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1 3 hepatitis, grade 3 pneumonia, and grade 4 myocarditis).
2 cohol, pericarditis, pulmonary embolism, and myocarditis).
3 creasing occurrence of high-risk ICI-related myocarditis.
4 eroids and discontinuation of ICIs in severe myocarditis.
5 dysfunction in mice with acute CVB3-induced myocarditis.
6 that it may be a target for the treatment of myocarditis.
7 me of immune checkpoint inhibitor-associated myocarditis.
8 it for recurrent VT after the acute phase of myocarditis.
9 mune-mediated myocardial injury described as myocarditis.
10 in cardiac tissue of patients and mice with myocarditis.
11 is dispensable for the development of acute myocarditis.
12 lated cardiomyopathy is frequently caused by myocarditis.
13 selecting features enabling the diagnosis of myocarditis.
14 cute respiratory distress syndrome and 3 had myocarditis.
15 ) imaging is commonly used to diagnose acute myocarditis.
16 sed cardiomyopathy and clinical suspicion of myocarditis.
17 unmet need to identify high-risk patients in myocarditis.
18 ands, both TS1 TEM and TN induced late-onset myocarditis.
19 respiratory distress syndrome and fulminant myocarditis.
20 to unravel the role of NOD2 in CVB3-induced myocarditis.
21 arameters do not sufficiently reflect LGE in myocarditis.
22 teria is used to make the diagnosis of acute myocarditis.
23 characterized by hypertrophy, fibrosis, and myocarditis.
24 observed in the subgroup (n=130) with viral myocarditis.
25 ic T cell responses during subclinical viral myocarditis.
26 r a spectrum of pathogenesis including viral myocarditis.
27 gnetic resonance to detect and monitor acute myocarditis.
28 nt LGE has been shown to be a risk marker in myocarditis.
29 eir role in Coxsackievirus B3 (CVB3)-induced myocarditis.
30 sk stratification in patients with suspected myocarditis.
31 ts increased susceptibility to virus-induced myocarditis.
32 , to investigate viruses in 33 patients with myocarditis.
33 cell epitopes that induce varying degrees of myocarditis.
34 ory response during the pathogenesis of CVB3 myocarditis.
35 ting diagnostic tools for risk assessment in myocarditis.
36 ation (2000-2015) with a listed diagnosis of myocarditis.
37 yocarditis, moderate myocarditis, and severe myocarditis.
38 une responses could be helpful in diagnosing myocarditis.
39 agnostic accuracy in patients with suspected myocarditis.
40 rdiomyocytes and pericytes, leading to viral myocarditis.
41 bsets of the inflammatory response in murine myocarditis.
42 severe heart failure at HT in children with myocarditis.
43 g cause of death in humans, can emanate from myocarditis.
44 d, consecutive patient cohort with suspected myocarditis.
45 ed 299 patients (0.7%) with the diagnosis of myocarditis.
46 tly different from control animals in severe myocarditis.
47 ra may be a suitable treatment for fulminant myocarditis.
48 id cell compartment, are protective in viral myocarditis.
49 tly between patients with and without active myocarditis.
50 iagnosed initially as cardiac sarcoidosis or myocarditis.
51 itis, colitis, hypophysitis, thyroiditis, or myocarditis.
52 wed high accuracy for the diagnosis of acute myocarditis.
53 mia recurrences in a cohort of patients with myocarditis.
54 focus on virus-induced and virus-associated myocarditis.
55 ced T1 shortening for the diagnosis of acute myocarditis.
56 ted viral sequences in up to 67% of cases of myocarditis.
57 antibodies (AIDAs) are autoimmune markers in myocarditis.
58 with cardiac events among patients with ICI myocarditis.
59 ) had GCM and 4 patients (13%) had fulminant myocarditis.
60 ic and regular VA are associated with healed myocarditis.
61 There are no data on the use of GLS in ICI myocarditis.
62 GCM or in blood samples from other types of myocarditis.
63 imental TnI-AM and in 2 cases of ICI-related myocarditis.
64 r 12 months in patients with suspected acute myocarditis.
