title: MRI monitoring of function, perfusion and viability in microembolized moderately ischemic myocardium.
abstract: Assessment of microembolization after coronary interventions is clinically challenging, thus we longitudinally investigated microemboli effects on moderately ischemic myocardium using MRI and histopathology. Twenty-four pigs (8/group) were divided into: group I (no intervention), group II (45 min LAD occlusion) and group III (45 min LAD occlusion with microembolization). Cine, perfusion and delayed contrast enhanced MRI (DE-MRI), using 1.5T MRI, were used for assessment at 3 days and 5 weeks. Triphenyltetrazolium-chloride (TTC) and Masson-trichrome were used as gold standard references for macro and microscopic quantification of myocardial infarction (MI). Cine MRI showed differential increase in end systolic volume (1.3 ± 0.08 ml/kg group II and 1.6 ± 0.1 ml/kg group III) and decrease in ejection fraction (45 ± 2 and 36 ± 2%, respectively) compared with controls at 3 days (2.1 ± 0.1 ml ESV and 50 ± 1% EF, P < 0.05). At 5 weeks group III, but not II, showed persistent perfusion deficits, wall thinning in the LAD territory and compensatory hypertrophy in remote myocardium. DE-MRI MI at 3 days was significantly smaller in group II (3.3 ± 2.2 g) than III (9.8 ± 0.6 g), at 5 weeks, MI were smaller by 60% (1.3 ± 0.9 g) and 22% (7.7 ± 0.5 g), respectively. TTC MI was similar to DE-MRI in group II (1.6 ± 1.0 g) and III (9.2 ± 1.6 g), but not microscopy (2.8 ± 0.4 and 10.5 ± 1.5 g, respectively). The effects of moderate ischemia with and without microembolization on myocardium could be differentiated using multiple MRI sequences. MRI demonstrated that microemboli in moderately ischemic myocardium, but not solely ischemia, prolonged ventricular dysfunction, created perfusion deficits, poor infarct resorption and enhanced compensatory hypertrophy, while moderate ischemia alone caused minor LV changes.
authors.affiliation: University of California, San Francisco, San Francisco, CA, USA.
authors.forename: Loi
authors.initials: L
authors.lastname: Do
authors.forename: Mark W
authors.initials: MW
authors.lastname: Wilson
authors.forename: Roland
authors.initials: R
authors.lastname: Krug
authors.forename: Steven W
authors.initials: SW
authors.lastname: Hetts
authors.forename: Maythem
authors.initials: M
authors.lastname: Saeed
mesh_terms: D000818:Animals; D001706:Biopsy; D003326:Coronary Circulation; D004195:Disease Models, Animal; D004617:Embolism / Q000175:diagnosis / Q000209:etiology* / Q000503:physiopathology; D019028:Magnetic Resonance Imaging, Cine; D017202:Myocardial Ischemia / Q000175:diagnosis* / Q000209:etiology / Q000503:physiopathology; D055414:Myocardial Perfusion Imaging / Q000379:methods*; D009206:Myocardium / Q000473:pathology; D062645:Percutaneous Coronary Intervention / Q000009:adverse effects*; D011237:Predictive Value of Tests; D013318:Stroke Volume; D013552:Swine; D013997:Time Factors; D014022:Tissue Survival; D018487:Ventricular Dysfunction, Left / Q000175:diagnosis / Q000209:etiology / Q000503:physiopathology; D016277:Ventricular Function, Left