Lipomatous metaplasia identified in rabbits with reperfused myocardial infarction by 3.0 T magnetic resonance imaging and histopathology

Abstract

BackgroundCardiac lipomatous metaplasia (LM) occurs in patients with chronic ischemic heart disease and heart failure with unclear mechanisms. We studied coronary occlusion/reperfusion-induced myocardial infarction (MI) in rabbits during a 9-months follow-up using 3.0 T magnetic resonance scanner, and confirmed the presence of MI in acute phase and LM in chronic phase using histopathology.MethodsMI was surgically induced in 10 rabbits by 90-min coronary artery occlusion and reperfusion. Forty-eight hours later, multiparametric cardiac magnetic resonance imaging (cMRI) was performed at a 3.0 T clinical scanner for MI diagnosis and cardiac function analysis. Afterwards, seven rabbits were scarified for histochemical staining with triphenyltetrazolium chloride (TTC), and hematoxylin-eosin (HE), and 3 were scanned with cMRI at 2 days, 2 weeks, 2 months and 9 months for longitudinal observations of morphological and functional changes, and the fate of the animals. Post-mortem TTC, HE and Masson's trichrome (MTC) were studied for chronic stage of MI.ResultsThe size of acute MI correlated well between cMRI and TTC staining (r2=0.83). Global cardiac morphology-function analysis showed significant correlation between increasing acute MI size and decreasing ejection fraction (p<0.001). During 9 months, cMRI documented evolving morphological and functional changes from acute MI to chronic scar transformation and fat deposition with a definite diagnosis of LM established by histopathology.ConclusionsAcute MI and chronic LM were induced in rabbits and monitored with 3.0 T MRI. Studies on this platform may help investigate the mechanisms and therapeutic interventions for LM.

Experimental Study on the Effect of Intravenous Stem Cell Therapy on Intestinal Ischemia Reperfusion Induced Myocardial Injury

“…Fibroblasts and fibrocytes were commonly found among the degenerated fibers in I/R group. This finding can correlate to morphological and functional changes from acute myocardial infarction to chronic scar transformation (21). Sections in the cardiac muscle of rats in SC therapy group showed some obviously congested capillaries between the fibers.…”

An Under-Recognized Sequela of Myocardial Infarction: Lipomatous Metaplasia

“…Following a myocardial infarction, myofibroblasts lay connective tissue that serves as a protective agent against future myocardial rupture and prevents dilation of the infarcted area [ 2 ]. However, in the case of lipomatous metaplasia, the myofibroblasts instead differentiate into adipose tissue through mechanisms that are still poorly understood [ 2 ].…”

“…Following a myocardial infarction, myofibroblasts lay connective tissue that serves as a protective agent against future myocardial rupture and prevents dilation of the infarcted area [ 2 ]. However, in the case of lipomatous metaplasia, the myofibroblasts instead differentiate into adipose tissue through mechanisms that are still poorly understood [ 2 ]. Given the findings in various studies and this case report, the most efficient modality for diagnosis of lipomatous metaplasia is T1-weighted cardiac MRI with and without fat suppression [ 3 , 4 ].…”

Cross-Sectional Imaging to Evaluate the Risk of Rupture in Abdominal Aortic Aneurysms

“…Fatty replacement (lipomatous metaplasia) is a rare and unreported feature of AAA. It may represent a cause of biomechanical weakening of the wall [ 66 ] but is mainly a marker of stabilization, as in other cardiovascular disease [ 67 ], although it has not been specifically evaluated so far. Fat is detected as low-attenuation tissue relative to water on X-ray techniques.…”