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Right Ventricular Dysfunction following Acute Myocardial Infarction in the Absence of Pulmonary Hypertension in the Mouse

BACKGROUND: Cardiac remodelling after AMI is characterized by molecular and cellular mechanisms involving both the ischemic and non-ischemic myocardium. The extent of right ventricular (RV) dilatation and dysfunction and its relation to pulmonary hypertension (PH) following AMI are unknown. The aim...

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Detalles Bibliográficos
Autores principales: Toldo, Stefano, Bogaard, Herman J., Van Tassell, Benjamin W., Mezzaroma, Eleonora, Seropian, Ignacio M., Robati, Roshanak, Salloum, Fadi N., Voelkel, Norbert F., Abbate, Antonio
Formato: Texto
Lenguaje:English
Publicado: Public Library of Science 2011
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3063789/
https://www.ncbi.nlm.nih.gov/pubmed/21455304
http://dx.doi.org/10.1371/journal.pone.0018102
Descripción
Sumario:BACKGROUND: Cardiac remodelling after AMI is characterized by molecular and cellular mechanisms involving both the ischemic and non-ischemic myocardium. The extent of right ventricular (RV) dilatation and dysfunction and its relation to pulmonary hypertension (PH) following AMI are unknown. The aim of the current study was to evaluate changes in dimensions and function of the RV following acute myocardial infarction (AMI) involving the left ventricle (LV). METHODS: We assessed changes in RV dimensions and function 1 week following experimental AMI involving the LV free wall in 10 mice and assessed for LV and RV dimensions and function and for the presence and degree of PH. RESULTS: RV fractional area change and tricuspidal annular plane systolic excursion significantly declined by 33% (P = 0.021) and 28% (P = 0.001) respectively. Right ventricular systolic pressure measured invasively in the mouse was within the normal values and unchanged following AMI. CONCLUSION: AMI involving the LV and sparing the RV induces a significant acute decline in RV systolic function in the absence of pulmonary hypertension in the mouse indicating that RV dysfunction developed independent of changes in RV afterload.