Abstract 19100: Transmural and Lateral Remodeling of the Post-infarction Scar Tissue: Serial Cardiac Magnetic Resonance Imaging Study From the Metocard-Cnic Trial

Background: The remodeling process that occurs following an acute myocardial infarction produces changes in the myocardial scar and the surrounding tissue. The spatial evolution of the scar has not been yet characterized using MRI. Purpose: To describe the spatial behavior of myocardial scar on its transmural and lateral dimensions following an acute myocardial infarction. Methods: A total of 220 patients with acutely reperfused anterior STEMI (METOCARD-CNIC trial population) were studied. All the patients underwent cardiac MRI at day 7 and 6 months after presentation. The spatial distribution of the scar was analyzed using short axis late gadolinium enhancement images. Endo and epicardial contours of each LV short axis slice was traced, and each one was divided by 100 cords for analysis (Figure 1A). The lateral extension was defined as the percentage of cords with enhancement in every slice, and the transmural extension as the percentage of enhancement within each cord, nested in the lateral extension (Figure 1B). All slices were weighed according to their relative mass. Data were compared by paired t test. Results: Six months after STEMI, myocardial scar was smaller in both dimensions (Figure 1C). Mean ± SEM lateral scar, as a percentage of cords affected, at 7 days and 6 months were, respectively, 27.9 ± 1.1 and 22.2 ± 1.0 (p < 0.001). Transmurality also decreased significantly, mean percentage at day 7 was 46.8 ± 1.5 and at 6 months 35.4 ± 1.4 (p < 0.001). All these changes were accompanied by an increase in LV end-diastolic volume (171.47 ± 2.5 and 190.61 ± 2.9 (p < 0.001)). Conclusions: The myocardial scar remodeling process following a STEMI includes a reduction in both its transmural and lateral extensions.

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Abstract 18987: Wavefront Progression of Necrosis During Myocardial Infarction Revisited: The Wave Expands From Endo to Epi as Well as From Center to Lateral Borders

Circulation ◽

10.1161/circ.132.suppl_3.18987 ◽

2015 ◽

Vol 132 (suppl_3) ◽

Author(s):

Rebeca Lorca ◽

Marta Jimenez-Blanco ◽

Jose Manuel García-Ruiz ◽

Gonzalo Pizarro ◽

Rodrigo Fernández-Jiménez ◽

...

Keyword(s):

Myocardial Infarction ◽

Coronary Occlusion ◽

Myocardial Necrosis ◽

Short Axis Slice ◽

Relative Mass ◽

Control Group ◽

Lateral Extension ◽

Lateral Direction ◽

Acute Coronary Occlusion

Background and purpose: The widely accepted wavefront theory of myocardial necrosis during acute coronary occlusion describes its progression as a wavefront from endo towards epicardium. The lateral affection of the myocardium would be predetermined by the location of the coronary occlusion. At the time this phenomenon was firstly described, advanced imaging technology was not available. Current cardiac magnetic resonance (CMR) is able to accurately characterize the necrosis progression in vivo. Methods: A total of 220 patients with reperfused anterior STEMI (METOCARD-CNIC trial population) were studied. All the patients underwent cine, T2-weighted and late gadolinium enhancement CMR at day 5-7 after STEMI. Endo- and epicardial contours of each LV short axis slice was traced, and each one was divided by 100 cords for analysis. Infarct size was characterized in its 2 dimensions: lateral (defined as the percentage of cords with enhancement in every slice) and transmural extension (percentage of enhancement within each cord, nested in the lateral extension). All slices were weighed according to their relative mass. We compared these parameters between the cardioprotected metoprolol group and the control group. Results: A strong lineal correlation between transmural and lateral infarct extension was observed (r: 0.88, p<0.001). We found that despite the edema lateral extension was larger than the IS lateral extension, this difference decreased as the transmurality affection increased. Finally, the infarct reduction exerted by metoprolol was derived from both the transmural and lateral extensions of IS. Conclusions: The transmural and lateral extension of necrosis after myocardial infarction are directly correlated. A proven cardioprotective therapy prevented the necrosis progression in both dimensions. These findings cannot be explained by the classical wavefront theory, suggesting that the necrotic wavefront progresses also in the lateral direction.

