Acute necrotizing eosinophilic myocarditis presenting with cardiogenic shock after mRNA booster dose for COVID-19: Case report and review of literature
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ABSTRACT:
SUBMITTER: Abete R
PROVIDER: S-EPMC9911929 | biostudies-literature | 2022 Oct
REPOSITORIES: biostudies-literature
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Project description:BackgroundSARS-CoV2, also known as COVID-19, is a specific strain of coronavirus that is responsible for an ongoing global pandemic. COVID-19 primarily targets the respiratory system via droplet transmission, causing symptoms similar to influenza, including fever, cough, and shortness of breath. It is now known to impact other organ systems, causing significant cardiovascular and gastrointestinal illness, among others.Case summaryWe describe two cases of COVID-19 induced myocarditis presenting with cardiogenic shock. These cases highlight the importance of understanding the lethal cardiac complications of COVID-19 infection, as well as its presentation, diagnosis, pathophysiology, and potential treatment options. These two cases involve patients without underlying cardiovascular disease risk factors who experienced prolonged symptoms of COVID-19 infection. Both patients presented with cardiogenic shock more than one week after symptom onset and diagnosis. These cases demonstrate the late presentation of myocarditis and cardiogenic shock, treated with corticosteroids and inotropes, with subsequent recovery of cardiac function.DiscussionThe cases highlight the importance of recognizing late presentation viral myocarditis secondary to COVID-19 infection, even in patients without underlying cardiac disease.
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Project description:Necrotizing eosinophilic myocarditis is a rare but potentially fatal condition that requires prompt recognition and treatment. We describe a case of a young athlete presenting with chest pain and breathlessness, with evidence of rapidly deteriorating cardiac function. The condition was successfully treated with corticosteroids, with no evidence of residual myocardial damage. This is the first reported case to demonstrate the utility of cardiac magnetic resonance imaging for diagnosis and monitoring response to treatment. It also highlights the value of endomyocardial biopsy in establishing a tissue diagnosis in cases of fulminant myocarditis, in order to direct treatment appropriately.
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Project description:Eosinophilic granulomatosis with polyangiitis (EGPA) is a systemic vasculitis involving small-to-medium-sized vessels characterized by asthma, vasculitis, and peripheral eosinophilia. EGPA-associated eosinophilic myocarditis (EM) occurs rarely, yet can be fatal if left untreated. Moreover, the accurate diagnosis of EGPA-associated EM without vasculitis is exceptionally difficult because of the overlapping features with EM of other causes. We report a case of probable EGPA with subclinical neurological involvement that presented with acute EM. The constellation of peripheral eosinophilia, left ventricular dysfunction, and normal epicardial coronary arteries raised suspicion of acute EM, which was confirmed by cardiac magnetic resonance (CMR) investigation and endomyocardial biopsy (EMB). Prompt systemic administration of corticosteroids completely restored and normalized myocardial structure and function. Although the patient's history suggested the presumed hypersensitivity myocarditis, EMB revealed EM without vasculitis, not hypersensitivity, leading to a tentative diagnosis of idiopathic hypereosinophilic syndrome. Interestingly, the characteristic findings of vasculitis on CMR imaging strongly suggested EGPA-associated EM. Although the patient had no clinical neurological manifestations, a nerve conduction study confirmed mononeuritis multiplex, leading to the final diagnosis of probable EGPA. Therefore, this case highlights the diagnostic challenge associated with EGPA and the diagnostic synergy of CMR and EMB for an exploratory diagnosis of EGPA-associated EM.
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Project description:Vaccination with mRNA vaccines against coronavirus disease 2019 (COVID-19) has been associated with a risk of developing myocarditis and pericarditis, with an estimated standardized incidence ratio of myocarditis being 5.34 (95% CI, 4.48 to 6.40) as compared to the expected incidence based on historical data according to a large national study in Israel. Most cases of myocarditis in vaccine recipients occur in young males, particularly following the second dose, and the presentation is usually mild. Recently, the third (booster) dose has been shown to reduce confirmed infections and severe illness even against common variants of the virus. In Israel, over 4.4 million citizens (more than 45% of the population) have been vaccinated with the third dose of Pfizer-BioNTech vaccine BNT162b2. Herein, we report the first case of a histologically confirmed severe myocarditis following the third dose of BNT162b2 COVID-19 vaccine.
