title: Prevention of left ventricular remodelling after acute myocardial infarction: an update.
abstract: Left ventricular remodelling is a progressive process, which starts immediately after acute myocardial infarction and evolves in the chronic phase of heart failure. It is characterized by left ventricular chamber dilatation and increased wall stress, which results in alteration of the contractile properties of the non-infarct zone and impairment of the systolic and diastolic performances of the left ventricle. Neurohormonal activation and increased sympathetic stimulation are among the factors that have been linked to the development and progression of left ventricular dysfunction after acute myocardial infarction. The present review will address recent insights from new patents and experimental studies of drugs, which ought to prevent left ventricular remodelling. Angiotensin-Converting Enzyme Inhibitors, Angiotensin Receptor Blockers and Beta-Blockers have been proven effective in modulating the process of remodelling and in reducing the occurrence of adverse events. However, in most of the trials high risk patients have been excluded, and uncertainty still exists regarding a number of clinically relevant questions. Data from experimental studies have identified new targets for interventions to prevent reverse left ventricular remodelling, i.e. stem cell transfer, activation of cardiac and leukocyte-dependent oxidant stress pathways, inflammatory pathway activation, matrix-metalloproteinase activation.
authors.affiliation: Dipartimento Cardiovascolare, Ospedali Riuniti di Bergamo, Bergamo, Italy. roberta_rossini@yahoo.it
authors.forename: Roberta
authors.initials: R
authors.lastname: Rossini
authors.forename: Michele
authors.initials: M
authors.lastname: Senni
authors.forename: Giuseppe
authors.initials: G
authors.lastname: Musumeci
authors.forename: Paolo
authors.initials: P
authors.lastname: Ferrazzi
authors.forename: Antonello
authors.initials: A
authors.lastname: Gavazzi
mesh_terms: D000319:Adrenergic beta-Antagonists / Q000494:pharmacology / Q000627:therapeutic use; D057911:Angiotensin Receptor Antagonists / Q000494:pharmacology / Q000627:therapeutic use; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology / Q000627:therapeutic use; D000975:Antioxidants / Q000627:therapeutic use; D020536:Enzyme Activators / Q000494:pharmacology / Q000627:therapeutic use; D006333:Heart Failure / Q000503:physiopathology / Q000517:prevention & control; D006801:Humans; D017379:Hypertrophy, Left Ventricular / Q000209:etiology* / Q000503:physiopathology / Q000517:prevention & control*; D020782:Matrix Metalloproteinases / Q000378:metabolism; D000451:Mineralocorticoid Receptor Antagonists / Q000627:therapeutic use; D009203:Myocardial Infarction / Q000150:complications* / Q000188:drug therapy* / Q000503:physiopathology / Q000517:prevention & control; D033581:Stem Cell Transplantation; D016277:Ventricular Function, Left / Q000187:drug effects; D020257:Ventricular Remodeling / Q000187:drug effects*
chemical_list: D000319:Adrenergic beta-Antagonists; D057911:Angiotensin Receptor Antagonists; D000806:Angiotensin-Converting Enzyme Inhibitors; D000975:Antioxidants; D020536:Enzyme Activators; D000451:Mineralocorticoid Receptor Antagonists; D020782:Matrix Metalloproteinases