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1 myopathies, including heart muscle diseases (cardiomyopathy).
2 l leads to myocyte instability and a dilated cardiomyopathy.
3 Erk5 expression in Erk5-CKO hearts prevents cardiomyopathy.
4 on the genetic basis of this rare and morbid cardiomyopathy.
5 hypertrophy and in human hearts with dilated cardiomyopathy.
6 e have been linked to muscular dystrophy and cardiomyopathy.
7 umulative variant hypothesis in hypertrophic cardiomyopathy.
8 icion of genetically determined hypertrophic cardiomyopathy.
9 ncluding pulmonary arterial hypertension and cardiomyopathy.
10 cause mortality in patients with nonischemic cardiomyopathy.
11 a candidate gene for muscular dystrophy and cardiomyopathy.
12 ze and improves cardiac function in ischemic cardiomyopathy.
13 d LVNC in the absence of a family history of cardiomyopathy.
14 hythmias in patients with idiopathic dilated cardiomyopathy.
15 ntically delivered in patients with ischemic cardiomyopathy.
16 ce, including specifically those with atrial cardiomyopathy.
17 underpins the lasting and severe effects of cardiomyopathy.
18 cle (LV) ultimately transitions to a dilated cardiomyopathy.
19 arrhythmogenesis and remodeling, leading to cardiomyopathy.
20 unctional Pg is a hallmark of arrhythmogenic cardiomyopathy.
21 c remodeling from ARVC and post-inflammatory cardiomyopathy.
22 decades as a reversible form of nonischemic cardiomyopathy.
23 revention ICDs) in patients with nonischemic cardiomyopathy.
24 t MSCs (itMSCs) in patients with nonischemic cardiomyopathy.
25 latives, and 9 with noncompaction or dilated cardiomyopathy.
26 evaluation of all patients with hypertrophic cardiomyopathy.
27 behavior in an animal model of hypertrophic cardiomyopathy.
28 may increase risk for human arrhythmias and cardiomyopathy.
29 rate of children with chronic HF and dilated cardiomyopathy.
30 B species were found in type 1 diabetes and cardiomyopathy.
31 utic solutions to treat CVD such as ischemic cardiomyopathy.
32 l) in at least 100 patients with nonischemic cardiomyopathy.
33 se mortality among patients with nonischemic cardiomyopathy.
34 VCL knockout mice prior to the appearance of cardiomyopathy.
35 ly prevented the development of hypertrophic cardiomyopathy.
36 as Chagasic, other nonischemic, or ischemic cardiomyopathy.
37 fibroadipocytes, as in human arrhythmogenic cardiomyopathy.
38 imal models of both AMI and chronic ischemic cardiomyopathy.
39 nvolved in the development of HIV-associated cardiomyopathy.
40 that leads to chronic remodeling and dilated cardiomyopathy.
41 m for mitochondrial dysfunction in lipotoxic cardiomyopathy.
42 isease mimicking nonobstructive hypertrophic cardiomyopathy.
43 and none to arrhythmogenic right ventricular cardiomyopathy.
44 d cDKOs), which develops adult-onset dilated cardiomyopathy.
45 matic PVCs, and 29 (4.7%) had IVA-associated cardiomyopathy.
46 ontribute to the pathophysiology of diabetic cardiomyopathy.
47 dense regions of myocardium, in postinfarct cardiomyopathy.
48 serve as therapeutic targets in inflammatory cardiomyopathies.
49 c remodeling from ARVC and post-inflammatory cardiomyopathies.
50 omes of patients with ischemic or idiopathic cardiomyopathies.
51 idemiology, cause, and outcomes of pediatric cardiomyopathies.
52 ted in about one-third of idiopathic dilated cardiomyopathies.
53 oing cardiac transplantation are affected by cardiomyopathies.
54 pathogenesis and pathobiology of individual cardiomyopathies.
55 his gene as an important cause of structural cardiomyopathies.
56 s are the leading cause of inherited primary cardiomyopathies.
57 mpared with those with LVNC and co-occurring cardiomyopathy (0% versus 12%, respectively; P<0.01).
