Resumo Fundamento: As matrizes metaloproteinases (MMPs) podem afetar o volume extracelular (VEC) e seus compartimentos, e isso pode oferecer informações mais detalhadas sobre o mecanismo de remodelação adversa (RA) do ventrículo esquerdo (VE) após o infarto agudo do miocárdio (IM). Objetivos: Investigar o papel que as alterações (Δ) nos compartimentos de VEC (volume matriz (MVi) e volume celular (CVi)) desempenham no desenvolvimento de RA após o IM, e sua relação com as expressões de MMP-2. Métodos: Um total de noventa e dois pacientes com primeiro IM passaram por exames de imagens por ressonância magnética cardiovascular 3 Tesla realizados 2 semanas (linha de base) e 6 meses após o IM. Medimos o mapeamento T1 com sequências MOLLI. O VEC foi obtido após o realce pelo gadolínio. O VEC e a massa do VE foram usados para calcular o MVi e o CVi. A RA foi definida como um aumento de ≥ 12% no volume diastólico final do VE em 6 meses. As MMPs foram medidas usando-se um sistema de imunoensaio multiplex em grânulos no primeiro dia (linha de base) e 2 semanas após o IM. Um P valor <0,05 foi aceito como estatisticamente significativo. Resultados: Os níveis de linha de base de MVi média e VEC médio foram mais altos no grupo com RA em comparação com o grupo sem RA (42,9±6,4 vs. 39,3±8,2 %, p= 0,037; 65,2±13,7 vs. 56,7±14,7 mL/m2, p=0,010; respectivamente). Os níveis de CVi eram semelhantes entre os grupos. Foi encontrada uma correlação positiva entre os níveis de linha de base de MMP-2 e os níveis de linha de base de VEC (r=0,535, p<0,001) e MVi (r=0,549, p<0,001). O aumento dos níveis de ΔMVi foi um preditor independente da RA (RC=1,03, p=0,010). O ΔMVi teve um desempenho diagnóstico superior quando comparado ao ΔVEC na previsão do (ΔAUC: 0,215±0,07, p<0,001). Conclusão: Níveis altos de MVi estão associados à RA, e o ΔMVi foi um preditor independente de RA. Isso pode estar associado à liberação de MMP-2 devido ao aumento da resposta inflamatória.

Abstract Background: Matrix metalloproteinases (MMPs) can affect myocardial extracellular volume (ECV) and its compartments, and this can provide more detailed information about the mechanism of adverse left ventricular (LV) remodeling (AR) after acute myocardial infarction (MI). Objectives: To investigate the role of changes (Δ) in ECV compartments (matrix volume (MVi) and cell volume (CVi)) in the development of AR after MI, and their relationship with MMP-2 expressions. Methods: Ninety-two first MI patients who underwent 3 Tesla cardiovascular magnetic resonance imaging performed 2 weeks (baseline) and 6 months post-MI. We measured T1 mapping with MOLLI sequences. ECV was performed post-gadolinium enhancement. ECV and LV mass were used to calculate MVi and CVi. AR was defined as an increase of ≥ 12% in LV end-diastolic volume in 6 months. MMPs were measured using a bead-based multiplex immunoassay system at first day (baseline) and 2 weeks post-MI. P <0.05 was accepted as statistically significant. Results: Mean ECV and mean MVi baseline levels were higher in AR group compared to without AR group (42.9±6.4 vs 39.3±8.2%, p= 0.037; 65.2±13.7 vs 56.7±14.7 mL/m2, p=0.010; respectively). CVi levels was similar between groups. A positive correlation was found between baseline levels of MMP-2 and baseline levels of ECV (r=0.535, p<0.001) and MVi (r=0.549, p<0.001). Increased ΔMVi levels was independently predictor of AR (OR=1.03, p=0.010). ΔMVi had superior diagnostic performance compared to ΔECV in predicting AR (ΔAUC: 0.215±0.07, p<0.001). Conclusion: High MVi levels are associated with AR, and ΔMVi was independently predictor of AR. This may be associated with MMP-2 release due to increased inflammatory response.

ABSTRACT Background: Inflammation plays a critical role in cardiac remodeling after myocardial infarction (MI). Monocyte to high-density lipoprotein-cholesterol (HDL-C) ratio (MHR) has emerged as a potential indicator of inflammation. Objectives: The study aimed to investigate the prognostic role of MHR at the time of hospital admission in late cardiac remodeling and subsequent 1-year mortality in an academic training and research hospital. Methods: This prospective multicenter study included 231 patients with acute ST-elevation MI. Left ventricular (LV) functions and volumes were assessed by cardiac magnetic resonance (CMR) imaging at 2 weeks and 6 months post-MI. The definition of adverse cardiac remodeling (AR) was based on the increase of LV end-diastolic volume by ≥ 12% at 6 months post-MI. All patients were followed for survival for 1 year after the second CMR imaging measurements. Results: At 6 months post-MI, 20 patients (23.8%) exhibited AR. The median MHR was higher in the AR group compared to the group without AR (2.2 vs. 1.5, p < 0.001). A positive correlation was found between MHR and infarct size in the groups with and without AR. High MHR was an independent predictor of AR (OR: 3.21, p = 0.002). The cut-off value of MHR in predicting AR was found to be >1.6 with 92.7% sensitivity and 70.1% specificity (AUC ± SE: 0.839 ± 0.03, p < 0.001). Mortality risk was 5.62-fold higher in the group with MHR of >1.6 (HR: 5.62, p < 0.001). Conclusions: These results indicate that admission MHR is a useful tool to predict patients with AR who are at risk of progression to heart failure and mortality after MI.