J Cardiol 2005 Jun; 45（6）: 277 – 279

Cardiovascular Imaging In-a-Month
Reduced Left Ventricular Ejection Fraction in an 82-Year-Old Woman
With Aortic Stenosis●Takuya

TANIGUCHI, MD

Tatsuya

KAWASAKI, MD

Tadaaki

KAMITANI, MD

ShingoKAWASAKI, MD

HirokiSUGIHARA, MD

CASE
An 82-year-old woman presented with a history of progressive dyspnea persistingfor several days. The diagnosis of severe aortic stenosis was established some years
ago. However, she had firmly declined the recommendation of aortic valve replacement. On admission, electrocardiography showed ST-segment depression in leads Ⅰ,aⅤL, and Ⅴ3 to Ⅴ6. Echocardiography revealed that the aortic valve area of 0.6 cm2
remained unchanged, but the left ventricular ejection fraction was reduced to 44%
compared to 70% some months before. She died of progressive heart failure.
Autopsy disclosed tricuspid stenotic aortic valves with calcification probably due toage-related degeneration, and circumferential discoloration in the subendocardial
layers of the left ventricle with coronary artery stenosis of ＜ 50% in diameter
（Fig.
1）.

Fig. 1──────────────────────────────────────────────
松下記念病院 循環器科
〔谷口琢也，川崎達也，神谷匡昭，川崎信吾，杉原洋樹〕: 〒 570−8540 大阪府守口市外島町 5−55
Department of Cardiology, Matsushita Memorial Hospital, Osaka
Address for correspondence : TANIGUCHI T, MD, Department of Cardiology, Matsushita Memorial Hospital, Sotojima-cho 5−55,
Moriguchi, Osaka 570−8540 ; E-mail : cytokine@nike.eonet.ne.jp
Manuscript received February 24, 2005 ; revised April 4, 2005 ; accepted April 5, 2005277

278

Taniguchi, Kawasaki, Kamitani et al

Point of Diagnosis
Key Words : Aortic valve stenosis ; Myocardial infarction, pathophysiology ; Pathology

Histological examination confirmed that the circumferential discoloration in the subendocardial
layers of the left ventricle was myocardial infarction（Fig. 2）
. In general, subendocardium is predisposed to myocardial ischemia, possibly leading tomyocardial infarction, even in the absence of significant coronary lesions1）. Subendocardial infarction seems not to be uncommon in patients withaortic stenosis due to marked myocardial hypertrophy and raised ventricular pressure1−3）. In this case,the onset of subendocardial infarction was unidentifiable because neither prolonged chest pain nor cardiac enzyme leakage had occurred during the clinical course. However, subendocardial infarction
could develop silently in patients with aortic stenosis4）. Silent myocardial infarction may have lead tothe left ventricular dysfunction in the presentpatient.

Acknowledgement
We thank Atsushi Tatebe, MD, for the pathologic
diagnosis.
References
1）Levine HD : Subendocardial infarction in retrospect :Pathologic, cardiographic, and ancillary features.
Circulation 1985 ; 72 : 790−8002）Hutchins GM, Kuhajda FP, Moore GW : Myocardial injury
in patients with aortic stenosis. Am J Cardiovasc Pathol
1987 ; 1 : 31−373）Kodama-Takahashi K, Ohshima K, Kurata A, Yamamoto
K, Uemura S, Watanabe S, Iwata T, Kawachi K :Myocardial infarction in a patient with severe aortic stenosis and normal coronary arteriograms : Involvement of thecircumferential subendocardial wall of the left ventricle.
Circ J 2003 ; 67 : 891−8944）Sarda L, Faraggi M, Brochet E, Vissuzaine C, Delahaya N,
Le Guludec D : Acute diffuse myocyte necrosis evidenced
with 111In-antimyosin antibody scintigraphy in a patientwith aortic stenosis. J Nucl Cardiol 1997 ; 4 : 426−427

Diagnosis : Subendocardial infarction with aorticstenosis

Fig. 2J Cardiol 2005 Jun; 45（6）: 277 – 279

Cardiovascular Imaging In-a-Month
Fig. 1 Photograph of heart sections
Transverse sections of the heart at the level of apical,
mid, and basal ventricles show circumferential discoloration in the subendocardial layers of the left ventricle.

J Cardiol 2005 Jun; 45（6）: 277 – 279

279

Fig. 2 Photomicrograph of the subendocardium
Wavy fibers are preferentially distributed in thesubendocardium（hematoxylin-eosin stain, objective× 4）.