scholarly journals Impact of Papillary Muscle Infarction on Ischemic Mitral Regurgitation Assessed by Magnetic Resonance Imaging

2017 ◽  
Vol 190 (01) ◽  
pp. 42-50 ◽  
Author(s):  
Christiane Bretschneider ◽  
Hannah-Klara Heinrich ◽  
Achim Seeger ◽  
Christof Burgstahler ◽  
Stephan Miller ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Mitral Regurgitation ◽  
Left Ventricular Function ◽  
Ventricular Function ◽  
Papillary Muscle ◽  
Left Ventricular ◽  
Ischemic Mitral Regurgitation ◽  
Chronic Myocardial Infarction ◽  
End Diastolic Volume ◽  
Significant Difference

Objective Ischemic mitral regurgitation is a predictor of heart failure resulting in increased mortality in patients with chronic myocardial infarction. It is uncertain whether the presence of papillary muscle (PM) infarction contributes to the development of mitral regurgitation in patients with chronic myocardial infarction (MI). The aim of the present study was to assess the correlation of PM infarction depicted by MRI with mitral regurgitation and left ventricular function. Methods and Materials 48 patients with chronic MI and recent MRI and echocardiography were retrospectively included. The location and extent of MI depicted by MRI were correlated with left ventricular function assessed by MRI and mitral regurgitation assessed by echocardiography. The presence, location and extent of PM infarction depicted by late gadolinium enhancement (LGE-) MRI were correlated with functional parameters and compared with patients with chronic MI but no PM involvement. Results PM infarction was found in 11 of 48 patients (23 %) using LGE-MRI. 8/11 patients (73 %) with PM infarction and 22/37 patients (59 %) without PM involvement in MI had ischemic mitral regurgitation. There was no significant difference between location, extent of MI and presence of mitral regurgitation between patients with and without PM involvement in myocardial infarction. In 4/4 patients with complete and in 4/7 patients with partial PM infarction, mitral regurgitation was present. The normalized mean left ventricular end-diastolic volume was increased in patients with ischemic mitral regurgitation. Conclusion The presence of PM infarction does not correlate with ischemic mitral regurgitation. In patients with complete PM infarction and consequent discontinuity of viable tissue in the PM-chorda-mitral valve complex, the probability of developing ischemic mitral regurgitation seems to be increased. However, the severity of mitral regurgitation is not increased compared to patients with partial or no PM infarction. Key points  Citation Format

Myocardial T2* Is Not Affected by the Structural Effects of Myocardial Fibrosis, Ageing or Impaired Left Ventricular Function.

Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 1675-1675
Author(s):  
Paul Kirk ◽  
Dudley J. Pennell
Keyword(s):  
Myocardial Infarction ◽  
Iron Overload ◽  
Left Ventricular Function ◽  
Ventricular Function ◽  
Age Distribution ◽  
Left Ventricular ◽  
Lv Function ◽  
Chronic Myocardial Infarction ◽  
Myocardial Iron ◽  
The Mean

Abstract Background The myocardial T2* technique has been validated as a reproducible non-invasive measurement of myocardial iron load and is now widely used for measurement of myocardial iron in iron overload diseases such as thalassaemia. The reduction in myocardial T2* seen in iron overload conditions is substantially greater than is seen in any other clinical circumstance, but there has been no direct comparison of myocardial T2* in normals and other conditions such as increasing age, myocardial infarction or impairment in left ventricular function. We aimed therefore to compare the findings in patients affected by these conditions with normals. Method A total of 38 patients in total were scanned using the myocardial T2* technique. Fifteen patients had normal hearts, 18 had impaired LV function and 6 had chronic myocardial infarction affecting the anteroseptal wall, where myocardial T2* measurements are normally made. Results The mean myocardial T2* in normals was 36.0 +/− 6.4 ms, yielding a lower limit of normal of 23ms. In patients with impaired LV function, the mean myocardial T2* was 39.0 +/− 11.7ms (p= 0.37 vs normals). In patients with anteroseptal myocardial infarction, the mean myocardial T2* was 34.7ms +/− 3.9ms (p= 0.64 vs normals). The frequency distribution of the myocardial T2* values are shown in figure 1. These approximate to normal, and are very similar in distribution. In addition, the age distribution of myocardial T2* in the 15 normals is shown in figure 2. There was no significant relation between myocardial T2* and age (r2 = 0.066, p=0.82). Conclusion There is no significant reduction in myocardial T2* associated with fibrosis from chronic myocardial infarction, impairment of left ventricular function, or increasing age. This suggests that structural changes associated with remodelling, infarction and fibrosis, and ageing do not have significant effects on the absolute measure of myocardial T2*, and in particular do not cause a reduction below 20ms as is seen in myocardial overload conditions. Thus these date suggest that myocardial T2* is robust to these structural alterations, and that myocardial iron overload can be ascertained from reduced myocardial T2* values, in a similar manner to that which can be achieved in normals. Figure 1 Figure 1. Figure 2 Figure 2.

Left ventricular function measurements in a mouse myocardial infarction model

2016 ◽  
Vol 55 (03) ◽  
pp. 115-122 ◽  
Author(s):  
Geert Hendrikx ◽  
Matthias Bauwens ◽  
Roel Wierts ◽  
Mark Post ◽  
Felix Mottaghy
Keyword(s):  
Myocardial Infarction ◽  
Myocardial Perfusion ◽  
Left Ventricular Function ◽  
Infarct Size ◽  
Ventricular Function ◽  
Left Ventricular ◽  
3D Echocardiography ◽  
Tetrazolium Chloride ◽  
Systolic Volume ◽  
End Diastolic Volume

SummaryAim: To assess the accuracy of ECG-gated micro (µ)-SPECT in a mouse myocardial infarction (MI) model in comparison to 3D-echocardiography. Animals, methods: In a mouse (Swiss mice) MI model we compared the accuracy of technetium-99m sestamibi (99mTc-sestamibi) myocardial perfusion, electrocardiogram (ECG) gated µSPECT to 3D-echocardiography in determining left ventricular function. 3D-echocardiography and myocardial perfusion ECG-gated µSPECT data were acquired in the same animal at baseline (n = 11) and 7 (n = 8) and 35 (n = 9) days post ligation of the left anterior descending coronary artery (LAD). Sham operated mice were used as a control (8, 6 and 7 mice respectively). Additionally, after day 35 µSPECT scans, hearts were harvested and 2,3,5-triphenyl-2H-tetrazolium chloride (TTC) staining and autoradiography was performed to determine infarct size. Results: In both infarcted and sham-operated mice we consistently found comparable values for the end-diastolic volume (EDV), end-systolic volume (ESV) and ejection fraction (EF) obtained by 3D-echocardiography and ECG-gated µSPECT. Excellent correlations between measurements from 3D-echocardiography and ECG-gated µSPECT were found for EDV, ESV and EF (r = 0.9532, r = 0.9693 respectively and r = 0.9581) in infarcted mice. Furthermore, comparable infarct size values were found at day 35 post MI by TTC staining and autoradiography (27.71 ± 1.80% and 29.20 ± 1.18% with p = 0.43). Conclusion: We have demonstrated that ECG-gated µSPECT imaging provides reliable left ventricular function measurements in a mouse MI model. Obtained results were comparable to the highly accurate 3D-echocardiography. This, in addition to the opportunity to simultaneously image multiple biological processes during a single acquisition makes µSPECT imaging a serious option for studying cardiovascular disease in small animals.

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