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*Corresponding author, Phone: ＋81-985-85-2810, Fax: ＋81-985-85-7614, E-mail: yasada＠fc.miyazaki-u.ac.jp

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Magn Reson Med Sci, Vol. 10, No. 4, pp. 255–258, 2011

CASE REPORT

Cardiac Rupture in Acute Myocardial Infarction: Post-mortem MR Imaging

Yasuyoshi KUROIWA1,2, Atsushi YAMASHITA2, Kensaku NISHIHIRA3, Yoshisato SHIBATA3,Yunosuke MATSUURA2, Masaji MAEDA1, and Yujiro ASADA2*

1Department of Radiological Technology, Koga General Hospital, Miyazaki, Japan2Department of Pathology, Faculty of Medicine, University of Miyazaki

5200 Kihara, Kiyotake, Miyazaki 889–1692, Japan3Miyazaki Medical Association Hospital, Miyazaki, Japan

(Received April 13, 2011; Accepted June 1, 2011)

We assessed acute myocardial infarction (AMI) with cardiac rupture in an autopsy usingmagnetic resonance (MR) imaging in vitro and histological staining. Cardiac MR imagingin vitro generated high resolution images of myocardial thinning, rupture, and epicardialhemorrhage. High signal intensity (SI) on T1 weighted images (WI) and low SI on T2WI ofthe rupture site corresponded with acute myocardial necrosis, edema, and hemorrhage. Arupture site rich in erythrocytes after AMI might aŠect SI on T1 and T2WI in cardiac MRimaging.

Keywords: autopsy, hemorrhage, rupture, signal intensity

Introduction

Noninvasive imaging plays a central role in diag-nosing heart disease, assessing prognosis, and mon-itoring the eŠects of therapy. Improvements inspeed, imaging quality, reliability, and range of ap-plications of cardiac magnetic resonance (MR)imaging permit its comprehensive assessment of pa-tients with heart disease and have made it an im-portant means of assessing myocardial anatomy,regional and global function, and viability.1 Cardi-ac rupture is a serious complication of acute my-ocardial infarction (AMI), and detailed MR fea-tures of this event remain unknown despite a fewcase reports of its visualization using cardiac MRimaging.2–4 We herein characterize the MR featuresof cardiac rupture using MR imaging in vitro andhistological assessment of AMI in an autopsiedcase.

Case Report

A 79-year-old woman with hypertension and ahistory of smoking consulted a primary care physi-cian for morning onset of sudden chest pain. Elec-trocardiography showed ST elevation in leads I,aVL, V1 to V6, and she was transferred to our

hospital with a diagnosis of AMI. Cardiac ultra-sonography revealed left ventricular hypertrophy,thinning of the apex to the anteroseptal wall withdecreased wall motion, and pericardial eŠusions.She died of cardiac shock 4 hours after the onset ofchest pain. We received written informed consentfrom a family member to perform an autopsy.Gross observation revealed a small ˆssure at the an-terior wall with hemopericardium and epicardialhemorrhage, indicating cardiac rupture. The heartwas then ˆxed in 10z formaldehyde for 24 hours atroom temperature, rinsed with water, and sub-merged in water in a plastic container. Cardiac MRimaging in vitro proceeded using a 1.5-tesla super-conducting system combined with an 8-channelknee-phased array coil (Signa Excite HDxt, GEMedical Systems, Waukesha, WI, USA). We ac-quired 3-dimensional (3D) fast spin echo (FSE)cube sequence T2-weighted images (T2WI) with fatsuppression, 1.500-ms repetition time (TR), and90-ms echo time (TE). Other parameters included:number of excitations (NEX), 6; echo train length(ETL), 110; receiver bandwidth (BW), 62.5 kHz;and acceleration factor (Acc), 2.8. We acquired 3Dfast spoiled gradient-recalled acquisition in thesteady state (GRASS) sequence (SPGR) T1-weight-ed images (T1WI) with fat suppression and pa-rameters: TR, 14.8 ms; TE, 2 ms; and ‰ip angle(FA), 159; NEX, 2; and BW, 62.5 kHz. FurtherMR imaging parameters included: ˆeld of view

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Fig. 1. Representative macroscopic and corre-sponding magnetic resonance (MR) images of theheart. (A) Axial section of the heart shows left ven-tricular hypertrophy, thinning of the anteroseptalwall with cardiac rupture (long arrow), and my-ocardial and epicardial hemorrhage (short arrows);a, anterior wall; p, posterior wall; lt, left; rt, right.Corresponding MR images show left ventricularhypertrophy, thinning anteroseptal wall with cardiacrupture (long arrows). The ruptured anterior wallshows high signal intensity (SI) on T1-weighted imag-ing (T1WI) (B) and iso SI on T2WI (C) (asterisks).The ruptured septal wall shows high to iso SI onT1WI (B) and low SI on T2WI (C) (cross symbols).The outer side shows iso SI on T1WI (B) and high SIon T2WI (C) (arrow heads). Epicardial hemorrhageshows high SI on T1WI and low SI on T2WI (short ar-rows).

