The impact of thyroid disorders on cardiovascular disease is not entirely well known. Thyroid hormones have multiple beneficial and harmful effects that are important to know when it comes to providing the best care to our patients.
The relationship between thyroid dysfunction and heart disease has long established well. We know that patients with hyperthyroidism or established clinical hypothyroidism are at increased risk of developing cardiomyopathies or cardiac arrhythmias. However, we are not currently so clear about what clinical decisions we should make to patients with heart disease or arrhythmias with subclinical thyroid dysfunction.
At the physiological level the relationship of the thyroid and cardiovascular system is narrow. We found thyroid receptors in the myocardium and endothelium capable of inducing different etiopathogenic mechanisms: regulation of myocyte contractility acting on myosin, modulation of calcium concentration in the sarcoplasmatic reticle, gene expression promote hypertrophy and fibrosis as well as the expression of membrane channels and proteins in atrial myocytes, which are responsible for heart rate control and for regulating parasympathetic tone.
Alterations in thyroid function promote dyslipemia and thrombogenesis. Thus, hypothyroid patients have an increased risk of atherogenesis due to increased elevation of LDL cholesterol and lipoprotein to. Similarly, patients with thyroid dysfunction most often have hypertension, increased intimate-media thickness, ateroma plaques, arterial stiffness and aortic calcification, which increases their cardiovascular risk. In addition, hyperthyroidism appears to play thrombogenic role through the elevation of the fibrinogen. On the other hand, in hypothyroidism we find a state of hypercoagulability associated with an increase in levels of activated factor VII and plasminogen activator factor. All these alterations are not usually found in euthyroid subjects.
At the vascular level thyroid function is also essential for the control of resistances and vascular tone. There are receptors for thyroid hormones in both muscle and endothelium. These vascular actions carried out by thyroid hormone receptors appear to be mediated by nitric oxide and not only occur at the level of systemic circulation, but also appear to influence the development of hypertension in lung circulation.
Thyroid hormones can have cardioprotective role, activating cytoprotective mechanisms, angiogenesis factors, and metabolic adaptations in cardiac tissue that decrease cardiac remodeling or facilitate reperfusion of areas of ischemic tissue. For example, they decrease the expression of the p53 tumor suppressor gene activated during a infarction by avoiding the mitochondrial apoptosis pathway. On the other hand, they seem to increase the expression of the hypoxia inducible factor and all this seems to decrease the area of ischemic gloom in the myocardium. Similarly in heart failure thyroid hormones have an anti-apoptotic effect that decreases interstitial fibrosis seen in hypothyroid cardiomyopathy.
These abnormalities in cardiovascular etiopathogenia are present with both hyperthyroidism and subclinical hypothyroidism.
In relation to ischemic heart disease finding reduced levels of T3 at the acute moment is very common (1 in 5 patients). Low T3 levels are associated with higher rate of post-ischemic fatal events, and in addition those patients with normal T3 levels have less alteration of contractility while better maintaining left ventricle systolic function. In terms of heart failure having low levels of T3 is also very prevalent and constitutes an independent predictor of systolic dysfunction. Similarly, when comparing these patients with euthyroids with similar systolic function, higher mortality is observed in the former. In some studies where hormonal deficits have been replaced, cardiovascular activity has been seen to improve and neuroendocrine activation decreased with less vasoconstriction, lower water retention and sodium, less aldosterone and reduced levels of natriuretic peptides. However, other substitute work has had to be discontinued by increased mortality. This leads to the search for the population subgroup that actually benefits from this treatment for which new studies are needed.
As we have seen in this review and in the light of the updated literature presented by the authors, for normal cardiovascular functioning, an adequate evaluation of thyroid function is important since very subtle changes in it can already worsen cardiovascular prognosis. Or put another way, we need to make sure that our patients with heart disease (whether chronic or acute) are in a situation of euthyroidism with optimized TSH values. Since it appears normal thyroid function may have a cardioprotective component against heart failure and acute coronary syndrome, although this data still needs to be contrasted with new studies and clinical trials.