scholarly journals Predictive role of quantification of myocardial fibrosis using delayed contrast-enhanced magnetic resonance imaging in nonischemic dilated cardiomyopathies: a systematic review and meta-analysis

2021 ◽  
Vol 26 (12) ◽  
pp. 4776
Author(s):  
E Z Golukhova ◽  
S A Aleksandrova ◽  
B Sh Berdibekov

Aim. The present study aims to provide a systematic review and meta-analysis to investigate the prognostic role of assessing the severity of myocardial fibrosis using delayed contrast-enhanced magnetic resonance imaging in nonischemic dilated cardiomyopathies.Material and methods. We searched PubMed, Google Scholar for studies that examined the predictive value of quantifying late gadolinium enhancement (LGE) areas in patients with nonischemic dilated cardiomyopathy. Unadjusted hazard ratios (HR) from studies with similar scoring criteria were pooled for meta-analysis.Results. Nine studies were retrieved from 782 publications for this systematic review and meta-analysis. In total, 2389 patients (mean age, 51,9 years; mean follow-up, 39,3 months) were included in the analysis. Meta-analysis showed the extent of LGE was associated with an increased risk of arrhythmic end point (HR: 1,09/1% LGE; 95% CI: 1,02-1,18; p=0,01), major adverse cardiovascular events (HR: 1,07/1% LGE; 95% CI: 1,01-1,13; p=0,03) and all-cause mortality (HR: 1,09/1% LGE; 95% CI: 1,04-1,13; p<0,0001).Conclusion. The severity of LGE by cardiac magnetic resonance predicts arrhythmic events (ventricular arrhythmia and sudden death), major adverse cardiovascular events and all-cause mortality. Assessment of LGE can be used as an effective tool for stratifying risk in patients with nonischemic dilated cardiomyopathy. 

2021 ◽  
Author(s):  
Luiz Sergio Fernandes de Carvalho ◽  
Ana Claudia Cavalcante Nogueira ◽  
Riobaldo Marcelo Ribeiro Cintra ◽  
Isabella Bonilha ◽  
Beatriz Luchiari ◽  
...  

Abstract Background: Among individuals with type 2 diabetes mellitus (T2DM), RCTs designed to investigate the cardiovascular effects of achieving HbA1c ≤7.0% by using insulin and sulfonylureas were unable to prevent the incidence of major adverse cardiovascular events (MACE) defined as CV death, non-fatal myocardial infarction, and non-fatal stroke. Intense glucose-lowering with newer antidiabetic therapies (ADTs) including SGLT2i, GLP1-RA, pioglitazone and DPP4i show lower risk of hypoglycemia and could lead to additive effect in preventing MACE. In this context, this study was designed to assess the impact of the HbA1c levels achieved with newer ADTs on the risk of MACE. Methods. We searched MEDLINE/PubMed, Cochrane and ClinicalTrials.gov. RCTs published up to January/2021 reporting the occurrence of MACE and all-cause mortality in individuals with T2DM, including a sample size ≥100 individuals in each study arm and follow-up ≥24 weeks, were selected. Data was extracted by four independent observers following PRISMA guidelines. We performed a systematic review and additive-effects network meta-analysis with random effects and a multivariate meta-regression to assess the impact of achieved HbA1c on incident MACE. Results. A total of 122 RCTs were included with 139 treatment arms, 256,990 individuals, and 689,346 individuals-years who were randomized to an active treatment vs. control group. Therapy with SGLT2i, GLP1-RA, or pioglitazone similarly reduced the risk of MACE compared to placebo (HR 0.88 [95%CI 0.83, 0.94, p<0.001], 0.89 [95% CI 0.85, 0.94, p<0.0001], and 0.86 [95% CI 0.76, 0.98, p=0.025], respectively). The achievement of HbA1c≤7.0% in RCTs with SGLT2i, DPP4i, TZD, or GLP1-RA in the active arm was associated with an adjusted HR of 0.91 (95% CI 0.80, 0.97; p=0.039) compared with HbA1c>7.0%. All-cause mortality was not influenced by HbA1c thresholds.Conclusions: Achieving lower glucose levels with newer ADTs is linearly associated with a reduced risk of MACEs, without affecting all-cause mortality. Targeting HbA1c between 6.5 and 7% with SGLT2i, GLP1A, pioglitazone or DPP4i brings cardiovascular benefits considering the available RCT evidence.Study registration: PROSPERO CRD42020200649


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