Circulating concentrations of proinflammatory cytolcines in mild or moderate heart failure secondary to ischemic or idiopathic dilated cardiomyopathy

Munger, Mark; Johnson, Barbara; Amber, Ina J.; Callahan, Karleen S.; Gilbert, Edward M.

doi:10.1016/s0002-9149(97)89206-5

Cited by 226 publications

(141 citation statements)

References 17 publications

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“…Recent studies have demonstrated that the development of DCM is accompanied by increased circulating levels of these specific cytokines. 37,38 Thus increased levels of specific cytokines with the development of DCM may modulate MMP species abundance. The MMPs are a family of metalloproteinases in which catalytic activity is influenced by substrate product stoichiometry.…”

Section: Discussionmentioning

confidence: 99%

“…Several recent studies have examined the use of synthetic MMP inhibitors in various disease states. 38,44,45 For example, Wang et al 45 recently reported that MMP inhibitor treatment reduced adenocarcinoma growth, spread, and metastasis in mice. Thus pharmacologic inhibition of MMP activity may directly influence extracellular remodeling in several disease states.…”

Section: Discussionmentioning

confidence: 99%

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Increased Matrix Metalloproteinase Activity and Selective Upregulation in LV Myocardium From Patients With End-Stage Dilated Cardiomyopathy

et al. 1998

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Background-One of the hallmarks of dilated cardiomyopathy (DCM) is left ventricular (LV) remodeling. The matrix metalloproteinases (MMPs) are a family of enzymes that contribute to extracellular remodeling in several disease states. Additionally, a family of inhibitors called tissue inhibitors of MMPs (TIMPs) has been shown to exist and to tightly regulate MMP activity. However, the types of MMPs and TIMPs expressed within the normal and DCM LV myocardium and the relation to MMP activity remain unexplored. Methods and Results-Relative LV myocardial MMP activity was determined in the normal (nϭ8) and idiopathic DCM (nϭ7) human LV myocardium by substrate zymography. Relative LV myocardial abundance of interstitial collagenase (MMP-1), stromelysin (MMP-3), 72 kD gelatinase (MMP-2), 92 kD gelatinase (MMP-9), TIMP-1, and TIMP-2 were measured with quantitative immunoblotting. LV myocardial MMP zymographic activity increased with DCM compared with normal (984Ϯ149 versus 413Ϯ64 pixels, PϽ.05). With DCM, LV myocardial abundance of MMP-1 decreased to 16Ϯ6% (PϽ.05), MMP-3 increased to 563Ϯ212% (PϽ.05), MMP-9 increased to 422Ϯ64% (PϽ.05), and MMP-2 was unchanged when compared with normal. LV myocardial abundance of TIMP-1 and TIMP-2 increased by Ͼ500% with DCM. A high-molecular-weight immunoreactive band for both TIMP-1 and TIMP-2, suggesting a TIMP/MMP complex, was increased Ͼ600% with DCM. Conclusions-This study demonstrated increased LV myocardial MMP activity and evidence for independent regulatory mechanisms of MMP and TIMP expression with DCM. These findings suggest that selective inhibition of MMP species within the LV myocardium may provide a novel therapeutic target in patients with DCM.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Increased Matrix Metalloproteinase Activity and Selective Upregulation in LV Myocardium From Patients With End-Stage Dilated Cardiomyopathy

et al. 1998

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“…Interleukin-6 and coronary heart disease: Recently, increased levels of circulating IL-6 and CRP have been also associated with high risk of all-cause mortality in older people. 7,23) Serum levels of IL-6, along with other cytokines, have also been associated with unfavorable clinical outcomes in patients hospitalized for unstable angina.…”

