Inflammatory Mediators and Clinical Outcome in Patients With Advanced Heart Failure Receiving Cardiac Resynchronization Therapy

Belperio, John A.; Horwich, Tamara B.; Abraham, William T.; Fonarow, Gregg C.; Gorcsan, John; Bersohn, Malcolm; Singh, Jagmeet P.; Sonel, Ali F.; Lee, Li Yin; Halilovic, Jasmina; Kadish, Alan H.; Shalaby, Alaa

doi:10.1016/j.amjcard.2015.11.049

Cited by 16 publications

(9 citation statements)

References 26 publications

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“…It is hypothesized that CRT reduces inflammation and that it may be one of the several factors responsible for improving the symptoms of HF. However, the available literature reports conflicting results and suggests that the role of CRT in reducing inflammation is not uniform, rather it shows variations due to different interactions occurring during the disease process [27,28]. It was also found in the present study that no significant change occured in the levels of inflammatory biomarkers, except in IL-6.…”

Section: Responderscontrasting

confidence: 52%

Evaluating the effects of cardiac resynchronization therapy on pathophysiological pathways of heart failure using surrogate biomarkers

et al. 2018

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Section: Responderscontrasting

confidence: 52%

Evaluating the effects of cardiac resynchronization therapy on pathophysiological pathways of heart failure using surrogate biomarkers

et al. 2018

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“…Reverse remodeling in CRT responders has been proved to be closely associated with cardiac fibrotic environment driven by inflammatory cytokines . It is reported that midwall fibrosis is an independent predictor of mortality and morbidity in patients with DCM undergoing CRT .…”

Section: Discussionmentioning

confidence: 99%

Effect of Cardiac Resynchronization Therapy on Myocardial Fibrosis and Relevant Cytokines in a Canine Model With Experimental Heart Failure

Wang

Gong

Chen

et al. 2017

Cardiovasc electrophysiol

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“…Obviously, the electrical signal also induces anti-inflammatory effects at the molecular level, which in turn affect the extracellular matrix and cardiomyocyte function. 24 Another approach is treating heart failure by applying a high-energy electrical stimulus during the refractory phase of the cardiac cycle, as is intended with the CCM device. One relevant observed effect is an increase in the level of myocyte calcium in the cytosol during systole, which accompanies moderate clinical improvement.…”

Section: Application Of Electrical Signalmentioning

confidence: 99%

Bioelectrical signals improve cardiac function and modify gene expression of extracellular matrix components

et al. 2017

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AimsBeyond the influence of stimulating devices on cardiac excitation, their use in treating patients with heart failure has positive effects on the myocardium at the molecular level. Electrical signals can induce a wide spectrum of effects in living tissue. Therefore, we sought to determine whether applying electrical microcurrent directly to failing hearts leads to functional improvement.Methods and resultsSixteen male spontaneously hypertensive rats (SHRs) with heart failure underwent application of a patch electrode to the left ventricular epicardium and placement of a subcutaneous counter electrode. The electrode delivered a 0.35 μA microcurrent to nine of the SHRs for 45 ± 3 days; the other seven SHRs were used as controls. At baseline and before the SHRs were humanely put to death, we measured the left ventricular ejection fraction (LVEF) and the thickness of the LV posterior wall during systole and diastole (LVPWs/d). We used quantitative PCR to determine extracellular matrix parameters [collagen I–III, matrix metalloproteinase (MMP)‐2, MMP‐9, tissue inhibitor of metalloproteinases 3 (TIMP3), TIMP4, connexins (Cxs) 40/43/45, transforming growth factor (TGF)‐β, and interleukin (IL)‐6].Among SHRs undergoing microcurrent application, LVEF normalized (mean decrease, 22.8%; P = 0.009), and LVPWs decreased (mean, 35.3%; P = 0.001). Compared with the control group, the SHRs receiving microcurrent exhibited a mean decrease in the gene expression of collagen I (10.6%, P = 0.003), TIMP3 (18.5%, P = 0.005), Cx43 (14.3%, P = 0.003), Cx45 (12.7%, P = 0.020), TGF‐β (13.0%, P = 0.005), and IL‐6 (53.7%, P = 0.000). Microcurrent application induced no changes in the expression of collagen III, MMP‐2, MMP‐9, TIMP4, or Cx40.ConclusionsApplying microcurrent to the LV epicardium of SHRs leads to statistically significant functional improvement and alterations in the levels of inflammatory and extracellular matrix components.

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Inflammatory Mediators and Clinical Outcome in Patients With Advanced Heart Failure Receiving Cardiac Resynchronization Therapy

Cited by 16 publications

References 26 publications

Evaluating the effects of cardiac resynchronization therapy on pathophysiological pathways of heart failure using surrogate biomarkers

Evaluating the effects of cardiac resynchronization therapy on pathophysiological pathways of heart failure using surrogate biomarkers

Effect of Cardiac Resynchronization Therapy on Myocardial Fibrosis and Relevant Cytokines in a Canine Model With Experimental Heart Failure

Bioelectrical signals improve cardiac function and modify gene expression of extracellular matrix components

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