65 ntly higher need for mechanical ventilation (myocarditis 11% versus NICM 2% versus ICM 4%; P<0.001),
66 Conclusion: In a rat model of autoimmune myocarditis, (18)F-FOL shows specific uptake in inflamed
67 iventricular mechanical circulatory support (myocarditis 19% versus NICM 2%, versus ICM 2%; P<0.001),
68 en patients with clinical diagnosis of acute myocarditis (25 years [23-38 years]; 78% males) were pro
70 hy (ICM), myocarditis patients were younger (myocarditis 43.4+/-14.2 years, NICM 49.8+/-12.4 years, a
71 01) and more frequently listed as status 1A (myocarditis 44% versus NICM 21% versus ICM 21%; P<0.001)
72 ), and extracoroporeal membrane oxygenation (myocarditis 5% versus NICM 0.4% versus ICM 1%; P<0.001).
75 significantly higher in patients with active myocarditis (65 ms [Q1-Q3, 61-70 ms]) than in patients w
77 ved vasopressor support, 53% had evidence of myocarditis, 80% were admitted to an intensive care unit
78 ead human diseases, including poliomyelitis, myocarditis, acute flaccid myelitis and the common cold.
82 cement (LGE) has not been clarified in acute myocarditis (AM) with preserved left ventricular (LV) ej
89 B-viruses (CVB) are frequent causes of acute myocarditis and dilated cardiomyopathy, but an effective
90 arditis, which can be a precursor of chronic myocarditis and dilated cardiomyopathy, leading causes o
91 tantially contributes to the pathogenesis of myocarditis and drives cardiac inflammation, probably vi
92 to discriminate between patients with acute myocarditis and healthy controls was 86% for T2>52 ms, 7
93 bits the development of chronic CVB3-induced myocarditis and improves the cardiac function to a level
94 the pathogenesis, diagnosis and treatment of myocarditis and inflammatory cardiomyopathy, with a spec
96 e role of histology that defines subtypes of myocarditis and its prognostic and therapeutic implicati
98 nosis of acute or chronic heart failure-like myocarditis and might be superior to Lake Louise criteri
99 S100A8 and S100A9 aggravate CVB3-induced myocarditis and might serve as therapeutic targets in in
101 te phase is associated with high parasitism, myocarditis and profound myocardial gene expression chan
102 ally for patchy diseases such as lymphocytic myocarditis and sarcoidosis) using the gold-standard Dal
103 myocarditis, and Stevens-Johnson syndrome); myocarditis and Stevens-Johnson syndrome were considered
104 cardial inflammation in rats with autoimmune myocarditis and studied the expression of FR-beta in hum
105 NCT02177630) with clinical suspicion for myocarditis and symptoms of heart failure were prospecti
106 ntricular ejection fraction 49 +/- 14%) with myocarditis and VA at index hospitalization, including v
107 lysis in 130 adult patients with acute viral myocarditis and viral prodrome within 2 weeks from the o
109 om ITAMY (ITalian multicenter study on Acute MYocarditis) and evaluated CMR results from 386 patients
110 ary (arrhythmias, myocardial infarction, and myocarditis) and secondary (myocardial injury/biomarker
114 is groups, including dilated cardiomyopathy, myocarditis, and ischemic and nonischemic cardiomyopathi
115 MB versus MBIso both in moderate and severe myocarditis, and MBCD4 signal correlated with CD4+ T-lym
116 atients with cardiac sarcoidosis, giant cell myocarditis, and myocarditis associated with connective
117 of Kawasaki's disease, toxic shock syndrome, myocarditis, and potential MIS-C in hospitalized patient
118 festations include encephalitis, meningitis, myocarditis, and sepsis, which can lead to serious neuro
121 e each of unknown cause, neutropenic sepsis, myocarditis, and Stevens-Johnson syndrome); myocarditis
122 lications including acute myocardial injury, myocarditis, arrhythmias, and venous thromboembolism.