65 mous LMNA VUS, demonstrated segregation with cardiomyopathy affection status and altered cardiac LMNA
66 its are characteristic of the desmin-related cardiomyopathies and crystallin cardiomyopathic diseases
72 s were used to examine a family with dilated cardiomyopathy and atrial and ventricular arrhythmias.
75 obtained from patients with newly diagnosed cardiomyopathy and clinical suspicion of myocarditis.
78 elopmental delay, failure to thrive, dilated cardiomyopathy and epilepsy, ultimately leading to death
80 esponsiveness in a model of familial dilated cardiomyopathy and improve cardiac function and morpholo
81 mmation in patients with nonischemic dilated cardiomyopathy and inflammatory cardiomyopathy (iCMP).
84 dverse outcome in patients with hypertrophic cardiomyopathy and may help to optimize risk stratificat
85 stability encountered in muscle diseases and cardiomyopathy and may underlie potential target treatme
87 , two deaths were attributed to hypertrophic cardiomyopathy and none to arrhythmogenic right ventricu
89 Regular surveillance and early treatment for cardiomyopathy and respiratory muscle weakness is advoca
90 umab 100 mg group; the patient had alcoholic cardiomyopathy and steatohepatitis, and adjudication was
92 abradine in paediatric patients with dilated cardiomyopathy and symptomatic chronic heart failure fro
94 n contributes to the pathophysiology of LMNA cardiomyopathy and that drugs activating beta-catenin ma
96 37 patients with prior (>12-month) takotsubo cardiomyopathy, and 37 age-, sex-, and comorbidity-match
97 ction occurs in 20% of children with dilated cardiomyopathy, and 40% die or undergo transplantation.
100 ted with fatal infantile lactic acidosis and cardiomyopathy, and was found to have profoundly decreas
104 uble mutations in patients with hypertrophic cardiomyopathy are much less common than previously esti
105 uble mutations in patients with hypertrophic cardiomyopathy are not rare and are associated with a mo
110 They review evidence implicating atrial cardiomyopathy as an independent contributor to the risk
111 nonsynonymous or splice-site variations in 6 cardiomyopathy-associated genes (BAG3, DSP, PKP2, RYR2,
113 ycardia syndromes) should also be considered cardiomyopathies because of electric myocyte dysfunction
114 variants are misinterpreted as hypertrophic cardiomyopathy because of the lack of extracardiac organ
115 S identified variants in genes implicated in cardiomyopathy but not included in prior panel testing:
116 ts cause hypertrophic (HCM) or dilated (DCM) cardiomyopathy by disrupting sarcomere contraction and r
117 endent cardiac phenotypes, including dilated cardiomyopathy, cardiac conduction disturbance, atrial f
122 e also propose potential mechanisms by which cardiomyopathy-causing mutations may lead to proteasome
123 The regulation is putatively impaired by cardiomyopathy-causing mutations that affect the intramo
124 nfected patients will develop chronic Chagas cardiomyopathy (CCC), an inflammatory cardiomyopathy cha
125 ost frequently occurred because hypertrophic cardiomyopathy centers had access to different privately
126 in variant classification among hypertrophic cardiomyopathy centers is largely attributable to privat
128 Chagas cardiomyopathy (CCC), an inflammatory cardiomyopathy characterized by hypertrophy, fibrosis, a
129 Restrictive cardiomyopathy (RCM) is a rare cardiomyopathy characterized by impaired diastolic ventr
130 5.98-66.97; P=0.02) and improved Kansas City Cardiomyopathy clinical summary (+5.22, 95% confidence i
131 3 ATTR-ACT study (Tafamidis in Transthyretin Cardiomyopathy Clinical Trial), an international, multic
135 them with samples from patients with dilated cardiomyopathy (DCM) and inflammatory cardiomyopathy (IC
141 trophic cardiomyopathy (HCM) and two dilated cardiomyopathy (DCM) mutants were studied by biochemical
143 Peripartum cardiomyopathy (PPCM) and dilated cardiomyopathy (DCM) show similarities in clinical prese
150 ty control, we used a mouse model of dilated cardiomyopathy driven by cardiac restricted overexpressi
151 evalence in arrhythmogenic right ventricular cardiomyopathy/dysplasia (ARVC/D) varies depending on st
