Thyroid Dysfunction and Arterial Stiffness. Does the Restoration of Thyroid Function Tests Offer any Benefit?

Abstract

A growing body of evidence suggests that hypothyroidism and hyperthyroidism, either as overt or subclinical states, are associated with increased risk for cardiovascular disease (CVD). Except for the increased prevalence of lipid disorders, coagulation abnormalities, endothelial dysfunction, cardiac arrhythmias, ventricular hypertrophy and hypertension have been proposed as the most plausible pathways for this association, increased arterial stiffness (AS) may also play a role. Increased AS has emerged recently as an early indicator of CVD in various studies. On the other hand, thyroid dysfunction, mainly hypothyroidism (overt and subclinical) seems to be associated with increased AS, although data are heterogeneous, emerging from different populations, with various methodologies of AS assessment and with variable periods of observation. Restoration of thyroid function with L-thyroxin replacement seems to reverse AS parameters, whereas data on the effect of normalization of thyroid function in hyperthyroidism on AS are inconsistent. The present review provides insights on the association between AS and thyroid dysfunction and discusses the available data about potential benefits of the restoration of thyroid function on AS.

Cardiac manifestations in hyperthyroidism

“…Clinical and preclinical evidence supporting the role of either overt or subclinical hyperthyroidism on arterial stiffness is scarce and in some aspects contradictory, as reviewed by Anagnostis et al . [ 118 ], but some small observation studies points towards a direct relation between these two variables [ 119 ]. Also, it seems that non-selective betablockers and restoring thyroid function improves arterial stiffness, systolic blood pressure and adverse cardiovascular events [ 115 ].…”

“…Also, it seems that non-selective betablockers and restoring thyroid function improves arterial stiffness, systolic blood pressure and adverse cardiovascular events [ 115 ]. Some of the limitations of these studies are that most of patients included had Grave’s disease, which is a autoimmune phenomenon that could affect the vasculature through other mechanisms [ 118 , 120 ].…”

The effect of L-thyroxine substitution on lipid profile, glucose homeostasis, inflammation and coagulation in patients with subclinical hypothyroidism

“…This association is evident mainly in patients < 65 years old . Even higher TSH levels within the normal range may be associated with increased CVD risk, since an increase of 1 mIU/l in TSH levels was found to be associated with a 33% higher risk for the occurrence of myocardial infarction, after adjustment for possible confounders . The proposed underlying mechanisms for this association are the specific alterations in cardiovascular haemodynamics existing in SH, such as impaired left ventricular systolic and diastolic function, increased systemic vascular resistance (SVR), cardiac contractility and carotid intima‐media thickness (c‐IMT), endothelial dysfunction and increased overall risk for atherosclerosis .…”

Pulsatility Index in Carotid Arteries is Increased in Levothyroxine-Treated Hashimoto Disease

“…Unfortunately, we do not have the values of thyroid function parameters of HT females from before the implementation of L-T4 therapy, but all of them used to be hypothyroid. Although many studies proved that L-T4 treatment in hypothyroid patients had beneficial effect on arterial stiffness and we have previously reported the decrease of homocysteine levels in L-T4 treated HT females, we suggest that arterial changes might only partially be reversible [26,27]. Under this scenario, the impaired arterial elastic properties in treated hypothyroid HT females resulted from the past history of hypothyroidism.…”