Prognostic significance of quantitative assessment of focal myocardial fibrosis in patients with heart failure with preserved ejection fraction

Kato, Shingo; Saito, Nozomu; Kirigaya, Hidekuni; Gyotoku, Daiki; Iinuma, Naoki; Kusakawa, Yuka; Iguchi, Kenta; Nakatani, Tatsuya; Fukui, Kazuki; Futaki, Masaaki; Iwasawa, Tae; Taguri, Masataka; Kimura, Kazuo; Umemura, Satoshi

doi:10.1016/j.ijcard.2015.05.048

Cited by 61 publications

(35 citation statements)

References 35 publications

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“…In other cardiomyopathies, the nding of non-ischemic LGE lesions is associated with prognosis, and if such is the case in T2DM this now has to be established. Non-ischemic LGE lesions have in other patient groups been correlated to heart failure, arrhythmias, and sudden cardiac death (24,26,27). The nonischemic LGE lesions found in our study were related to parameters associated with impaired diastolic function, in itself an important prognostic factor.…”

Section: Discussionsupporting

confidence: 59%

Distinct non-ischemic myocardial late gadolinium enhancement lesions in patients with type 2 diabetes

Bojer

Sørensen

Vejlstrup

et al. 2020

Preprint

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Background: Cardiovascular magnetic resonance imaging (CMR) have described localised non-ischemic late gadolinium enhancement (LGE) lesions of prognostic importance in various non-ischemic cardiomyopathies. Ischemic LGE lesions are prevalent in diabetes (DM), but non-ischemic LGE lesions have not previously been described or systematically studied in DM. Methods: 296 patients with type 2 DM (T2DM) and 25 sex-matched control subjects underwent echocardiography and CMR including adenosine-stress perfusion, T1-mapping and LGE. Results: 264 patients and all control subjects completed the CMR protocol. 78.4% of patients with T2DM had no LGE lesions; 11.0% had ischemic LGE lesions only; 9.5% had non-ischemic LGE lesions only; and 1.1% had both one ischemic and one non-ischemic lesion. The non-ischemic LGE lesions were situated mid-myocardial in the basal lateral or the basal inferolateral part of the left ventricle and the affected segments showed normal to high wall thickness and normal contraction. Patients with non-ischemic LGE lesions in comparison with patients without LGE lesions had increased myocardial mass (150±34 vs. 133±33 g, P=0.02), average E/e’(9.9 IQR8.7-12.6 vs. 8.8 IQR7.4-10.7, P=0.04), left atrial maximal volume (102 IQR84.6-115.2 vs. 91 IQR75.2-100.0 mL, P=0.049), NT-proBNP (8.9 IQR5.9-19.7 vs. 5.9 IQR5.9-10.1 µmol/L, P=0.02) and high-sensitive troponin (15.6 IQR13.0-26.1 vs. 13.0 IQR13.0-14.6 ng/L, P=0.007) and a higher prevalence of retinopathy (48 vs. 25 %, p=0.009) and autonomic neuropathy (52 vs. 30.5%, P=0.005).Conclusion A specific LGE pattern with lesions in the basal lateral or the basal inferolateral part of the left ventricle was found in patients with type 2 diabetes.Clinical trial registration: www.clinicaltrials.gov. Unique identifier: NCT02684331.

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Section: Discussionsupporting

confidence: 59%

Distinct non-ischemic myocardial late gadolinium enhancement lesions in patients with type 2 diabetes

Bojer

Sørensen

Vejlstrup

et al. 2020

Preprint

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“…In addition, the presence of LGE and its extent in myocardial tissue relates to overall cardiovascular outcomes (Groves et al, 1989; Duan et al, 2015; Kato et al, 2015; Barbier et al, 2016; Birnie et al, 2016; Liu et al, 2016; Raina et al, 2016). Our team (Liu et al, 2016) reported that the amount of LGE from high-scale threshold on CMR correlated positively with the likelihood for adverse cardiovascular outcomes in patients with end stage C&D heart failure (adjusted hazard ratio, 1.46/10% increase in LGE; P = 0.002).…”

