ライフサイエンスコーパス: myocarditis

1 3 hepatitis, grade 3 pneumonia, and grade 4 myocarditis).

2 sed cardiomyopathy and clinical suspicion of myocarditis.

3 to unravel the role of NOD2 in CVB3-induced myocarditis.

4 agnostic accuracy in patients with suspected myocarditis.

5 bsets of the inflammatory response in murine myocarditis.

6 severe heart failure at HT in children with myocarditis.

7 g cause of death in humans, can emanate from myocarditis.

8 d, consecutive patient cohort with suspected myocarditis.

9 ed 299 patients (0.7%) with the diagnosis of myocarditis.

10 tly different from control animals in severe myocarditis.

11 ra may be a suitable treatment for fulminant myocarditis.

12 id cell compartment, are protective in viral myocarditis.

13 tly between patients with and without active myocarditis.

14 arameters do not sufficiently reflect LGE in myocarditis.

15 teria is used to make the diagnosis of acute myocarditis.

16 hanisms of this important cause of pediatric myocarditis.

17 denoviruses are frequent causes of pediatric myocarditis.

18 standard was the clinical evidence for acute myocarditis.

19 characterized by hypertrophy, fibrosis, and myocarditis.

20 hematical models as they apply to autoimmune myocarditis.

21 oaches in patients suspected of having acute myocarditis.

22 mation and outcome in a mouse model of viral myocarditis.

23 review how autoimmunity is induced in viral myocarditis.

24 and cardiac proteins causes autoimmunity in myocarditis.

25 are frequently needed to diagnose giant-cell myocarditis.

26 of the sarcolemma play a role in CV-mediated myocarditis.

27 1 in cardiomyocytes had reduced CVB3-induced myocarditis.

28 actosylceramide showed significantly reduced myocarditis.

29 tes, qualifying this disease as eosinophilic myocarditis.

30 obal myocardium edema in patients with acute myocarditis.

31 An infection with CVB3 leads to myocarditis.

32 n determine the sexual dimorphism in EAE and myocarditis.

33 on of inflammatory cells in a mouse model of myocarditis.

34 2 (PAR2) in coxsackievirus B3 (CVB3)-induced myocarditis.

35 ardiac inflammation and injury in infectious myocarditis.

36 toreactive T cell responses in two models of myocarditis.

37 ruzi control and protection from fatal acute myocarditis.

38 cruzi infection, a known inducer of lymphoid myocarditis.

39 observed in the subgroup (n=130) with viral myocarditis.

40 characteristic of both human and mouse viral myocarditis.

41 from chronic MI and identification of acute myocarditis.

42 icant therapeutic challenge in patients with myocarditis.

43 is a potential therapeutic target for viral myocarditis.

44 ic T cell responses during subclinical viral myocarditis.

45 unmet need to identify high-risk patients in myocarditis.

46 gnetic resonance to detect and monitor acute myocarditis.

47 nt LGE has been shown to be a risk marker in myocarditis.

48 eir role in Coxsackievirus B3 (CVB3)-induced myocarditis.

49 sk stratification in patients with suspected myocarditis.

50 ts increased susceptibility to virus-induced myocarditis.

51 ands, both TS1 TEM and TN induced late-onset myocarditis.

52 cell epitopes that induce varying degrees of myocarditis.

53 ory response during the pathogenesis of CVB3 myocarditis.

54 ting diagnostic tools for risk assessment in myocarditis.

55 ation (2000-2015) with a listed diagnosis of myocarditis.

56 yocarditis, moderate myocarditis, and severe myocarditis.

57 une responses could be helpful in diagnosing myocarditis.

58 ntly higher need for mechanical ventilation (myocarditis 11% versus NICM 2% versus ICM 4%; P<0.001),

59 tages were found in patients with HCM (16%), myocarditis (15%), and hypertension (14%) but without re

60 iventricular mechanical circulatory support (myocarditis 19% versus NICM 2%, versus ICM 2%; P<0.001),

61 en patients with clinical diagnosis of acute myocarditis (25 years [23-38 years]; 78% males) were pro

62 ur work involved 51 patients with giant cell myocarditis (35 women) aged 52+/-12 years.