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(FOV), 180×180 mm; matrix, 224×224; slicethickness, 1.2 mm. The table and ˆgures showcardiac MR imaging and corresponding macro- andmicroscopic ˆndings. MR imaging revealed leftventricular concentric hypertrophy and a thin an-teroseptal wall with cardiac rupture and hemor-rhage, ˆndings identical to macroscopic ˆndings ofthe axial section of the heart (Fig. 1A). The an-terior wall at the rupture site (asterisks) showedhigh signal intensity (SI) on T1WI (Fig. 1B) and isoSI on T2WI (Fig. 1C). The septal wall at the rup-ture site (cross symbols) showed high to iso SI onT1WI (Fig. 1B) and low SI on T2WI (Fig. 1C). Theouter side (arrow heads) showed iso SI on T1WI(Fig. 1B) and high SI on T2WI (Fig. 1C), whereasthe epicardial hemorrhage showed high SI on T1WIand low SI on T2WI (Fig. 1B and C, short arrows).Myocardial hemorrhage, thin and wavy cardio-myocytes, and edema were histological features ofthe ruptured anteroseptal wall (Fig. 2C) that werecompatible with the features of the early phase ofAMI with hemorrhage. The area with high SI onT2WI showed edema without necrotic change (Fig.2D) compared with the unaŠected myocardium(Fig. 2B). The myocardial hemorrhage in the areawith iso SI on T2WI (Fig. 2E) was widely im-munopositive for glycophorin A, (DAKO, Glos-trup, Denmark), a marker of erythrocytes, com-pared with the area of high SI on T2WI (Fig. 2F).Staining for ˆbrosis (Mallory-Azan) and hemo-seridin deposition (Berlin blue) were negative in theinfarcted area. Microscopically, hypertrophic car-diomyocytes in the area without infarction withoutmyocyte disarray or obvious ˆbrosis suggested sys-temic hypertension. Histological cross-section ofthe left anterior descending artery revealed plaqueerosion of an advanced atherosclerotic lesion withocclusive thrombus formation, and the thrombuswas considered the cause of the AMI with cardiacrupture at the anteroseptal wall.

Discussion

Cardiac MR imaging in vitro generated highresolution images of myocardial thinning, rupture,and epicardial hemorrhage in a patient with AMI.High SI on T1WI and low SI on T2WI at the rup-ture site corresponded to acute myocardial necro-sis, edema, and hemorrhage.

MR ˆndings of the infarcted lesion were heter-ogeneous with high to iso SI on T1WI and low toiso SI on T2WI at the rupture site or iso SI on T1WIand high SI on T2WI in the outer side (Table). Pub-lished case reports of cardiac rupture describehypoenhancement of the aŠected ventricular wall

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Fig. 2. Magnetic resonance T2-weighted imaging (T2WI) and representativemicrophotographs of the myocardium. Axial T2WI of the heart (A). Para‹nsections were stained with Mallory-Azan (B, C, D) or immunostained withglycophorin A (E, F). Area of iso SI (black arrow) on T2WI shows thin, wavycardiomyocytes, edema, and myocardial hemorrhage (C), compared with un-aŠected myocardium (B). Area of high SI (white arrow) on T2WI shows edemawithout necrotic change (D). Immunohistochemical staining for glycophorin Ashows myocardial hemorrhage in area of low SI (black arrow in A) (E) but nothigh SI (white arrow in A) (F).

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caused by arterial obstruction or late gadoliniumenhancement in cardiac MR imaging,2–4 but de-tailed MR ˆndings of cardiac rupture have not beenreported. T2-weighted images can reveal areas ofhigh SI caused by edema in patients with AMI,5,6

and the high SI on T2WI and edema at the outerside of the lesion of our patient were compatiblewith these ˆndings. The diŠerent ˆndings in theruptured myocardium might be caused by thepresence of myocardial hemorrhage because theMR ˆndings of epicardial hemorrhage were similar.Others have demonstrated that the proportions of

oxy-, deoxy- and methemoglobin generated byerythrocyte degradation aŠect relaxation rates andMR images and that changes in the proportions ofhemoglobin contribute to age-related changes inMR signals in hematoma.7,8 Therefore, the heter-ogeneous MR ˆndings of the ruptured myocardiummight be mainly aŠected by deoxy- and methemo-globin in extravasated erythrocytes. Furthermore,the absence of hemosiderin deposition in the lesionwas compatible with the early phase of hemor-rhage.

Cardiac ultrasonography cannot easily distin-

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Table. Cardiac magnetic resonance imaging and corresponding macro- and microscopic ˆndings

Symbols in Fig. 1 T1WI T2WI Macroscopic Microscopic

Rupture site*(anterior wall) high SI iso SI

thinning, hemorrhage necrosis, edema, hemorrhage†(septal wall) high to iso SI low SIOuter side arrow head iso SI high SI no remarkable change edemaEpicardium short arrow high SI low SI hemorrhage hemorrhage

SI (signal intensity)

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guish acute myocardial thinning in AMI from thethin ˆbrous wall that results from old myocardialinfarction (OMI). The necrotic myocardium at thefocus of a large transmural myocardial infarctionundergoes thinning and ultimate replacement by ˆ-brous tissue. Late gadolinium-enhanced MR imag-ing is widely used to assess myocardial viability inpatients with myocardial infarction,9,10 but AMIand OMI both demonstrate late enhancement. T2-weighted imaging is considered useful to distin-guish them; as described, high signal intensity onT2WI can detect tissue edema in patients with AMI,and areas of low to high SI were combined on T2WIof the infarcted lesion described herein. Myocardialthinning with an area of low to iso SI on T2WImight have re‰ected myocardial hemorrhage (Ta-ble).

Although this study was in vitro, MR imagingrevealed left ventricular hypertrophy and thinningof the anteroseptal wall with cardiac rupture andhemorrhage, ˆndings identical to the macroscopicfeatures. Two of 3 reports of cardiac rupture visu-alized by cardiac MR imaging describe either my-ocardial thinning or ˆssuring.2,3 Improved speedand image quality and technical advances in soft-ware have enabled the use of cardiac MR imagingfor diagnosing cardiac rupture.

In summary, cardiac MR imaging in vitro gener-ated high resolution images of myocardial thin-ning, rupture, and epicardial hemorrhage in a pa-tient with acute myocardial infarction. Myocardialhemorrhage after AMI might aŠect SI on T1WI andT2WI in cardiac MR imaging.

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