Remodelling after an Infarct: Crosstalk between Life and Death

Ferrari, Roberto; Malagù, Michele; Biscaglia, Simone; Fucili, Alessandro; Rizzo, Paola

doi:10.1159/000445882

Cited by 12 publications

(24 citation statements)

References 40 publications

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“…This curve of NT-proBNP-Time re ect that Sacubitril/Valsartan could be a vital medicine in reducing NT-proBNP to a certain extent. ANP and BNP act via natriuretic peptide G protein-coupled transmembrane receptors activating cGMP as second messenger which, in turn, exerts natriuretic, diuretic and vasodilating action [18] . Some of the peptides substrate for neprylisin are known to play a role in HF, such as natriuretic peptides, angiotensin, endothelin, bradykinin, substance P, aldosterone, and arginine vasopressin.…”

Section: Discussionmentioning

confidence: 99%

Use of Sacubitril/Valsartan in a Chronic Heart Failure Patient with Reduced Ejection Fraction Accompany Dilated Cardiomyopathy and Myocardial Indensification: A Case Report

Dai¹,

Zhang²,

Xiao³

2020

Preprint

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Rationale: Dilated cardiomyopathy (DCM) is a progressive cardiac disease characterized by ventricular dilation and contractile dysfunction and is the third most common cause of heart failure and the most common cause of heart transplantation. Heart failure (HF) and atrial fibrillation (AF) often coexist and share a mutually beneficial relationship. The presence of atrial fibrillation increases the tendency for heart failure, which can worsen its severity and increase the risk of stroke. DCM、AF and HF are causal to each other in pathophysiological view. However, how these pathogens translates upon acute decompensation heart failure(ADHF) is unknown. Control acute attack of chronic heart failure is the first step of treatment.Case summary: Herein, we described a 68-year-old man with acute decompensated heart failure (ADHF) with severe DCM and atrial fibrillation who was treated with Sacubitril/Valsartan and had a reduced ejection fraction. The patient’s echocardiography features had a significant improvement under taking Sacubitril/Valsartan. Sacubitril/Valsartan may act as an intermediary that balancing of the good and the bad neuroendocrine response.Discussion: DCM is a major cardiomyopathy and a major cause of heart transplantation. DCM’s clinical prognosis is poor, additionally, along with myocardial indensification, early diagnosis and treatment is helpful to prolong the patients' life. The emergence of Sacubitril/Valsartan represents the advent of a new strategy for treating HFrEF. Its beneficial effects are related in part, at least, to an improvement of echocardiographic features and positive modulation of the neuroendocrine response to HF.

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Section: Discussionmentioning

confidence: 99%

Use of Sacubitril/Valsartan in a Chronic Heart Failure Patient with Reduced Ejection Fraction Accompany Dilated Cardiomyopathy and Myocardial Indensification: A Case Report

Dai¹,

Zhang²,

Xiao³

2020

Preprint

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“…arginine vasopressin system, renin-angiotensin-aldosterone system [RAAS], and adrenergic activation). 1,3,[5][6][7][8][9][10][11][12][13][14][15][16][17] Temporally, classical remodeling might be further categorized into 2 phases17: the early phase (within the first 3 days after AMI) primarily characterized by infarct expansion (leading to wall thinning and chamber dilatation), and the late phase (beyond 3 days) characterized by myocyte hypertrophy as well as diffuse fibrosis involving the infarcted and remote myocardial segments. 17 However, the abovementioned conventional insights have been already discussed in detail elsewhere 1,3,[5][6][7][8][9][10][11][12][13][14][15][16][17] and hence are not within the scope of this review.…”

Section: Classical (Early) Myocardial Remodeling After Ami: Novel Insmentioning

confidence: 99%

“…4 However, a couple of reports have exclusively regarded "late AMR" as a variety of morphological changes representing later stages of classical early AMR (characterized by compensatory hypertrophy and dysfunction involving remote myocardium and usually arising 1 month after AMI) rather than a distinct phenomenon with a de novo presentation. 8,9 Notably, these late changes were also suggested to serve as the fundamental determinants of prognosis among AMI survivors. 9 Surprisingly, there has been no clear-cut and uniform categorization of myocardial remodeling suggested so far based on temporal trends and characteristics along with no mention of late AMR as a separate clinical and pathophysiological entity in the post-AMI setting.…”

Section: Introductionmentioning

confidence: 99%

“…8,9 Notably, these late changes were also suggested to serve as the fundamental determinants of prognosis among AMI survivors. 9 Surprisingly, there has been no clear-cut and uniform categorization of myocardial remodeling suggested so far based on temporal trends and characteristics along with no mention of late AMR as a separate clinical and pathophysiological entity in the post-AMI setting. However, late AMR should not be regarded simply as the late stage of classical early AMR, but as a late-onset phenomenon (with a significant latent period) with diverse mechanisms and implications as compared with its early counterpart in the setting of AMI (including its particular association with persistent systemic inflammation).…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Late Versus Early Myocardial Remodeling After Acute Myocardial Infarction: A Comparative Review on Mechanistic Insights and Clinical Implications

Yalta

Yilmaz

Yalta

et al. 2019

J Cardiovasc Pharmacol Ther

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In the setting of acute myocardial infarction (AMI), adverse myocardial remodeling (AMR) has been universally regarded as an early-onset phenomenon generally arising within the first few weeks (usually within days in the infarct zone) following myocardial injury. On the other hand, onset of cardiac morphological changes in this setting may potentially extend far beyond this time frame (usually beyond several months after the index AMI), suggesting a prolonged latent period in certain cases. In clinical practice, this delayed form of post-AMI remodeling, namely late AMR, has emerged as an interesting and underrecognized phenomenon with poorly understood mechanisms. Notably, systemic inflammation and associated growth factors seem to play a pivotal role in this setting. Accordingly, the present article primarily aims to discuss potential mechanisms and clinical implications of late AMR (in a comparative manner with its classical early counterpart) among AMI survivors along with a particular emphasis on potential benefits of certain anti-inflammatory strategies in this setting.

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“…This year, the focus of the Keynote Lecture was reperfusion injury and was presented by Prof. Roberto Ferrari, Dean of the University of Ferrara School of Medicine, one of the world's preeminent figures in this area. Prof. Ferrari has committed his lecture to a written review, published in two parts in the previous [1] and in this issue [2] of Cardiology . We believe this is the definitive current statement on the pathophysiology of reperfusion injury, pointing to approaches for evaluation and therapy.…”

mentioning

confidence: 99%