Inflammation as a Driver of Adverse Left Ventricular Remodeling After Acute Myocardial Infarction

Westman, Peter C.; Lipinski, Michael J.; Luger, Dror; Waksman, Ron; Bonow, Robert O.; Wu, Edwin; Epstein, Stephen E.

doi:10.1016/j.jacc.2016.01.073

Cited by 388 publications

(360 citation statements)

References 75 publications

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“…The mechanism of harmful heart remodelling after a MI includes numerous cellular, extracellular and neurohumoral components 8 and in most cases, the size of scar formed is proportionate to the severity of heart remodelling, but it has also been demonstrated that size of scar need not translate into severe heart remodelling. 9 …”

Section: Introductionmentioning

confidence: 99%

Improvements in long standing cardiac pathologies by individualized homeopathic remedies: A case series

Tenzera¹,

Djindjić

Mihajlovic-Elez³

et al. 2018

SAGE Open Medical Case Reports

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We present three cases of cardiac arrest at different stages of pathology. Acute myocardial infarction and resulting heart failure is emerging as the leading cause of mortality. In the long run, acute episodes and cardiac remodelling can cause considerable damage and result in heart failure. In these cases, individualized homeopathic therapy was instituted along with the conventional medicines and the results were encouraging. The changes in the laboratory diagnostic parameters (single-photon emission computed tomography, electrocardiograph, echocardiography and ejection fraction as the case may be) are demonstrated over time. The key result seen in all three cases was the preservation of general well-being while the haemodynamic states also improved. While the three cases provide evidence of positive outcomes for homeopathic therapy, more extensive studies are required in a hospital setting to establish the real extent to which this therapy may be employed.

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Section: Introductionmentioning

confidence: 99%

Improvements in long standing cardiac pathologies by individualized homeopathic remedies: A case series

Tenzera¹,

Djindjić

Mihajlovic-Elez³

et al. 2018

SAGE Open Medical Case Reports

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“…Inflammation is at the center stage of pathologic cardiac remodeling and heart failure. 29,30 Previous reports have shown that lessened T-cell activation is correlated with diminished cardiac inflammation in the setting of POL. 5,6 We presented that TMRKO mice manifested reduced cardiac inflammation in parallel with improved cardiac remodeling, as well as decreased T-cell accumulation and activation in the heart after POL.…”

Section: Discussionmentioning

confidence: 99%

“…29, 30 We next determined whether TMRKO affected cardiac inflammation. Accumulation of myeloid cells in the heart was first analyzed using flow cytometry ( Figure S5).…”

Section: T-cell Mr Deficiency Decreases Aac-induced Cardiac Inflammatmentioning

confidence: 99%

Mineralocorticoid Receptor Deficiency in T Cells Attenuates Pressure Overload–Induced Cardiac Hypertrophy and Dysfunction Through Modulating T-Cell Activation

Sun

et al. 2017

Hypertension

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Although antagonists of mineralocorticoid receptor (MR) have been widely used to treat heart failure, the underlying mechanisms are incompletely understood. Recent reports show that T cells play important roles in pathologic cardiac hypertrophy and heart failure. However, it is unclear whether and how MR functions in T cells under these pathologic conditions. We found that MR antagonist suppressed abdominal aortic constriction–induced cardiac hypertrophy and decreased the accumulation and activation of CD4 + and CD8 + T cells in mouse heart. T-cell MR knockout mice manifested suppressed cardiac hypertrophy, fibrosis, and dysfunction compared with littermate control mice after abdominal aortic constriction. T-cell MR knockout mice had less cardiac inflammatory response, which was illustrated by decreased accumulation of myeloid cells and reduced expression of inflammatory cytokines. Less amounts and activation of T cells were observed in the heart of T-cell MR knockout mice after abdominal aortic constriction. In vitro studies showed that both MR antagonism and deficiency repressed activation of T cells, whereas MR overexpression elevated activation of T cells. These results demonstrated that MR blockade in T cells protected against abdominal aortic constriction–induced cardiac hypertrophy and dysfunction. Mechanistically, MR directly regulated T-cell activation and modulated cardiac inflammation. Targeting MR in T cells specifically may be a feasible strategy for more effective treatment of pathologic cardiac hypertrophy and heart failure.

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“…

A long‐term, inappropriate, and excessive inflammatory process contributes importantly to the progressive myocardial deterioration that occurs after AMI and that occurs in patients with HF.

The concept that the progressive deterioration of cardiac function seen in both AMI and HF is in part caused by an excessive persistent inflammatory response has a compelling experimental basis supporting its validity 11, 12. For example, in the setting of AMI, there is a subgroup of patients whose progressive deterioration in left ventricular function is not caused solely by the AMI‐induced magnitude of myocardial damage, but involves other mechanisms 13. Chronic inflammation has been postulated as being one of these mechanisms responsible for progressive myocardial dysfunction in AMI, and also in HF 11, 12, 13, 14, 15

…”

mentioning

confidence: 99%

“…For example, in the setting of AMI, there is a subgroup of patients whose progressive deterioration in left ventricular function is not caused solely by the AMI‐induced magnitude of myocardial damage, but involves other mechanisms 13. Chronic inflammation has been postulated as being one of these mechanisms responsible for progressive myocardial dysfunction in AMI, and also in HF 11, 12, 13, 14, 15

Systemic anti‐inflammatory effects of MSCs constitute one of the major mechanisms by which MSCs may improve left ventricular function.

Any myocardial benefit provided by stem cell administration is undoubtedly not caused by repopulating the damaged myocardium with new myocytes, but rather by paracrine activities with a diverse array of beneficial effects 12, 16, 17.

…”

mentioning

confidence: 99%

Persistent Inflammation, Stem Cell–Induced Systemic Anti‐Inflammatory Effects, and Need for Repeated Stem Cell Injections: Critical Concepts Influencing Optimal Stem Cell Strategies for Treating Acute Myocardial Infarction and Heart Failure

Epstein

Lipinski

Luger

2018

JAHA

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Inflammation as a Driver of Adverse Left Ventricular Remodeling After Acute Myocardial Infarction

Cited by 388 publications

References 75 publications

Improvements in long standing cardiac pathologies by individualized homeopathic remedies: A case series

Improvements in long standing cardiac pathologies by individualized homeopathic remedies: A case series

Mineralocorticoid Receptor Deficiency in T Cells Attenuates Pressure Overload–Induced Cardiac Hypertrophy and Dysfunction Through Modulating T-Cell Activation

Persistent Inflammation, Stem Cell–Induced Systemic Anti‐Inflammatory Effects, and Need for Repeated Stem Cell Injections: Critical Concepts Influencing Optimal Stem Cell Strategies for Treating Acute Myocardial Infarction and Heart Failure

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