152 th inherited left ventricular arrhythmogenic cardiomyopathy/dysplasia and a high incidence of adverse
153 h inherited arrhythmogenic right ventricular cardiomyopathy/dysplasia, although their cellular and mo
155 at are significantly associated with dilated cardiomyopathy (false discovery corrected P</=0.05), wit
156 e survival of children with familial dilated cardiomyopathy (FDCM) to that of children with idiopathi
157 m cells (hMSCs) have been tested in ischemic cardiomyopathy, few studies exist in chronic nonischemic
158 erter defibrillator in patients with dilated cardiomyopathy for the primary prevention of sudden card
160 These data do not suggest an indication for cardiomyopathy gene panel testing in individuals with is
162 th LVNC, we sought to determine the yield of cardiomyopathy gene panel testing, distinguish the yield
165 t an evaluation of cardiac channelopathy and cardiomyopathy genes in a large, demographically diverse
166 nd surveillance of cardiac channelopathy and cardiomyopathy genes represents the latest molecular aut
167 olecular autopsy for electrical disorder and cardiomyopathy genes, using ACMG guidelines for variant
169 athy who had undergone targeted hypertrophic cardiomyopathy genetic testing (either multigene panel o
170 may prove to reduce stroke risk from atrial cardiomyopathy given its parallels to atrial fibrillatio
171 um biomarkers, patients with prior takotsubo cardiomyopathy had impaired cardiac deformation indices
172 ractory symptoms of obstructive hypertrophic cardiomyopathy has long been debated and is primarily ce
177 tations in the TNT1 region, six hypertrophic cardiomyopathy (HCM) and two dilated cardiomyopathy (DCM
182 Yield of causative variants in hypertrophic cardiomyopathy (HCM) is increased in some probands, sugg
184 common sustained arrhythmia in hypertrophic cardiomyopathy (HCM), is capable of producing symptoms t
185 on, which is exhibited in human hypertrophic cardiomyopathy (HCM), to investigate the influence of HC
188 Proteasome impairment has been detected in cardiomyopathies, heart failure, myocardial ischaemia, a
189 s more at risk of ischemic heart disease and cardiomyopathy/heart failure death, respectively, than e
190 ), 10 patients with hypertrophic obstructive cardiomyopathy (HOCM), 10 patients with aortic valve ste
191 rter defibrillator (ICD) therapy in ischemic cardiomyopathy (ICM) and nonischemic cardiomyopathy (NIC
195 to that of children with idiopathic dilated cardiomyopathy (IDCM) has produced conflicting results.
198 atients developing neurological deficits and cardiomyopathy in the long-term, among other complicatio
199 rare variants in patients with hypertrophic cardiomyopathy in the setting of comprehensive and targe
200 myopathy, ischemic heart disease, or dilated cardiomyopathy, in comparison to nonfailing hearts.
201 advances were achieved in the nosography of cardiomyopathies, influencing the definition and taxonom
204 The new catchphrase in the evaluation of cardiomyopathies is multimodality imaging, which is purp
210 commendations for patients with hypertrophic cardiomyopathy is challenging because of concern about t
214 in viral RNA replication.IMPORTANCE Dilated cardiomyopathy is the most common indication for heart t
217 n are reported in patients with hypertrophic cardiomyopathy, ischemic heart disease, diabetes mellitu
218 on of genes with altered abundance in septic cardiomyopathy, ischemic heart disease, or dilated cardi
219 ed evolution of a sarcomeric to infiltrative cardiomyopathy, leading to an ominous outcome in which t
220 , those with DM had higher rates of ischemic cardiomyopathy, LVAD implantation as destination therapy
223 c & Translational Research, Cardiac Failure, Cardiomyopathies/Myocardial & Pericardial Diseases, Cong
224 schemic cardiomyopathy (ICM) and nonischemic cardiomyopathy (NICM) patients and to evaluate 4 LGE bor
228 d with progressive external ophthalmoplegia, cardiomyopathy, nonsyndromic intellectual disability, ap
229 ommon; restrictive, noncompaction, and mixed cardiomyopathies occur infrequently; and arrhythmogenic
232 ciate with a life-threatening arrhythmogenic cardiomyopathy, often of right ventricular predominance.
