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1 S probable by FDG PET cases were found to be arrhythmogenic cardiomyopathy.
2 iants identified were in genes implicated in arrhythmogenic cardiomyopathy.
3 iomyopathy, hypertrophic cardiomyopathy, and arrhythmogenic cardiomyopathy.
4 therapy on conduction in patients with PKP2 arrhythmogenic cardiomyopathy.
5 M20 cardiomyopathy as a highly penetrant and arrhythmogenic cardiomyopathy.
6 cause loss of junctional Pg is a hallmark of arrhythmogenic cardiomyopathy.
7 excess cardiac fibroadipocytes, as in human arrhythmogenic cardiomyopathy.
8 2 (PKP2), is the most common causal gene for arrhythmogenic cardiomyopathy.
9 and drug screens for effective therapies in arrhythmogenic cardiomyopathy.
10 in is the first sarcomeric protein linked to arrhythmogenic cardiomyopathy.
11 ed phenotype of an early onset biventricular arrhythmogenic cardiomyopathy.
12 es has prompted proposal of the broader term arrhythmogenic cardiomyopathy.
13 ar mechanisms underlying the pathogenesis of arrhythmogenic cardiomyopathy.
14 ci were involved in myocardial structure and arrhythmogenic cardiomyopathy.
15 opathy (DCM), with a high risk of developing arrhythmogenic cardiomyopathy.
16 ause hypertrophic, dilated, restrictive, and arrhythmogenic cardiomyopathies.
17 and the development of high-risk dilated and arrhythmogenic cardiomyopathies.
18 3.5%), whereas other forms were less common: arrhythmogenic cardiomyopathy (7.0%), hypertrophic cardi
20 of titin's spring region is associated with arrhythmogenic cardiomyopathy, a disease characterized b
21 Desmoglein 2 gene (DSG2) mutations cause arrhythmogenic cardiomyopathy (AC) in human and transgen
30 only exhibit both dilated cardiomyopathy and arrhythmogenic cardiomyopathy, accounting for a signific
31 that cause dilated cardiomyopathy (DCM) and arrhythmogenic cardiomyopathy (ACM) convey high risks fo
32 In recent years, it has become evident that arrhythmogenic cardiomyopathy (ACM) displays a wide spec
33 ressive loss of cardiac systolic function in arrhythmogenic cardiomyopathy (ACM) has recently gained
47 in iPSC-cardiac myocytes from patients with arrhythmogenic cardiomyopathy (ACM) under basal conditio
48 ted and acquired cardiomyopathies, including arrhythmogenic cardiomyopathy (ACM), a genetic heart dis
50 ar enlargement and systolic dysfunction; and arrhythmogenic cardiomyopathy (ACM), with right, left, o
53 disorders such as hypertrophic, dilated, and arrhythmogenic cardiomyopathies and hypercholesterolemia
54 milies, including hypertrophic, dilated, and arrhythmogenic cardiomyopathies and inherited arrhythmia
55 cardiomyocytes, are the predominant cause of arrhythmogenic cardiomyopathy and can be identified in a
56 r early cardiac arrhythmias in patients with arrhythmogenic cardiomyopathy and cardiocutaneous syndro
57 is review highlights current knowledge about arrhythmogenic cardiomyopathy and considers clinical, pa
58 ith Naxos disease, which is characterized by arrhythmogenic cardiomyopathy and the cutaneous disorder
59 ht ventricular cardiomyopathy, left-dominant arrhythmogenic cardiomyopathy, and biventricular arrhyth
60 y of long-QT syndrome, Brugada syndrome, and arrhythmogenic cardiomyopathy, and in the study of funct
62 ncompaction, restrictive cardiomyopathy, and arrhythmogenic cardiomyopathy, are discussed in less det
66 as sarcomeric, force generation disease; and arrhythmogenic cardiomyopathy as desmosome, cell junctio
67 Cardiomyocyte ILK deletion produces a lethal arrhythmogenic cardiomyopathy associated with important
68 NC (FLNC(LOF)) would have increased odds for arrhythmogenic cardiomyopathy-associated phenotypes vers
