[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.

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