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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

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