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The effect of intra-aortic balloon counterpulsation on left ventricular functional recovery early after acute myocardial infarction: a randomized experimental magnetic resonance imaging study

European Heart Journal ◽

10.1093/eurheartj/ehi137 ◽

2005 ◽

Vol 26 (12) ◽

pp. 1235-1241 ◽

Cited By ~ 28

Author(s):

Clerio F. Azevedo ◽

Luciano C. Amado ◽

Dara L. Kraitchman ◽

Bernhard L. Gerber ◽

Thor Edvardsen ◽

...

Keyword(s):

Magnetic Resonance Imaging ◽

Myocardial Infarction ◽

Acute Myocardial Infarction ◽

Magnetic Resonance ◽

Imaging Study ◽

Left Ventricular ◽

Magnetic Resonance Imaging Study ◽

Resonance Imaging ◽

Intra Aortic Balloon Counterpulsation ◽

Balloon Counterpulsation

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Prognostic impact of unrecognized myocardial scar in the non-culprit territories by cardiac magnetic resonance imaging in patients with acute myocardial infarction

European Heart Journal - Cardiovascular Imaging ◽

10.1093/ehjci/jex194 ◽

2017 ◽

Vol 19 (1) ◽

pp. 108-116 ◽

Cited By ~ 6

Author(s):

Taku Omori ◽

Tairo Kurita ◽

Kaoru Dohi ◽

Akihiro Takasaki ◽

Tomoyuki Nakata ◽

...

Keyword(s):

Magnetic Resonance Imaging ◽

Myocardial Infarction ◽

Acute Myocardial Infarction ◽

Cardiac Magnetic Resonance ◽

Magnetic Resonance ◽

Cardiac Magnetic Resonance Imaging ◽

Myocardial Scar ◽

Prognostic Impact ◽

Resonance Imaging

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A PET/CT-follow-up imaging study to differentiate takotsubo cardiomyopathy from acute myocardial infarction

The International Journal of Cardiovascular Imaging ◽

10.1007/s10554-013-0311-x ◽

2013 ◽

Vol 30 (1) ◽

pp. 207-209 ◽

Cited By ~ 8

Author(s):

Jelena R. Ghadri ◽

Svetlana Dougoud ◽

Willibald Maier ◽

Philipp A. Kaufmann ◽

Oliver Gaemperli ◽

...

Keyword(s):

Myocardial Infarction ◽

Acute Myocardial Infarction ◽

Takotsubo Cardiomyopathy ◽

Imaging Study ◽

Pet Ct

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Reduced regional flow in the left ventricle after anterior acute myocardial infarction: a case control study using 4D flow MRI

BMC Medical Imaging ◽

10.1186/s12880-019-0404-7 ◽

2019 ◽

Vol 19 (1) ◽

Cited By ~ 1

Author(s):

Philip A. Corrado ◽

Jacob A. Macdonald ◽

Christopher J. François ◽

Niti R. Aggarwal ◽

Jonathan W. Weinsaft ◽

...

Keyword(s):

