Identificación de la relación Entre Componentes de la Inmunidad Celular y Factores Inflamatorios y neuroendócrinos Como Determinantes Del pronóstico clínico en el síndrome Coronario Agudo

Introduction According to data from the World Health Organization, cardiovascular disease is the leading cause of death worldwide. It is estimated that in 2015, 18 million people died from this cause, representing 31% of all deaths recorded globally. The majority of these deaths (7.4 million) were due to coronary heart disease. Additionally, cardiovascular disease represents the highest burden of disease, defined by disability-adjusted life years (DALY), with 4,800 DALY per 100,000 inhabitants.

From a clinical perspective, the topic that concerns us within cardiovascular disease is acute coronary syndrome (ACS), which refers to a group of signs and symptoms compatible with acute myocardial ischemia. In this context, for decades, to optimize diagnosis and provide timely treatment, ACS has been subclassified into acute myocardial infarction with (STEMI) and without ST-segment elevation (NSTEMI) and unstable angina (UA).

Among the broad spectrum of ACS, the least severe form is UA, where symptoms suggest myocardial ischemia but there is no biochemical evidence of myocardial infarction. At the other extreme is acute myocardial infarction, whose clinical definition is based on the presence of acute myocardial damage detected by the elevation of cardiac biomarkers (troponin) in the context of evidence of acute myocardial ischemia. It is classified into five types, with type 1, caused by atherothrombotic coronary disease, being the focus of this study. This type is often precipitated by the rupture or erosion of an atherosclerotic plaque.

Background and Rationale Years of exhaustive clinical research have resulted in therapies that reduced mortality and complication rates of ACS, ranging from the creation of the Coronary Care Unit, anticoagulation therapies, beta-blockers, renin-angiotensin-aldosterone system inhibitors, antiplatelet therapies, to reperfusion, whether mechanical or pharmacological. However, in recent years, we have not been able to make a qualitative leap in the pathophysiological approach to coronary disease to create new paradigms in therapeutics. Thus, it is imperative to seek new horizons, new pathophysiological hypotheses, addressing topics such as inflammation, immune response, immunothrombosis, and stress response in the context of ACS.

It is undeniable that inflammation and stress are risk factors for developing ACS. Additionally, ACS triggers both an acute inflammatory response and a stress response, with cortisol being one of the main effectors of the latter, possessing anti-inflammatory effects. However, we currently lack a deep understanding of the mechanisms governing this interesting dialogue between inflammation and stress in the context of ACS. Some authors have described that a higher degree of inflammation is associated with worse outcomes in ACS patients. Recently, we described that this poor outcome is related to plasma cortisol levels.