**Abbreviations**

*Cardiac Diseases - Novel Aspects of Cardiac Risk, Cardiorenal Pathology and Cardiac Interventions*

During AMI, the levels of catecholamines and cortisol increase, insulin decreases, and blood glucagon increase. This leads to a notable increase in blood glucose and decreased glucose utilization by cells. Free fatty acids and their metabolites are increased that increase myocardial damage by different mechanisms (direct inhibition of glucose oxidation, increased demand for O2, direct toxicity). Insulin can reverse some of these mechanisms by inducing the production of ATP from aerobic glucose metabolism in the myocyte. Several studies mentioned in these guidelines demonstrated benefits in patients with hyperglycemia who received insulin infusion for strict glycemic control during the event. These guidelines establish that the normalization of insulin glycemia is a class I indication with a level of evidence B for patients with complicated AMI and class IIa with a level of evidence

These guidelines mention, scarcely, that to reduce myocardial damage beyond reperfusion therapy, some strategies that include pharmacological and mechanical therapies have been demonstrating the potential to reduce the size of AMI by decreasing the impact of reperfusion injury in small clinical trials. But there is no large-scale clinical study that has demonstrated clinical benefit. Therefore, they make no recommendation regarding measures to limit reperfusion injury or any other therapy to

The use of B blockers and nitrates is favorable to reduce myocardial damage caused by primary and secondary ischemia, reducing the imbalance between supply and demand of O2 and nutrients until reperfusion. Beside, these drugs are useful to optimize the conditions of pre- and post-loading of LV, decrease heart rate and blood pressure, and thus limit the damage caused by mechanical stress. A wide variety of potent platelet antiplatelets such as clopidogrel, prasugrel, or ticagrelor added to the routine use of aspirin were shown to reduce the recurrence of ischemic events after reperfusion (secondary ischemia). Although it is not clearly established by evidence from clinical trials, thromboaspiration; potent vasodilators at the microvasculature level such as adenosine and calcium blockers, among others; and the use of IIb–IIIa glycoprotein inhibitors may be effective in prevention and treatment of no-reflow. The phenomenon of no-reflow can cause ischemia (secondary ischemia) to continue beyond the recanalization of the epicardial artery. However, reperfusion inflammation and injury are not prevented or treated in daily practice.

The development of reperfusion therapies for AMI was shown to reduce mortality strongly. There are possibilities to optimize its use. Health teams must continue fighting to shorten the system times and detect the best strategy according to the context in which they operate. There are working groups that carry out research in basic sciences, translational research, and clinical research and are making advances in myocardial protection. Cyclosporine and colchicine are currently evaluated for their ability to reduce the damage caused by inflammation. Developed treatments

reduce myocardial damage during the event, beyond reperfusion [63].

B for patients with uncomplicated AMI [59–61, 62].

**5. Current reperfusion adjuvant therapy status**

*4.1.4 Glycemia control*

**4.2 ESC guides 2017**

**250**

**6. Perspectives**

