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Cortisol-Mediated Stress Response and Mortality in Acute Coronary Syndrome

2020; Elsevier BV; Volume: 46; Issue: 3 Linguagem: Inglês

10.1016/j.cpcardiol.2020.100623

1535-6280

Martín Aladio, Diego Costa, Maia Matsudo, Alejo Pérez de la Hoz, Diego González, Alejandra Brignoli, Sandra Swieszkowski, Ricardo Pérez de la Hoz,

Adrenal Hormones and Disorders

Acute coronary syndrome is a frequent cause of morbidity and mortality, and a known stress response trigger. We aim to investigate the association between cortisol, as a primary stress hormone, and prognosis/mortality in this scenario. Single-center, prospective, observational, and analytical study in patients admitted for acute coronary syndrome. Clinical characteristics and prognosis markers were registered, along with serum cortisol levels on admission and in-hospital mortality. Cortisol levels were higher in patients with a depressed ST segment (18.22 ± 13.38 μg/dL), compared to those with an isoelectric ST segment (12.66 ± 10.47 μg/dL), and highest in patients with an elevated ST segment (22.61 ± 14.45 μg/dL), with P< 0.001. Also, cortisol was significantly increased in patients with elevated troponin I values (18.90 ± 14.19 μg/dL vs 11.87 ± 8.21 μg/dL, P< 0.001). Patients with Killip-Kimball class I or II had a lower mean serum cortisol (14.66 ± 10.82 μg/dL) than those with class III or IV (41.34 ± 15.57 μg/dL), P< 0.001. Finally, we found that patients who died during hospitalization had higher cortisol on admission: 36.39 ± 17.85 μg/dL vs 15.26 ± 11.59 μg/dL, P= 0.003. Cortisol was directly related to the electrocardiographic presentation of ACS and with the maximum troponin I value. This indicates that serum cortisol levels parallel the extension of ischemia and myocardial injury, and in this way affect the clinical prognosis, evidenced by the Killip-Kimball class and the increase in mortality.