(24.6% vs. 17.9%; p = 0.006), major complications (35.3% to 29.3%), and death (21% vs. 12%; odds ratio: 0.52; 95% confidence interval: 0.38-0.71; p = 0.004). also decreased. Conclusion: The Infarction Code strategy improved treatment, times of medical attention and decreased complications and death in these patients.

Objective: To evaluate the prognostic of interleukin 6 levels, in patients with acute myocardial infarction with No Reflow phenomenon. Methods:Consecutive patients with acute ST elevation myocardial infarction diagnosis, with ≤12 hours of evolution, and treated with primary angioplasty were included. The intracoronary interleukin 6 was measured before and after the procedure. The patients were classified into two groups: group I (Success or Reflow) and II (Failure or No Reflow) respectively. The early outcome variables were evaluated during the hospitalization.Results: A total of 45 patients were studied, the average age was 62 ± 11 years, 26 patients in the group I, and 19 in the group II, without differences in the traditional risk factor, or in the evolution time. Compared to group 1, the complications were more frequent in the group II, compared to group I: hypotension (7.7% vs. 63%, p<0.0001), arrhythmias (7.7% vs. 47%, p=0.017) y hospital death (0% vs. 32%, p=0.001). The ejection fraction was lower in the group II (45.6 ± 9.2% vs. 34.8 ± 11.3%, p=0.009). The interleukin 6 levels were higher in the group II (8.7 ± 6.4 vs. 16.8 pg/mL, p=0.032). Conclusion:The levels of Interleukin 6 intra-coronary are associated with the phenomenon of No Reflow, plus complications and early death.

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Despite significant improvements in the treatment of virtually all cardiac disorders, heart failure (HF) is an exception, its prevalence is increasing, and only small extensions occur in survival. Several pathogenetic mechanisms appear to be operative in HF. These include higher overhead hemodynamic dysfunction associated with ventricular ischemia, remodeling with neurohumoral excessive stimulation, myocyte cycling abnormal calcium, inadequate or excessive proliferation of the extracellular matrix, accelerated apoptosis and genetic mutations. HF can present with reduced ejection fraction (EF), HFrEF, or with preserved EF (HFpEF). The interplay between diverse organ systems contributing to HF is mediated by the activation of counteracting neurohormonal pathways focused to re-establishing hemodynamic homeostasis. Cardiorenal Syndrome is a specific condition which is characterized by a rapid or chronic worsening of cardiac function leading to acute or chronic kidney injury (A/CKI) and /or the reciprocal organ dysfunction sequence can be possible. Even though its pathophysiology is complex and not still completely understood, oxidative stress and endothelial dysfunction seems to play a pivotal role. New Pathways between heart and kidney and its early recognition can also be targeted for more effective and beneficial HF treatments.