Section: )mentioning

confidence: 99%

Interleukin-6 and Cardiovascular Diseases

2004

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SUMMARYInflammatory cytokines are important for both cardiovascular scientists and practicing clinicians. Interleukin-6 (IL-6) has been emphasized by reports of elevated circulating as well as intracardiac IL-6 levels in patients with congestive heart failure (CHF). IL-6 may contribute to the progression of myocardial damage and dysfunction in chronic heart failure syndrome resulting from different causes. As the cause of CHF in cardiomyopathy, myocarditis, allograft rejection, and left ventricular assist device (LVADs) conditions, circulating IL-6 levels are associated with the severity of left ventricular dysfunction, and are also strong predictors of subsequent clinical outcomes. Continuous and excessive production of IL-6 promotes myocardial injury by breaking down both cytokine networks and viral clearance under viral myocarditis. Although IL-6 is likely important in the process of viral antigen presentation, early activation of immune responses and attenuation of viral replication also appear to be significant in an animal model of viral myocarditis. IL-6 can cause cardiac hypertrophy through the IL-6 signal transducing receptor component, glycoprotein 130. There are several interesting cases of cardiac myxoma complicated with mediastinal lymphadenopathy or left ventricular hypertrophy. Increased expression of IL-6 is observed in the myocardium of all donor hearts showing marked dysfunction. Myocardial IL-6 concentrations are also significantly higher in LVAD candidates compared with advanced heart failure patients. Although the IL-6 family plays a central role in the pathophysiology of cardiovascular diseases, it remains to be determined whether the IL-6 family is beneficial or detrimental. Future study will be needed to resolve this question. (Jpn Heart J 2004; 45: 183-193)

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“…In the present study, we observed elevated levels of this cytokine only in 6.9% of patients; this result is similar to that reported by van Riemsdijk-van Overbeeke et al 31 , who failed to detect serum levels of free TNFα in HF patients notwithstanding their finding of elevated levels of TNFα soluble receptors with increased binding capacity, which explained the low TNFα bioavailability. Additionally, no change in the levels of this cytokine when compared to control healthy individuals was reported in two other studies done in patients with mild or moderate heart failure [32][33] .…”

Section: Discussionmentioning

confidence: 80%

Prevalence of Trypanosoma cruzi antibodies and inflammatory markers in uncompensated heart failure

Bravo-Tobar

Parra²,

Pérez

et al. 2011

Rev. Soc. Bras. Med. Trop.

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Introduction: Heart failure (HF) represents the final stage of chronic chagasic cardiomyopathy (CChC). The diagnosis of CChC is based on the demonstration of anti-Trypanosoma cruzi antibodies (aTcAg) and clinical and epidemiological data. In Venezuela, there are no data about the prevalence of chagasic HF. The aim of this study was to determine the epidemiological, clinical, and inflammatory risk factors associated with seronegative or seropositive HF patients. Methods: We performed a cross-sectional study in the Venezuelan central-west states among a healthy rural population and in patients admitted to the emergency room with uncompensated HF. Results: The seroprevalence rates of Trypanosoma cruzi antibodies were 11.2% and 40.1% in the healthy population and in HF patients, respectively. Seropositivity in healthy individuals was associated with age, knowledge on triatomine vectors, and having seen wild reservoirs in the house; in HF patients, with contact with the vector and previous clinical diagnosis of Chagas' disease; and in both groups taken together, with age, knowledge on triatomines, and HF. Seropositive patients had prolonged QRS, decreased ejection fraction, and high serum magnesium, all significant as compared with HF seronegative cases. Left atrium enlargement and ventricular hypertrophy were most frequently observed in HF seronegative patients. CRP, IL6, ILβ1, IL2, and FNTα were elevated in 94.5%, 48%, 17.8%, 13.7%, and 6.9% of HF patients, respectively, but only IL2 levels were associated with chagasic HF. Conclusions: There is a high prevalence of aTcAg in HF patients from the central-west region of Venezuela, and their epidemiological, clinical, and inflammatory features are discreetly different as compared with those of seronegative cases.

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Circulating concentrations of proinflammatory cytolcines in mild or moderate heart failure secondary to ischemic or idiopathic dilated cardiomyopathy

Cited by 226 publications

References 17 publications

Increased Matrix Metalloproteinase Activity and Selective Upregulation in LV Myocardium From Patients With End-Stage Dilated Cardiomyopathy

Increased Matrix Metalloproteinase Activity and Selective Upregulation in LV Myocardium From Patients With End-Stage Dilated Cardiomyopathy

Interleukin-6 and Cardiovascular Diseases

Prevalence of Trypanosoma cruzi antibodies and inflammatory markers in uncompensated heart failure

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