Espessura íntima-média carotídea como marcador de risco cardiovascular em pacientes com hipotireoidismo subclínico

Abstract

RESUMOO hipotireoidismo subclínico (HS) já foi associado a aumento do risco cardiovascular. Na avaliação desse risco, a medida da espessura íntima-média (EIM) carotídea por ultra-sonografia é capaz de detectar alterações iniciais da aterosclerose. O objetivo deste estudo foi avaliar a EIM carotídea em pacientes com HS e sua associação com um provável aumento do risco cardiovascular. Não foi encontrada diferença significativa nas medidas da EIM das pacientes com HS e das controles. Os resultados encontrados nos dois grupos estudados foram, respectivamente: 0,573 ± 0,070 mm vs. 0,576 ± 0,068 mm para as caróti-das comuns (p= 0,904) e 0,602 ± 0,079 mm vs. 0,617 ± 0,102 mm para as bifurcações (p= 0,714). Mesmo após estratificação das pacientes de acordo com o TSH e com a presença ou não de auto-imunidade, a diferença entre os sub-grupos permaneceu sem significância estatística. As medidas da EIM nesses grupos nos sítios avaliados foram: TSH 4-8 mUI/L: 0,579 ± 0,070 mm e 0,586 ± 0,063 mm; TSH > 8 mUI/L: 0,569 ± 0,073 mm e 0,616 ± 0,091 mm; anti-TPO+: 0,585 ± 0,070 mm e 0,621 ± 0,085 mm; anti-TPO-: 0,554 ± 0,072 mm e 0,571 ± 0,066 mm. Também não houve diferença no lipidograma e nas dosagens de apoproteína B e de lipoproteína (a). Este fato sugere que o HS, quando leve, sem alterações metabólicas associadas, não promove aumento do risco cardiovascular. Subclinical hypothyroidism (SH) has been associated with an increased risk for coronary disease. Carotid intima-media thickness (IMT), as assessed by ultrasonography, is a precise marker of atherosclerotic changes and can be used as an endpoint for cardiovascular events. Aims of this study were to determine carotid IMT in a group of patients with SH and its possible association with an increase in cardiovascular risk. There were no significant differences in mean carotid IMT between patients and controls. Results of both groups were, respectively: common carotid arteries, 0.573 ± 0.070 mm and 0.576 ± 0.068 mm (p= 0.904); carotid bifurcation, 0.602 ± 0.079 mm and 0.617 ± 0.102 mm (p= 0.714). Similar results were obtained when analyzing subgroups with serum TSH < or > 8 mIU/L and with positive or negative titers of TPOAb. The mean carotid IMT in these subgroups were: TSH 4-8 mIU/L: 0.579 ± 0.070 mm and 0.586 ± 0.063 mm; TSH > 8 mIU/L: 0.569 ± 0.073 mm and 0.616 ± 0.091 mm; TPOAb+: 0.585 ± 0.070 mm and 0.621 ± 0.085 mm; TPOAb-: 0.554 ± 0.072 mm and 0.571 ± 0.066 mm. No differences in the lipid profile and in the apoprotein B and lipoprotein (a) levels between the groups were found. These findings suggest that mild SH with no related metabolic changes is not associated with an increase in cardiovascular risk, as assessed by carotid IMT. (Arq Bras Endocrinol Metab 2007;51/3:472-477)

Normal flow-mediated vasodilatation of the brachial artery and carotid artery intima-media thickness in subclinical hypothyroidism

“…Levothyroxine replacement therapy reduced both LDL-C and mean IMT, suggesting that lipid infiltration of the arterial wall may represent the main mechanism underlying the increase in IMT in SHT. We previously reported no significant differences in mean carotid IMT in a group of subclinical hypothyroid patients compared to a euthyroid group, suggesting that mild SHT is not associated with an increase in cardiovascular risk when assessed by carotid IMT (38).…”

Non-invasive markers of cardiovascular risk in patients with subclinical hypothyroidism: A systematic review and meta-analysis of 27 case control studies

“…The NOS for quality assessment of the included studies yielded a median value of 6. There were 23 high-quality articles in our meta-analysis 28 , 29 , 31 – 37 , 40 , 42 – 54 .…”

Evaluation of endothelial function in exogenous subclinical hyperthyroidism and the effect of treatment

“…[212223] These results suggesting that subclinical hyperthyroidism and SHy is not associated with an increase in cardiovascular risk when assessed by carotid IMT. [23] There is not clear in thyroid dysfunction what the causative agent of endothelial damage is, but seems thyroid autoantibodies induce decreased endothelial NO synthesis or inflammation. [24]…”