9 research outputs found
Mineralocorticoid receptor antagonist spironolactone improves left ventricular remodeling in patients with congestive heart failure and acute myocardial infarction
Left Ventricular Hypertrophy and Geometry in Untreated Essential Hypertension is Associated With Blood Levels of Aldosterone and Procollagen Type III Amino-Terminal Peptide
Effects of Enalapril on the Collagen Matrix in Cardiomyopathic Syrian Hamsters (BIO 14.6 and 53.58)
Effect of Manidipine Hydrochloride, a Calcium Antagonist, on Isoproterenol-Induced Left Ventricular Hypertrophy
Angiotensin Blockade Inhibits Osteopontin Expression in Non-infarcted Myocardium After Myocardial Infarction
Influence of Plasma Aldosterone on Left Ventricular Geometry and Diastolic Function in Treated Essential Hypertension
Extracellular Matrix Biomarkers of Adverse Remodeling after Myocardial Infarction
Approximately every minute, someone will die from a myocardial infarction (MI). A MI is the result of an obstruction of blood supply causing the heart to undergo complex structural and functional changes in the left ventricular wall, known as ventricular remodeling. Cardiomyocytes undergo necrosis rapidly after the onset of injury, leading to early accumulation of neutrophils, activation of metalloproteinases, and degradation of the stromal tissue, eventually leading to formation of a collagen scar. Circulating factors related to inflammatory and fibrotic responses are key predictors of extracellular matrix (ECM) changes that occur after MI. Changes in the collagen network of the ECM can alter myocardial stiffness, consequently leading to cardiac hypertrophy, fibrosis, and LV dysfunction. Proteins and peptides of the ECM are promising biomarkers for MI. This book chapter provides an overview of key ECM biomarkers involved in adverse remodeling post-MI and their practical applications