å¡ CASE REPORT å¡
Transient Increase in Wall Thickness of the Left Ventricular Apex after Stunned Myocardium: A Case Report Kanji Iga, Katsuji Kitaguchi, Kenjiro Hori, Tadashi Matumura, Hiromitu Gen, Go Tomonaga and Toshitake Tamamura A case of transiently increased wall thickness in the left ventricular apex after stunned myocardium due to severe attack of vasospastic angina is described. "Ace of spades" configur ation, documented by left ventriculogram and increased apical wall thickness of the left This transiently increased left ventricular mass may have been due to to myocardial which ventricle, as revealed by two-dimensional echocardiograms returned normal inedema, 2 months. is occasionally seen in the recovery course of active myocarditis. (Internal Medicine 31: 122-124, 1992) Key words: transient apical wall thickening, apical hypertrophic cardiomyopathy (APH) , myocardial ischemia
Introduction A case of transiently increased apical wall thickness of the left ventricle in the recovery phase from the severe ischemic attack is reported. The purpose of this paper is to discuss the cause of this transiently increased left ventricular mass. Case Report A 64-yr-old man was admitted to our hospital because of oppressive chest sensation. The oppressive chest sensation, dating back about 6 months previously, only occurred early in the morning and 2-3 times a week. On the day of admission, the oppressive chest sensation had lasted for 12h on and off. There was no elevation in creatine-phosphokinase (CK) in the serial blood tests after admission. He has had no history of Serial electrocardiograms (ECG) are shown in Fig. 1; hypertension. an ECG, taken 4yr prior to admission was normal and a giant negative T wave was seen in I, aVL and chest leads on the day of admission. Two-dimensional echocardiog raphy revealed aneurysm in the cardiac apex. After admission, calcium antagonist and isosorbite dinitrate FromDepartment of Cardiology, Tenri Hospital, Tenri Received for publication December 7, 1990; Accepted for publication Reprint requests should be addressed to Kanji Iga, MD, Department 122
were administered and the oppressive chest sensation disappeared. The wall motion of the left ventricle re turned to normal in 10 days, however, the left ventricular apical wall thickness, revealed by two-dimensional echo cardiography became increased. Cardiac catheterization was performed 3wk after admission; the cardiac index was 3.621/min/m2 and left ventricular end-diastolic pressure was 9mmHg. Left ventriculography showed "ace of spades" configuration on end-diastole with an ejection fraction of 67% (Fig. 2). Coronary angiography revealed no abnormalities. An ergonovine test was not done. Treadmill stress test, done in the morning when the patient was off medication showed ST segment elevation in leads 1, aVL and V5 in the third stage of a modified Bruce protocol accompanied by oppressive chest sensation. However, he had accomplished the fifth stage of modified Bruce protocol without symptoms or ST changes when the patient was on medication. Two dimensional echocardiography (Fig. 3) showed gradual regression of the thickened left ventricular apical wall after 2 months. Levo-phase left ventriculography, taken 6 months after the severe ischemic attack showed that the "ace of spades" configuration had disappeared com pletely and an electrocardiogram performed at the same Maytime 13, was 1991 normalized (Figs. 1-3).
of Cardiology,
Tenri Hospital,
Internal
200 Mishima-cho, Medicine
Tenri 632, Japan
Vol. 31, No. 1 (January.
