Abstract and Introduction
Abstract
Context: Aortic stiffness is an emerging predictor of cardiovascular morbidity and mortality. Current data about the effect of subclinical and overt thyroid hormone disorders on aortic stiffness are often conflicting.
Objective: Primary outcome was to investigate if subclinical and overt thyroid hormone disorders were associated with aortic stiffness. Secondary outcome was to identify disease effect modifiers.
Methods: Data sources were PubMed, Google Scholar, SCOPUS, Web of Sciences, and the Cochrane Library. Eligible studies included reports of pulse wave velocity (PWV), which is the gold standard method for measuring aortic stiffness, in patients with subclinical and overt thyroid disorders. Two investigators independently identified eligible studies and extracted data. Pooled mean difference was the summary effect measure. Data were presented in forest plots with outlier and influential case diagnostics. Univariate meta-regression analysis was used to identify effect modifiers.
Results: Eleven observational studies were selected, including 1239 patients with subclinical hypothyroidism, 81 patients with overt hypothyroidism, 338 patients with thyrotoxicosis, and 12 715 controls. PWV was significantly higher in subclinical (P < .001) and overt hypothyroidism (P < .001), as well as in patients with thyrotoxicosis (P = .027) compared with controls. Age was an effect modifier in hypothyroid patients.
Conclusion: This study shows that both overt and subclinical hypothyroidism as well as thyrotoxicosis were associated with an increase of aortic stiffness. The impact of treatment of these conditions on aortic stiffness should be assessed in clinical trials.
Introduction
The cardiovascular system is one of the main targets of thyroid hormone actions.[1,2] Overt changes in circulating thyroid hormones can significantly affect cardiovascular function and homeostasis, as thyroid hormone excess or deficiency can induce or exacerbate atrial and ventricular arrhythmias, cardiomyopathy,[3,4] heart failure, arteriosclerosis, and atheroma formation. Consistent with these actions, both hypothyroidism and/or thyrotoxicosis are regarded as a cardiovascular risk factor in the general population.[2] Also subclinical hypothyroidism, which affects >10% of European and American postmenopausal women,[5,6] as shown in the Rotterdam or Colorado cohort studies, has been associated with an increased risk of cardiovascular morbidity[5] and mortality,[7,8] particularly in those with a thyrotropin (TSH) concentration of 10 mIU/L.[8]
Arteriosclerosis, which corresponds to an age-related stiffening of the vessels, is a process consisting of a gradual fatigue fracture of elastic fibers within the arterial wall, with a resultant transfer of wall stress to collagen fibers over time, leading to the development of arterial stiffness.[9] This process should not be confused with atherosclerosis, which is characterized by vascular wall inflammation and plaque formation,[10] although they can be associated. Arterial stiffness determines the rate at which the pulse pressure wave travels along the vessels (the higher is the stiffness the higher is the pulse wave velocity [PWV]), such that the measurement of PWV represents the gold standard method for its assessment.[11,12] The pulse wave has 2 components: a forward travelling wave and a reflected wave, which travels from the periphery to the aortic root in diastole. In case of an increase in arterial stiffness, the reflected wave returns earlier, which raises aortic pressure during systole, systolic and pulse pressure, and it promotes left ventricular hypertrophy as well as subendocardial ischemia[9,13] with other hemodynamic consequences.[9,14] Aortic stiffness is an important emerging predictor of all-cause mortality in the general population.[15,16] A meta-analysis on 17 635 subjects demonstrated that aortic stiffness could predict future fatal and nonfatal coronary and stroke events, with a hazard ratio of 1.3 after adjustments for established cardiovascular risk factors.[17]
During the last decades, several works have evaluated the impact of hypothyroidism and/or thyrotoxicosis on arterial stiffness, with different methods and conflicting results,[18–21] such as in patients with subclinical hypothyroidism[18,19] and thyrotoxicosis.[20,21] The aim of this study was to evaluate the association between thyroid hormone deficiency and excess (be it overt or subclinical) and central arterial stiffness, as assessed by PWV, and to identify potential effect modifiers.
J Endo Soc. 2022;6(4) © 2022 Endocrine Society