63 hy (ICM), myocarditis patients were younger (myocarditis 43.4+/-14.2 years, NICM 49.8+/-12.4 years, a

64 01) and more frequently listed as status 1A (myocarditis 44% versus NICM 21% versus ICM 21%; P<0.001)

65 ), and extracoroporeal membrane oxygenation (myocarditis 5% versus NICM 0.4% versus ICM 1%; P<0.001).

66 , 61-70 ms]) than in patients without active myocarditis (59 ms [Q1-Q3, 55-64 ms]; P<0.01).

67 significantly higher in patients with active myocarditis (65 ms [Q1-Q3, 61-70 ms]) than in patients w

68 Patients with myocarditis (7.7%), postpartum cardiomyopathy (4.4%), an

69 is one of the most prevalent causes of acute myocarditis, a disease that frequently is identified onl

70 on is one of the most common causes of acute myocarditis, a serious and sometimes fatal disease.

71 ibited a reduced viral load and developed no myocarditis after infection with CVB3.

72 diverged depending on the susceptibility to myocarditis after viral infection in mice.

73 cement (LGE) has not been clarified in acute myocarditis (AM) with preserved left ventricular (LV) ej

74 quencing of 42 unrelated children with acute myocarditis (AM), some with proven viral causes.

75 (1) our experience in diagnosing giant-cell myocarditis and (2) the outcome of patients on combined

76 Overall, 137 children with myocarditis and 1249 with idiopathic dilated cardiomyopa

77 We identified 221 children with myocarditis and 1583 with idiopathic dilated cardiomyopa

78 Thirteen patients with acute myocarditis and a control group of seven healthy adults

79 for confirming or rejecting the diagnosis of myocarditis and are superior to the LLC.

80 as accompanied by a profound exacerbation of myocarditis and by a significant increase in mortality a

81 a profound acceleration and exacerbation of myocarditis and by a significant increase in mortality.

82 ropic strain of T. cruzi displayed increased myocarditis and cardiac fibrosis compared to WT controls

83 odel to determine the role of eosinophils in myocarditis and DCMi.

84 tion and prevents the progression to chronic myocarditis and dilated cardiomyopathy (DCM) by inhibiti

85 development of autoimmune coxsackievirus B3 myocarditis and dilated cardiomyopathy in male BALB/c mi

86 years) with a history of biopsy-proven viral myocarditis and drug-refractory VT; 5 patients presented

87 ponses are elevated during acute and chronic myocarditis and have been found to contribute to cardiac

88 to discriminate between patients with acute myocarditis and healthy controls was 86% for T2>52 ms, 7

89 utic strategy in the treatment of autoimmune myocarditis and inflammatory cardiomyopathy.

90 in coxsackievirus B3-induced (CVB3-induced) myocarditis and influenza A infection.

91 c alpha myosin heavy chain (alphaMYHC) cause myocarditis and mice tolerized to alphaMYHC are protecte

92 S100A8 and S100A9 aggravate CVB3-induced myocarditis and might serve as therapeutic targets in in

93 common cause of acute and chronic infectious myocarditis and pancreatitis.

94 single treatments in inhibiting CVB3-induced myocarditis and preventing cardiac dysfunction.

95 te phase is associated with high parasitism, myocarditis and profound myocardial gene expression chan

96 dysplasia/cardiomyopathy in 6 patients, for myocarditis and sarcoidosis in 1 patient each.

97 ally for patchy diseases such as lymphocytic myocarditis and sarcoidosis) using the gold-standard Dal

98 ors promotes CD4+ T-cell-mediated autoimmune myocarditis and subsequent inflammatory cardiomyopathy.

99 ic processes of coxsackievirus-induced viral myocarditis and to screen antiviral therapeutics for eff

100 fies myocardial involvement in patients with myocarditis and TTCM.

101 lysis in 130 adult patients with acute viral myocarditis and viral prodrome within 2 weeks from the o

102 ranging from mild elevation of biomarkers to myocarditis and/or pericarditis.

103 om ITAMY (ITalian multicenter study on Acute MYocarditis) and evaluated CMR results from 386 patients

104 ed heart failure, biventricular failure, and myocarditis), and explore management considerations for

105 cardiomyocytes, limiting viral replication, myocarditis, and death.