70 rdium has revealed mechanistic insights into arrhythmogenic cardiomyopathy but cardiac samples are di
71 spectrum of phenotypic manifestations within arrhythmogenic cardiomyopathy, but data on genotype-spec
72 Inherited primary arrhythmia syndromes and arrhythmogenic cardiomyopathies can lead to sudden cardi
73 inally hailed as a putative gold standard in arrhythmogenic cardiomyopathy, cardiovascular magnetic r
75 pping phenotype of dilated and left-dominant arrhythmogenic cardiomyopathies complicated by frequent
78 C-derived cardiomyocytes from a patient with arrhythmogenic cardiomyopathy due to mutations in the de
80 anish family with inherited left ventricular arrhythmogenic cardiomyopathy/dysplasia and a high incid
81 nts presented data consistent with inherited arrhythmogenic cardiomyopathy/dysplasia phenotype with v
82 auses predominant inherited left ventricular arrhythmogenic cardiomyopathy/dysplasia with a high inci
83 histochemistry was compatible with inherited arrhythmogenic cardiomyopathy/dysplasia, and the functio
87 yopathy in the right ventricle, the scope of arrhythmogenic cardiomyopathy has broadened to include t
88 indicates that ventricular myocytes in PKP2 arrhythmogenic cardiomyopathy have greatly reduced elect
89 esmoplakin (DSPtv) are an important cause of arrhythmogenic cardiomyopathy; however the genetic archi
90 In contrast, pathogenic mutations that cause arrhythmogenic cardiomyopathies in patients significantl
91 magnetic resonance assessment include proven arrhythmogenic cardiomyopathy in the family, unexplained
92 mias are well-recognized as presentation for arrhythmogenic cardiomyopathy in the right ventricle, th
94 e in ARVC (Heart Rhythm Society consensus on arrhythmogenic cardiomyopathy, International Task Force
95 ALVC) is an under-characterized phenotype of arrhythmogenic cardiomyopathy involving the LV ab initio
104 d with the development of a distinct form of arrhythmogenic cardiomyopathy known as DSP cardiomyopath
106 tion) and nonischemic (previous myocarditis, arrhythmogenic cardiomyopathy, lipomatous hypertrophy of
107 These include hypertrophic cardiomyopathy, arrhythmogenic cardiomyopathy, long QT syndrome, Brugada
108 anding of the pathogenesis of this aspect of arrhythmogenic cardiomyopathy may shed light onto the ba
109 were detected in 163 cases (22%), including arrhythmogenic cardiomyopathy (n = 36; 5%), hypertrophic
110 5% CI, 1.1-5.6]; P=0.048), and left-dominant arrhythmogenic cardiomyopathy (odds ratio, 4.2 [95% CI,
111 human PKP2 associate with a life-threatening arrhythmogenic cardiomyopathy, often of right ventricula
112 nderstanding of the pathogenic mechanisms of arrhythmogenic cardiomyopathy over the past decade have
114 both of which are presumably present in PKP2 arrhythmogenic cardiomyopathy patients undergoing gene t
115 kedly diminished in buccal mucosa cells from arrhythmogenic cardiomyopathy patients with known desmos
116 ssociated with the development of a distinct arrhythmogenic cardiomyopathy phenotype not fully captur
119 [IQR: 15.8-44.4 years]) from the Netherlands Arrhythmogenic Cardiomyopathy Registry without definite
120 DSP cardiomyopathy is a distinct subset of arrhythmogenic cardiomyopathy, reported primarily in adu
121 on of Jup in cardiomyocytes in mice leads to arrhythmogenic cardiomyopathy similar to Naxos disease i
123 ythmogenic cardiomyopathy, and biventricular arrhythmogenic cardiomyopathy were examined in this stud
124 lar junction proteins are the major cause of arrhythmogenic cardiomyopathy, whereas recessive mutatio
125 ntly garnered attention as a likely cause of arrhythmogenic cardiomyopathy, which is considered an ac
126 re responsible for a subset of patients with arrhythmogenic cardiomyopathy who exhibit cardiac arrhyt