Graves' Disease and Cardiac Complications

*Abdulla Arslan and Hakan Altay*

### **Abstract**

Graves' Disease is an autoimmune thyroid disease and a common cause of hyperthyroidism. Thyroid hormones have multiple adverse effect on cardiovascular system through many direct and indirect mechanisms. They increases heart rate, cardiac contractility, systolic and mean pulmonary artery pressure, cardiac output, diastolic relaxation, and myocardial oxygen consumption, whereas decrease systemic vascular resistance and diastolic pressure. All these hemodynamic changes in cardiovascular system can eventually lead to heart failure, tachyarrhythmias, systemic and pulmonary hypertension, if left untreated. Cardiovascular complications of Graves' Disease are frequent and important cause of increased morbidity and mortality. This chapter reviews the cardiovascular complications of Graves' hyperthyroidism with underlying mechanisms and treatment.

**Keywords:** Graves' Disease, cardiac complications, heart failure, thyrotoxicosis, pulmonary hypertension

#### **1. Introduction**

Robert Graves identified the association of goiter, palpitations, and exophthalmos in 1835 [1]. Although the cause of Graves' hyperthyroidism was initially thought to be thyrotropin, it was later understood that Graves' hyperthyroidism was clearly caused by thyroid stimulating antibodies-IgG- which bind to and activate to thyrotropin receptors on thyroid cells [2]. Although the incidence is not known exactly, manifest hyperthyroidism is common and affects 2–5% of the population [3]. Approximately 60–80% of hyperthyroidism cases have Graves' Disease due to regional factors, particularly iodine intake. Over a period of 20 years, the incidence in women is around 0.5 per 1000 annually and the most frequent onset age gap is 40–60; hence, Graves' Disease is most common autoimmune disorder in the United States [4]. Graves' Disease rate in men is between 1/5 and 1/10 and equal to women; however, the disease is unusual in children. The prevalence is lower in African-Americans in reference to Asians and Whites [5]. Graves' Disease has similarities with autoimmune hypothyroidism, including high serum concentrations of antibodies against thyroglobulin, thyroid peroxidase, and possibly the sodium-iodide cotransporter in thyroid tissue. These antibodies' concentrations vary among patients, and the antibodies themselves may modify the stimulatory effects of thyroid-stimulating antibodies. In some patients, the simultaneous production of antibodies that block the thyrotropin receptor reduces the stimulatory action of thyroid-stimulating antibodies. For these reasons there is no direct correlation between serum concentrations of thyroid-stimulating antibodies and serum thyroid hormone concentrations in patients with Graves' hyperthyroidism [6].

Thyroid hormones have major effects on the heart and cardiovascular system through many mechanisms. They increase heart rate, cardiac contractility, systolic and mean pulmonary artery pressure, cardiac output, diastolic relaxation, and myocardial oxygen consumption, and reduce systemic vascular resistance and diastolic pressure [7]. Cardiovascular symptoms have been showing some signs of patients clinical presentation for the physicians: palpitations, exercise intolerance, dyspnoea, angina-like chest pain, peripheral edema and congestive heart failure are common symptoms of hyperthyroidism [8, 9]. In hyperthyroid patients mortality is increased by 20% and the major causes of death are cardiac problems [10].
