[Cardiovascular effects of hyperthyroidism and their treatment]

The most striking clinical effects of hyperthyroidism are on the heart. These effects concern both heart rate and function. The increased contractility is mainly based on the indirect inotropic effect of peripheral vasodilation as a consequence of hyperthyroidism. Although contractility at rest is enhanced in hyperthyroidism, cardiac reserve is decreased due to diminished chronotropic, inotropic and vasodilatory reserve. In hyperthyroid patients, the clinical impression is often that of a hyperadrenergic circulation. However, the sensitivity of the heart for catecholamines is not increased. The diminution of palpitations by beta-adrenergic blockers in hyperthyroid patients is due to both a decrease in heart rate and atrial extrasystoles, and is not the consequence of a normalisation of cardiac contractility. Heart failure is almost exclusively found in patients with pre-existing cardiac disease. In the case of serious heart failure a rapid reduction of circulating thyroid hormone by means of thyreostatics is important as well. There is no consensus as to whether patients with thyrotoxic atrial fibrillation should be treated with oral anticoagulants. However, most experts recommend oral anticoagulants for elderly patients (> 60 years) or patients with additional risk factors for embolism.