AI Article Synopsis
- Neurohormonal systems activate early in acute coronary syndromes to help maintain blood circulation, but long-term activation of these stress hormones can be harmful.
- Cortisol levels peak at 8 hours after symptoms start, with consistently high levels linked to poorer outcomes, while catecholamines surge significantly within 30 minutes of ischemia, worsening heart damage.
- Stress-related high blood sugar leads to inflammation, vascular issues, and increased risk of blood clots, and notably, hyperglycemia in non-diabetic patients is associated with higher in-hospital and 12-month mortality rates.
Article Abstract
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. Stress hyperglycaemia induces inflammation and endothelial dysfunction, and also has procoagulant and prothrombotic effects. Patients with hyperglycaemia and no diabetes elevated in-hospital and 12-month mortality rates. Hyperglycaemia in patients without diabetes has been shown to be an appropriate independent mortality prognostic factor in this type of patient.
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Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6159413 | PMC |
| http://dx.doi.org/10.15420/ecr.2017:19:3 | DOI Listing |
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