Therapeutic plasma exchange a potential strategy for patients with advanced heart failure

Torre‐Amione, Guillermo; Orrego, Carlos M.; Khalil, Nashwa; Kottner-Assad, Christian; Leveque, Christopher; Celis, René; Youker, Keith A.; Estep, Jerry D.

doi:10.1002/jca.20264

Cited by 23 publications

(21 citation statements)

References 41 publications

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“…Patients treated with therapeutic plasma exchange demonstrated improved LVEF as well as improvements in quality of life as measured by the Minnesota Living with Heart Failure Questionnaire. In addition, a reduction of the presence of immunoglobulin G in myocardium toward normal was demonstrated, as well as a decrease in myocyte hypertrophy [65]. The previously mentioned therapies raise the question of the importance of antigen presentation and immune complex activation of the inflammatory response in HF.…”

Section: Therapeutic Plasma Exchangementioning

confidence: 96%

Immune Modulation in Heart Failure: Past Challenges and Future Hopes

Flores‐Arredondo

García‐Rivas

Torre‐Amione

2011

Curr Heart Fail Rep

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Immune-modulation therapy has had great success in various inflammatory diseases. Despite the promising results of preliminary studies in anti-tumor necrosis factor-α therapies, large randomized studies have lacked positive clinical outcomes in patients with heart failure. These results have led to the idea that therapies directed toward specific inflammatory mediators may not be the answer and lead us toward the development of novel anti-inflammatory strategies that may involve a broader spectrum of inflammatory mediators. Therapeutic plasma exchange has been demonstrated as a safe treatment, and preliminary outcomes led us to develop new treatment schemes.

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Section: Therapeutic Plasma Exchangementioning

confidence: 96%

Immune Modulation in Heart Failure: Past Challenges and Future Hopes

Flores‐Arredondo

García‐Rivas

Torre‐Amione

2011

Curr Heart Fail Rep

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“…The few trials using immunoadsorption therapy in patients with dilated cardiomyopathy, where autoantibodies are thought to play a role in pathogenesis, were promising 119, 120 . Therapeutic plasma exchange, where large amounts of plasma are removed from the circulation and replaced with 5% albumin, potassium chloride, calcium gluconate, and then terminally supplemented with immunoglobulins to replace the removed proteins, is being tested 121 .…”

Section: Fibrosismentioning

confidence: 99%

Pathological Ventricular Remodeling

2013

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Despite declines in heart failure morbidity and mortality with current therapies, re-hospitalization rates remain distressingly high, impacting substantially on individuals, society, and the economy. As a result, the need for new therapeutic advances and novel medical devices is urgent. Disease-related left ventricular remodeling is a complex process involving cardiac myocyte growth and death, vascular rarefaction, fibrosis, inflammation, and electrophysiological remodeling. As these events are highly inter-related, targeting one single molecule or process may not be sufficient. Here, we review molecular and cellular mechanisms governing pathological ventricular remodeling.

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“…The evidence in support of B‐cell activation after myocardial injury is as follows: First, in patients with acute HF, there is activation of B‐cells. Markers of B‐cell activation increase in hospitalized patients with HFrEF and return to normal after treatment . Second, a variety of anticardiac antibodies have been found in patients after myocardial infarction (MI) and in patients with various forms of HF; in these settings, the initial myocardial injury was not immunologically mediated, suggesting that after myocardial ischemia or necrosis new antigens are exposed that trigger an immune response and antibody production.…”

Section: Introductionmentioning

confidence: 99%

“…Markers of B-cell activation increase in hospitalized patients with HFrEF and return to normal after treatment. 5 Second, a variety of anticardiac antibodies have been found in patients after myocardial infarction (MI) and in patients with various forms of HF [6][7][8][9] ; in these settings, the initial myocardial injury was not immunologically mediated, suggesting that after myocardial ischemia or necrosis new antigens are exposed that trigger an immune response and antibody production. Third, a large proportion of patients with end-stage cardiomyopathy, regardless of the etiology, have anticardiac antibodies deposited in the myocardium.…”

mentioning

confidence: 99%

“…And, finally, limited clinical observations suggest that strategies to remove antibodies may have an impact on the course of HF. 5,13 For example, studies using immune adsorption in patients with nonischemic cardiomyopathy that have circulating anti-beta-receptor antibodies appear to improve clinically as well as recover cardiac function. 14 Also, as a proof of principle, therapeutic plasma exchange in patients with HF has been performed and appears to be safe.…”

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confidence: 99%

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Full Expression of Cardiomyopathy Is Partly Dependent on B‐Cells: A Pathway That Involves Cytokine Activation, Immunoglobulin Deposition, and Activation of Apoptosis

Cordero‐Reyes

Youker

Trevino

et al. 2016

JAHA

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BackgroundLimited information exists on the role of B‐cell‐dependent mechanisms in the progression of heart failure (HF). However, in failing human myocardium, there is evidence of deposition of activated complement components as well as anticardiac antibodies. We aimed to determine the contribution of B‐cells in HF progression using a nonsurgical mouse model of nonischemic cardiomyopathy (CMP).Methods and Results CMP protocol involved the use of l‐NAME and NaCl in the drinking water and angiotensin‐II infusion for 35 days. At day 35, mice were analyzed by cardiac magnetic resonance imaging, gene expression, and histology. Mice (12 weeks old) were divided into 4 groups, all in C57BL/6 background: wild‐type (WT) CMP; severe combined immunodeficiency (SCID) CMP (T‐ and B‐cell deficient); CD22− CMP (B‐cell depleted); and Nude CMP (T‐cell deficient), with their respective controls. We performed B‐cell depletion and reconstitution protocols. The protective effect of B‐cell depletion was demonstrated by a significant reduction of cell hypertrophy and collagen deposition and a preserved ejection fraction in the CD22− CMP group compared to WT CMP. Once SCID mice underwent B‐cell reconstitution with isolated CMP B‐cells, the CMP phenotype was restored. Furthermore, deposition of IgG3 and apoptosis in the myocardium follows the development of CMP; in addition, in vitro studies demonstrated that activated B‐cells stimulate collagen production by cardiac fibroblasts.ConclusionsThe absence of B‐cells in this model of HF resulted in less hypertrophy and collagen deposition, preservation of left ventricular function, and, in association with these changes, a reduction in expression of proinflammatory cytokines, immunoglobulin G deposition, and apoptosis in the myocardium. Taken together, these data suggest that B‐cells play a contributory role in an angiotensin‐II‐induced HF model.

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Therapeutic plasma exchange a potential strategy for patients with advanced heart failure

Abstract: These data collectively suggest a role of humoral immunity in the progression of heart failure.

Cited by 23 publications

References 41 publications

Immune Modulation in Heart Failure: Past Challenges and Future Hopes

Immune Modulation in Heart Failure: Past Challenges and Future Hopes

Pathological Ventricular Remodeling

Full Expression of Cardiomyopathy Is Partly Dependent on B‐Cells: A Pathway That Involves Cytokine Activation, Immunoglobulin Deposition, and Activation of Apoptosis

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