123 rent standard Lake Louise criteria (LLC) for myocarditis as well as native T1, calculation of extrace
124 iac sarcoidosis, giant cell myocarditis, and myocarditis associated with connective tissue disorders
125 ods for detection and risk stratification of myocarditis associated with immune checkpoint inhibitors
127 was significantly elevated in patients with myocarditis at FU0 (2.2 [2.0-2.3] versus 1.6 [1.5-1.7];
128 rarely develop life-threatening acute viral myocarditis (AVM), given that the causal viral infection
131 ed that NMRI mice develop pronounced chronic myocarditis between day 18 and day 28 after infection wi
132 ositive patients compared with patients with myocarditis but without evidence of persistent CVB3 infe
133 arrhythmias are characteristic of giant cell myocarditis, but their true incidence, predictors, and o
134 re studied after the induction of autoimmune myocarditis by immunization with alpha-myosin-peptide; 2
137 & Translational Research, Cardiac Failure & Myocarditis, Cardiomyopathies/Congenital & Genetics, Car
138 by speckle tracking at presentation with ICI myocarditis (cases, n = 101) to that from patients recei
141 , was also present in 2 cases of ICI-related myocarditis, demonstrating the activation of heart-speci
142 of two patients with melanoma in whom fatal myocarditis developed after treatment with ipilimumab an
144 ejection fraction 52% +/- 9%) had history of myocarditis diagnosed by endomyocardial biopsy (59%) and
146 After adjustment for severity of illness, myocarditis does not confer additional risk for wait-lis
147 with metastatic melanoma who developed fatal myocarditis during ipilimumab and nivolumab combination
148 s study, we used the experimental autoimmune myocarditis (EAM) model to determine the role of eosinop
149 of NET formation in experimental autoimmune myocarditis (EAM) of mice substantially reduces inflamma
151 model of TnI-induced experimental autoimmune myocarditis (EAM), we demonstrated that both local and s
154 lowing viruses in the blood of patients with myocarditis: Epstein Barr virus (n=11, 41%), human pegiv
157 amatic presentation, patients with fulminant myocarditis (FM) might have better outcome than those wi
158 refore, establishing a uniform definition of myocarditis for application in clinical trials of cancer
161 pite higher allosensitization, patients with myocarditis had similar post-transplant rejection, retra
166 he human heart long after the signs of acute myocarditis have abated are still not completely underst
169 ore, efforts to detect viruses implicated in myocarditis have been unsuccessful in more accessible sa
170 regarding athletic participation after acute myocarditis have heightened the importance of early diag
171 Among children listed for HT, those with myocarditis have more severe heart failure than children
172 on of immune checkpoint inhibitor-associated myocarditis, have made ascertainment and identification
173 nd regular VA was found in AM patients after myocarditis healing (42%), as well as in PM patients (al
174 sulting from virus infection is the cause of myocarditis; however, the precise mechanism by which inf
178 demonstrate that ANT1 can induce autoimmune myocarditis in A/J mice by generating autoreactive T cel
181 ntial to aid in the management of autoimmune myocarditis in humans, possibly including patients with
183 esonance (CMR) techniques to identify active myocarditis in patients with recent-onset heart failure.
