ABC | Volume 110, Nº2, February 2018

Original Article Soeiro et al TSH versus SCA Arq Bras Cardiol. 2018; 110(2):113-118 Specifically, hypothyroidism reduces cardiac output, blood volume, chronotropism and inotropism, and increases systemic vascular resistance, diastolic blood pressure, vascular wall thickness and stiffness, and afterload. The increase in peripheral resistance mainly induces left ventricular systolic dysfunction and abnormal relaxation, without modification of heart rate. Changes in arterial wall elasticity are involved in the progression of atherosclerotic processes. Effects on vascular endothelial function alter blood flow, and nitric oxide plays an important role in this process. Hypothyroidism decreases glomerular filtration rate, which influences circulating cholesterol levels and favors the development of type II diabetes complications. 2,3,16,17 These findings could partially justify the higher occurrence of ACS in this group of patients, and perhaps their worse prognosis. In addition, this mechanism could be associated with the development of cardiogenic shock, well described in our study. In 2005, Walsh et al. 18 studied the relationship between thyroid hormone and cardiovascular events in 1,981 healthy individuals in Australia. In a cross-sectional study, they examined the prevalence of coronary heart disease in subjects with and without subclinical thyroid dysfunction. In a longitudinal study, they examined the risk of cardiovascular mortality and coronary heart disease events (fatal and nonfatal). Subjects with subclinical hypothyroidism (n = 119) had a significantly higher prevalence of coronary heart disease than euthyroid subjects (OR = 1.8; 95% CI: 1.0 - 3.1; p = 0.04). In the longitudinal analysis of subjects with subclinical hypothyroidism, 33 coronary heart disease events were observed as compared to 14.7 expected (HR = 1.7; 95% CI: 1.2 - 2.4; p = 0.01). 18 Another study 1 in 2005 investigatedwhether thyroid hormone levels had any predictive value for mortality in patients presenting to the emergency department with AMI. Three groups of patients admitted to the emergency department within the 11-month study period: 95 patients with chest pain and diagnosed AMI; 26 patients with chest pain and no AMI; and 114 controls with no evidence of any major disease. Cardiac enzymes and thyroid hormones were analyzed and compared between groups to examine the effects of historical and demographic factors. Sixteen patients with AMI (16.8%) died within the study period. Troponin and creatine kinase M-type subunit levels were significantly higher among non-survivors as compared with survivors. Survivors in the AMI group had higher levels of triiodothyronine and total thyroxine and lower free thyroxine levels, while non-survivors in the AMI group had higher TSH and lower triiodothyronine, total thyroxine and free thyroxine levels than controls. In logistic regression, TSH levels were not significantly different between survivors and non-survivors (1.08 mIU/L vs. 1.84 mIU/L, p = 0.1). The conclusion was that triiodothyronine and lower free thyroxine appeared to be independent prognostic factors in patients with AMI. 1 In our study, we showed a trend towards higher levels of troponin and TSH. However, correlation until this moment was not significant. Differences might appear with a larger sample. On the other hand, in 2014, Him et al. 19 retrospectively reviewed the relationship between thyroid hormone levels and AMI severity in 40 patients with STEMI, and the extent of transmural involvement was evaluated via contrast-en- hanced cardiac magnetic resonance imaging. The high triiodothyronine group (≥ 68.3 ng/dL) exhibited a significantly greater transmural involvement (late transmural enhancement > 75% after administration of gadolinium contrast agent) than did the low triiodothyronine group (60% vs. 15%, p = 0.003). However, a significant difference was not evident between the high- and low-TSH and free thyroxine groups. When the triiodothyronine cut-off level was set to 68.3 ng/dL using a receiver operating characteristic curve, the sensitivity was 80% and the specificity was 68% in terms of differentiating between those with and without transmural involvement. 19 Friberg et al. 20 have described a possible rapid down‑regulation of thyroid hormones in patients withAMI. Forty-seven consecutive euthyroid patients withAMI were studied prospectively during the first 5 days, and again 6 and 12 weeks after AMI. They observed that the thyroid system was rapidly down-regulated with maximal changes appearing 24 to 36 hours after onset of symptoms. Levels of TSH declined 51% (p < 0.001) between the first 6 hours and the 24 to 36-hour period. The authors also described a strong relationship between inflammation (high levels of C-reactive protein and cytokine interleukin 6) and a greater down‑regulation of the thyroid system. Alternatively, MACE were high among patients with themost pronounced TSHdepression, indicating that the down-regulation observed after AMI may be maladaptive. Lower TSH levels measured at 5 days significantly correlated with mortality in one year (1.0 mIU/L vs. 1.6 mIU/L, p = 0.04, respectively, between dead and alive patients). 20 This difference from our results may be because we did not assess TSH levels on the first and fifth days after ACS in our study. Our analysis of only the initial sample at hospital admission was not included in that study by Friberg et al. 20 Another study has investigated whether changes in plasma thyroid hormone levels were associated with the recovery of cardiac function in patients with AMI. A total of 47 patients with AMI and early reperfusion therapy were included in this study. Cardiac function was assessed by echocardiography; left ventricular ejection fraction and function recovery were evaluated 48 hours and 6 months after AMI. A strong correlation was found between function recovery and total triiodothyronine levels (r = 0.64, p = 10 -6 ) 6 months after AMI. Furthermore, multivariate regression analysis revealed that triiodothyronine at 6 months was an independent determinant of ventricular function recovery. TSH levels were not significantly different between the two groups (with and without ventricular function recovery) during the acute phase of myocardial infarction, but at 6 months, TSH levels were significantly higher in the group without recovery as compared with the group with better recovery of ventricular function (2.9 vs. 1.46, p < 0.05). 21 A study published in 2016 assessed a prospective 3-year cohort with 2430 patients submitted to percutaneous coronary intervention with versus without hypothyroidism. The authors related a higher number of MACE (myocardial infarction, stroke, revascularization) in patients with hypothyroidism or TSH> 5.0 mIU/L (HR = 1.28, p = 0.0001). 22 These data were similar to our findings, but they evaluate long-term prognosis. However, the association with worse prognosis was the same, including the similar value of TSH described. 116