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.

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.

[MINOCA, infarction with normal coronaries. The fall of the paradigm ?].

Myocardial infarction is the leading cause of death in the world, being the coronary atherosclerotic obstruction the main finding. Although 6% of all the patients had no significant coronary arteries disease on coronary angiography, defined by lumen vascular obstruction greater than 50%. This type of cases was defined by the term MINOCA (myocardial infarction with non-obstructive coronary arteries).

Neuroendocrine System Regulatory Mechanisms: Acute Coronary Syndrome and Stress Hyperglycaemia.

Neurohormonal systems are activated in the early phase of acute coronary syndromes to preserve circulatory homeostasis, but prolonged action of these stress hormones might be deleterious. Cortisol reaches its peak at 8 hours after the onset of symptoms, and individuals who have continued elevated levels present a worse prognosis. Catecholamines reach 100-1,000-fold their normal plasma concentration within 30 minutes of ischaemia, therefore inducing the propagation of myocardial damage.