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Open AccessJournal ArticleDOI

The inflammatory response in myocardial injury, repair, and remodelling.

TLDR
Biomarker-based approaches are needed to identify patients with distinct pathophysiologic responses and to rationally implement inflammation-modulating strategies in patients with myocardial infarction.
Abstract
Myocardial infarction triggers an intense inflammatory response that is essential for cardiac repair, but which is also implicated in the pathogenesis of postinfarction remodelling and heart failure. Signals in the infarcted myocardium activate toll-like receptor signalling, while complement activation and generation of reactive oxygen species induce cytokine and chemokine upregulation. Leukocytes recruited to the infarcted area, remove dead cells and matrix debris by phagocytosis, while preparing the area for scar formation. Timely repression of the inflammatory response is critical for effective healing, and is followed by activation of myofibroblasts that secrete matrix proteins in the infarcted area. Members of the transforming growth factor β family are critically involved in suppression of inflammation and activation of a profibrotic programme. Translation of these concepts to the clinic requires an understanding of the pathophysiological complexity and heterogeneity of postinfarction remodelling in patients with myocardial infarction. Individuals with an overactive and prolonged postinfarction inflammatory response might exhibit left ventricular dilatation and systolic dysfunction and might benefit from targeted anti-IL-1 or anti-chemokine therapies, whereas patients with an exaggerated fibrogenic reaction can develop heart failure with preserved ejection fraction and might require inhibition of the Smad3 (mothers against decapentaplegic homolog 3) cascade. Biomarker-based approaches are needed to identify patients with distinct pathophysiologic responses and to rationally implement inflammation-modulating strategies.

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Journal ArticleDOI

Innate immune response in the pathogenesis of heart failure in survivors of myocardial infarction

TL;DR: This review presents short- and long-term features of post-MI in human hearts and animal models, and indicates that blunting of this innate immune cardiomyocyte response may offer new hope for the management of HF.
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Usefulness of Enzyme-Free and Enzyme-Resistant Detection of Complement Component 5 to Evaluate Acute Myocardial Infarction

TL;DR: In this paper , the traditional antibody-based target recognition and enzyme-based signal amplification are replaced with synthetic probe and metal ion-catalyzed cross-linking reaction for detecting complement component 5 (C5) protein.
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Temporal cascade of inflammatory cytokines and cell-type populations in monocyte chemotactic protein-1 (MCP-1)-mediated aneurysm healing.

TL;DR: The sequential cascade of aneurysm healing occurred in stages characteristic of normal wound healing and is consistent with an inflammatory model of injury, repair, and remodeling.
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Monoamine oxidase-dependent histamine catabolism accounts for post-ischemic cardiac redox imbalance and injury.

TL;DR: It is demonstrated that exogenous histamine is transported into isolated cardiomyocytes and triggers a rise in the levels of reactive oxygen species (ROS) and pargyline pretreatment induced intracellular accumulation of N1-methylhistamine along with decrease in ROS levels.
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Left ventricular end-systolic volume as the major determinant of survival after recovery from myocardial infarction.

TL;DR: Volume, ejection fractions, and severity of coronary arterial occlusions and stenoses in 605 male patients under 60 years of age at 1 to 2 months after a first or recurrent myocardial infarction showed that end-systolic volume had greater predictive value for survival than end-diastolic volume or ejection fraction.
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Cardiac remodeling—concepts and clinical implications: a consensus paper from an international forum on cardiac remodeling

TL;DR: Left ventricular end-diastolic and end-systolic volume and ejection fraction data provide support for the beneficial effects of therapeutic agents such as angiotensin-converting enzyme (ACE) inhibitors and beta-adrenergic blocking agents on the remodeling process.
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