Eosinophilic Myocarditis

Cheung, Christopher C.; Constantine, Maggie; Ahmadi, Amir Ali; Shiau, Carolyn J; Chen, Luke Y C

doi:10.1016/j.amjms.2017.04.002

Cited by 65 publications

(87 citation statements)

References 55 publications

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“…Eosinophils are a subtype of myeloid cells that participate in the immunologic response to parasites and hypersensitivity reactions. 1 Hypereosinophilia, defined as an absolute eosinophilic count of 1.5 × 10 9 /L or greater, has a wide differential diagnosis (Box 1). 2 Importantly, these cells can infiltrate tissues and cause end-organ damage, resulting in a rare condition known as hypereosinophilic syndrome, which has an estimated annual incidence of 0.035 per 100 000.…”

Section: Discussionmentioning

confidence: 99%

“…2 Importantly, these cells can infiltrate tissues and cause end-organ damage, resulting in a rare condition known as hypereosinophilic syndrome, which has an estimated annual incidence of 0.035 per 100 000. 1,3,6 Although this multisystem condition most commonly involves the skin, gastrointestinal tract and the lungs, hypereosinophilic syndrome can result in cardiac manifestations in about 20%-50% of cases. 1,6 Eosinophilic cardiac disease -also known as Loeffler endocarditis, eosinophilic myocarditis or fibroplastic endocarditis -is a major source of morbidity and mortality in hypereosinophilic syndrome.…”

Section: Discussionmentioning

confidence: 99%

“…1,3,6 Although this multisystem condition most commonly involves the skin, gastrointestinal tract and the lungs, hypereosinophilic syndrome can result in cardiac manifestations in about 20%-50% of cases. 1,6 Eosinophilic cardiac disease -also known as Loeffler endocarditis, eosinophilic myocarditis or fibroplastic endocarditis -is a major source of morbidity and mortality in hypereosinophilic syndrome. 4,6 Most cases of eosinophilic myocarditis described in the literature have presented with symptoms of cardiac failure.…”

Section: Discussionmentioning

confidence: 99%

“…Unfortunately, these imaging changes remain inconsistent in the early phases of eosinophilic myocarditis. 1,6 More importantly, patients presenting with cognitive dysfunction may not be able to follow the commands needed to effectively conduct an MRI examination. Therefore, endomyocardial biopsy remains the gold standard diagnostic modality for eosinophilic myocarditis.…”

Section: Discussionmentioning

confidence: 99%

“…Corticosteroids, at 0.5-1.0 mg/kg for about 2 weeks and tapered over 2-3 months to a maintenance dose of 5-10 mg/d, are the cornerstone of treatment for idiopathic cases to decrease hypereosinophilia and the resulting end-organ damage, but evidence is limited to small case series. 1,2,6 Second-line options include hydroxyurea and interferon-α. 1 Monitoring with echocardiography or cardiac MRI is indicated every 6 months in cases of sustained hypereosinophilia, and more frequently if cardiac disease is discovered.…”

Section: Discussionmentioning

confidence: 99%

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Eosinophilic myocarditis presenting with hypoactive delirium and cardioembolic stroke

Chan

Gibson

2019

CMAJ

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A 64-year-old woman with normal baseline functioning presented to hospital with an altered level of consciousness. She had a history of hypertension (perindopril 8 mg/d), gout (allopurinol 200 mg/d) and anxiety (sertraline 100 mg/d). She was brought to the hospital by her husband because of a 3-day history of being in a hypoactive state with urinary and stool incontinence. Her husband reported no preceding infectious, allergic or constitutional symptoms. Family history and rheumatologic review of systems were noncontributory, and the patient had no recent history of rashes. There had been no out-of-country travel in the preceding 2 years.On admission, the patient's temperature was 36.3°C, she had a regular heart rate of 103 beats/min, her blood pressure was 128/78 mm Hg and oxygen saturation was 95% on room air. Her glucose level was 5.7 (normal 3.3-11.0) mmol/L. The patient's score on the Glasgow Coma Scale was 15/15, but she was inattentive and oriented to only her name. A neurologic examination was limited owing to lack of cooperation. The patient's neck was supple. Pupils were equal and reactive, with no gaze preference or nystagmus. She was unable to squeeze her left hand, and had hypertonia of the left lower extremity and a unilateral upgoing Babinski sign. On the right side, she had antigravity strength. She was hyperreflexic (graded at 3/4) throughout. There were no features of heart failure. The examination was otherwise unremarkable.Initial laboratory investigations showed a normal complete blood count except for an elevated leukocyte count of 15.7 × 10 9 /L owing to an eosinophil count of 6.3 (normal < 0.7) × 10 9 /L. The patient's complete blood count had been normal 4 months earlier. Electrolytes, creatinine, lipase, liver enzymes and vitamin B 12 levels were within the normal ranges, and thyroid-stimulating hormone was minimally elevated at 4.07 (normal 0.20-4.00) mIU/L. Importantly, her C-reactive protein (CRP) level was substantially elevated at 110.3 (normal < 8) mg/L, and serial troponin levels ranged from 1620 to 1780 (normal < 14) ng/L without any clear trend. Electrocardiography showed sinus tachycardia with nonspecific ST and T wave changes in the inferolateral leads. Chest radiography and computed tomography angiography of the head and neck were both normal. Magnetic resonance imaging (MRI), however, showed multiple foci of restricted diffusion within the cerebral hemispheres, basal ganglia and posterior fossa, suggestive of cardioembolic phenomena (Figure 1).The patient was initially given heparin for possible cardioembolic stroke, and ceftriaxone, vancomycin and acyclovir for potential infectious endocarditis or meningoencephalitis. An extensive infectious workup was undertaken. Urinalysis was clear. Blood, stool (including ova and parasites) and urine cultures were negative. Cerebrospinal fluid (CSF) analysis showed a leukocyte count of 1 × 10 6 /L and a CSF protein level of 0.47 (normal 0.15-0.45) g/L but was negative for culture and viral testing. HIV testing was not performed owing to...

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Eosinophilic myocarditis presenting with hypoactive delirium and cardioembolic stroke

Chan

Gibson

2019

CMAJ

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Chest Pain in a Middle-aged Woman With Asthma

2020

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CAR‐T cell therapeutic avenue for fighting cardiac fibrosis: Roadblocks and perspectives

Abdalla,

Miao,

Ahmed

et al. 2024

Cell Biochemistry & Function

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Heart diseases remain the primary cause of human mortality in the world. Although conventional therapeutic opportunities fail to halt or recover cardiac fibrosis, the promising clinical results and therapeutic efficacy of engineered chimeric antigen receptor (CAR) T cell therapy show several advancements. However, the current models of CAR‐T cells need further improvement since the T cells are associated with the triggering of excessive inflammatory cytokines that directly affect cardiac functions. Thus, the current study highlights the critical function of heart immune cells in tissue fibrosis and repair. The study also confirms CAR‐T cell as an emerging therapeutic for treating cardiac fibrosis, explores the current roadblocks to CAR‐T cell therapy, and considers future outlooks for research development.

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Eosinophilic Myocarditis

Cited by 65 publications

References 55 publications

Eosinophilic myocarditis presenting with hypoactive delirium and cardioembolic stroke

Eosinophilic myocarditis presenting with hypoactive delirium and cardioembolic stroke

Chest Pain in a Middle-aged Woman With Asthma

CAR‐T cell therapeutic avenue for fighting cardiac fibrosis: Roadblocks and perspectives

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