Takotsubo Cardiomyopathy in COVID-19

Giustino, Gennaro; Croft, Lori B.; Oates, Connor P.; Rahman, Karishma; Lerakis, Stamatios; Reddy, Vivek Y.; Goldman, Martin E.

doi:10.1016/j.jacc.2020.05.068

Cited by 127 publications

(148 citation statements)

References 3 publications

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“…Takotsubo cardiomyopathy, a reversible condition, occurs due to physical and emotional stress that affects the left ventricle. Several reports have shown Takotsubo cardiomyopathy in COVID-19 patients (180)(181)(182)(183)(184)(185). Correspondingly, this condition is also reported in influenza-infected patients (186)(187)(188)(189).…”

Section: Comparison Of Cardiovascular Conditions Associated With Sarsmentioning

confidence: 74%

Immune Mechanisms in Cardiovascular Diseases Associated With Viral Infection

2020

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Influenza virus infection causes 3-5 million cases of severe illness and 250,000-500,000 deaths worldwide annually. Although pneumonia is the most common complication associated with influenza, there are several reports demonstrating increased risk for cardiovascular diseases. Several clinical case reports, as well as both prospective and retrospective studies, have shown that influenza can trigger cardiovascular events including myocardial infarction (MI), myocarditis, ventricular arrhythmia, and heart failure. A recent study has demonstrated that influenza-infected patients are at highest risk of having MI during the first seven days of diagnosis. Influenza virus infection induces a variety of pro-inflammatory cytokines and chemokines and recruitment of immune cells as part of the host immune response. Understanding the cellular and molecular mechanisms involved in influenza-associated cardiovascular diseases will help to improve treatment plans. This review discusses the direct and indirect effects of influenza virus infection on triggering cardiovascular events. Further, we discussed the similarities and differences in epidemiological and pathogenic mechanisms involved in cardiovascular events associated with coronavirus disease 2019 (COVID-19) compared to influenza infection.

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Section: Comparison Of Cardiovascular Conditions Associated With Sarsmentioning

confidence: 74%

Immune Mechanisms in Cardiovascular Diseases Associated With Viral Infection

2020

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“…A total of 777 records were collected by the databases and manual searching. After the exclusion of the duplicates, review articles, case reports, pre‐printed versions without peer‐review, and irrelevant studies by title or abstract screening, 187 studies remained for full‐text review; 52 studies 6,17‐67 were finally included into the meta‐analysis, and 18 studies were included in the qualitative synthesis (Figure 1). A total of 52 records involving 10 614 COVID‐19 patients confirmed between December 25, 2019, and June 1, 2020, were included.…”

Section: Resultsmentioning

confidence: 99%

Ferritin in the coronavirus disease 2019 (COVID‐19): A systematic review and meta‐analysis

Cheng

et al. 2020

Clinical Laboratory Analysis

313

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Objective The coronavirus disease 2019 (COVID‐19) has rapidly developed into a pandemic. Increased levels of ferritin due to cytokine storm and secondary hemophagocytic lymphohistiocytosis were found in severe COVID‐19 patients. Therefore, the aim of this study was to determine the role of ferritin in COVID‐19. Methods Studies investigating ferritin in COVID‐19 were collected from PubMed, EMBASE, CNKI, SinoMed, and WANFANG. A meta‐analysis was performed to compare the ferritin level between different patient groups: non‐survivors versus survivors; more severe versus less severe; with comorbidity versus without comorbidity; ICU versus non‐ICU; with mechanical ventilation versus without mechanical ventilation. Results A total of 52 records involving 10 614 COVID‐19‐confirmed patients between December 25, 2019, and June 1, 2020, were included in this meta‐analysis, and 18 studies were included in the qualitative synthesis. The ferritin level was significantly increased in severe patients compared with the level in non‐severe patients [WMD 397.77 (95% CI 306.51‐489.02), P < .001]. Non‐survivors had a significantly higher ferritin level compared with the one in survivors [WMD 677.17 (95% CI 391.01‐963.33), P < .001]. Patients with one or more comorbidities including diabetes, thrombotic complication, and cancer had significantly higher levels of ferritin than those without (P < .01). Severe acute liver injury was significantly associated with high levels of ferritin, and its level was associated with intensive supportive care, including ICU transfer and mechanical ventilation. Conclusions Ferritin was associated with poor prognosis and could predict the worsening of COVID‐19 patients.

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“…In patients with myocarditis or inflammatory cardiomyopathies, inflammation is the primary cause of heart failure [5]. Moreover, cytokine-mediated inflammation has been implicated in acute stress-induced cardiomyopathy [6], an enigmatic entity that may be associated with major emotional or physical stress [7], and may also be a rare cause of myocardial injury in patients with coronavirus disease 2019 (COVID-19) [8,9]. In most other cases, activation of an inflammatory program reflects a reparative or protective response to other primary injurious processes.…”

Section: Introductionmentioning

confidence: 99%

Inflammatory Cytokines and Chemokines as Therapeutic Targets in Heart Failure

Hanna

Frangogiannis

2020

Cardiovasc Drugs Ther

231

170

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Heart failure exhibits remarkable pathophysiologic heterogeneity. A large body of evidence suggests that regardless of the underlying etiology, heart failure is associated with induction of cytokines and chemokines that may contribute to the pathogenesis of adverse remodeling, and systolic and diastolic dysfunction. The pro-inflammatory cytokines tumor necrosis factor (TNF)-α, interleukin (IL)-1, and IL-6 have been extensively implicated in the pathogenesis of heart failure. Inflammatory cytokines modulate phenotype and function of all myocardial cells, suppressing contractile function in cardiomyocytes, inducing inflammatory activation in macrophages, stimulating microvascular inflammation and dysfunction, and promoting a matrixdegrading phenotype in fibroblasts. Moreover, cytokine-induced growth factor synthesis may exert chronic fibrogenic actions contributing to the pathogenesis of heart failure with preserved ejection fraction (HFpEF). In addition to their role in adverse cardiac remodeling, some inflammatory cytokines may also exert protective actions on cardiomyocytes under conditions of stress. Chemokines, such as CCL2, are also upregulated in failing hearts and may stimulate recruitment of pro-inflammatory leukocytes, promoting myocardial injury, fibrotic remodeling, and dysfunction. Although experimental evidence suggests that cytokine and chemokine targeting may hold therapeutic promise in heart failure, clinical translation remains challenging. This review manuscript summarizes our knowledge on the role of TNF-α, IL-1, IL-6, and CCL2 in the pathogenesis of heart failure, and discusses the promises and challenges of targeted anti-cytokine therapy. Dissection of protective and maladaptive cellular actions of cytokines in the failing heart, and identification of patient subsets with overactive or dysregulated myocardial inflammatory responses are required for design of successful therapeutic approaches.

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Takotsubo Cardiomyopathy in COVID-19

Cited by 127 publications

References 3 publications

Immune Mechanisms in Cardiovascular Diseases Associated With Viral Infection

Immune Mechanisms in Cardiovascular Diseases Associated With Viral Infection

Ferritin in the coronavirus disease 2019 (COVID‐19): A systematic review and meta‐analysis

Inflammatory Cytokines and Chemokines as Therapeutic Targets in Heart Failure

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