Sub-Clinical Hypothyroidism and Its Association With Increased Cardiovascular Mortality: Call For Action!

Abstract

Thyroid hormones play an important role in regulating different functions regarding metabolism and performance in multiple organs. Any change in the thyroid hormones axis can lead to profound effect on the vital organ stability especially the cardiovascular system. Hypothyroidism is classified according to the clinical presentation as overt and subclinical. Currently, there exists a paucity of evidence on the beneficial effects of thyroxine hormone replacement on cardiovascular mortality outcomes in subclinical hypothyroidism. Also, the clinical relevance of measuring and treating supra-normal thyroid-stimulating hormone levels in newly diagnosed heart failure patients with preserved ejection fraction requires further study. Here we review the current evidence regarding the prognostic significance of sub-clinical hypothyroidism in patients with heart failure with preserved ejection fraction.

The current debate over treatment of subclinical hypothyroidism to prevent cardiovascular complications

“…The decreased levels of thyroid hormones in SCH are associated with several adverse cardiovascular hemodynamic effects that include: decreased cardiac output, decreased myocardial contractility, decreased filling pressure and systolic dysfunction, impaired diastolic ventricular filling and relaxation, increase in peripheral vascular resistance because of endothelial dysfunction from the decreased availability of NO, atherosclerosis and increase in SBP and DBP 2,7‐8,30‐32 . As a consequence of these hemodynamic and metabolic abnormalities of SCH, there is an increased incidence of CVD, HF and CV mortality 10,27,29,33‐36 . Regarding the basic mechanism by which SCH affects myocardial function and the development of HF, this has been attributed to mitochondrial dysfunction and quality control (MQC).…”

“…The thyroid hormones exert their effects through their receptors α and β located in the myocardial and vascular endothelial tissues and modulate their cardiovascular function 6‐8 . Minor changes in thyroid hormone levels could have an adverse impact on the cardiometabolic effects in the body that include increases in serum cholesterol and glucose levels, endothelial dysfunction through decreased availability of nitric oxide (NO), causing arterial stiffness and increase in peripheral vascular resistance and blood pressure (BP), all being significant risk factors for CVD and HF 9‐13 . However, there is currently a debate in the literature regarding the adverse cardiometabolic effects of SCH and its treatment 14‐16 .…”

Polypharmacy: What About Undertreated Medication-Induced Hypothyroidism?

“…I am currently interested in the consequences of undertreated medication-induced hypothyroidism, especially considering the association of even subclinical hypothyroidism with mortality. [4][5][6][7] From my perspective, the value of the article 1 would increase greatly if one could know both the rate and cause of death in persons taking levothyroxine alone and in each of the listed groups: levothyroxine + antacids, levothyroxine + calcium, levothyroxine + iron, or levothyroxine + antacids + calcium + iron. I expect that mortality is relatively high in the last group and relatively low in the levothyroxine-alone group.…”

Uric Acid and NT-proBNP as Biomarkers of Cardiovascular Dysfunction in Hyperthyroidism and Hypothyroidism

“…Moreover, after the discovery of the general physiological and pathological responses to stress, both in case of negative and positive *email: scozma2005@yahoo.com; Phone: 0748 167030 #These authors contributed equally to this work and should be regarded as first author responses, the stress concept was involved in the pathogenesis of many morbid, endocrine, metabolic or cardiovascular conditions. Clinical and subclinical thyroid changes are accompanied by autoimmune phenomena that can contribute to worsening of cardiovascular reactions and dysregulation of other endocrine systems, such as the hypothalamic-pituitary-adrenocortical axis [10][11][12][13][14]. Cardiovascular laboratory parameters have been insufficiently studied in the presence of certain endocrine dysfunctions.…”