Heart failure with preserved ejection fraction

Alsamara, Mershed; Alharethi, Rami

doi:10.1586/14779072.2014.911086

Cited by 7 publications

(3 citation statements)

References 62 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Chagas heart disease is characterized by marked inflammation and fibrosis of the heart, along with cardiac edema, myofibrillar destruction, chamber dilation, and loss of contractile function. The etiology of Chagas heart disease is not fully understood and likely multifactorial, with a contribution of an autoimmune response due in part to molecular mimicry between antigenic determinants of T. cruzi and human (cardiac) antigens [ 62 , 63 ]. With heart failure in Chagas disease, myocardial levels of CD8 + and CD4 + T cells are increased, with a predominance of CD8 + T cells [ 61 , 64 , 65 ].…”

Section: Myocarditis and Chagas Heart Diseasementioning

confidence: 99%

The CXCL10/CXCR3 Axis and Cardiac Inflammation: Implications for Immunotherapy to Treat Infectious and Noninfectious Diseases of the Heart

Altara

Mallat

Booz

et al. 2016

Journal of Immunology Research

View full text Add to dashboard Cite

Accumulating evidence reveals involvement of T lymphocytes and adaptive immunity in the chronic inflammation associated with infectious and noninfectious diseases of the heart, including coronary artery disease, Kawasaki disease, myocarditis, dilated cardiomyopathies, Chagas, hypertensive left ventricular (LV) hypertrophy, and nonischemic heart failure. Chemokine CXCL10 is elevated in cardiovascular diseases, along with increased cardiac infiltration of proinflammatory Th1 and cytotoxic T cells. CXCL10 is a chemoattractant for these T cells and polarizing factor for the proinflammatory phenotype. Thus, targeting the CXCL10 receptor CXCR3 is a promising therapeutic approach to treating cardiac inflammation. Due to biased signaling CXCR3 also couples to anti-inflammatory signaling and immunosuppressive regulatory T cell formation when activated by CXCL11. Numbers and functionality of regulatory T cells are reduced in patients with cardiac inflammation, supporting the utility of biased agonists or biologicals to simultaneously block the pro-inflammatory and activate the anti-inflammatory actions of CXCR3. Other immunotherapy strategies to boost regulatory T cell actions include intravenous immunoglobulin (IVIG) therapy, adoptive transfer, immunoadsorption, and low-dose interleukin-2/interleukin-2 antibody complexes. Pharmacological approaches include sphingosine 1-phosphate receptor 1 agonists and vitamin D supplementation. A combined strategy of switching CXCR3 signaling from pro- to anti-inflammatory and improving Treg functionality is predicted to synergistically lessen adverse cardiac remodeling.

show abstract

Section: Myocarditis and Chagas Heart Diseasementioning

confidence: 99%

The CXCL10/CXCR3 Axis and Cardiac Inflammation: Implications for Immunotherapy to Treat Infectious and Noninfectious Diseases of the Heart

Altara

Mallat

Booz

et al. 2016

Journal of Immunology Research

View full text Add to dashboard Cite

show abstract

“…Hypertension, diabetes mellitus and obesity comprise traditional cardiovascular risk factors that are associated with diastolic dysfunction [6]. However, these metabolic abnormalities fail to account for all changes in diastolic function [7].…”

Section: Introductionmentioning

confidence: 99%

Associations of inflammatory markers with impaired left ventricular diastolic and systolic function in collagen-induced arthritis

et al. 2020

View full text Add to dashboard Cite

Background High-grade inflammation may play a pivotal role in the pathogenesis of left ventricular (LV) dysfunction. Evidence to support a role of systemic inflammation in mediating impaired LV function in experimental models of rheumatoid arthritis (RA) remains limited. The aim of the present study was to determine the effects of high-grade systemic inflammation on LV diastolic and systolic function in collagen-induced arthritis (CIA).

show abstract

“…Thus, HFpEF is one of the largest unmet needs in cardiovascular medicine, and there is a substantial requirement for new therapeutic approaches and strategies that target mechanisms specific for HFpEF (16). A general feature in HFpEF patients is the presence of several comorbidities (Figure 1) including HTN, anemia, atrial fibrillation (AF), obesity, and diabetes (7, 14, 16, 24–30). Moreover, comorbidities negatively affect prognosis to a greater extent in individuals with HFpEF than with HFrEF and have a greater impact on physical impairment as well (31).…”

Section: Introductionmentioning

confidence: 99%

Targeting Obesity and Diabetes to Treat Heart Failure with Preserved Ejection Fraction

et al. 2017

View full text Add to dashboard Cite

Heart failure with preserved ejection fraction (HFpEF) is a major unmet medical need that is characterized by the presence of multiple cardiovascular and non-cardiovascular comorbidities. Foremost among these comorbidities are obesity and diabetes, which are not only risk factors for the development of HFpEF, but worsen symptoms and outcome. Coronary microvascular inflammation with endothelial dysfunction is a common denominator among HFpEF, obesity, and diabetes that likely explains at least in part the etiology of HFpEF and its synergistic relationship with obesity and diabetes. Thus, pharmacological strategies to supplement nitric oxide and subsequent cyclic guanosine monophosphate (cGMP)—protein kinase G (PKG) signaling may have therapeutic promise. Other potential approaches include exercise and lifestyle modifications, as well as targeting endothelial cell mineralocorticoid receptors, non-coding RNAs, sodium glucose transporter 2 inhibitors, and enhancers of natriuretic peptide protective NO-independent cGMP-initiated and alternative signaling, such as LCZ696 and phosphodiesterase-9 inhibitors. Additionally, understanding the role of adipokines in HFpEF may lead to new treatments. Identifying novel drug targets based on the shared underlying microvascular disease process may improve the quality of life and lifespan of those afflicted with both HFpEF and obesity or diabetes, or even prevent its occurrence.

show abstract

Heart failure with preserved ejection fraction

Cited by 7 publications

References 62 publications

The CXCL10/CXCR3 Axis and Cardiac Inflammation: Implications for Immunotherapy to Treat Infectious and Noninfectious Diseases of the Heart

The CXCL10/CXCR3 Axis and Cardiac Inflammation: Implications for Immunotherapy to Treat Infectious and Noninfectious Diseases of the Heart

Associations of inflammatory markers with impaired left ventricular diastolic and systolic function in collagen-induced arthritis

Targeting Obesity and Diabetes to Treat Heart Failure with Preserved Ejection Fraction

Contact Info

Product

Resources

About