1992)
Transient LV Apical Hypertrophy
Fig. 1. Serial electrocardiograms. No abnormalities were found in 1984. On the day of admission (Aug. 31, 1988), deep symmetrical T waves were seen on 1, aVL and chest leads. On Jan. 19, 1988, the T wave changes were normalized. Discussion As the coronary angiography showed no significant stenosis and the morning exercise test revealed ST seg ment elevation with typical angina pectoris, it is clear that the diagnosis of this patient was vasospastic angina. The ischemic attack before this admission was severe enough to induce stunned myocardium (1). In the recov ery course from stunned myocardium, transiently in creased left ventricular mass in the apex was increased observed. Two-dimensional echocardiography showed wall thickness in the apex without any change of echo intensity in the myocardium. Left ventriculography, done 3 wk after the severe ischemic attack revealed "ace of spades" configuration at end-diastole, similar to apical hypertrophic cardiomyopathy (2). As the ejection frac tion was normal , concomitant apical hypertrophic cardio myopathy could not be ruled out at the time of the cardiac catheterization. As two-dimensional echocardiog raphy and left ventriculography, done about 6 months after the severe ischemic attack showed the disappear ance of the thickened apical wall, apical hypertrophic 20, 1988 (upper panel) showed concave configuration against the long Fig. ventriculograms. Left ventriculography on Sept. axis 2. of Serial the leftleft ventricle which is known as the "ace of spades" (arrows). Digital subtraction left ventriculography on Feb. 21, 1989 (lower panel) showed disappearance of this abnormal configuration at end-diastole. Internal
Medicine
Vol. 31, No. 1 (January
1992)
123
Iga et al cardiomyopathy was unlikely. A transient increase in left ventricular mass has been observed in the recovery course from active myocarditis (3, 4). Echocardiography shows diffuse and increasing wall thickness in the left ventricle. As the echo-intensity of the involved myocardium in these patients was high, Transient wall thickening of the left ven edema of increased the myocardium was speculated. tricular apex, seen in this patient could be explained by the same mechanism as in the recovery process from the severe myocardial ischemia. References 1) Braunwald E, Rutherfold JD. Reversible ischemic left ventricular dysfunction: Evidence for "hibernating myocardium." J Am Coll Cardiol 8: 1467, 1986 2) Yamaguchui H, Ishimura S, Nagasaki et al. Hypertrophic cardio myopathy with giant negative T wave (apical type): Ventriculog raphic and echocardiographic feature in 30 patients. Am J Cardiol 44: 401, 1979 3) Chandraratna PN, Bradley WG, Kortman KE, et al. Detection of acute myocarditis using nuclear magnetic resonance imaging. Am J Med 83: 1144, 1987 4) Nishida S, Ito A, Tuchiya A, et al. Acute idiopathic myocarditis having myocardial inflammatory swelling demonstrated by echo cardiography: A case report. J Cardiol 15: 909, 1985 (in Japanese).
Fig. 3. Serial two-dimensional echocardiograms. All panels are at end-diastolic phase. Left ventricular apical aneurysm, present on Aug. 31, 1988 (upper panel) disappeared on Feb. 16, 1989 (lower panel) via a phase of increased apical wall thickness of the left ventricle on Sept. 12, 1988 (middle panel).
124
Internal
Medicine
Vol. 31, No. 1 (January
1992)
Transient Increase in Wall Thickness of the Left Ventricular Apex after Stunned Myocardium: A Case Report Kanji Iga, Katsuji Kitaguchi, Kenjiro Hori, Tadashi Matumura, Hiromitu Gen, Go Tomonaga and Toshitake Tamamura A case of transiently increased wall thickness in the left ventricular apex after stunned myocardium due to severe attack of vasospastic angina is described. "Ace of spades" configur ation, documented by left ventriculogram and increased apical wall thickness of the left This transiently increased left ventricular mass may have been due to to myocardial which ventricle, as revealed by two-dimensional echocardiograms returned normal inedema, 2 months. is occasionally seen in the recovery course of active myocarditis. (Internal Medicine 31: 122-124, 1992) Key words: transient apical wall thickening, apical hypertrophic cardiomyopathy (APH) , myocardial ischemia
Introduction A case of transiently increased apical wall thickness of the left ventricle in the recovery phase from the severe ischemic attack is reported. The purpose of this paper is to discuss the cause of this transiently increased left ventricular mass. Case Report A 64-yr-old man was admitted to our hospital because of oppressive chest sensation. The oppressive chest sensation, dating back about 6 months previously, only occurred early in the morning and 2-3 times a week. On the day of admission, the oppressive chest sensation had lasted for 12h on and off. There was no elevation in creatine-phosphokinase (CK) in the serial blood tests after admission. He has had no history of Serial electrocardiograms (ECG) are shown in Fig. 1; hypertension. an ECG, taken 4yr prior to admission was normal and a giant negative T wave was seen in I, aVL and chest leads on the day of admission. Two-dimensional echocardiog raphy revealed aneurysm in the cardiac apex. After admission, calcium antagonist and isosorbite dinitrate FromDepartment of Cardiology, Tenri Hospital, Tenri Received for publication December 7, 1990; Accepted for publication Reprint requests should be addressed to Kanji Iga, MD, Department 122
were administered and the oppressive chest sensation disappeared. The wall motion of the left ventricle re turned to normal in 10 days, however, the left ventricular apical wall thickness, revealed by two-dimensional echo cardiography became increased. Cardiac catheterization was performed 3wk after admission; the cardiac index was 3.621/min/m2 and left ventricular end-diastolic pressure was 9mmHg. Left ventriculography showed "ace of spades" configuration on end-diastole with an ejection fraction of 67% (Fig. 2). Coronary angiography revealed no abnormalities. An ergonovine test was not done. Treadmill stress test, done in the morning when the patient was off medication showed ST segment elevation in leads 1, aVL and V5 in the third stage of a modified Bruce protocol accompanied by oppressive chest sensation. However, he had accomplished the fifth stage of modified Bruce protocol without symptoms or ST changes when the patient was on medication. Two dimensional echocardiography (Fig. 3) showed gradual regression of the thickened left ventricular apical wall after 2 months. Levo-phase left ventriculography, taken 6 months after the severe ischemic attack showed that the "ace of spades" configuration had disappeared com pletely and an electrocardiogram performed at the same Maytime 13, was 1991 normalized (Figs. 1-3).
