scholarly journals Expedient assessment of post-infarct remodeling by native cardiac magnetic resonance imaging in mice

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Cajetan Immanuel Lang ◽  
Praveen Vasudevan ◽  
Piet Döring ◽  
Ralf Gäbel ◽  
Heiko Lemcke ◽  
...  

AbstractNovel therapeutic strategies aiming at improving the healing process after an acute myocardial infarction are currently under intense investigation. The mouse model plays a central role for deciphering the underlying mechanisms on a molecular and cellular level. Therefore, we intended to assess in-vivo post-infarct remodeling as comprehensively as possible using an expedient native magnetic resonance imaging (MRI) in the two most prominent infarct models, permanent ligation (PL) of the left anterior descending artery (LAD) versus ischemia reperfusion (I/R). Mice were subjected to either permanent or transient (45 min) occlusion of the LAD. After 3 weeks, examinations were performed with a 7-Tesla small animal MRI system. Data analysis was performed with the freely available software Segment. PL resulted in a massive dilation of the left ventricle, accompanied by hypertrophy of the non-infarcted myocardium and a decline of contractile function. These effects were less pronounced following I/R compared to healthy animals. Single plane assessments were not sufficient to capture the specific differences of left ventricular (LV) properties between the two infarct models. Bulls-eye plots were found to be an ideal tool for qualitative LV wall assessment, whereas a multi-slice sector-based analysis of wall regions is ideal to determine differences in hypertrophy, lateral wall thinning and wall thickening on a quantitative level. We combine the use of polar map-based analysis of LV wall properties with volumetric measurements using simple CINE CMR imaging. Our strategy represents a versatile and easily available tool for serial assessment of the LV during the remodeling process. Our study contributes to a better understanding of the effects of novel therapies targeting the healing of damaged myocardium.

2005 ◽  
Vol 83 (12) ◽  
pp. 1109-1115 ◽  
Author(s):  
Fabrice Prunier ◽  
Laurent Marescaux ◽  
Florence Franconi ◽  
Alain Thia ◽  
Pierre Legras ◽  
...  

In vivo assessment of treatment efficacy on postinfarct left ventricular (LV) remodeling is crucial for experimental studies. We examined the technical feasibility of serial magnetic resonance imaging (MRI) for monitoring early postinfarct remodeling in rats. MRI studies were performed with a 7-Tesla unit, 1, 3, 8, 15, and 30 days after myocardial infarction (MI) or sham operation, to measure LV mass, volume, and the ejection fraction (EF). Three groups of animals were analyzed: sham-operated rats (n = 6), MI rats receiving lisinopril (n = 11), and MI rats receiving placebo (n = 8). LV dilation occurred on day 3 in both MI groups. LV end-systolic and end-diastolic volumes were significantly lower in lisinopril-treated rats than in placebo-treated rats at days 15 and 30. EF was lower in both MI groups than in the sham group at all time points, and did not differ between the MI groups during follow-up. Less LV hypertrophy was observed in rats receiving lisinopril than in rats receiving placebo at days 15 and 30. We found acceptable within- and between-observer agreement and an excellent correlation between MRI and ex vivo LV mass (r = 0.96; p < 0.001). We demonstrated the ability of MRI to detect the early beneficial impact of angiotensin-converting enzyme (ACE) inhibitors on LV remodeling. Accurate and noninvasive, MRI is the tool of choice to document response to treatment targeting postinfarction LV remodeling in rats.


2014 ◽  
Vol 25 (1) ◽  
pp. 187-190 ◽  
Author(s):  
Carol A. Wittlieb-Weber ◽  
Matthew A. Harris ◽  
Joseph W. Rossano

AbstractWe describe a case of influenza A myocarditis and transient left ventricular wall thickening in a 14-year-old girl presenting with acute heart failure. Admission echocardiogram revealed significant left ventricular hypertrophy with depressed left ventricular systolic function. The aetiology of the ventricular thickening was demonstrated to be myocardial oedema using cardiac magnetic resonance imaging. The natural course of this unusual clinical presentation of acute myocarditis and the importance of cardiac magnetic resonance imaging in this challenging clinical setting are discussed.


2017 ◽  
Vol 312 (5) ◽  
pp. H1068-H1075 ◽  
Author(s):  
Xiao-Ming Gao ◽  
Qi-Zhu Wu ◽  
Helen Kiriazis ◽  
Yidan Su ◽  
Li-Ping Han ◽  
...  