106 is groups, including dilated cardiomyopathy, myocarditis, and ischemic and nonischemic cardiomyopathi

107 MB versus MBIso both in moderate and severe myocarditis, and MBCD4 signal correlated with CD4+ T-lym

108 piral load for uncomplicated, renal failure, myocarditis, and multi-organ failure patients were 8616,

109 atients with cardiac sarcoidosis, giant cell myocarditis, and myocarditis associated with connective

110 estinal perforation), one patient because of myocarditis, and one patient because of multiorgan failu

111 of the right subclavian artery, one case of myocarditis, and one pulmonary malignancy with pulmonary

112 lammatory mediator during adenovirus-induced myocarditis, and persistent adenovirus infection may con

113 s were grouped into no myocarditis, moderate myocarditis, and severe myocarditis.

114 s known about the pathogenesis of adenovirus myocarditis, and the species specificity of human adenov

115 ally and robustly in experimental autoimmune myocarditis, and thus allowed for an unprecedented insig

116 e long-term mortality in patients with viral myocarditis, and to establish the prognostic value of va

117 cenarios, such as suspected hypersensitivity myocarditis, anthracycline cardiomyopathy, cardiac tumor

118 ) and SAPS II, whereas immunosuppression and myocarditis as the reason for ECMO support were associat

119 rent standard Lake Louise criteria (LLC) for myocarditis as well as native T1, calculation of extrace

120 diseases caused by picornaviruses, including myocarditis, aseptic meningitis, encephalitis, hepatitis

121 iac sarcoidosis, giant cell myocarditis, and myocarditis associated with connective tissue disorders

122 ldren and adults is often the consequence of myocarditis associated with Coxsackievirus (CV) infectio

123 was significantly elevated in patients with myocarditis at FU0 (2.2 [2.0-2.3] versus 1.6 [1.5-1.7];

124 rarely develop life-threatening acute viral myocarditis (AVM), given that the causal viral infection

125 confirming that NKT cells are protective for myocarditis but pathogenic in the liver.

126 fected C57Bl/6 male mice developed increased myocarditis but reduced hepatic injury compared with inf

127 ositive patients compared with patients with myocarditis but without evidence of persistent CVB3 infe

128 arrhythmias are characteristic of giant cell myocarditis, but their true incidence, predictors, and o

129 re studied after the induction of autoimmune myocarditis by immunization with alpha-myosin-peptide; 2

130 Th2 responses reduce acute myocarditis by inhibiting Th1 responses via regulatory T

131 hat Th1-type immunity protects against acute myocarditis by reducing viral replication and prevents t

132 Myocarditis can cause dilated cardiomyopathy resulting i

133 Studying the pathogenesis of myocarditis caused by different viruses is essential in

134 al biopsies from patients with CVB3-positive myocarditis compared with controls, respectively.

135 pathic) and can be mechanistically caused by myocarditis, conduction abnormalities, focal direct inju

136 ory microRNA-155 is upregulated during acute myocarditis, contributes to the adverse inflammatory res

137 gic encephalomyelitis (EAE) and experimental myocarditis, correlates with the natural variation in co

138 acute cardiac remodeling leading to chronic myocarditis/DCM.

139 of two patients with melanoma in whom fatal myocarditis developed after treatment with ipilimumab an

140 Myocarditis development also required donor bone marrow

141 Finally, patients with myocarditis displayed increased local and systemic HMGB1

142 After adjustment for severity of illness, myocarditis does not confer additional risk for wait-lis

143 with metastatic melanoma who developed fatal myocarditis during ipilimumab and nivolumab combination

144 eutic agent for the treatment of acute viral myocarditis during the viremic phase.

145 s study, we used the experimental autoimmune myocarditis (EAM) model to determine the role of eosinop

146 Experimental autoimmune myocarditis (EAM) was initiated in BALB/c mice by immuni

147 ice developed severe experimental autoimmune myocarditis (EAM), in which mice are immunized with card

148 model of TnI-induced experimental autoimmune myocarditis (EAM), we demonstrated that both local and s

149 Eosinophilic myocarditis (EM) is an acute life-threatening inflammato

150 Patients with giant-cell myocarditis, eosinophilic myocarditis, or cardiac sarcoi

151 her key heart disease-related processes like myocarditis, fibrosis, hypertrophy and arrhythmia.

