ABC | Volume 110, Nº2, February 2018

Original Article Soeiro et al TSH versus SCA Arq Bras Cardiol. 2018; 110(2):113-118 Figure 1 – Classification of ACS according to TSH levels. NSTEMI: Non-ST-elevation myocardial infarction; STEMI: ST-elevation myocardial infarction; TSH: thyrotropin. 80% 70% 60% 50% 40% 30% 20% 10% 0% 90% TSH ≤ 4 mlU/L TSH > 4 mlU/L 82% 18% 76% 24% NSTEMI STEMI Table 2 – Results of multivariate analysis of in-hospital outcomes comparing groups I and II TSH ≤ 4 mIU/L TSH > 4 mIU/L OR 95% CI p Reinfarction 1.3% 0% 0.2 0.11 – 3.45 0.37 Cardiogenic Shock 6.1% 13.6% 1.72 1.25 – 4.68 0.029 Bleeding 6.5% 15.3% 3.36 1.31 – 8.65 0.012 Stroke 0.9% 0% 0.9 0.15 – 9.32 0.9 Mortality 3.1% 8.5% 2.32 0.63 – 8.48 0.2 MACE 17.9% 37.4% 3.05 1.43 – 6.42 0.004 CI: confidence interval; MACE: major adverse cardiac events; TSH: thyrotropin. (14.80% vs. 27.12%, respectively, OR = 3.05, p = 0.004), cardiogenic shock (4.77% vs. 6.05%, respectively, OR = 4.77, p = 0.02) and bleeding (12.09% vs. 15.25%, respectively, OR = 3.36, p = 0.012). Discussion The major finding of this study supports data previously published, showing that in-hospital MACE of patients with ACS were associated with higher levels of TSH. In addition, we also showed a relationship between TSH and cardiogenic shock and bleeding. There are many possible pathophysiological explanations for the uncertain relationship between worse prognosis and thyroid hormones in cardiovascular diseases. Numerous studies have focused on the impact of subclinical thyroid dysfunction on the development of cardiovascular disease, especially ACS. However, we do not know if the TSH levels are higher prior to ACS or if they become higher at the moment of ACS. 2,3,7-11 Triiodothyronine functions through interactions with isoform type α receptors, α 1 or α 2, and type β receptors, β 1, β 2 or β 3. 2,3,12,13 Regarding their cardiac distribution, these receptors are located both on atrial cells, as well as on ventricular cells. 2,3,12-14 By binding to these receptors, thyroid hormones accelerate myosin synthesis and influence sarcoplasmic reticulum activity, movement through the ionic Ca and K channels, response of adrenergic receptors, transmembrane ion gradients, and the levels of ATP and of atrial natriuretic peptide. 2,3,12-14 The effects of thyroid hormones can be categorized as genomic or non-genomic, and can structurally and functionally influence cardiovascular proteins. 2,3 Acting on α receptors, triiodothyronine plays a role in the process of increasing myocardial contractility and enhancing myosin production. Acting on β receptors, they influence diastolic processes and left ventricular relaxation. The mainmechanism is that of reducing the high levels of cytosolic calciumduring systole. On a vascular level, triiodothyronine plays an essential role in the maintenance and renewal of endothelial integrity, in peripheral arterial resistance and in modulating the arterial response to the renin-angiotensin-aldosterone mechanism activation. 2,3,15 This hormone also controls the macrophage response to the deposition of lipids in the vascular wall. 2,3 Apart from these direct effects, thyroid hormones play an important role in the development of cardiovascular pathology by other mechanisms, such as influencing the coagulation process by controlling the levels of activated factor VII and the ratio of activated factor VII and anti-activated factor VII antibody. 2,3 115