Ventricular remodeling in a mouse model of myocardial infarction. 1998

R D Patten, and M J Aronovitz, and L Deras-Mejia, and N G Pandian, and G G Hanak, and J J Smith, and M E Mendelsohn, and M A Konstam
Division of Cardiology, Molecular Cardiology Research Institute, New England Medical Center, Boston, Massachusetts, USA.

We investigated the suitability of studying ventricular remodeling in a mouse model of myocardial infarction (MI). We performed left coronary ligation (n = 22) or a sham procedure (n = 21) on normal C57BL/6J mice. Six weeks later, animals underwent echocardiography and hemodynamic evaluation. Left ventricular (LV) volume at a common distending pressure was calculated from passive pressure-volume curves. The MI group exhibited lower systolic blood pressure (P < 0.05), higher LV end-diastolic pressure (P < 0.05), and lower peak first derivative of LV pressure (dP/dt, P < 0.05) than the sham group. Mice with moderate (< 40%, n = 11) and large (> or = 40%, n = 11) MIs displayed increased LV mass-to-body weight ratio (P < 0.02 and P < 0.01, respectively, vs. sham group), whereas only the large-MI group exhibited increased right ventricular mass-to-body weight ratio (P < 0.01). LV volumes were increased in the moderate-MI group (P = 0.059 vs. sham group) and to a much greater extent in the large-MI group (P < 0.0001 vs. sham group). The moderate- and large-MI groups also exhibited increases in LV end-diastolic diameter (P < 0.03 and P < 0.0001, respectively, vs. sham group) and LV end-systolic diameter (P < 0.01 and P < 0.0001, respectively, vs. sham group) with decreased fractional shortening (P < 0.01 for both). These data demonstrate ventricular remodeling in a mouse model of MI and confirm the feasibility of quantifying indexes of remodeling in vivo and postmortem. This model will be of particular usefulness when applied to transgenic strains.

UI MeSH Term Description Entries
D008297 Male Males
D008810 Mice, Inbred C57BL One of the first INBRED MOUSE STRAINS to be sequenced. This strain is commonly used as genetic background for transgenic mouse models. Refractory to many tumors, this strain is also preferred model for studying role of genetic variations in development of diseases. Mice, C57BL,Mouse, C57BL,Mouse, Inbred C57BL,C57BL Mice,C57BL Mice, Inbred,C57BL Mouse,C57BL Mouse, Inbred,Inbred C57BL Mice,Inbred C57BL Mouse
D009203 Myocardial Infarction NECROSIS of the MYOCARDIUM caused by an obstruction of the blood supply to the heart (CORONARY CIRCULATION). Cardiovascular Stroke,Heart Attack,Myocardial Infarct,Cardiovascular Strokes,Heart Attacks,Infarct, Myocardial,Infarction, Myocardial,Infarctions, Myocardial,Infarcts, Myocardial,Myocardial Infarctions,Myocardial Infarcts,Stroke, Cardiovascular,Strokes, Cardiovascular
D001835 Body Weight The mass or quantity of heaviness of an individual. It is expressed by units of pounds or kilograms. Body Weights,Weight, Body,Weights, Body
D004195 Disease Models, Animal Naturally-occurring or experimentally-induced animal diseases with pathological processes analogous to human diseases. Animal Disease Model,Animal Disease Models,Disease Model, Animal
D006352 Heart Ventricles The lower right and left chambers of the heart. The right ventricle pumps venous BLOOD into the LUNGS and the left ventricle pumps oxygenated blood into the systemic arterial circulation. Cardiac Ventricle,Cardiac Ventricles,Heart Ventricle,Left Ventricle,Right Ventricle,Left Ventricles,Right Ventricles,Ventricle, Cardiac,Ventricle, Heart,Ventricle, Left,Ventricle, Right,Ventricles, Cardiac,Ventricles, Heart,Ventricles, Left,Ventricles, Right
D006439 Hemodynamics The movement and the forces involved in the movement of the blood through the CARDIOVASCULAR SYSTEM. Hemodynamic
D000818 Animals Unicellular or multicellular, heterotrophic organisms, that have sensation and the power of voluntary movement. Under the older five kingdom paradigm, Animalia was one of the kingdoms. Under the modern three domain model, Animalia represents one of the many groups in the domain EUKARYOTA. Animal,Metazoa,Animalia
D017379 Hypertrophy, Left Ventricular Enlargement of the LEFT VENTRICLE of the heart. This increase in ventricular mass is attributed to sustained abnormal pressure or volume loads and is a contributor to cardiovascular morbidity and mortality. Left Ventricular Hypertrophy,Ventricular Hypertrophy, Left,Hypertrophies, Left Ventricular,Left Ventricular Hypertrophies,Ventricular Hypertrophies, Left
D051379 Mice The common name for the genus Mus. Mice, House,Mus,Mus musculus,Mice, Laboratory,Mouse,Mouse, House,Mouse, Laboratory,Mouse, Swiss,Mus domesticus,Mus musculus domesticus,Swiss Mice,House Mice,House Mouse,Laboratory Mice,Laboratory Mouse,Mice, Swiss,Swiss Mouse,domesticus, Mus musculus

Related Publications

R D Patten, and M J Aronovitz, and L Deras-Mejia, and N G Pandian, and G G Hanak, and J J Smith, and M E Mendelsohn, and M A Konstam
June 2002, Journal of the American Society of Echocardiography : official publication of the American Society of Echocardiography,
R D Patten, and M J Aronovitz, and L Deras-Mejia, and N G Pandian, and G G Hanak, and J J Smith, and M E Mendelsohn, and M A Konstam
January 1993, Advances in experimental medicine and biology,
R D Patten, and M J Aronovitz, and L Deras-Mejia, and N G Pandian, and G G Hanak, and J J Smith, and M E Mendelsohn, and M A Konstam
June 1991, Archives des maladies du coeur et des vaisseaux,
R D Patten, and M J Aronovitz, and L Deras-Mejia, and N G Pandian, and G G Hanak, and J J Smith, and M E Mendelsohn, and M A Konstam
October 1992, The American journal of cardiology,
R D Patten, and M J Aronovitz, and L Deras-Mejia, and N G Pandian, and G G Hanak, and J J Smith, and M E Mendelsohn, and M A Konstam
December 2002, Journal of cardiac failure,
R D Patten, and M J Aronovitz, and L Deras-Mejia, and N G Pandian, and G G Hanak, and J J Smith, and M E Mendelsohn, and M A Konstam
June 2006, Journal of cardiac failure,
R D Patten, and M J Aronovitz, and L Deras-Mejia, and N G Pandian, and G G Hanak, and J J Smith, and M E Mendelsohn, and M A Konstam
April 2021, JACC. Basic to translational science,
R D Patten, and M J Aronovitz, and L Deras-Mejia, and N G Pandian, and G G Hanak, and J J Smith, and M E Mendelsohn, and M A Konstam
September 1999, Thrombosis and haemostasis,
R D Patten, and M J Aronovitz, and L Deras-Mejia, and N G Pandian, and G G Hanak, and J J Smith, and M E Mendelsohn, and M A Konstam
December 1994, Cardiologia (Rome, Italy),
R D Patten, and M J Aronovitz, and L Deras-Mejia, and N G Pandian, and G G Hanak, and J J Smith, and M E Mendelsohn, and M A Konstam
March 2005, Nihon rinsho. Japanese journal of clinical medicine,
Copied contents to your clipboard!