Chronic Heart Failure and Inflammation

Dick, Sarah A.; Epelman, Slava

doi:10.1161/circresaha.116.308030

Cited by 496 publications

(377 citation statements)

References 178 publications

Supporting

Mentioning

352

Contrasting

Unclassified

Order By: Relevance

“…34 It is well-recognized that proinflammatory cytokines, particularly TNF-α, are upregulated in patients with chronic heart failure. Furthermore, animal models have demonstrated that proinflammatory cytokines, including IL-6 and TNF-α (Table 2), are increased during heart failure progression.…”

Section: Inflammationmentioning

confidence: 99%

“…Furthermore, animal models have demonstrated that proinflammatory cytokines, including IL-6 and TNF-α (Table 2), are increased during heart failure progression. 34 Demonstrating this in humans, hsCRP is independently associated with mortality in patients admitted with decompensated heart failure.148 However, negative results from clinical trials of treatments targeting inflammation cast doubt over the issue of whether these inflammatory pathways are causal. …”

mentioning

confidence: 99%

See 1 more Smart Citation

Novel Risk Markers and Risk Assessments for Cardiovascular Disease

Thomas

Lip

2017

Circulation Research

111

View full text Add to dashboard Cite

Abstract:The use of risk markers has transformed cardiovascular medicine, exemplified by the routine assessment of troponin, for both diagnosis and assessment of prognosis in patients with chest pain. Clinical risk factors form the basis for risk assessment of cardiovascular disease and the addition of biochemical, cellular, and imaging parameters offers further refinement. Identifying novel risk factors may allow greater risk stratification and a steady, but gradual progression toward precision medicine. Indeed, the generation of data in this area of research is explosive and when combined with new technologies and techniques provides the potential for more refined, targeted approaches to cardiovascular medicine. Although discussing the most recent developments in this field, this review article aims to strike a balance between novelty and validity by focusing on recent large samplesize studies that have been validated in a separate cohort in most cases. Risk markers related to atherosclerosis, thrombosis, inflammation, cardiac injury, and fibrosis are introduced in the context of their pathophysiology. Rapidly developing new areas, such as assessment of micro-RNA, are also explored. Subsequently the prognostic ability of these risk markers in coronary artery disease, heart failure, and atrial fibrillation is discussed in detail. ( addition to these roles in the pathogenesis of coronary artery disease, lipid-related molecules have been identified to be markers of inflammation and oxidative stress (Table 1). Thrombosis-Related Risk MarkersAfter atherosclerotic plaque rupture, platelets adhere to exposed subendothelial components, such as collagen and von Willebrand factor, which promotes platelet activation and aggregation. 10 In addition, platelet activation is potentiated by exposure to released soluble agonists, such as thrombin and ADP.10 Activated platelets then further release ADP, which acts on platelet P2Y 12 ADP receptors and has a central role in amplifying the response of platelets to the initial stimulus. 10 Platelet reactivity to various agonists, including ADP, has been studied extensively in the context of acute coronary syndrome (ACS; Table 2). 11 The VerifyNow and Multiplate pointof-care tests allow for the measurement of platelet aggregation in response to stimulation, and it has been shown that high platelet reactivity is associated with adverse cardiovascular events. 26 Platelet microparticles are released on platelet activation, and their role in cardiovascular disease is an area of active investigation (Table 2). 15 Circulating microparticles are released from cells undergoing activation or apoptosis and are a type of small plasma membrane vesicle that retain defined properties from their original cell lineage. 15 Platelet activation and aggregation lead to the activation of the coagulation cascade and the formation of a stable crosslinked fibrin clot. The balance between prothrombotic factors and endogenous fibrinolysis determines whether the thrombus propagates or instead proceeds to dis...