233 sarcomere hypercontractility of hypertrophic cardiomyopathy, one of the most prevalent heritable card
235 ETHODS AND Clinical data of all hypertrophic cardiomyopathy patients with 2 rare genetic variants wer
236 eter to predict new-onset AF in hypertrophic cardiomyopathy patients with LA diameter <45 mm, which t
240 ur findings demonstrate that after takotsubo cardiomyopathy, patients develop a persistent, long-term
241 e each important determinants of the dilated cardiomyopathy phenotype and are controlled by genetic f
243 an occur in isolation or can co-occur with a cardiomyopathy phenotype or cardiovascular malformation.
244 among patients with dilated and restrictive cardiomyopathies, pointed to this gene as an important c
247 isk factor for the development of peripartum cardiomyopathy (PPCM), but it is unknown whether preecla
249 ed on 358 consecutive genotyped hypertrophic cardiomyopathy probands at 5 tertiary hypertrophic cardi
250 changes preceded the onset of iron overload cardiomyopathy, providing an early biomarker of disease
251 h, 1 year, and 2 years using the Kansas City Cardiomyopathy Questionnaire (KCCQ) (23 items covering p
252 uality-of-life measurements, the Kansas City Cardiomyopathy Questionnaire (KCCQ) overall summary and
253 and health status as assessed by Kansas City Cardiomyopathy Questionnaire (KCCQ, range 0-100, higher
254 ducation (P<0.01), including the Kansas City Cardiomyopathy Questionnaire (P=0.009), depressive sympt
255 and 1 year after TAVR using the Kansas City Cardiomyopathy Questionnaire overall summary (KCCQ-OS) s
257 EQ-5D-3L visual analog scale and Kansas City Cardiomyopathy Questionnaire-12 summary scores pre-impla
261 METHODS AND Thirty patients with ischemic cardiomyopathy received in a blinded manner either 20 mi
266 ients clinically diagnosed with hypertrophic cardiomyopathy resulted in identification of 8 individua
268 young white adults raises the possibility of cardiomyopathy, specifically arrhythmogenic right ventri
270 ntric hypertrophy does progress to a dilated cardiomyopathy, such a transition would occur over a muc
271 2P/H222P mouse, a small animal model of LMNA cardiomyopathy, suggested decreased WNT/beta-catenin sig
272 pression differs between adult and pediatric cardiomyopathies, suggesting that treatment response may
273 a patient suffering from idiopathic dilated cardiomyopathy, suggesting that such mutant viruses may
274 Tachycardiomyopathy or tachycardia-induced cardiomyopathy (TCM) has been known for decades as a rev
275 pe gene SYNE1 in a child with severe dilated cardiomyopathy that underwent transplant, as well as in
276 emic cardiomyopathy, 150 nonischemic dilated cardiomyopathy), the mean left ventricular ejection frac
277 ential for treating metabolic stress-induced cardiomyopathy.The mechanistic link between metabolic st
278 in mice with large infarcts, and in ischemic cardiomyopathy, they improve LV function, effects appare
279 cts the peripheral nerves, and transthyretin cardiomyopathy (TTR-CM), which primarily affects the hea
282 tients with ischemic or non-ischemic dilated cardiomyopathy undergoing prophylactic ICD implantation
285 , traditionally associated with hypertrophic cardiomyopathy, was the commonest pattern of ventricular
286 echanism driving the development of diabetic cardiomyopathy, we studied a unique model of T2DM: lipod
287 variants in genes associated with inherited cardiomyopathies were significantly enriched in AM-AVM p
288 lterations in messenger RNA levels in septic cardiomyopathy were both distinct from and more profound
289 >/=2) variants in patients with hypertrophic cardiomyopathy were described 10 years ago with a preval
290 evels in explanted human hearts with dilated cardiomyopathy were elevated despite ACE inhibition with
293 Gottingen swine with experimental ischemic cardiomyopathy were randomized to receive transendocardi
296 this review, left ventricular noncompaction cardiomyopathy, which is often caused by mutations in sa
297 ODS AND Forty-one patients with hypertrophic cardiomyopathy who had undergone targeted hypertrophic c
300 ggest UPS dysfunction is a common feature of cardiomyopathies, with an emphasis on hypertrophic cardi
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