Wide-spread myocardial remodeling after acute myocardial infarction in rat. Features for heart failure progression

2008 ◽  
Vol 48 (2-3) ◽  
pp. 100-108 ◽  
Author(s):  
Tadeusz F. Krzemiński ◽  
Jerzy K. Nożyński ◽  
Joanna Grzyb ◽  
Maurycy Porc
Keyword(s):  
Myocardial Infarction ◽  
Heart Failure ◽  
Acute Myocardial Infarction ◽  
Myocardial Remodeling ◽  
Wide Spread ◽  
Heart Failure Progression

scholarly journals A Review of the Molecular Mechanisms Underlying the Development and Progression of Cardiac Remodeling

2017 ◽  
Vol 2017 ◽  
pp. 1-16 ◽  
Author(s):  
Leonardo Schirone ◽  
Maurizio Forte ◽  
Silvia Palmerio ◽  
Derek Yee ◽  
Cristina Nocella ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Heart Failure ◽  
Cardiac Remodeling ◽  
Molecular Mechanisms ◽  
Volume Overload ◽  
Cardiac Complications ◽  
Compensatory Mechanism ◽  
Myocardial Remodeling ◽  
Heart Failure Progression ◽  
Complex Signaling

Pathological molecular mechanisms involved in myocardial remodeling contribute to alter the existing structure of the heart, leading to cardiac dysfunction. Among the complex signaling network that characterizes myocardial remodeling, the distinct processes are myocyte loss, cardiac hypertrophy, alteration of extracellular matrix homeostasis, fibrosis, defective autophagy, metabolic abnormalities, and mitochondrial dysfunction. Several pathophysiological stimuli, such as pressure and volume overload, trigger the remodeling cascade, a process that initially confers protection to the heart as a compensatory mechanism. Yet chronic inflammation after myocardial infarction also leads to cardiac remodeling that, when prolonged, leads to heart failure progression. Here, we review the molecular pathways involved in cardiac remodeling, with particular emphasis on those associated with myocardial infarction. A better understanding of cell signaling involved in cardiac remodeling may support the development of new therapeutic strategies towards the treatment of heart failure and reduction of cardiac complications. We will also discuss data derived from gene therapy approaches for modulating key mediators of cardiac remodeling.

Cytokine Profile of Mononuclear Cells in Patients with Acute Myocardial Infarction, Complicated by Heart Failure

2013 ◽  
Vol 4 (3) ◽  
pp. 253-259
Author(s):  
Tatyana I. Gavrilenko ◽  
Alexandr N. Parkhomenko ◽  
Natalia A. Ryzhkova ◽  
Sergey N. Kozhukhov ◽  
Lyudmyla V. Yakushko
Keyword(s):  
Myocardial Infarction ◽  
Heart Failure ◽  
Acute Myocardial Infarction ◽  
Mononuclear Cells ◽  
Cytokine Profile

Predictors of Left Ventricular Remodeling Post Acute Myocardial Infarction. Protocol for a Clinical Study

2019 ◽  
Vol 4 (3) ◽  
pp. 120-123
Author(s):  
Ioana Cîrneală ◽  
Diana Opincariu ◽  
István Kovács ◽  
Monica Chițu ◽  
Imre Benedek
Keyword(s):  
Myocardial Infarction ◽  
Heart Failure ◽  
Acute Myocardial Infarction ◽  
Speckle Tracking ◽  
Ventricular Remodeling ◽  
Speckle Tracking Echocardiography ◽  
Left Ventricular Remodeling ◽  
Left Ventricular ◽  
Serum Biomarkers ◽  
Remodeling Index

Abstract Heart failure is a clinical syndrome that appears as a consequence of a structural disease, and the most common cause of left ventricular systolic dysfunction results from myocardial ischemia. Cardiac remodeling and neuroendocrine activation are the major compensatory mechanisms in heart failure. The main objective of the study is to identify the association between serum biomarkers illustrating the extent of myocardial necrosis (highly sensitive troponin as-says), left ventricular dysfunction (NT-proBNP), and systemic inflammatory response (illustrated via serum levels of hsCRP and interleukins) during the acute phase of a myocardial infarction, and the left ventricular remodeling process at 6 months following the acute event, quantified via speckle tracking echocardiography. The study will include 400 patients diagnosed with acute myocardial infarction without signs and symptoms of heart failure at the time of enrollment that will undergo a complex clinical examination and speckle tracking echocardiography. Serum samples from the peripheral blood will be collected in order to determine the inflammatory serum biomarkers. After 6 months, patients will be divided into 2 groups according to the development of ventricular remodeling, quantified by speckle tracking echocardiography: group 1 will consist of patients with a remodeling index lower than 15%, and group 2 will consist of patients with a remodeling index higher than 15%. All clinical and imaging data obtained at the baseline will be compared between these two groups in order to determine the features associated with a higher risk of deleterious ventricular remodeling and heart failure.

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