184 l inflammation and leukocyte infiltration in myocarditis in the absence of a detectable decline in le
186 del will enable fundamental studies of viral myocarditis, including IFN-gamma modulation as a therape
189 , we demonstrate that the induction of acute myocarditis involves the engagement of CD43 cytoplasmic
192 mes from randomized clinical trials in which myocarditis is a rare event that is investigator reporte
196 HT and used Cox models to determine whether myocarditis is independently associated with wait-list m
202 rders in which inflammation of the heart (or myocarditis) is the proximate cause of myocardial dysfun
204 sone group (cardiac arrest, cardiac failure, myocarditis, large intestine perforation, pneumonia, and
206 at treatments tailored to specific causes of myocarditis may impact clinical outcomes when added to g
208 summarize the common terminology related to myocarditis meanwhile highlighting some areas of controv
209 - 23 ms in HTN subjects; p < 0.05), areas of myocarditis (median 22% LV with T1 >990 ms, as compared
210 TnI-AM or after establishment of autoimmune myocarditis, mice were treated with the immunoproteasome
211 uncertain but is suspected to be related to myocarditis, microvascular injury, systemic cytokine-med
214 athies in developed countries is lymphocytic myocarditis most commonly caused by a viral pathogenesis
215 ence of intervention-related adverse events (myocarditis, myocardial rupture, neoplasm, hypersensitiv
217 n participants with acute heart failure-like myocarditis (n = 31; mean age, 47 years +/- 17; 10 women
218 In patients with chronic heart failure-like myocarditis (n = 40; mean age, 48 years +/- 13; 12 women
224 th T2 and T1 mapping reliably detected acute myocarditis, only T2 mapping discriminated between acute
225 and November 2016 with a diagnosis of acute myocarditis (onset of symptoms <1 month) of whom 55 requ
228 larly, myocardial fibrosis in the absence of myocarditis or left ventricular hypertrophy, or other kn
229 acids from viruses previously implicated in myocarditis or other human illnesses were detected in re
232 ts with giant-cell myocarditis, eosinophilic myocarditis, or cardiac sarcoidosis and those <15 years
233 re responsible for human diseases, including myocarditis, pancreatitis, acute flaccid paralysis, and
234 important human causative pathogen for viral myocarditis, pancreatitis, and meningitis, has evolved d
235 hy (NICM) and ischemic cardiomyopathy (ICM), myocarditis patients were younger (myocarditis 43.4+/-14
240 GLS among control subjects on an ICI without myocarditis (pre-ICI vs. on ICI, 20.6 +/- 2.0% vs. 20.5
242 GLS was strongly associated with MACE in ICI myocarditis presenting with either a preserved or reduce
243 Twenty-nine patients were examined with a myocarditis protocol (group A), 10 patients with a stres
244 eeds to be fully defined, described cases of myocarditis range from syndromes with mild signs and sym
246 87 patients from the ITAMY (ITAlian study in MYocarditis) registry, CMR was performed within the firs
255 e complex with patients presenting with AMI, myocarditis simulating an ST-elevation myocardial infarc
257 drial proteins can be target autoantigens in myocarditis, supporting the notion that the antigens rel
258 A nonischemic pattern of CMR abnormalities (myocarditis, takotsubo syndrome, or nonischemic cardiomy
259 onal definition of cancer therapy-associated myocarditis that may facilitate case ascertainment and r
260 mmation, which is characterized by a diffuse myocarditis that precedes the development of coronary va
262 arkers are commonly interpreted as resolving myocarditis, this assumption has not been confirmed as o
264 conclusion, eosinophils drive progression of myocarditis to DCMi, cause severe DCMi when present in l
265 ation can be used effectively in adults with myocarditis to support the circulation while awaiting my
266 out the risk stratification of patients with myocarditis undergoing ventricular tachycardia (VT) abla
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
279 portance in the pathogenesis of CVB3-induced myocarditis, we aimed to unravel the role of NOD2 in CVB
280 condition for the development of the chronic myocarditis, we hypothesized that CD73 activity may coun
285 is, acute respiratory distress syndrome, and myocarditis were the clinical prototypes, but there were
286 Four active COVID-19 cases showed focal myocarditis, whereas 1 case of cleared COVID-19 showed e
287 p B enteroviruses are common causes of acute myocarditis, which can be a precursor of chronic myocard
288 s known about the pathogenesis of adenovirus myocarditis, which is a significant impediment to the de
289 red during the study (pulmonary embolism and myocarditis while taking amantadine, and a multiple scle
290 Previous studies suggest that children with myocarditis who receive heart transplantation (HT) may b
291 hortening of 70% or greater identified acute myocarditis with 93% sensitivity, 100% specificity, and
292 fractory cardiac electrical instability, and myocarditis with a robust presence of T-cell and macroph
293 old woman who was hospitalized for fulminant myocarditis with biventricular failure and cardiogenic s
295 ave made ascertainment and identification of myocarditis with high specificity challenging in clinica
296 iotoxicity spectrum has broadened to include myocarditis with immune checkpoint inhibitors and cardia
298 ophilic IL-5Tg mice resulted in eosinophilic myocarditis with severe ventricular and atrial inflammat
299 n, we treated a patient with fulminant viral myocarditis with the interleukin-1 receptor blocking age
300 late heart failure pathogenesis during viral myocarditis, yet their identities and functions remain p