Cardiac microvascular obstruction (MVO) after ischemia-reperfusion (I/R) has been well studied, but microvascular leakage (MVL) remains largely unexplored. We characterized MVL in the mouse I/R model by histology, biochemistry, and cardiac magnetic resonance (CMR) imaging. I/R was induced surgically in mice. MVL was determined by administrating the microvascular permeability tracer Evans blue (EB) and/or gadolinium-diethylenetriaminepentaacetic acid contrast. The size of MVL, infarction, and MVO in the heart was quantified histologically. Myocardial EB was extracted and quantified chromatographically. Serial CMR images were acquired from euthanized mice to determine late gadolinium enhancement (LGE) for comparison with MVL quantified by histology. I/R resulted in MVL with its severity dependent on the ischemic duration and reaching its maximum at 24–48 h after reperfusion. The size of MVL correlated with the degree of left ventricular dilatation and reduction in ejection fraction. Within the risk zone, the area of MVL (75 ± 2%) was greater than that of infarct (47 ± 4%, P < 0.01) or MVO (36 ± 4%, P < 0.01). Contour analysis of paired CMR-LGE by CMR and histological MVL images revealed a high degree of spatial colocalization ( r = 0.959, P < 0.0001). These data indicate that microvascular barrier function is damaged after I/R leading to MVL. Histological and biochemical means are able to characterize MVL by size and severity while CMR-LGE is a potential diagnostic tool for MVL. The size of ischemic myocardium exhibiting MVL was greater than that of infarction and MVO, implying a role of MVL in postinfarct pathophysiology. NEW & NOTEWORTHY We characterized, for the first time, the features of microvascular leakage (MVL) as a consequence of reperfused myocardial infarction. The size of ischemic myocardium exhibiting MVL was significantly greater than that of infarction or no reflow. We made a proof-of-concept finding on the diagnostic potential of MVL by cardiac magnetic resonance imaging.


2021 ◽  
Vol 42 (Supplement_1) ◽  
Author(s):  
N Funabashi ◽  
Y Kobayashi

Abstract Background Left ventricular (LV) wall thickening and diastolic dysfunction on a transthoracic echocardiogram (TTE) without high voltage R wave in V5 leads on ECG leads to a diagnosis of cardiac amyloidosis. A final diagnosis is made by endomyocardial biopsy. However, amyloid sometimes invade the right ventricle (RV), and left (LA) and right (RA) atria to cause ECG changes such as sick sinus syndrome (SSS), arrhythmia, and QRS wave axis deviation. Purpose To predict sites of wall thickening and abnormal late enhancement (LE) on cardiac computed tomography (CT) and magnetic resonance imaging (MRI), suggesting amyloid invasion, using cardiac rhythm and other ECG findings in patients with cardiac amyloidosis confirmed by biopsy. Methods A total of 26 patients (11 females) with suspected cardiac amyloidosis, showing LV wall thickening by TTE without a high voltage R wave in V5 leads on ECG, underwent cardiac enhanced CT. LV wall thickening on CT in the early phase led to late phase acquisition to detect LE. Five patients (3 females, mean age 73 years) were diagnosed with cardiac amyloidosis: complicated multiple myeloma, 2; senile ATTR (transthyretin) amyloidosis, 1; immunoglobulin light chain (AL) amyloidosis 1; and transthyretin mutation, 1. Four patients underwent cardiac MRI. Results Two patients (cases 1 and 2) had SSS (junctional rhythm), one had atrial tachycardia, and the remaining two (cases 4 and 5) had a normal sinus rhythm. In case 1, ECG showed a left axis QRS wave deviation, no low voltage R wave in limb leads and a mild LA load. Wall thickening in the basal interventricular septum (IVS), LV inferior-posterior wall, LA on CT, LE in the endocardium in whole LV, RV, and RA on CT, and LE in the endocardium in whole LV, RV, LA, and IVS on MRI were observed. In case 2, ECG showed a normal QRS wave axis, no low voltage R wave in limb leads, no LA load, wall thickening in whole LV, RV, LA, and IVS on CT, and unclear (CT) or no (MRI) LE. In case 3, ECG showed a normal QRS wave axis, with low voltage R wave in limb leads, no LA load, wall thickening in LA and basal IVS on CT, LE in LA and basal IVS on CT, and LE in LA only on MRI. In case 4, ECG showed left axis QRS wave deviation, a low voltage R wave in limb leads, and no LA load, wall thickening in the LA and RV moderator band on CT, unclear LE on CT, and LE in whole LV, endocardium in the RV, and whole IVS on MRI. In case 5, ECG showed a right axis QRS wave deviation, low voltage R wave in limb leads, and a mild LA load, wall thickening in the IVS, LV lateral wall, LV anterior wall, RA, RV outflow tract, and RA appendage, and no LE on CT (MRI not performed). Conclusions This pilot study of a few patients with cardiac amyloidosis revealed few links between cardiac rhythm and other ECG findings with sites of wall thickening and abnormal LE. However, a longer-term study of more patients may lead to detecting an association between these variables with this methodology. FUNDunding Acknowledgement Type of funding sources: None.


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