause increased preload with low systemic vascular resistance, a high heart rate, and increased cardiac muscle oxygen consumption. In the short term hyperthyroidism these effects result in an increased heart rate and high cardiac output.
Decreased exercise capacity
Despite the high cardiac output, hyperthyroid patients have a greatly reduced exercise tolerance. This counter-intuitive effect is due to reduced cardiovascular reserve, which eventually leads to reduced cardiac output during physical exercise. Because the mechanisms of cardiac-output-reserve (an increase in heart rate, blood volume, and cardiac contractility) are already a maximal use, there is a direct correlation with reduced exercise capacity.
The adverse cardiac events caused by hyperthyroidism:
The EGRET trial did confirm in a population based study that regardless of which treatments were used, patients had a 10% increase in overall major cardiac adverse effects (MACE)
Hyperthyroidism is associated with atrial arrhythmias, dysfunction of the sinus node, and supraventricular ectopic beats. Untreated patients with Graves disease or toxic multinodular goiter have a high incidence of premature ventricular contractions (PVCs).
Atrial fibrillation (AF) is a condition of an irregular and fast heart which can lead to a stroke and usually requires blood thinners to treat. Paroxysmal atrial fibrillation refers to recurrent episodes that are less than a week in duration and persistent atrial fibrillation refers to episodes that last more that 1 week. Persistent atrial fibrillation is common with hyperthyroidism and can occur in patients with overt or subclinical hyperthyroidism. Patients at risk are mean, the elderly, and those with underlying heart disease. Atrial fibrillation is directly correlated with the degree of TSH suppression and occurs in 10-28% of patients with thyrotoxicosis, compared to 0.5-9% in the general population. These heart rhythms may persist when treated with antithyroid drugs. The factors that are associated with a return to normal heart rhythm are young age, those with newly diagnosed atrial fibrillation, those with lower blood pressures, and if the patient becomes hypothyroid.
Congestive heart failure
This is a condition that can be caused by long-term untreated hyperthyroidism. Because the heart muscle is beating so strongly, it enlarges, leading to reduced ability to push blood forward. The risk of congestive heart failure (CHF) is increased in patients with age >60, those with long-term untreated hyperthyroidism, and those with pre-existing heart disease. CHF may be the first manifestation of hyperthyroidism in elderly patients who are unaware of their hyperthyroid state. Rate-related cardiomyopathy and dilated cardiomyopathy are other forms of CHF due to hyperthyroidism.
Cardiac valve disease
The likelihood of valve degeneration is increased in patients with Graves disease but not in those with toxic multinodular goiter. A cardiac ultrasound may be indicated in patients with Graves who also have a murmur on clinical examination.
1. von Olshausen, K. et al. Cardiac arrhythmias and heart rate in hyperthyroidism. Am. J. Cardiol. 63, 930–933 (1989).
2. Kahaly, G. J. & Dillmann, w. H. Thyroid hormone action in the heart. Endocr. Rev. 26, 704–728 (2005).
3. Flynn, r. w., MacDonald, T. M., Jung, T. r., Morris, A. D. & Leese, G. P. Mortality and vascular outcomes in patients treated for thyroid dysfunction. J. Clin. Endocrinol. Metab. 91, 2159–2164 (2006