Prognostic value of myocardial extracellular volume fraction evaluation based on cardiac magnetic resonance T1 mapping with T1 long and short in hypertrophic cardiomyopathy

Li, Yuancheng; Liu, Xiuming; Yang, Fan; Wang, Jie; Xu, Yuanwei; Fang, Tingting; Pu, Lutong; Zhou, Xiaoyue; Han, Yuchi; Chen, Yu‐Cheng

doi:10.1007/s00330-020-07650-7

Cited by 39 publications

(19 citation statements)

References 43 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Myocardial fibrosis is a common feature shared by different insults, including myocardial ischemia, which facilitates the development of heart failure by causing contractile dysfunction and arrhythmogenicity [ 18 ]. Different studies have shown that a higher degree of fibrosis and lesion size are associated with shorter long-term survival in patients with heart failure and other cardiac pathologies [ 19 , 20 ]. Our data show that patients with acute MI presented with more than 40% of the myocardium occupied by fibrosis, which was accompanied by a reduction in cardiac function.…”

Section: Discussionmentioning

confidence: 99%

Mitochondrial Oxidative Stress Promotes Cardiac Remodeling in Myocardial Infarction through the Activation of Endoplasmic Reticulum Stress

et al. 2022

View full text Add to dashboard Cite

We have evaluated cardiac function and fibrosis in infarcted male Wistar rats treated with MitoQ (50 mg/kg/day) or vehicle for 4 weeks. A cohort of patients admitted with a first episode of acute MI were also analyzed with cardiac magnetic resonance and T1 mapping during admission and at a 12-month follow-up. Infarcted animals presented cardiac hypertrophy and a reduction in the left ventricular ejection fraction (LVEF) and E- and A-waves (E/A) ratio when compared to controls. Myocardial infarction (MI) rats also showed cardiac fibrosis and endoplasmic reticulum (ER) stress activation. Binding immunoglobulin protein (BiP) levels, a marker of ER stress, were correlated with collagen I levels. MitoQ reduced oxidative stress and prevented all these changes without affecting the infarct size. The LVEF and E/A ratio in patients with MI were 57.6 ± 7.9% and 0.96 ± 0.34, respectively. No major changes in cardiac function, extracellular volume fraction (ECV), or LV mass were observed at follow-up. Interestingly, the myeloperoxidase (MPO) levels were associated with the ECV in basal conditions. BiP staining and collagen content were also higher in cardiac samples from autopsies of patients who had suffered an MI than in those who had died from other causes. These results show the interactions between mitochondrial oxidative stress and ER stress, which can result in the development of diffuse fibrosis in the context of MI.

show abstract

Section: Discussionmentioning

confidence: 99%

Mitochondrial Oxidative Stress Promotes Cardiac Remodeling in Myocardial Infarction through the Activation of Endoplasmic Reticulum Stress

et al. 2022

View full text Add to dashboard Cite

show abstract

“…A plausible explanation for the better clinical correlation and discrimination performance of ECV than native T1 mapping is that ECV could be normalized by comparing changes in T1 relaxation rates in the blood pool before and after contrast administration and was highly accurate and reproducible, while native T1 could be affected by intracellular water content, field strengths, the CMR system acquisition sequence, and individual conditions [ 40 , 41 ]. All the above suggest a potential value for ECV in clinical severity assessment and a possible prognostic role in patients with ES.…”

Section: Discussionmentioning

confidence: 99%

Detection and evaluation of myocardial fibrosis in Eisenmenger syndrome using cardiovascular magnetic resonance late gadolinium enhancement and T1 mapping

Gong

Guo

Wan

et al. 2022

Journal of Cardiovascular Magnetic Resonance

Self Cite

View full text Add to dashboard Cite

Background Myocardial fibrosis is a common pathophysiological process involved in many cardiovascular diseases. However, limited prior studies suggested no association between focal myocardial fibrosis detected by cardiovascular magnetic resonance (CMR) late gadolinium enhancement (LGE) and disease severity in Eisenmenger syndrome (ES). This study aimed to explore potential associations between myocardial fibrosis evaluated by the CMR LGE and T1 mapping and risk stratification profiles including exercise tolerance, serum biomarkers, hemodynamics, and right ventricular (RV) function in these patients. Methods Forty-five adults with ES and 30 healthy subjects were included. All subjects underwent a contrast-enhanced 3T CMR. Focal replacement fibrosis was visualized on LGE images. The locations of LGE were recorded. After excluding LGE in ventricular insertion point (VIP), ES patients were divided into myocardial LGE-positive (LGE+) and LGE-negative (LGE−) subgroups. Regions of interest in the septal myocardium were manually contoured in the T1 mapping images to determine the diffuse myocardial fibrosis. The relationships between myocardial fibrosis and 6-min walk test (6MWT), N-terminal pro-brain natriuretic peptide (NT-pro BNP), hematocrit, mean pulmonary arterial pressure (mPAP), pulmonary vascular resistance index (PVRI), RV/left ventricular end-systolic volume (RV/LV ESV), RV ejection fraction (RVEF), and risk stratification were analyzed. Results Myocardial LGE (excluding VIP) was common in ES (16/45, 35.6%), and often located in the septum (12/45, 26.7%). The clinical characteristics, hemodynamics, CMR morphology and function, and extracellular volume fraction (ECV) were similar in the LGE+ and LGE− groups (all P > 0.05). ECV was significantly higher in ES patients (28.6 ± 5.9% vs. 25.6 ± 2.2%, P < 0.05) and those with LGE− ES (28.3 ± 5.9% vs. 25.6 ± 2.2%, P < 0.05) than healthy controls. We found significant correlations between ECV and log NT-pro BNP, hematocrit, mPAP, PVRI, RV/LV ESV, and RVEF (all P < 0.05), and correlations trends between ECV and 6MWT (P = 0.06) in ES patients. An ECV threshold of 29.0% performed well in differentiating patients with high-risk ES from those with intermediate or low risk (area under curve 0.857, P < 0.001). Conclusions Myocardial fibrosis is a common feature of ES. ECV may serve as an important imaging marker for ES disease severity.

