Hershman describes hypothyroidism as a disorder which results from a deficit of the action of thyroid hormone (2009, p. 435). This condition affects the development and function of all tissues of the body, an important example of which is the heart. The thyroid hormone is responsible for the crucial regulation of calcium flux into the sarcomeres of myocytes (Rao, 2007, p. 202). The most common effect of deficient thyroid-hormone action on any tissue is well known; a decrease in the basal metabolic rate.
For the heart, this decrease most commonly causes a decrease in heart rate. Other manifestations may include “decreased cardiac output, flabby myocardium, pericardial effusion and impaired endothelial function” (Hershman, 2009, p. 435). However, for the profoundly hypothyroid patient, the most frequent cause of cardiac anomalies is impaired diastolic relaxation (Klein, 2005, p. 777). Although the fall in rate of metabolism is ubiquitous in hypothyroidism, the heart experiences a disproportionate change in demand and supply of oxygen, the supply drops faster than the demand.
On the other hand, patients of coronary heart disease who have later developed hypothyroidism have been given either low doses of T4, or no medication at all by some practitioners (Klein, 2005, p. 777); the lowered cardiac load associated with hypothyroidism helps in lowering the stress on the heart. Nonetheless, the adverse effects of hypothyroidism on the heart and on metabolism generally far outweigh this small concession (Klein, 2005, p. 777). Another complication associated with hypothyroidism is hypertension.
The main feature of pathophysiology that results in this manifestation is the increased vascular resistance due to absence of the vasodilating action of T3 (Klein, 2005, p. 776). This brand of hypertension shows decreased sensitivity to salt intake as compared to other forms of hypertension (Klein, 2005, p. 776). Hypertension in a profoundly hypothyroid patient is especially ominous. The increase serum levels of cholesterol and lipoprotein (a), associated with the low metabolic rate, combined with the increased vascular resistance may lead to coronary heart disease (Klein, 2005, p. 77).
However, it’s the subclinical counterpart of hypothyroidism that represents a major challenge; the lack of clear cut symptoms makes the diagnosis of this latent condition difficult. In a recent study, subclinical hypothyroidism was claimed to be an independent risk factor for heart disease in women in their 60s and 70s (Hak et al. , 2000). The main pathophysiological feature is the delayed relaxation of the left ventricle after contractions, exacerbated by endothelial dysfunction and a stiffness of the arteries (Biondi, 2009, p. 24).
Serum thyroid stimulating hormone, TSH, and serum free T4 are an appropriate starting point in acquiring a diagnosis of hypothyroidism (Hershman, 2009, p. 436). Myoglobin levels in blood and urine are also excellent indicators of injury to cardiac tissue (Klein, 2005, p. 777). Serum creatine kinase levels may also be increased, but troponin levels remain normal (Rao, 2007, p. 202). In subclinical hypothyroidism, TSH levels are moderately increased while T4 levels remain normal. ECG shows a general decrease in amplitude and the T wave may be inverted (Rao, 2007, p. 202).
The treatment of both the latent and overt forms of hypothyroidism, in relation to the heart, involves the maintenance of steady thyroid hormone levels. Levothyroxine is the drug of choice; in patients with a known heart condition, the dosage of the drug should be given incrementally to reach a stable normal level (Rao, 2007, p. 202). In elderly patients, some degree of cardiac ischemia is assumed present and the dosage is always increased gradually (Hershman, 2009, p. 438). Beta-blockers can be administered to counter the deleterious effect hormone therapy on cardiac ischemia, unless counter-indicated (Rao, 2007, p. 203).
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