Neurohumoral response and stress hyperglycemia in myocardial infarction.

Background: Hyperglycemia is associated with an increased risk for death in acute coronary syndromes. This could be related to underlying glucose metabolism abnormalities or be caused by a counter-regulatory stress response. However, there is a paucity of data on the relationship between stress hormones, hyperglycemia, and clinical outcomes in myocardial infarction. Methods: Single-center, prospective, observational study. Patients admitted to the coronary care unit with a diagnosis of myocardial infarction were included. On admission, blood samples were obtained to measure serum glucose, cortisol, and catecholamines. A second sample was obtained at 8 AM after 48 h from admission. Results: There was a mild and positive correlation between serum cortisol and glucose (Spearman's rho = 0.24, p = 0.005), and no significant correlation was found between glucose and catecholamines. A similar correlation between cortisol and glucose among diabetics and non-diabetics was observed. Significantly higher serum cortisol and glucose levels were present in patients who developed heart failure or died during hospitalization. The association between glycemia and mortality lost significance in multivariate analysis, with a significant interaction term with cortisol (p = 0.003). Conclusion: Cortisol is a key responsible for stress hyperglycemia, and its deleterious effects on the cardiovascular system could be the cause for worst outcomes associated with hyperglycemia in ACS. Further research is warranted to ascertain this relationship and to investigate potential therapeutic targets.

Cortisol-Mediated Stress Response and Mortality in Acute Coronary Syndrome.

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.