Myocardial Infarction ◽

Acute Myocardial Infarction ◽

Linear Models ◽

Left Ventricular ◽

Short Axis ◽

Flow Data ◽

4D Flow Mri ◽

4D Flow ◽

Regional Flow ◽

Flow Mri

Abstract Background Acute myocardial infarction (AMI) alters left ventricular (LV) hemodynamics, resulting in decreased global LV ejection fraction and global LV kinetic energy. We hypothesize that anterior AMI effects localized alterations in LV flow and developed a regional approach to analyze these local changes with 4D flow MRI. Methods 4D flow cardiac magnetic resonance (CMR) data was compared between 12 anterior AMI patients (11 males; 66 ± 12yo; prospectively acquired in 2016–2017) and 19 healthy volunteers (10 males; 40 ± 16yo; retrospective from 2010 to 2011 study). The LV cavity was contoured on short axis cine steady-state free procession CMR and partitioned into three regions: base, mid-ventricle, and apex. 4D flow data was registered to the short axis segmentation. Peak systolic and diastolic through-plane flows were compared region-by-region between groups using linear models of flow with age, sex, and heart rate as covariates. Results Peak systolic flow was reduced in anterior AMI subjects compared to controls in the LV mid-ventricle (fitted reduction = 3.9 L/min; P = 0.01) and apex (fitted reduction = 1.4 L/min; P = 0.02). Peak diastolic flow was also lower in anterior AMI subjects compared to controls in the apex (fitted reduction = 2.4 L/min; P = 0.01). Conclusions A regional method to analyze 4D LV flow data was applied in anterior AMI patients and controls. Anterior AMI patients had reduced regional flow relative to controls.

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Histochemical and immunohistochemical analyses of the myocardial scar fallowing acute myocardial infarction

Vojnosanitetski pregled ◽

10.2298/vsp110110008t ◽

2012 ◽

Vol 69 (7) ◽

pp. 581-588 ◽

Cited By ~ 1

Author(s):

Vujadin Tatic ◽

Saso Rafajlovski ◽

Vladimir Kanjuh ◽

Radoslav Gajanin ◽

Dusan Suscevic ◽

...

Keyword(s):

Myocardial Infarction ◽

Acute Myocardial Infarction ◽

Smooth Muscle ◽

Smooth Muscle Cells ◽

Muscle Fibers ◽

Myocardial Scar ◽

Oval Cells ◽

Ki 67 ◽

Alpha Actin ◽

Immunohistochemical Analyses

Background/Aim. The heart has traditionally been considered as a static organ without capacity of regeneration after trauma. Currently, the more and more often asked question is whether the heart has any intrinsic capacities to regenerate myocytes after myocardial infarction. The aim of this study was to present the existence of the preserved muscle fibers in the myocardial scar following myocardial infarction as well as the presence of numerous cells of various size and form that differently reacted to the used immunohistochemical antibodies. Methods. Histological, histochemical and immunohistochemical analyses of myocardial sections taken from 177 patients who had died of acute myocardial infarction and had the myocardial scar following myocardial infarction, were carried out. More sections taken both from the site of acute infarction and scar were examined by the following methods: hematoxylin-eosin (HE), periodic acid schiff (PAS), PAS-diastasis, Masson trichrom, Malory, van Gieson, vimentin, desmin, myosin, myoglobin, alpha actin, smoth muscle actin (SMA), p53, leukocyte common antigen (LCA), proliferating cell nuclear antigen (PCNA), Ki-67, actin HHF35, CD34, CD31, CD45, CD45Ro, CD8, CD20. Results. In all sections taken from the scar region, larger or smaller islets of the preserved muscle fibers with the signs of hypertrophy were found. In the scar, a large number of cells of various size and form: spindle, oval, elongated with abundant cytoplasm, small with one nucleus and cells with scanty cytoplasm, were found. The present cells differently reacted to histochemical and immunohistochemical methods. Large oval cells showed negative reaction to lymphocytic and leukocytic markers, and positive to alpha actin, actin HHF35, Ki-67, myosin, myoglobin and desmin. Elongated cells were also positive to those markers. Small mononuclear cells showed positive reaction to lymphocytic markers. Endothelial and smooth muscle cells in the blood vessel walls were positive to CD34 and CD31, and smooth muscle cells to SMA. Oval and elongated cells were positive to PCNA and Ki-67. The preserved muscle fibers in the scar were positive to myosin, myoglobin and desmin as well as elongated and oval cells. Other cells were negative to these markers. Conclusion. Our findings speak that myocardial regeneration is maybe possible and develops in human ischemic heart damages and that the myocardium is not a static organ without capacity of cell regeneration.

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