Cardiac magnetic resonance (MR) imaging with late gadolinium enhancement (LGE) is used to detect and assess the myocardial damage seen with a variety of cardiomyopathies. Gadolinium-based contrast material accumulates in the expanded interstitial space of the myocardium. Areas with LGE correspond to replacement fibrosis, fibrofatty change, epithelioid granuloma, inflammatory cell infiltration, cardiomyocyte necrosis, and amyloid deposition-conditions that represent a focal increase in interstitial space. Areas without LGE correspond to interstitial or plexiform fibrosis, mildly degenerated cardiomyocytes, inflammatory cell infiltration, and diffuse amyloid deposition-conditions that represent diffuse increases in interstitial space. LGE MR imaging cannot depict these diffuse changes and does not enable quantitative evaluation of this increased interstitial space because on inversion-recovery MR images, the inversion time is adjusted to null the signal from normal-appearing or the least enhancing regions of the myocardium. Thus, the absence of LGE does not always indicate normal myocardial tissue. The use of current T1 mapping techniques enables one to overcome these drawbacks of LGE imaging, detect diffuse myocardial abnormalities, and perform quantitative analysis of the interstitial space. The authors describe the histopathologic and corresponding cardiac MR imaging findings of hypertrophic cardiomyopathy, dilated cardiomyopathy, arrhythmogenic right ventricular cardiomyopathy, cardiac sarcoidosis, giant cell myocarditis, and cardiac amyloidosis-mainly those seen on LGE MR images-as assessed by using whole-heart specimens obtained from autopsy or transplantation. RSNA, 2017.
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.
Identification of the Adamkiewicz artery (AKA) using CT angiography (CTA) is crucial in patients with thoracic aortic aneurysm (TAA) or aortic dissection (AD). The purpose of this study was to compare the AKA detection rate of intravenous injection with a 64-slice MDCT (IV64) versus a 16-slice MDCT (IV16) as well as by CTA using intra-arterial injection with a 16-slice MDCT (IA16). A retrospective review of 160 consecutive patients who underwent CTA was performed. There were 108 TAA and 52 AD cases, 105 of whom were examined with IV64, 15 with IV16, and 40 with IA16. The AKA detectability for each imaging method was assessed, and the factors influencing the detectability were analyzed by multivariate analysis. The detection rates for IV64, IV16, and IA16 were 85.7, 60.0, and 80.0 %, respectively, with IV64 being more sensitive than IV16 (P = 0.025). The detection rate for AD patients was 66.7 % with IV64, which was similar to IV16 (57.1 %) and IA16 (66.8 %). On the other hand, the detection rate for TAA patients was 93.3 % with IV64, which was higher than IV16 (62.5 %, P = 0.021) and similar to IA16 (88.0 %). Multivariate analysis demonstrated the independent factors for AKA detectability were TAA versus AD (P = 0.005, Odds ratio = 3.98) and IV64 versus IV16 (P = 0.037, Odds ratio = 4.03). The detection rate was higher for IV64 than for IV16, especially for TAA patients, while the rate was similar between IV64 and invasive IA16. A 64-slice MDCT thus provides a less invasive visualization of the AKA.
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