152 amatic presentation, patients with fulminant myocarditis (FM) might have better outcome than those wi

153 We have developed a mouse model of myocarditis following mouse adenovirus 1 (MAV-1) infecti

154 Viral myocarditis follows a fatal course in approximately 30%

155 Clinical and experimental myocarditis follows microbial infections, but autoimmuni

156 Giant cell myocarditis (GCM) typically causes fulminant heart failu

157 In the myocarditis group, 17% (4 of 23) died of acute rejection

158 Children with lymphocytic myocarditis had better survival and a higher rate of ech

159 Additionally, patients with myocarditis had higher likelihood of delisting for clini

160 pite higher allosensitization, patients with myocarditis had similar post-transplant rejection, retra

161 Myocarditis has also been named inflammatory cardiomyopa

162 Viral myocarditis has been proposed to be divided into 3 phase

163 e, overall mortality from cardiomyopathy and myocarditis has decreased since 2005.

164 he human heart long after the signs of acute myocarditis have abated are still not completely underst

165 series nor clinical trials on this specific myocarditis have been reported.

166 regarding athletic participation after acute myocarditis have heightened the importance of early diag

167 Among children listed for HT, those with myocarditis have more severe heart failure than children

168 d countries, viral infections commonly cause myocarditis; however, in the developing world, rheumatic

169 quired Zika acute infection complicated with myocarditis imported in Mainland France.

170 Endomyocardial biopsy revealed active myocarditis in 16 (52%) of 31 patients.

171 AM-guided biopsy diagnosed ARVC in 11 (46%), myocarditis in 8 (33%), and idiopathic RVOT-VAs in 5 (21

172 demonstrate that ANT1 can induce autoimmune myocarditis in A/J mice by generating autoreactive T cel

173 Necroscopic findings were compatible to myocarditis in both, and immunohistochemistry for dengue

174 provided >90% control of parasite burden and myocarditis in chagasic mice.

175 rus B, which has been linked to diabetes and myocarditis in humans.

176 raction values for assessing the activity of myocarditis in patients with recent-onset heart failure

177 esonance (CMR) techniques to identify active myocarditis in patients with recent-onset heart failure.

178 longs to the genus Cardiovirus and can cause myocarditis in susceptible mouse strains.

179 l inflammation and leukocyte infiltration in myocarditis in the absence of a detectable decline in le

180 n for 147 patients with a diagnosis of acute myocarditis in the Extracorporeal Life Support Organizat

181 ttractive therapeutic approach against viral myocarditis in the future.

182 l cells prevented exacerbation of autoimmune myocarditis in vivo.

183 del will enable fundamental studies of viral myocarditis, including IFN-gamma modulation as a therape

184 Using this novel model for viral myocarditis induced with Theiler's murine encephalomyeli

185 The myocarditis-inducing ability of ANT1 21-40 was associate

186 Eosinophils were dispensable for myocarditis induction but were required for progression

187 Myocarditis is a diverse group of heart-specific immune

188 Myocarditis is a leading cause of sudden cardiac failure

189 Viral myocarditis is a life-threatening illness that may lead

190 Viral myocarditis is among the most common causes of heart fai

191 Myocarditis is an inflammatory disease of the cardiac mu

192 ge of clinical symptoms, biopsy-proven viral myocarditis is associated with a long-term mortality of

193 Diagnosing myocarditis is challenged by nonspecific clinical signs

194 Active myocarditis is characterized by large heterogeneity of c

195 f chronic dilated cardiomyopathy after viral myocarditis is complex and determined by host and viral

196 HT and used Cox models to determine whether myocarditis is independently associated with wait-list m

197 Myocarditis is inflammation of the heart muscle that can

198 RECENT FINDINGS: Acute CVB3 myocarditis is known to be increased by Th1 immune respo

199 A major causative agent for viral myocarditis is the B3 strain of coxsackievirus, a positi

200 The true incidence of myocarditis is unknown to the limited utilization and th

201 rders in which inflammation of the heart (or myocarditis) is the proximate cause of myocardial dysfun

202 Cardiac tests for diagnosing myocarditis lack sensitivity or specificity.

203 ell and lymphocytic infiltrates, lymphocytic myocarditis-like foci, cardiomyocyte necrosis, and cardi

204 rhythmias, ischemia, and pericarditis and/or myocarditis-like syndromes, or they can be chronic, such

205 Patients with the diagnosis of myocarditis listed for orthotopic heart transplantation

206 sample of patients with biopsy-proven active myocarditis, looking for accessible and valid early pred

207 Myocarditis may result from both infectious and noninfec

208 Twenty four patients with acute myocarditis (mean age +/- standard deviation, 34.7 years

209 - 23 ms in HTN subjects; p < 0.05), areas of myocarditis (median 22% LV with T1 >990 ms, as compared

210 uses are significant human pathogens causing myocarditis, meningitis, and encephalitis.

