ArticleHeart and vessels2016
Late gadolinium enhancement in cardiac amyloidosis: attributable both to interstitial amyloid deposition and subendocardial fibrosis caused by ischemia.
Article in Heart and vessels, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 37 citations in OpenAlex.
- Optimizing TI selection in LGE imaging: pharmacokinetically standardized synthetic LGE and clinical cohort validation of a fixed 400 ms TI for LGE quantification.The international journal of cardiovascular imaging · 2026Article
- Imaging features of wild-type transthyretin amyloid cardiomyopathy in gated and non-gated contrast-enhanced CT.European radiology · 2025Article
- Arrhythmias and Device Therapies in Cardiac Amyloidosis.Journal of clinical medicine · 2024Review
- Arrhythmic Manifestations of Cardiac Amyloidosis: Challenges in Risk Stratification and Clinical Management.Journal of clinical medicine · 2023Review
- Prevalence, incidence and clinical outcomes of epicardial coronary artery disease among transthyretin amyloidosis cardiomyopathy patients.BMC cardiovascular disorders · 2023Article
- The major factor of left ventricular systolic dysfunction in patients with cardiac amyloidosis: Amyloid overload or microcirculation impairment?Frontiers in cardiovascular medicine · 2023Article
- Emerging from the Darkness. Sudden Cardiac Death in Cardiac Amyloidosis.Reviews in cardiovascular medicine · 2022Review
- An Unusual Case of Heart Failure: Sometimes When You Hear Hoof Beats You Should Think of Zebras.Cureus · 2021Article
- Cardiac amyloidosis CT sign.Clinical research in cardiology : official journal of the German Cardiac Society · 2021Article
- Amyloid Deposits and Fibrosis on Left Ventricular Endomyocardial Biopsy Correlate With Extracellular Volume in Cardiac Amyloidosis.Journal of the American Heart Association · 2021Article
- Electrophysiological Manifestations of Cardiac Amyloidosis:JACC. CardioOncology · 2021Review
- Performance ofJournal of nuclear cardiology : official publication of the American Society of Nuclear Cardiology · 2020Article
- Emerging Therapeutics for the Treatment of Light Chain and Transthyretin Amyloidosis.JACC. Basic to translational science · 2019Review
- Right ventricular involvement evaluated by cardiac magnetic resonance imaging predicts mortality in patients with light chain amyloidosis.Heart and vessels · 2018Article
- Regional differences in prognostic value of cardiac valve plane displacement in systemic light-chain amyloidosis.Journal of cardiovascular magnetic resonance : official journal of the Society for Cardiovascular Magnetic Resonance · 2017Article
- Reduced trans-mitral A-wave velocity predicts the presence of wild-type transthyretin amyloidosis in elderly patients with left ventricular hypertrophy.Heart and vessels · 2017Article
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Gadolinium contrast agents used for late gadolinium enhancement (LGE) distribute in the extracellular space. Global diffuse myocardial LGE pronounced in the subendocardial layers is common in cardiac amyloidosis. However, the pathophysiological basis of these findings has not been sufficiently explained. A 64-year-old man was admitted to our hospital with leg edema and nocturnal dyspnea. Bence Jones protein was positive in the urine, and an endomyocardial and skin biopsy showed light-chain (AL) amyloidosis. He died of ventricular fibrillation 3 months later. 9 days before death, the patient was examined by cardiac magnetic resonance (CMR) imaging on a 3-T system. We acquired LGE data at 2, 5, 10, and 20 min after the injection of gadolinium contrast agents, with a fixed inversion time of 350 ms. Myocardial LGE developed sequentially. The myocardium was diffusely enhanced at 2 min, except for the subendocardium, but LGE had extended to almost the entire left ventricle at 5 min and predominantly localized to the subendocardial region at 10 and 20 min. An autopsy revealed massive and diffused amyloid deposits in perimyocytes throughout the myocardium. Old and recent ischemic findings, such as replacement fibrosis and coagulative myocyte necrosis, were evident in the subendocardium. In the intramural coronary arteries, mild amyloid deposits were present within the subepicardial to the mid layer of the left ventricle, but no stenotic lesions were evident. However, capillaries were obstructed by amyloid deposits in the subendocardium. In conclusion, the late phase of dynamic LGE (at 10 and 20 min) visualized in the subendocardium corresponded to the interstitial amyloid deposition and subendocardial fibrosis caused by ischemia in our patient.
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