Lack of thyroid hormones causes multiple alterations in the cardiovascular system. The most frequent changes in hypothyroid patients are increased systemic vascular resistance, diastolic dysfunction, reduced systolic function, and decreased cardiac preload. Bradycardia, cardiomegaly, and low voltage complexes on the electrocardiogram (ECG) are well- known features (Box 1). The decrease in pulse rate approximately parallels the decrease in the body’s metabolic rate. Myocardial contractility is reduced. The cardiac output at rest is decreased because of reduction in both stroke volume and heart rate, reflecting loss of the inotropic and chronotropic effects of thyroid hormones. The mechanism re sponsible for the impaired ventricular performance is multifactorial. The actions of thyroid hormone on the hearth are mediated by genomic and non- genomic mechanisms targeted to membrane proteins, cytoskeletal components, and organelles. The genomic actions are mediated by nuclear receptors alpha and beta. In animal models, low thyroid hormone concentrations alter the expression of myocyte- specific genes and the distribution of the heavy- chain isoforms of sarcomeric myosin and of the calcium- regulating proteins. Alterations in myocyte calcium uptake and release are responsible for the change in the inotropic state. Peripheral vascular resistance at rest is increased, and blood volume is reduced. These haemodynamic alterations cause narrowing of pulse pressure, prolongation of circulation time, and decreased blood flow to the tissues. In most tissues the decrease in blood flow is proportional to the decrease in oxygen consumption, so the arteriovenous oxygen difference remains normal or may be slightly increased. Slow peripheral circulation, and therefore more complete extraction of oxygen, as well as anaemia, may be responsible for the increased arteriovenous oxygen difference. Myocardial oxygen consumption is decreased, usually more than blood supply to the myocardium, so that angina is infrequent. In some patients a reduction in cardiac output greater than the decline in oxygen consumption indicates specific cardiac damage from the myxoedema.

Box1. Cardiovascular signs and symptoms in hypothyroidism

The haemodynamic alterations at rest resemble those of congestive heart failure, but cardiac output increases and peripheral vascular resistance decreases normally in response to exercise un less the hypothyroid state is severe. The non- pitting oedema observed in hypothyroid patients is due to an increase in protein distribution in the extravascular extracellular space resulting from increased capillary permeability.

Venous pressure is normal, but peripheral resistance is increased. The mechanism responsible for the increase in systemic vascular resistance is not known. Triiodothyronine (T3) may act as a vasodilator and in its absence vascular resistance may rise. Arterial blood pressure is often mildly increased. Hypertension is present in 10– 20% of patients with hypothyroidism. Diastolic hypertension is usually restored to normal after treatment. Three factors can contribute to systemic hypertension, increased peripheral resistance, increased arterial stiffness, and endothelial dysfunction.

Few symptoms referable to the cardiovascular system are referred in patients with hypothyroidism. Exertional dyspnoea and exercise intolerance are probably due to skeletal muscle dysfunction. There has been much discussion as to whether the hypercholesterolaemia that accompanies primary hypothyroidism accelerates the development of coronary atherosclerosis. An increased risk for atherosclerosis is supported by autopsy and epidemiological studies in patients with thyroid hormone deficiency and may be, in part, explained by the hypercholesterolaemia and marked increase in low- density lipoprotein (LDL). Moreover, diastolic hypertension, increased arterial stiffness and endothelial dysfunction, altered coagulability, and increased levels of C- reactive protein may further contribute to the increased cardiovascular risk (8, 9). Most autopsied myxoedematous individuals have severe atherosclerosis, but they are also usually 60 years of age or more. Occasionally angina pectoris is encountered in myxoedema. Sometimes angina or angina- like pain is present before treatment. This generally indicates the presence of significant coronary artery disease since there is inadequate myocardial oxygenation despite reduced cardiac output and oxygen utilization. Angina may also appear for the first time after treatment has been initiated, indicating that coronary f low is inadequate for resumption of normal cardiac function. The presence of a structural lesion must be strongly suspected.

On physical examination certain findings can suggest hypothyroidism. The heart rate is lowered, the pulse pressure is narrowed, and the carotid upstroke and left ventricular apical impulse are di minished. The heart sounds are diminished in intensity; this finding is due largely to effusion into the pericardial sac of fluid rich in protein and glycosaminoglycans.

