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Predisposição genética ao choque cardiogênico que complica o infarto agudo do miocárdio: revisão sistemática

Cardiologia
Imagem de arquivo, ilustrativa — não é do estudo. Capilares da prega ungueal do dedo, em capilaroscopia. Dmitry Stavtsev, Nikita Margaryants e Mikhail Volkov · CC BY 4.0 · Wikimedia Commons

Revisão sistemáticaNível 1 · Evidência consolidadaCurrent problems in cardiology16 out 20260 citações

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Resumo original em inglês

O que aconteceu

Cardiogenic shock (CS) complicates 5-10% of acute myocardial infarctions (AMI) and remains associated with in-hospital mortality of approximately 40-50%. The clinical predictors established do not fully explain why patients with comparable infarct severity have divergent outcomes, raising the hypothesis that host genetic factors modulate susceptibility to CS. Therefore, we conducted this systematic review to synthesize published evidence describing genetic variants associated with the development of CS complicating AMI.

PubMed, Embase, Scopus, and the Cochrane Library were searched from inception through Jun 2026, following PRISMA 2020 guidance. Eligible studies included any study type enrolling adults with AMI and reporting association of any specific genetic variants with CS.

O que encontraram

Of 480 records identified, 9 studies met inclusion criteria. Reported variants clustered into five biological pathways: inflammatory/cytokine signaling (TNF-α -308G>A, IFN-γ +874T>A, RANTES/CCL5 -403G>A), lipid metabolism (APOE ε2/ε3/ε4), thrombosis and fibrinolysis (PAI-1/SERPINE1 4G/4 G, MTHFR C677T/A1298C), clonal myeloproliferative disease (JAK2 V617F), and hypercoagulable/antioxidant pathways (protein C/S-related thrombophilia, PON1 Q192R). The APOE ε3/4 genotype and the TNF-2 allele showed the most direct associations with CS incidence and survival, respectively; JAK2 V617F and combined PAI-1/MTHFR variants were reported in severe, thrombus-driven case presentations of CS. RANTES and PON1 genotypes were not associated with CS occurrence, although circulating RANTES levels correlated with CS severity.

Por que isso importa

The available evidence is limited, but the variants reported to date span inflammatory, lipid, thrombotic, and myeloproliferative pathways, suggesting that genetic susceptibility to CS complicating AMI is polygenic and mechanistically heterogeneous, requiring prospective genetic association studies.

Resumo publicado sob licença CC BY. A tradução para o português ainda não chegou a este estudo.

O estudo original

Genetic predisposition to cardiogenic shock complicating acute myocardial infarction: a systematic review

Alaa Rahhal, Ans Alamami, Mostafa Najim, Mohanad Shehadeh, Abdul Rahman Arabi, Amr Omar, Mir B Basir, Ahmed Awaisu, Hazem Elewa

Descritores MeSH

  • Myocardial Infarction
  • Shock, Cardiogenic
  • Genetic Predisposition to Disease
  • Humans

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