show abstract

Section: Inflammationmentioning

confidence: 99%

mentioning

confidence: 99%

Novel Risk Markers and Risk Assessments for Cardiovascular Disease

Thomas

Lip

2017

Circulation Research

111

View full text Add to dashboard Cite

show abstract

“…For example, it is well known that HF is associated with a chronic state of inflammation11, 39 and the intestinal microbiome might not only be addressed as a target of systemic inflammation, but also as a trigger for this pathomechanism. Of note, this linkage has been proposed in several other inflammatory diseases such as rheumatoid arthritis 40.…”

Section: Discussionmentioning

confidence: 99%

Heart failure is associated with depletion of core intestinal microbiota

Luedde¹,

et al. 2017

View full text Add to dashboard Cite

AimsIn spite of current medical treatment approaches, mortality of chronic heart failure (HF) remains high and novel treatment modalities are thus urgently needed. A recent theory proposes a possible impact of the intestinal microbiome on the incidence and clinical course of heart failure. This study sought to systematically investigate, if there are specific changes of the intestinal microbiome in heart failure patients.Methods and resultsThe intestinal microbiome of 20 patients with heart failure with reduced ejection fraction due to ischemic or dilated cardiomyopathy was investigated by applying high‐throughput sequencing of the bacterial 16S rRNA gene. Microbial profiles were compared to those of matched controls in which heart failure was ruled out by clinical assessment and NT‐proBNP serum levels (n = 20). According to the Shannon diversity index (which measures the intra‐individual alpha‐diversity) based on the distribution of operational taxonomic units (OTUs), HF cases showed a nominally significantly lower diversity index compared to controls (P nom. = 0.01), and testing for genera abundance showed a tendency towards a decreased alpha diversity of HF patients. Beta‐diversity measures (inter‐individual diversity) revealed a highly significant separation of HF cases and controls, (e.g. P weighted UniFracv = 0.004). Assessing the individual abundance of core measurable microbiota (CMM), a significant decrease of Coriobacteriaceae, Erysipelotrichaceae and Ruminococcaceae was observed on the family level. In line with that, Blautia, Collinsella, uncl. Erysipelotrichaceae and uncl. Ruminococcaceae showed a significant decrease in HF cases compared to controls on the genus level.ConclusionsHeart failure patients showed a significantly decreased diversity of the intestinal microbiome as well as a downregulation of key intestinal bacterial groups. Our data point to an altered intestinal microbiome as a potential player in the pathogenesis and progression of heart failure.

show abstract

“…Relatively high or inappropriately normal hepcidin levels can be found also in ID patients with a concomitant inflammatory disorder [67,68]. The best studied condition in this sense is chronic heart failure (CHF), where low-grade chronic inflammation is known to play an important role [69]. ID is quite common in CHF, involving at least 30% of patients [70,71].…”

Section: Oral Iron Therapy In the Hepcidin Eramentioning

confidence: 99%

Modern iron replacement therapy: clinical and pathophysiological insights

et al. 2017

View full text Add to dashboard Cite

Iron deficiency, with or without anemia, is extremely frequent worldwide, representing a major public health problem. Iron replacement therapy dates back to the seventeenth century, and has progressed relatively slowly until recently. Both oral and intravenous traditional iron formulations are known to be far from ideal, mainly because of tolerability and safety issues, respectively. At the beginning of this century, the discovery of hepcidin/ferroportin axis has represented a turning point in the knowledge of the pathophysiology of iron metabolism disorders, ushering a new era. In the meantime, advances in the pharmaceutical technologies are producing newer iron formulations aimed at minimizing the problems inherent with traditional approaches. The pharmacokinetic of oral and parenteral iron is substantially different, and diversities have become even clearer in light of the hepcidin master role in regulating systemic iron homeostasis. Here we review how iron therapy is changing because of such important advances in both pathophysiology and pharmacology.

show abstract

Chronic Heart Failure and Inflammation

Cited by 496 publications

References 178 publications

Novel Risk Markers and Risk Assessments for Cardiovascular Disease

Novel Risk Markers and Risk Assessments for Cardiovascular Disease

Heart failure is associated with depletion of core intestinal microbiota

Modern iron replacement therapy: clinical and pathophysiological insights

Contact Info

Product

Resources

About