Clinical impact of the presence of macrophages in endomyocardial biopsies of patients with dilated cardiomyopathy

Nakayama, Takafumi; Sugano, Yasuo; Yokokawa, Tetsuro; Nagai, Toshiyuki; Matsuyama, Takehisa; Ohta‐Ogo, Keiko; Ikeda, Yoshihiko; Ishibashi‐Ueda, Hatsue; Nakatani, Takeshi; Ohte, Nobuyuki; Yasuda, Satoshi; Anzai, Toshihisa

doi:10.1002/ejhf.767

Cited by 74 publications

(59 citation statements)

References 39 publications

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“…Recent clinical and experimental evidence has suggested that immune activation and the consequential inflammatory response in the myocardium may be involved in the process of deteriorating cardiac function . Both pro‐inflammatory and anti‐inflammatory infiltrates were associated with poor prognosis in, for instance, dilated cardiomyopathy patients, leading to some profound pathophysiological implications regarding disease progression of cardiomyopathy . Regardless of the trigger of myocardial inflammation, the subsequent immune activation accompanied by a persistence of myocardial inflammatory infiltrates may be a causative factor of the deterioration in severe heart failure .…”

Section: Discussionmentioning

confidence: 99%

Intramyocardial inflammation predicts adverse outcome in patients with cardiac AL amyloidosis

Siegismund

Escher

Laßner

et al. 2017

European J of Heart Fail

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Our study reports for the first time a high incidence (48.1%) of intramyocardial inflammation in a series of patients with EMB-proven cardiac amyloidosis and could show that in patients with AL amyloidosis, intramyocardial inflammation correlated significantly with increased mortality. Our data have a direct clinical impact because one can hypothesize that additional immunomodulating/anti-inflammatory treatment regimens in patients with biopsy-proven inflammation of heart muscle tissue could be beneficial for patients suffering from cardiac AL amyloidosis.

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Section: Discussionmentioning

confidence: 99%

Intramyocardial inflammation predicts adverse outcome in patients with cardiac AL amyloidosis

Siegismund

Escher

Laßner

et al. 2017

European J of Heart Fail

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“…In this investigation, DCM was defined as systolic dysfunction [left ventricular ejection fraction (LVEF) < 45%] with ventricular dilation [left ventricular end-diastolic diameter (LVEDD) > 55 mm] in the absence of an apparent secondary cause of cardiomyopathy, such as coronary heart disease, hypertensive heart disease, or valvular heart disease [20]. The exclusion criteria included ischaemic cardiomyopathy, hypertrophic cardiomyopathy, hypertensive heart disease, a history of uncontrollable or untreated hypertension for at least a year before the documentation of LV Cellular Physiology and Biochemistry Cellular Physiology and Biochemistry dysfunction, and other secondary cardiomyopathies such as sarcoidosis and amyloidosis, the presence of significant coronary artery stenosis on angiography and non-ischaemic DCM secondary to valvular heart disease, systemic hypertension, cardiac surgery or acute myocarditis, excessive alcohol abuse, pregnancy, endocrine disease, active infectious disease or collagen disease, medical history of autoimmune disease [12,21]. All subjects gave written informed consent and the protocol was reviewed.…”

Section: Study Populationmentioning

confidence: 99%

Response Gene to Complement-32 Promotes the Imbalance of Treg/Th17 in Patients with Dilated Cardiomyopathy

Li¹,

Zhou²,

Tang³

et al. 2017

Cell Physiol Biochem

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Background/Aims: The imbalance of Treg/Th17 cells plays important role in the pathogenesis of dilated cardiomyopathy (DCM). Response gene to complement (RGC)-32 is a cell cycle regulator that plays an important role in cell proliferation. We evaluated whether the upregulation of RGC-32 was implicated in the homeostasis of Treg/Th17 cells in DCM. Methods:The levels of plasma RGC-32, IL-17 and TGF-β1, and the frequencies of circulating CD4 + RGC-32 + T cells, Th17 and Treg cells in patients with DCM were determined by Cytokinespecific sandwich ELISA and the flow cytometer (FCM), respectively. Results: A significant elevation of plasma RGC-32 in patients with DCM compared with healthy control (HC) subjects was observed. This upregulation was associated with an increase in frequency of Th17 and a decrease in frequency of Treg cells. To further assessed the role of RGC-32, we investigated the effects of RGC-32 up-or down-regulation on frequencies of Th17 and Treg cells in peripheral blood mononuclear cells (PBMCs) from subjects. Importantly, overexpression of RGC-32 was accompanied by an augmentation of Th17 and a reduction of Treg expression. Conclusion: In summary, our study demonstrated the up-regulation of RGC-32 contributed to the imbalance of Treg/Th17 cells in patients with DCM.

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“…Furthermore, myocardial inflammation may be seen in other forms of dilated cardiomyopathy as well, and its presence has been recently associated with adverse myocardial remodeling and disease progression. 40 Finally, the radiation exposure from a typical cardiac FDG PET/CT protocol, including a limited whole body FDG PET (skull-base through mid-thighs), is not trivial, however; with the development of three-dimensional acquisition and advent of more sensitive PET systems, it is expected that radiation exposure will continue to decrease substantially in the years to come. 41 …”

Section: Cardiac Fdg Petmentioning

confidence: 99%

Advanced cardiovascular imaging for the evaluation of cardiac sarcoidosis

Bravo

Singh

Carli

et al. 2019

Journal of Nuclear Cardiology

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Cardiac sarcoidosis (CS) remains an intriguing infiltrating disorder and one of the most important forms of inflammatory cardiomyopathy. Identification of patients with CS is of extreme importance because they are at higher risk of sudden death, and heart-failure progression. And while it remains a diagnostic conundrum, a great amount of experience has been accumulated over the last decade with the advent of fluorine-18 fluorodeoxyglucose positron emission tomography and cardiac magnetic resonance with late gadolinium enhancement imaging. They have both proven to be advanced imaging techniques that provide important, and often complementary, diagnostic and prognostic information for the management of CS. However, they have also shown to have limitations, and, thus, there is a continued need for developing more specific imaging probes for identifying cardiac inflammation. The aim of the present manuscript is to provide the reader with a better understanding of the histopathology of the disease, how this potentially relates to noninvasive imaging detection, and the best strategies available for the diagnosis and management of patients with CS.

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Clinical impact of the presence of macrophages in endomyocardial biopsies of patients with dilated cardiomyopathy

Abstract: It was found that DCM with increased myocardial immune activation was associated with poor long-term outcome. The association between M2 macrophages and collagen formation suggests the phenotypic polarization of macrophages toward M2 may be associated with ventricular remodelling in DCM.

Cited by 74 publications

References 39 publications

Intramyocardial inflammation predicts adverse outcome in patients with cardiac AL amyloidosis

Intramyocardial inflammation predicts adverse outcome in patients with cardiac AL amyloidosis

Response Gene to Complement-32 Promotes the Imbalance of Treg/Th17 in Patients with Dilated Cardiomyopathy

Advanced cardiovascular imaging for the evaluation of cardiac sarcoidosis

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