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1 ied (1.3 [0.49 mm(2)] vs. 1.0 [0.40 mm(2)]), fibrofatty (0.23 [0.15 mm(2)] vs. 0.11 [0.087 mm(2)]), a
2 [32.2] mm3 vs 5.6 [28.5] mm3; P = .002), and fibrofatty and necrotic core plaque volume (mean [SD], 4
6 6 sections each from 25 hearts with typical (fibrofatty) ARVC, 7 hearts with fat replacement of the r
7 ted with noncalcified (B = 0.28; P < 0.001), fibrofatty (B = 0.49; P < 0.001), and lipid-rich necroti
8 with noncalcified (beta = 0.28; P < 0.001), fibrofatty (beta = 0.49; P < 0.001), and lipid-rich necr
9 characterize plaque broadly as calcified or fibrofatty but was limited in its ability to more precis
10 cintigraphy, and finally, attenuation of the fibrofatty changes of the skin, the final consequences o
11 ed myocyte apoptosis in skeletal muscle; and fibrofatty connective tissue proliferation around joints
12 population, the mean percentage of fibrous, fibrofatty, dense calcified, and necrotic core plaques i
14 m RyR2(R176Q/+) mice revealed no evidence of fibrofatty infiltration or structural abnormalities char
16 Among whole hearts, the most common areas of fibrofatty infiltration were the left ventricular poster
17 als additional pathogenic potential, causing fibrofatty infiltration within the myocardium and drivin
20 se distinguished by endothelial dysfunction, fibrofatty material accumulation in the intima of the ar
22 acking is associated with the severity of LA fibrofatty myocardial remodeling at histologic analysis.
23 ion was found between PLAS and the degree of fibrofatty myocardial replacement at histologic analysis
25 plaque (median 76.1 vs 31.1, P = .003), and fibrofatty plaque (median 63.6 vs 27.6, P < .001) volume
26 ), mesenteric signs such as hyperemia (n=9), fibrofatty proliferation (n=8) and lymphadenopathy (n=28
30 muscle disorder characterized by myocardial fibrofatty replacement and an increased risk of sudden c
31 myopathy, characterized by right ventricular fibrofatty replacement and arrhythmias, causes sudden de
36 athy (ARVD/C) is a disorder characterized by fibrofatty replacement of cardiac myocytes that typicall
38 eritable myocardial disorder associated with fibrofatty replacement of myocardium and ventricular arr
39 lial arrhythmogenic disease characterized by fibrofatty replacement of myocytes with scattered foci o
40 ar cardiomyopathy (ARVC) is characterized by fibrofatty replacement of primarily the right ventricula
41 ogical features include loss of myocytes and fibrofatty replacement of right ventricular myocardium;
43 genetic myocardial disease characterized by fibrofatty replacement of the myocardium and a predispos
44 is a rare inherited disease characterized by fibrofatty replacement of the myocardium, associated wit
45 n inherited cardiac disease characterized by fibrofatty replacement of the myocardium, resulting in h
46 ized by dilation of the cardiac chambers and fibrofatty replacement of the myocardium, which results
47 rdiomyopathy characterized pathologically by fibrofatty replacement primarily of the RV and clinicall
48 lleviated the phenotypic ACM features (i.e., fibrofatty replacement, contractile dysfunction, and ven
52 ht ventricle, subepicardial left ventricular fibrofatty replacements (64%), myocyte atrophy (96%), an
55 nvolution were telangiectasias (145, 84.3%), fibrofatty tissue (81, 47.1%), and anetodermic skin (56,
56 osition in CAV may include early fibrous and fibrofatty tissue and late atheromatous calcification.
57 ncluding fibre size variability, presence of fibrofatty tissue of varying severity, without specific
58 r disorder characterized by myocyte loss and fibrofatty tissue replacement of the right ventricle.
59 d by progressive loss of cardiomyocytes with fibrofatty tissue replacement, systolic dysfunction, and
61 lcium progression, regression of fibrous and fibrofatty tissue, and excessive expansive remodeling, s