Interleukin-6 correlates with hemodynamic impairment during dobutamine administration in chronic heart failure

Deng, Mario C.; Erren, Michael; Lütgen, Andreas; Zimmermann, Pia; Brisse, B; Schmitz, Wilhelm; Assmann, Gerd; Breithardt, Günter; Scheld, Hans H.

doi:10.1016/s0167-5273(96)02805-7

Cited by 40 publications

(27 citation statements)

References 15 publications

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“…Alternatively, we may assume that the elevation of IL-6 during DSE may be the consequence of the acute hemodynamic impairment resulting from the development of extensive WMAs at DSE, and acute deterioration of systolic LV function has been shown to occur in patients with congestive heart failure. 23 However, the relation between increasing IL-6 levels at rest and increasing number of ischemic myocardial segments at peak DSE suggests Figure 1. Individual values of IL-6 and TF plasma levels at baseline (rest), peak DSE (peak stress), and 30 minutes after cessation of dobutamine (recovery) in patients with ischemic (A, C) or nonischemic (B, D) response at peak stress.…”

Section: Il-6 Levelsmentioning

confidence: 97%

“…19,20 Additionally, WMAs may persist during recovery, and the time to recovery has been linked to the severity of myocardial ischemia at peak stress, the presence of multivessel disease, and the absence of collateral circulation at angiography. 21 IL-6 has a direct negative inotropic action on human myocardium, 22 has been associated with elevated intracardiac pressures in patients with ischemic cardiomyopathy, 23 and is induced during experimental ischemic models. 16 However, the relation between IL-6 plasma levels and the extent of new or worsening WMAs after DSE has not been investigated.…”

Section: Editorial P 3215mentioning

confidence: 99%

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Myocardial Ischemia Induces Interleukin-6 and Tissue Factor Production in Patients With Coronary Artery Disease

et al. 2005

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Background-Interleukin-6 (IL-6) and macrophage colony stimulating factor plasma levels are elevated in acute coronary syndromes. IL-6 has an inherent negative inotropic action and, with tissue factor (TF), mediates the ischemiareperfusion myocardial injury. We hypothesized that inducible ischemia leads to cytokine production, TF expression, and consequently persistent left ventricular dysfunction after dobutamine stress echocardiography (DSE) in coronary artery disease patients. Methods and Results-DSE was performed in 103 patients with angiographically documented coronary artery disease.Blood samples were obtained at rest, at peak stress, and 30 minutes after cessation of dobutamine infusion for measurement of macrophage colony stimulating factor, IL-6, and TF. New or worsening wall motion abnormalities at peak stress and their duration into recovery were noted. Median IL-6 and TF levels were increased at peak stress and at 30 minutes into recovery compared with rest (2.7 and 2.4 versus 2.1 pg/mL for IL-6, 310 and 385 versus 266 pg/mL for TF [PϽ0.01] in patients with an ischemic response; nϭ55). Compared with rest, a greater release of IL-6 at peak stress and recovery was observed in patients with increasing number of ischemic segments at peak DSE (2 versus 3 to 4 versus 5 to 6 versus 7 to 8 segments; Pϭ0.03). The time to recovery of wall motion abnormalities was also associated with IL-6 levels at peak stress and recovery (rϭ0. 51 and rϭ0.39, PϽ0.05). Macrophage colony stimulating factor levels remained unchanged throughout DSE. Conclusions-Reversible ischemia induced during DSE increases IL-6 and TF plasma levels. IL-6 is related to the extent of left ventricular dysfunction at peak stress and to persistent LV dysfunction during recovery. (Circulation. 2005;112: 3272-3279.)

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Section: Il-6 Levelsmentioning

confidence: 97%

Section: Editorial P 3215mentioning

confidence: 99%

Myocardial Ischemia Induces Interleukin-6 and Tissue Factor Production in Patients With Coronary Artery Disease

et al. 2005

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“…32) It is not clear whether this increase of circulating cytokines is mainly an epiphenomenon of the severity of the underlying cardiac impairment, 33) but in vitro and in vivo investigations suggest that the proinflammatory cytokines might depress myocardial contractility. 34) In a previous report we showed that the expression of IL-6 and the coexpressed ANP in IL-6-positive myocardium were observed in heart from autopsy cases of acute myocardial infarction.…”

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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“…This triggers immune system activation that provides shortterm compensation for the failing heart in an attempt to reverse OD. However, this immune system activation also coincides with progressive OD in the kidneys, liver, bone marrow and brain, profound metabolic derangements, creating a milieu similar to systemic diseases (10)(11)(12)(13)(14)(15)(16).…”

Section: Pathophysiology and Neuro-endocrino-immunology Of Adhfmentioning

confidence: 99%

Current indications for transplantation: stratification of severe heart failure and shared decision-making

Vucicevic¹,

Honoris²,

Raia³

et al. 2018

Ann. Cardiothorac. Surg.

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Heart failure (HF) is a complex clinical syndrome that results from structural or functional cardiovascular disorders causing a mismatch between demand and supply of oxygenated blood and consecutive failure of the body's organs. For those patients with stage D HF, advanced therapies, such as mechanical circulatory support (MCS) or heart transplantation (HTx), are potentially life-saving options. The role of risk stratification of patients with stage D HF in a value-based healthcare framework is to predict which subset might benefit from advanced HF (AdHF) therapies, to improve outcomes related to the individual patient including mortality, morbidity and patient experience as well as to optimize health care delivery system outcomes such as costeffectiveness. Risk stratification and subsequent outcome prediction as well as therapeutic recommendationmaking need to be based on the comparative survival benefit rationale. A robust model needs to (I) have the power to discriminate (i.e., to correctly risk stratify patients); (II) calibrate (i.e., to show agreement between the predicted and observed risk); (III) to be applicable to the general population; and (IV) provide good external validation. The Seattle Heart Failure Model (SHFM) and the Heart Failure Survival Score (HFSS) are two of the most widely utilized scores. However, outcomes for patients with HF are highly variable which make clinical predictions challenging. Despite our clinical expertise and current prediction tools, the best short-and long-term survival for the individual patient, particularly the sickest patient, is not easy to identify because among the most severely ill, elderly and frail patients, most preoperative prediction tools have the tendency to be imprecise in estimating risk. They should be used as a guide in a clinical encounter grounded in a culture of shared decision-making, with the expert healthcare professional team as consultants and the patient as an empowered decision-maker in a trustful safe therapeutic relationship.

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Interleukin-6 correlates with hemodynamic impairment during dobutamine administration in chronic heart failure

Cited by 40 publications

References 15 publications

Myocardial Ischemia Induces Interleukin-6 and Tissue Factor Production in Patients With Coronary Artery Disease

Myocardial Ischemia Induces Interleukin-6 and Tissue Factor Production in Patients With Coronary Artery Disease

Interleukin-6 and Cardiovascular Diseases

Current indications for transplantation: stratification of severe heart failure and shared decision-making

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