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Project description:BackgroundAcute myocarditis is a common condition, with viral infections being the most common aetiology in North America and Europe. Influenza A myocarditis is however rare. As clinical manifestation may be fulminant, early recognition and management are paramount and may impact overall prognosis by hindering complications such as thromboembolism. A brief review of the literature, diagnostic modalities, work-up and treatment are discussed.Case summaryWe present the case of a 42-year-old, previously healthy woman with recent flu-like symptoms, developing decompensated heart failure (HF) and cardiogenic shock within a week, due to Influenza A myocarditis. Biventricular thrombi were identified. Pharmacological haemodynamic support, followed by HF therapy, allowed full recuperation of heart function. Intracavitary thrombi disappeared under unfractionated heparin with bridging to rivaroxaban.DiscussionFulminant myocarditis due to Influenza A is rare and, to the best of our knowledge, has not been associated with intracardiac thrombi formation. Echocardiography is the essential first-line imaging modality. Cardiac magnetic resonance plays a major role in the diagnosis of myocarditis and may preclude the need for an endomyocardial biopsy in selected cases. Coronary angiography may be required to rule out ischaemic aetiology. First-line therapy in fulminant disease is pharmacological and, if required, mechanical haemodynamic support. Standard HF therapy complete the therapeutic options and should be introduced as soon as possible. Complications such as intracardiac thrombi formation, require targeted treatment. Specific drug therapies targeting Influenza A have no proven benefit in myocarditis.
| S-EPMC8874847 | biostudies-literature
Project description:BackgroundAmyloidosis is a systemic infiltrative disease that can affect nearly every organ in the human body. It is characterized by the deposition of misfolded protein within various tissues and organs. Once there is cardiac involvement this portends a worse prognosis.Case summaryWe describe a case series of two patients with cardiac amyloidosis presenting as a cardiogenic shock. There were several missed opportunities in diagnosing cardiac amyloid prior to their fatal presentations. In the first case, a 65-year-old African-American male patient presented with worsening shortness of breath and signs of heart failure. Echocardiography revealed preserved ejection fraction. He was diagnosed with light chain subtype of cardiac amyloidosis, and rapidly deteriorated during his admission. Patient in the second case is a 75-year-old African-American female who presented with worsening heart failure and hypotension. Echocardiography revealed reduced ejection fraction. She was diagnosed with transthyretin cardiac amyloid. Her clinical status worsened during admission and she went into cardiogenic shock requiring multiple vasopressors.DiscussionThis case series discusses two incidences of cardiac amyloidosis presenting as cardiogenic shock in African-American patients. This article postulates that cardiac amyloidosis may be misdiagnosed for more common causes of heart failure especially among this demographic group. Once patients with cardiac amyloid present with cardiogenic shock their clinical course is typically rapidly fatal despite aggressive measures. Earlier detection is imperative to prevent poor outcomes.
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Project description:Giant cell myocarditis is a rare and often fatal disease. The most obvious presentation often described in the literature is one of rapid hemodynamic deterioration due to cardiogenic shock necessitating urgent consideration of mechanical circulatory support and heart transplantation. We present the case of a 60-year-old man whose initial presentation was consistent with myopericarditis but who went on to develop a rapid decline in left ventricular systolic function without overt hemodynamic compromise or dramatic symptomatology. Giant cell myocarditis was confirmed via endomyocardial biopsy. Combined immunosuppression with corticosteroids and calcineurin inhibitor resulted in resolution of symptoms and sustained recovery of left ventricular function one year later. Our case highlights that giant cell myocarditis does not always present with cardiogenic shock and should be considered in the evaluation of new onset cardiomyopathy of uncertain etiology as a timely diagnosis has distinct clinical implications on management and prognosis.
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Project description:Introduction. Hypereosinophilic syndrome (HES) is a rare disease characterized by unexplained peripheral eosinophilia along with evidence of end-organ damage. Cardiac involvement is the most life-threatening consequence and is frequently underreported with a prevalence of around 5%. The gold standard for diagnosis is myocardial biopsy, but less-invasive imaging such as cardiac MR (CMR) has been frequently used to help with the diagnosis. We are presenting a unique case of a patient diagnosed with Eosinophilic myocarditis (EM) supported by CMR with rapid improvement after starting steroid treatment. Case Presentation. A 67-year-old African American female with extensive cardiovascular disease history presenting with chest pain was diagnosed with EM secondary to hypereosinophilic syndrome (HES). Lab workup revealed absolute eosinophils of 4.70 × 103/μL (normal 0-0.75 × 103/μL). Transthoracic echocardiography showed mild reduction in left ventricular function and a large obliterating thrombus in the right ventricular apex. CMR showed increased signal intensity at the left ventricular and right ventricular apex, consistent with myocardial edema. Subsequently, the patient was placed on dexamethasone 10 mg daily with significant symptomatic improvement. Discussion. EM is a rare complication of hypereosinophilic syndrome and can mimic common cardiovascular diseases such as acute exacerbation of heart failure or myocardial infarction. A high index of suspicion is essential especially in the setting of suggestive lab workup. CMR is a promising noninvasive and cost-effective alternative for myocardial biopsy in diagnosis.
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