211 l outcomes, including hydrops fetalis, fetal myocarditis, meningoencephalitis, neurodevelopmental del

212 In a CVB3-induced mouse myocarditis model, both components applied individually

213 Animals were grouped into no myocarditis, moderate myocarditis, and severe myocarditi

214 zed granzyme B activity in hearts with acute myocarditis monitored by fluorescent molecular tomograph

215 athies in developed countries is lymphocytic myocarditis most commonly caused by a viral pathogenesis

216 safety end point was incidence of infectious myocarditis, myocardial rupture, neoplasm, hypersensitiv

217 (Magnetic Resonance Imaging in Myocarditis [MyoRacer]; NCT02177630).

218 Patients with acute myocarditis (n=514) were identified from April 2006 to M

219 al diagnosis includes myocardial infarction, myocarditis, neurogenic pulmonary edema, and nonischemic

220 r outcome than those with acute nonfulminant myocarditis (NFM).

221 Pharmacovigilance studies show that myocarditis occurred in 0.27% of patients treated with a

222 onance imaging in only 24% of patients, with myocarditis occurring in 33% and no significant abnormal

223 io 41.5, 95% confidence interval 35.4-48.8), myocarditis (odds ratio 36.6, 95% confidence interval 21

224 Giant-cell myocarditis often escapes diagnosis until autopsy or tra

225 rders and may be beneficial in chronic viral myocarditis once virus is cleared.

226 th T2 and T1 mapping reliably detected acute myocarditis, only T2 mapping discriminated between acute

227 and November 2016 with a diagnosis of acute myocarditis (onset of symptoms <1 month) of whom 55 requ

228 lar dysfunction resulting from KD-associated myocarditis or between patients with and without coronar

229 Patients with myocarditis or dilated cardiomyopathy develop autoantibo

230 larly, myocardial fibrosis in the absence of myocarditis or left ventricular hypertrophy, or other kn

231 Dilated cardiomyopathy (n=27), myocarditis or sarcoidosis (n=22), occult myocardial inf

232 Thirty patients with suspected myocarditis or TTCM, referred for cardiac magnetic reson

233 ts with giant-cell myocarditis, eosinophilic myocarditis, or cardiac sarcoidosis and those <15 years

234 irus B3 (CVB3) is a causative agent of viral myocarditis, pancreatitis, and meningitis in humans.

235 important human causative pathogen for viral myocarditis, pancreatitis, and meningitis, has evolved d

236 hy (NICM) and ischemic cardiomyopathy (ICM), myocarditis patients were younger (myocarditis 43.4+/-14

237 DCMi develops in up to 30% of myocarditis patients, but the mechanisms involved in dis

238 inflammation in all experimental autoimmune myocarditis-positive animals.

239 and endomyocardial biopsy can help identify myocarditis, predict risk of cardiovascular events, and

240 Giant cell myocarditis presented as nonfatal ventricular tachyarrhy

241 Because myocarditis presents with non-specific symptoms includin

242 The severity of myocarditis, prevalence of cardiac myocyte apoptosis, an

243 Twenty-nine patients were examined with a myocarditis protocol (group A), 10 patients with a stres

244 establish a mouse model of human adenovirus myocarditis, providing the means to study host and patho

245 Although most individuals with myocarditis recover spontaneously, some develop chronic

246 es (5, 14%), dilated cardiomyopathy (3, 8%), myocarditis related (3, 8%), aortic dissection (3, 8%),

247 Treatment of viral fulminant myocarditis relies on life support measures.

248 Although the prevalence of myocarditis remained stable between 1990 and 2013 at abo

249 Viral myocarditis remains a prominent infectious-inflammatory

250 y assessment tool in patients with suspected myocarditis remains limited.

251 90% (56%-100%), and 71% (48%-89%) for active myocarditis, respectively.

