[Acute coronary syndrome. Physiopathology and genetics]
Gilberto Vargas-Alarcón1, José Manuel Fragoso, Hilda Delgadillo
1Departamento de Biología Molecular, Instituto Nacional de Cardiología Ignacio Chávez, México, DF. gvargas63@yahoo.com
Insights
Acute coronary syndrome (ACS), a leading cause of death, involves oxidative, inflammatory, and thrombotic processes. This review examines ACS pathogenesis and candidate genes, noting inconsistent population study results.
Area of Science:
- Cardiology
- Genetics
- Pathophysiology
Context:
- Acute coronary syndrome (ACS) is a major cause of mortality in industrialized nations, accounting for up to 29% of deaths.
- ACS encompasses conditions like unstable angina and myocardial infarction, driven by complex pathophysiological mechanisms.
- The prevalence and impact of ACS underscore the need for a deeper understanding of its underlying causes.
Purpose:
- To review the physiopathogenesis of acute coronary syndrome (ACS).
- To discuss the role of candidate genes in ACS pathogenesis.
- To highlight inconsistencies in genetic association studies across different populations.
Summary:
- ACS pathogenesis involves intricate oxidative, inflammatory, and thrombotic processes.
- Various molecules influence ACS progression, and their encoding genes have been investigated for disease association.
- Genetic studies in ACS have yielded inconsistent findings in different populations, necessitating further research.
Impact:
- Provides a comprehensive overview of ACS pathophysiology.
- Identifies key candidate genes implicated in ACS development.
- Emphasizes the need for population-specific genetic analyses in ACS research.
Abstract:
The acute coronary syndrome (ACS) is characterized by a spectrum of arterial diseases that include unstable angina and myocardial infarction. In the last 10 years, ACS has become the cause of up to 29% of deaths in the industrialized countries, becoming the main cause of death, and it will most probably stay that way for the year 2020. The physiopathogenesis of ACS include oxidative, inflammatory, and thrombotic processes. Diverse molecules participate in the processes, increasing of decreasing the damage. The genes that encode these molecules have been associated with the disease. However, in some cases inconsistent results in different populations have been reported. In this review the physiopathogenesis and the role of several candidate genes involved in the pathogenesis of ACS are discussed.
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