show abstract

“…There were limited studies with regard to the relationship between T1 mapping and ECV with the adverse outcomes in HCM patients ( 3 ). Li et al have reported that ECV was a strong biomarker in predicting the adverse outcomes in 263 HCM patients during a mean follow-up of 28.3 months ( 23 ). Xu et al found that both native T1 mapping and ECV values were associated with SCD in 258 patients with HCM without the presence of LGE and LVOT obstruction ( 14 ).…”

Section: Discussionmentioning

confidence: 99%

Incremental Values of T1 Mapping in the Prediction of Sudden Cardiac Death Risk in Hypertrophic Cardiomyopathy: A Comparison With Two Guidelines

Qin

Min

Chen

et al. 2021

Front. Cardiovasc. Med.

View full text Add to dashboard Cite

Background: MRI native T1 mapping and extracellular volume fraction (ECV) are quantitative values that could reflect various myocardial tissue characterization. The role of these parameters in predicting the risk of sudden cardiac death (SCD) in hypertrophic cardiomyopathy (HCM) is still poorly understood.Aim: This study aims to investigate the ability of native T1 mapping and ECV values to predict major adverse cardiovascular events (MACE) in HCM, and its incremental values over the 2014 European Society of Cardiology (ESC) and enhanced American College of Cardiology/American Heart Association (ACC/AHA) guidelines.Methods: Between July 2016 and October 2020, HCM patients and healthy individuals with sex and age matched who underwent cardiac MRI were prospectively enrolled. The native T1 and ECV parameters were measured. The SCD risk was evaluated by the 2014 ESC guidelines and enhanced ACC/AHA guidelines. MACE included cardiac death, transplantation, heart failure admission, and implantable cardioverter-defibrillator implantation.Results: A total of 203 HCM patients (54.2 ± 14.9 years) and 101 healthy individuals (53.2 ± 14.7 years) were evaluated. During a median follow-up of 15 months, 25 patients (12.3%) had MACE. In multivariate Cox regression analysis, global native T1 mapping (hazard ratio (HR): 1.446; 95% confidence interval (CI): 1.195–1.749; P < 0.001) and non-sustained ventricular tachycardia (NSVT) (HR: 4.949; 95% CI, 2.033–12.047; P < 0.001) were independently associated with MACE. Ten of 86 patients (11.6%) with low SCD risk assessed by the two guidelines had MACE. In this subgroup of patients, multivariate Cox regression analysis showed that global native T1 mapping was independently associated with MACE (HR: 1.532; 95% CI: 1.221–1.922; P < 0.001). In 85 patients with conflicting results assessed by the two guidelines, end-stage systolic dysfunction was independently associated with MACE (HR: 7.942, 95% CI: 1.322–47.707, P = 0.023). In 32 patients with high SCD risk assessed by the two guidelines, NSVT was independently associated with MACE (HR: 9.779, 95% CI: 1.953–48.964, P = 0.006).Conclusion: The global native T1 mapping could provide incremental values and serve as potential supplements to the current guidelines in the prediction of MACE.

show abstract

Prognostic value of myocardial extracellular volume fraction evaluation based on cardiac magnetic resonance T1 mapping with T1 long and short in hypertrophic cardiomyopathy

Cited by 39 publications

References 43 publications

Mitochondrial Oxidative Stress Promotes Cardiac Remodeling in Myocardial Infarction through the Activation of Endoplasmic Reticulum Stress

Mitochondrial Oxidative Stress Promotes Cardiac Remodeling in Myocardial Infarction through the Activation of Endoplasmic Reticulum Stress

Detection and evaluation of myocardial fibrosis in Eisenmenger syndrome using cardiovascular magnetic resonance late gadolinium enhancement and T1 mapping

Incremental Values of T1 Mapping in the Prediction of Sudden Cardiac Death Risk in Hypertrophic Cardiomyopathy: A Comparison With Two Guidelines

Contact Info

Product

Resources

About