Hypothyroidism and its Relationship to Heart Disease and Cardiac Problems Essay

Hershman describes hypothyroid glandism as a disorder which results from a deficit of the action of thyroid ductless gland (2009, p. 435). This condition affects the development and function of all tissue papers of the body, an important example of which is the nitty-gritty. The thyroid hormone is responsible for the crucial regulation of calcium flux into the sarcomeres of myocytes (Rao, 2007, p. 202). The virtually common effect of deficient thyroid-hormone action on any tissue is well known a decrease in the basal metabolic rate.For the core, this decrease most commonly causes a decrease in heart rate. Other constructions 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 ghost cause of cardiac anomalies is impaired diastolic heartsease (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 new(prenominal) hand, patients of coronary heart complaint who have later genuine hypothyroidism have been abandoned either low doses of T4, or no medicinal drug at all by some practitioners (Klein, 2005, p. 777) the lowered cardiac charge up associated with hypothyroidism helps in lowering the stress on the heart. Nonetheless, the adverse effects of hypothyroidism on the heart and on metabolism world-widely far outweigh this grim concession (Klein, 2005, p. 777). Another complication associated with hypothyroidism is hypertension.The main feature of pathophysiology that results in this manifestation is the increase vascular resistance due to absence of the vasodilating action of T3 (Klein, 2005, p. 776). This give away of hypertension shows decreased sensitivity to salt intake as comp argond to other forms of hypertension (Klein, 2005, p. 776). H ypertension in a profoundly hypothyroid patient is peculiarly 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, its the subclinical counterpart of hypothyroidism that represents a major challenge the overlook of clear cut symptoms makes the diagnosing 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 level s in blood and urine are also excellent indicators of hurt 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 similitude 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 social disease 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 baneful effect hormone therapy on cardiac ischemia, unles s counter-indicated (Rao, 2007, p. 203).