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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Plaque rupture triggers a prothrombotic response that is counterbalanced by a fibrinolytic response. D-dimer serves as a marker of both processes. Inflammatory mediators are also released, evidenced with the rise of high-sensitive C reactive protein (hsCRP). Current evidence with these biomarkers has shown conflicting results. Determine an association between D-dimer and hsCRP within hospital and 1-year mortality in patients with acute coronary syndromes. In total, 127 patients were included. In-hospital mortality was 5.7%, and 1-year all-cause and cardiovascular mortality were 14.6 and 9.7%, respectively. The median of admission D-dimer for patients who died during hospital stay was higher than those who survived [4.59 (interquartile ranges (IQR) 1.94-6.05 mg/ml fibrinogen equivalent units (FEU)) vs. 0.56 (IQR 0.31-1.12 mg/ml FEU), P U 0.001]. At 1-year follow-up, the median of admission D-dimer for patients who died was significantly higher than those who survived: 1.55 (IQR 0.91-5.08 mg/ml FEU) vs. 0.53 (IQR 0.29-0.90 mg/ml FEU), P < 0.001. Positive D-dimer vs. negative D-dimer at admission analysis evidenced that almost 25% of the positive patients were dead at 1-year follow-up (22.4 vs. 2.4% negative D-dimer, P U 0.011). Multivariate logistic regression analysis showed that D-dimer has an independent association with 1-year mortality [odds ratio 1.06 (95% confidence interval 1.02-1.10), P U 0.006]. Positive significative correlations between D-dimer and hsCRP levels (R U 0.56, P < 0.001) were found. High levels of admission D-dimer were strongly associated with inhospital and 1-year mortality. Significant correlations with hsCRP could explain the inflammatory nature that led to poorer outcomes. D-dimer could be useful in risk stratification in acute coronary syndromes; however, a specific threshold should be defined for this type of patient.

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