Section: Clinical Diagnostic Methods and Prognostic Significancementioning

confidence: 99%

Current Understanding of the Pathophysiology of Myocardial Fibrosis and Its Quantitative Assessment in Heart Failure

et al. 2017

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Myocardial fibrosis is an important part of cardiac remodeling that leads to heart failure and death. Myocardial fibrosis results from increased myofibroblast activity and excessive extracellular matrix deposition. Various cells and molecules are involved in this process, providing targets for potential drug therapies. Currently, the main detection methods of myocardial fibrosis rely on serum markers, cardiac magnetic resonance imaging, and endomyocardial biopsy. This review summarizes our current knowledge regarding the pathophysiology, quantitative assessment, and novel therapeutic strategies of myocardial fibrosis.

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“…The pathophysiology of HFpEF has been postulated to involve myocardial fibrosis and myocyte hypertrophy, leading to impaired LV filling and decreased diastolic distensibility and stiffness. [34][35][36] The present study utilized a noninvasive diagnostic tool to evaluate coronary flow reserve (phasecontract cine-MRI of the coronary sinus), and this modality might allow more-accurate diagnosis of HFpEF. Distinguishing HFpEF from other etiologies of exertional shortness of breath, such as chronic pulmonary disorders, is of clinical interest.…”

Section: Clinical Implicationmentioning

confidence: 99%

Impairment of Coronary Flow Reserve Evaluated by Phase Contrast Cine‐Magnetic Resonance Imaging in Patients With Heart Failure With Preserved Ejection Fraction

Kato

Saito

Kirigaya

et al. 2016

JAHA

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108

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BackgroundPhase contrast (PC) cine‐magnetic resonance imaging (MRI) of the coronary sinus allows for noninvasive evaluation of coronary flow reserve (CFR), which is an index of left ventricular microvascular function. The objective of this study was to investigate coronary flow reserve in patients with heart failure with preserved ejection fraction (HFpEF).Methods and ResultsWe studied 25 patients with HFpEF (mean and SD of age: 73±7 years), 13 with hypertensive left ventricular hypertrophy (LVH) (67±10 years), and 18 controls (65±15 years). Breath‐hold PC cine‐MRI images of the coronary sinus were obtained to assess blood flow at rest and during ATP infusion. CFR was calculated as coronary sinus blood flow during ATP infusion divided by coronary sinus blood flow at rest. Impairment of CFR was defined as CFR <2.5 according to a previous study. The majority (76%) of HFpEF patients had decreased CFR. CFR was significantly decreased in HFpEF patients in comparison to hypertensive LVH patients and control subjects (CFR: 2.21±0.55 in HFpEF vs 3.05±0.74 in hypertensive LVH, 3.83±0.73 in controls; P<0.001 by 1‐way ANOVA). According to multivariable linear regression analysis, CFR independently and significantly correlated with serum brain natriuretic peptide level (β=−68.0; 95% CI, −116.2 to −19.7; P=0.007).Conclusions CFR was significantly lower in patients with HFpEF than in hypertensive LVH patients and controls. These results indicated that impairment of CFR might be a pathophysiological factor for HFpEF and might be related to HFpEF disease severity.

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Prognostic significance of quantitative assessment of focal myocardial fibrosis in patients with heart failure with preserved ejection fraction

Cited by 61 publications

References 35 publications

Distinct non-ischemic myocardial late gadolinium enhancement lesions in patients with type 2 diabetes

Distinct non-ischemic myocardial late gadolinium enhancement lesions in patients with type 2 diabetes

Current Understanding of the Pathophysiology of Myocardial Fibrosis and Its Quantitative Assessment in Heart Failure

Impairment of Coronary Flow Reserve Evaluated by Phase Contrast Cine‐Magnetic Resonance Imaging in Patients With Heart Failure With Preserved Ejection Fraction

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