The combination of a large heart, associated with typical haemodynamic and electrocardiographic alterations, and the serum enzyme changes (creatine kinase, aspartate aminotransferase, and lactate dehydrogenase may be increased) has been termed myxoedema heart. This term was introduced by Zondek in 1918. It embraced dilatation of the left and right sides of the heart, a slow indolent heart action with normal blood pressure, and lowering of the P and T waves of the electrocardiogram. Zondek found that after treatment with thyroid hormone there was a return of the dilated heart to near normal size, a more rapid pulse without change in blood pressure, and gradual return of the P and T waves to normal. Microscopic examination discloses myxoedematous changes of the myocardial fibres. The myocardium is pale and flabby. Histopathological examination of the myocardium reveals interstitial oedema and swelling of the muscle fibres with loss of striations. The cause of the cardiac enlargement has been disputed. It is not due to hypertrophy alone, since it would not disappear so rapidly with treatment. One factor may be a decrease in contractility of the heart muscle; this would require a lengthening of muscle fibres in order to perform the required work.

In myxoedema, when the heart does not return to a normal size under thyroid hormone administration, hypertrophy due to some other disease is present as a complication. The slow and progressive return to normal size under treatment requires between 3 weeks and 10 months for completion. This decrease in size, like the progressive elevation of the T waves, is of diagnostic value.

Electrocardiographic Changes

 Electrocardiographic changes include sinus bradycardia, prolongation of the P– R interval, low amplitude of the P wave and QRS complex, alterations of the ST segment, and flattened or inverted T waves. Although suggestive of myocardial ischaemia, these wave form changes often disappear during thyroxine (T4) treatment. Pericardial effusion is probably responsible for the low amplitude. Rarely, complete heart block may be present, but this disappears when the hypothyroidism is treated. In hypothyroidism, the atrial pacemaker function is normal and atrial ectopy is rare, but ventricular premature beats and occasionally ventricular tachycardia may occur. The syndrome of torsades de pointes with a long Q– T interval and ventricular tachycardia can occur with hypothyroidism, and resolve with T4 treatment alone.

Systolic Time Intervals and Echographic Findings

Systolic time intervals are altered, the pre- ejection period is pro longed, and the ratio of pre- ejection period to left ventricular ejection time is increased. Some patients have been reported to have asymmetrical hypertrophy of the intraventricular septum by echo cardiography that resolves with T4 treatment, but a recent study failed to show septal hypertrophy in any hypothyroid patient studied. Pericardial effusion occurs in one- third to one- half of patients with overt hypothyroidism. The effusion is more common and their volume is greater in patients with long- standing severe disease. Cardiac tamponade is very rare. More sophisticated techniques have been used to assess systolic and diastolic function and myocardial texture, such as cardiac MRI, tissue Doppler imaging, and ultrasonic myocardial textural analysis. By using magnetic resonance spectroscopy, an early cardiac bioenergetics impairment was demonstrated in patients with subclinical hypothyroidism which was reversible after L- thyroxine therapy.

Laboratory Tests

 The serum levels of creatine kinase, aspartate aminotransferase, and lactate dehydrogenase may be increased. Serum creatine kinase activity is high in as many as 30% of patients. Whereas the increase may reflect myocardial necrosis, in most patients the isoenzyme distribution indicates its origin from the skeletal rather than cardiac muscle. Prolongation of the half- life of creatine kinase in the circulation contributes to the elevated serum concentration.

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مواضيع ذات صلة

Organ System Manifestations of Hypothyroidism: Respiratory Changes

Organ System Manifestations of Hypothyroidism : Cutaneous Manifestations and Changes in the Connective Tissues

Thromboembolic Conditions

Conditions that Cause Excessive Bleeding in Humans

Absent Intrinsic Factor Secretion and Pernicious Anemia

Subclinical Hyperthyroidism

Thyrotoxic Periodic Paralysis: Clinical Features

Nutritional Causes of Folate Deficiency

Neurologic Dysfunction with Cobalamin Deficiency

Sclerosing Thyroiditis (Riedel’s Thyroiditis) : Clinical Features

Infectious Thyroiditis

Leukopenia