252 tional and deformation echocardiography, and myocarditis severity graded on histology.

253 tibody asialogangloside GM-1 did not augment myocarditis severity in eosinophil-deficient Deltadouble

254 ) at day 21 correlated with the histological myocarditis severity score.

255 -asialo GM1 antibody significantly increased myocarditis severity, and was accompanied by elevated fi

256 o S100A9 knockout CVB3 mice induced a severe myocarditis similar to wild-type CVB3 mice.

257 Rarer causes of myocarditis such as GCM should be sought in patients who

258 drial proteins can be target autoantigens in myocarditis, supporting the notion that the antigens rel

259 In myocarditis, T2 was 65.2+/-3.2 ms in the involved myocar

260 significantly longer in patients with acute myocarditis than in control subjects (1185.3 msec +/- 49

261 In giant cell myocarditis, the risk of life-threatening ventricular ar

262 arkers are commonly interpreted as resolving myocarditis, this assumption has not been confirmed as o

263 ty signal transducer IRAK4 exacerbates viral myocarditis through inhibition of interferon production

264 comparable symptoms, including inflammatory myocarditis, through chronic activation of the stimulato

265 conclusion, eosinophils drive progression of myocarditis to DCMi, cause severe DCMi when present in l

266 ation can be used effectively in adults with myocarditis to support the circulation while awaiting my

267 ents with histologically verified giant-cell myocarditis treated in our hospital since 1991.

268 Six hundred seventy patients with suspected myocarditis underwent CMR including late gadolinium enha

269 entricular function and clinically suspected myocarditis underwent endomyocardial biopsy and CMR at 1

270 imental cytotoxic CD8+ T lymphocyte-mediated myocarditis using fluorescence reflectance imaging, vali

271 expression was also induced in CVB3-induced myocarditis versus healthy control mice.

272 T-cell responses in experimental autoimmune myocarditis via nitric oxide.

273 Active myocarditis was defined by ongoing inflammation on endom

274 METHODS AND Myocarditis was diagnosed based on clinical presentation

275 nificantly contributes to the development of myocarditis was hypothesized by the first physician-scie

276 Myocarditis was induced after intraperitoneal inoculatio

277 Experimental autoimmune myocarditis was induced in BALB/c mice by immunization w

278 Experimental autoimmune myocarditis was induced in BALB/c mice.

279 ence-based component to prevent CVB3-induced myocarditis was investigated.

280 We found that microRNA-155 expression during myocarditis was localized primarily in infiltrating macr

281 However, in adjusted analysis, myocarditis was not associated with wait-list mortality

282 portance in the pathogenesis of CVB3-induced myocarditis, we aimed to unravel the role of NOD2 in CVB

283 condition for the development of the chronic myocarditis, we hypothesized that CD73 activity may coun

284 ace, smaller left ventricular dimension, and myocarditis were associated with death after transplanta

285 In unadjusted analysis, children with myocarditis were at higher risk of wait-list mortality (

286 2009, 82 patients with biopsy-proven active myocarditis were consecutively enrolled and followed-up

287 Children with myocarditis were more likely to be listed while on assis

288 bacteremia/sepsis, acute renal failure, and myocarditis were rare (each </= 2% of children) but asso

289 his discrepancy was particularly evident for myocarditis, whereas in infiltrative and storage disease

290 s known about the pathogenesis of adenovirus myocarditis, which is a significant impediment to the de

291 Previous studies suggest that children with myocarditis who receive heart transplantation (HT) may b

292 To induce myocarditis, wild-type (wt) and PAR2 knockout (ko) mice

293 fractory cardiac electrical instability, and myocarditis with a robust presence of T-cell and macroph

294 old woman who was hospitalized for fulminant myocarditis with biventricular failure and cardiogenic s

295 Most ChHD patients display diffuse myocarditis with fibrosis and hypertrophy.

296 vival of a consecutive cohort with suspected myocarditis with regard to CMR findings.

297 ophilic IL-5Tg mice resulted in eosinophilic myocarditis with severe ventricular and atrial inflammat

298 n, we treated a patient with fulminant viral myocarditis with the interleukin-1 receptor blocking age

299 Otherwise, myocarditis would commonly follow myocardial infarcts.

300 late heart failure pathogenesis during viral myocarditis, yet their identities and functions remain p