of Cardiology,
Tenri Hospital,
Internal
200 Mishima-cho, Medicine
Tenri 632, Japan
Vol. 31, No. 1 (January.
1992)
Transient LV Apical Hypertrophy
Fig. 1. Serial electrocardiograms. No abnormalities were found in 1984. On the day of admission (Aug. 31, 1988), deep symmetrical T waves were seen on 1, aVL and chest leads. On Jan. 19, 1988, the T wave changes were normalized. Discussion As the coronary angiography showed no significant stenosis and the morning exercise test revealed ST seg ment elevation with typical angina pectoris, it is clear that the diagnosis of this patient was vasospastic angina. The ischemic attack before this admission was severe enough to induce stunned myocardium (1). In the recov ery course from stunned myocardium, transiently in creased left ventricular mass in the apex was increased observed. Two-dimensional echocardiography showed wall thickness in the apex without any change of echo intensity in the myocardium. Left ventriculography, done 3 wk after the severe ischemic attack revealed "ace of spades" configuration at end-diastole, similar to apical hypertrophic cardiomyopathy (2). As the ejection frac tion was normal , concomitant apical hypertrophic cardio myopathy could not be ruled out at the time of the cardiac catheterization. As two-dimensional echocardiog raphy and left ventriculography, done about 6 months after the severe ischemic attack showed the disappear ance of the thickened apical wall, apical hypertrophic 20, 1988 (upper panel) showed concave configuration against the long Fig. ventriculograms. Left ventriculography on Sept. axis 2. of Serial the leftleft ventricle which is known as the "ace of spades" (arrows). Digital subtraction left ventriculography on Feb. 21, 1989 (lower panel) showed disappearance of this abnormal configuration at end-diastole. Internal
Medicine
Vol. 31, No. 1 (January
1992)
123
Iga et al cardiomyopathy was unlikely. A transient increase in left ventricular mass has been observed in the recovery course from active myocarditis (3, 4). Echocardiography shows diffuse and increasing wall thickness in the left ventricle. As the echo-intensity of the involved myocardium in these patients was high, Transient wall thickening of the left ven edema of increased the myocardium was speculated. tricular apex, seen in this patient could be explained by the same mechanism as in the recovery process from the severe myocardial ischemia. References 1) Braunwald E, Rutherfold JD. Reversible ischemic left ventricular dysfunction: Evidence for "hibernating myocardium." J Am Coll Cardiol 8: 1467, 1986 2) Yamaguchui H, Ishimura S, Nagasaki et al. Hypertrophic cardio myopathy with giant negative T wave (apical type): Ventriculog raphic and echocardiographic feature in 30 patients. Am J Cardiol 44: 401, 1979 3) Chandraratna PN, Bradley WG, Kortman KE, et al. Detection of acute myocarditis using nuclear magnetic resonance imaging. Am J Med 83: 1144, 1987 4) Nishida S, Ito A, Tuchiya A, et al. Acute idiopathic myocarditis having myocardial inflammatory swelling demonstrated by echo cardiography: A case report. J Cardiol 15: 909, 1985 (in Japanese).
Fig. 3. Serial two-dimensional echocardiograms. All panels are at end-diastolic phase. Left ventricular apical aneurysm, present on Aug. 31, 1988 (upper panel) disappeared on Feb. 16, 1989 (lower panel) via a phase of increased apical wall thickness of the left ventricle on Sept. 12, 1988 (middle panel).
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Medicine
Vol. 31, No. 1 (January
1992)
