Biomarkers of Heart Failure in Myocarditis and Dilated Cardiomyopathy

Fairweather, DeLisa; Abston, Eric; Coronado, Michael

doi:10.5772/19723

Cited by 8 publications

(8 citation statements)

References 141 publications

(211 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…24 To examine the effects of rIL-33 administration in an autoimmune model of viral-induced heart disease, we treated BALB/c mice with rIL-33, rST2 (to block IL-33 released during myocarditis) 25 or PBS ip every other day from day 1–9 pi and examined myocarditis at day 10 pi. We found that rIL-33 treatment significantly increased CVB3 myocarditis (Figure 1A and 1C, p =0.006) and pericarditis (Figure 1D) compared to PBS controls, while rST2 did not ( p =0.19).…”

Section: Resultsmentioning

confidence: 99%

IL-33 Independently Induces Eosinophilic Pericarditis and Cardiac Dilation

Abston

Barin

Čiháková

et al. 2012

Circ: Heart Failure

Self Cite

View full text Add to dashboard Cite

Background Interleukin (IL)-33 via its receptor ST2 protects the heart from myocardial infarct and hypertrophy in animal models, but paradoxically increases autoimmune disease. In this study we examined the effect of IL-33 or ST2 administration on autoimmune heart disease. Methods and Results We used pressure volume relationships and isoproterenol challenge to assess the effect of recombinant (r)IL-33 or rST2 (e.g. soluble ST2) administration on the development of autoimmune coxsackievirus (CVB3) myocarditis and dilated cardiomyopathy (DCM) in male BALB/c mice. rIL-33 treatment significantly increased acute perimyocarditis (p=0.006) and eosinophilia (p=1.3×10−5), impaired cardiac function (maximum ventricular power p=0.0002), and increased ventricular dilation (end diastolic volume p=0.01). rST2 treatment prevented eosinophilia and improved heart function compared to rIL-33 treatment (ejection fraction, p=0.009). Neither treatment altered viral replication. rIL-33 increased IL-4, IL-33, IL-1β and IL-6 levels in the heart during acute myocarditis. To determine whether IL-33 altered cardiac function on its own, we administered rIL-33 to undiseased mice and found that rIL-33 induced eosinophilic pericarditis and adversely affected heart function. We used cytokine knockout mice to determine that this effect was due to IL-33-mediated signaling but not IL-1β or IL-6. Conclusions We show for the first time that IL-33 induces eosinophilic pericarditis while sST2 prevents eosinophilia and improves systolic function, and that IL-33 independently adversely affects heart function via the IL-33 receptor.

show abstract

Section: Resultsmentioning

confidence: 99%

IL-33 Independently Induces Eosinophilic Pericarditis and Cardiac Dilation

Abston

Barin

Čiháková

et al. 2012

Circ: Heart Failure

Self Cite

View full text Add to dashboard Cite

show abstract

“…A number of enzymes, hormones, markers of heart stress or necrosis, cytokines, and other biological agents have been examined as biomarkers for heart failure. Although biomarkers are discussed in this review by category (for example those related to heart damage or inflammation), in fact many of these biomarkers interact or are related to each other which shows that the combination of biomarkers tends to provide the best risk assessment for cardiovascular disease [15].…”

Section: Biomarkers Of Coronary Heart Disease (Chd)mentioning

confidence: 99%

The Role Of hs-CRP In Predicting The Likelihood Of Coronary Heart Disease

Sitepu

Harahap

2020

idjpcr

View full text Add to dashboard Cite

Coronary Heart Disease (CHD) is a disorder of the cardiovascular system, characterized by atherosclerotic lesions. Inflammation is a strong predictor for coronary heart disease. High sensitivity C-Reactive Protein (hs-CRP) is an important biomarker, synthesized in the liver, can predict the severity of CHD. If the hs-CRP level is found to be low 3 mg / L, a person has the potential for severe vascular risk. Therefore, hs-CRP can be used as a predictor of primary CHD prevention, especially if the hs-CRP level is still low.

show abstract

“…AutoAbs against all of these major cardiac antigens are found during myocarditis [44]. Additionally, troponin I is used as a clinical biomarker for cardiovascular damage during myocardial infarction, myocarditis, and DCM [47, 48], indicating that troponin I is released systemically during acute myocarditis. However, there is a problem of “timing”.…”

Section: 4 Theoriesmentioning

confidence: 99%

Unresolved issues in theories of autoimmune disease using myocarditis as a framework

Root‐Bernstein

Fairweather

2015

Journal of Theoretical Biology

Self Cite

View full text Add to dashboard Cite

Many theories of autoimmune disease have been proposed since the discovery that the immune system can attack the body. These theories include the hidden or cryptic antigen theory, modified antigen theory, T cell bypass, T cell-B cell mismatch, epitope spread or drift, the bystander effect, molecular mimicry, anti-idiotype theory, antigenic complementarity, and dual-affinity T cell receptors. We critically review these theories and relevant mathematical models as they apply to autoimmune myocarditis. All theories share the common assumption that autoimmune diseases are triggered by environmental factors such as infections or chemical exposure. Most, but not all, theories and mathematical models are unifactorial assuming single-agent causation of disease. Experimental and clinical evidence and mathematical models exist to support some aspects of most theories, but evidence/models that support one theory almost invariably supports other theories as well. More importantly, every theory (and every model) lacks the ability to account for some key autoimmune disease phenomena such as the fundamental roles of innate immunity, sex differences in disease susceptibility, the necessity for adjuvants in experimental animal models, and the often paradoxical effect of exposure timing and dose on disease induction. We argue that a more comprehensive and integrated theory of autoimmunity associated with new mathematical models is needed and suggest specific experimental and clinical tests for each major theory that might help to clarify how they relate to clinical disease and reveal how theories are related.

show abstract

Biomarkers of Heart Failure in Myocarditis and Dilated Cardiomyopathy

Cited by 8 publications

References 141 publications

IL-33 Independently Induces Eosinophilic Pericarditis and Cardiac Dilation

IL-33 Independently Induces Eosinophilic Pericarditis and Cardiac Dilation

The Role Of hs-CRP In Predicting The Likelihood Of Coronary Heart Disease

Unresolved issues in theories of autoimmune disease using myocarditis as a framework

Contact Info

Product

Resources

About