title: Cardiac magnetic resonance imaging in small animal models of human heart failure.
abstract: The aim of this study was to test the feasibility of cine magnetic resonance imaging (MRI) for assessment of the infarcted rat and mouse heart and to compare the results with established methods. These models have been proven to predict genesis and prevention of heart failure in patients. The value of cine MRI was tested in studies investigating interventions to change the course of the remodeling process. MRI was performed for determination of left ventricular (LV) volumes and mass, myocardial infarct (MI) size and cardiac output. LV wet weight was determined after MRI. Rats underwent conventional hemodynamic measurements for determination of cardiac output and LV volumes by electromagnetic flowmeter and pressure-volume curves. Infarct size was determined by histology. MRI-acquired MI-size (18.5+/-2%) was smaller than that found by histology (22.8+/-2.5%, p<0.05) with close correlation (r=0.97). There was agreement in LV mass between MRI and wet weight (r=0.97, p<0.05) and in the MRI- and flowmeter measurements of cardiac output (r=0.80, p<0.05). Volume by MRI differed from pressure-volume curves with good correlation (r=0.96, p<0.05). In a serial study of mice after coronary ligation, LV hypertrophy at 8 weeks was detected (Sham 105.1+/-7.9 mg, MI 144.4+/-11.7 mg, p<0.05). Left ventricles were enlarged in infarcted mice (end-diastolic volume, week 8: Sham 63.5+/-4 microl, MI 94.2 microl, p<0.05). In conclusion, cine MRI is a valuable diagnostic tool applicable to the rat and mouse model of MI. Being non-invasive and exact it offers new insights into the remodeling process after MI because serial measurements are possible. The technique was applied to study several interventions and proved its usefulness.
authors.affiliation: Physikalisches Institut (EP5), Universität Würzburg, Am Hubland, 97074 Würzburg, Germany. m.nahrendorf@medizin.uni-wuerzburg.de
authors.forename: M
authors.initials: M
authors.lastname: Nahrendorf
authors.forename: K-H
authors.initials: KH
authors.lastname: Hiller
authors.forename: K
authors.initials: K
authors.lastname: Hu
authors.forename: G
authors.initials: G
authors.lastname: Ertl
authors.forename: A
authors.initials: A
authors.lastname: Haase
authors.forename: W R
authors.initials: WR
authors.lastname: Bauer
mesh_terms: D000818:Animals; D002302:Cardiac Output; D004195:Disease Models, Animal; D006333:Heart Failure / Q000175:diagnosis* / Q000188:drug therapy / Q000209:etiology / Q000503:physiopathology / Q000517:prevention & control; D006352:Heart Ventricles / Q000187:drug effects / Q000503:physiopathology; D006801:Humans; D007511:Ischemia; D019028:Magnetic Resonance Imaging, Cine / Q000379:methods*; D051379:Mice; D009203:Myocardial Infarction / Q000150:complications / Q000175:diagnosis* / Q000188:drug therapy / Q000503:physiopathology; D017202:Myocardial Ischemia / Q000150:complications / Q000175:diagnosis / Q000188:drug therapy / Q000503:physiopathology; D011725:Pyridines / Q000627:therapeutic use; D051381:Rats; D015203:Reproducibility of Results; D012680:Sensitivity and Specificity; D013045:Species Specificity; D013223:Statistics as Topic; D013318:Stroke Volume; D013739:Testosterone / Q000494:pharmacology; D018487:Ventricular Dysfunction, Left / Q000175:diagnosis* / Q000188:drug therapy / Q000209:etiology / Q000503:physiopathology; D020257:Ventricular Remodeling / Q000187:drug effects / Q000502:physiology
chemical_list: D011725:Pyridines; D013739:Testosterone; C086276:cerivastatin