Left ventricular apical aneurysm caused by takotsubo cardiomyopathy

Abstract

A 78-year-old woman with hypertension was admitted to our hospital with palpitation and chest discomfort. She had been nervous since she learned about a severe earthquake on the news. An electrocardiogram showed ST-segment elevation in leads I, aVL, and V2–6. Emergency coronary angiography demonstrated no significant coronary stenosis and left ventriculography revealed marked akinesis of apical left ventricle with hyperkinesis of the basal segments, indicating typical takotsubo cardiomyopathy. On day 24, an electrocardiogram showed diffuse T-wave inversion, but ST-segment elevation remained in V3–6. Cardiac magnetic resonance imaging revealed left ventricular apical aneurysm and epicardial late gadolinium enhancement in the apex, indicating takotsubo-inflicted myocardial injury. Although many previous reports show takotsubo cardiomyopathy is a reversible left ventricular systolic dysfunction with less significant complications, it should be reconsidered as benign disease with long-term complications.

Learning objective

Although many previous reports show takotsubo cardiomyopathy (TC) is a reversible left ventricular (LV) systolic dysfunction with less significant complications, our patient is a rare case of TC which led to LV apical aneurysm. It was believed that lack of late gadolinium enhancement (LGE) was necessary to diagnose TC, however we detected epicardial LGE in the LV apical wall and this finding might indicate nonreversible change in this case.

Introduction

Takotsubo cardiomyopathy (TC) is an acute and usually reversible heart failure syndrome first reported in 1990 in Japan by Sato et al. [1]. Although many previous reports show TC is a reversible left ventricular (LV) systolic dysfunction with less significant complications [2], here we present a rare case of TC which led to LV apical aneurysm.

Case report

A 78-year-old woman with hypertension was admitted to our hospital with palpitation and chest discomfort. She had been nervous since she learned about a severe earthquake on the news. An electrocardiogram (ECG) showed ST-segment elevation in leads I, II, III, aVF, and V2–6 (Fig. 1A, day 0). Emergency coronary angiography demonstrated no significant coronary stenosis (Fig. 1B-D) and left ventriculography [Fig. 2A (showing diastole) and B (showing systole)] revealed marked akinesis of apical left ventricle with hyperkinesis of the basal segments, indicating typical TC. On day 4, we detected biphasic T-wave in leads V3–6 (Fig. 1A, day 4). On day 7, transthoracic echocardiogram demonstrated dyskinesis in the LV apical wall with hyperkinesis of the basal segment [Fig. 2C (showing diastole) and D (showing systole, arrows show dyskinetic area)]. Peak creatine kinase (CK)/CK-MB and troponin T levels were 746/112 IU/L and 1647 ng/L at admission and these levels normalized 12 days after the cardiac event (Fig. 2E). On the other hand, peak N-terminal prohormone of brain natriuretic peptide (NT-proBNP) levels were 6370.0 pg/mL 20 days after the cardiac event (Fig. 2E). The pattern of these data also suggests TC. On day 24, an electrocardiogram showed diffuse T-wave inversion, but ST-segment elevation remained in V3–6 (Fig. 1A, day 24). Cardiac magnetic resonance imaging revealed LV apical aneurysm [Fig. 3A (showing diastole) and B (showing systole)] and epicardial late gadolinium enhancement (LGE) in the apex (Fig. 3C-D), indicating takotsubo-inflicted myocardial injury. LGE was detected in circumferential area of LV apical wall, which extended beyond a single epicardial vascular distribution, suggesting spastic or embolic event to the left anterior descending artery was unlikely to be the cause of LV apical aneurysm. On day 178, an electrocardiogram showed negative T-waves in V2–6 were shallower compared with those on day 24, but ST-segment elevation also remained in V3–6 (Fig. 1A, day 178). Furthermore, transthoracic echocardiogram after 6 months also demonstrated dyskinesis in the LV apical wall without hyperkinesis of the basal segment [Fig. 3E (showing diastole) and F (showing systole, arrows show dyskinetic area)], suggesting our patient is a rare case of TC which led to LV apical aneurysm.

Fig. 1.

(A) Representative 12‑lead electrocardiographic changes in our patient. (B-D) Coronary angiography demonstrated no significant coronary stenosis.

(B) Left coronary artery (anteroposterior (AP) cranial view). (C) Left coronary artery (AP caudal view). (D) Right coronary artery (left anterior oblique (LAO) view).

Fig. 2.

Left ventriculography revealed marked akinesis of the left ventricle with hyperkinesis of the basal segments, representative of takotsubo cardiomyopathy [diastole (A) and systole (B)]. Transthoracic echocardiogram after 7 days also demonstrated dyskinesis in the left ventricular apical wall with hyperkinesis of the basal segments [diastole (C) and systole (D)]. (E) Summary of the clinical course of the patient.

CK, creatine kinase; CK-MB, creatine kinase–MB subform; NTproBNP, N-terminal prohormone of brain natriuretic peptide; TropT, cardiac muscle troponin T.

Fig. 3.

On day 24, cardiac magnetic resonance imaging revealed left ventricular apical aneurysm [diastole (A) and systole (B)]. Cardiac resonance imaging also demonstrated epicardial late gadolinium enhancement (red arrows) in the left ventricular apical wall (C). The line in (C) shows the level of axial view (D) and red arrows also show epicardial late gadolinium enhancement. Transthoracic echocardiogram after 6 months also demonstrated dyskinesis in the left ventricular apical wall [diastole (E) and systole (F)].

Discussion

Although many previous reports show TC is a reversible LV systolic dysfunction with less significant complications [2], it should be reconsidered as a benign disease with long-term complications. It was believed that lack of LGE was necessary to diagnose TC, however a recent report demonstrated LGE can be seen in the patients diagnosed with TC [3]. A previous study used immunohistochemical evidence to reveal that LGE-positive areas in TC have increased collagen-1 which could be indicative of a fibrotic process [4]. Another study demonstrated that TC patients with LGE had a slower recovery of wall motion compared to those that did not show LGE [5]. We detected epicardial LGE in the LV apical wall (Fig. 3C,D) and this finding might indicate nonreversible change in this case.

The pattern of LGE is seen in patients with focal myocarditis. Corroboration between clinical presentation, ECG, and biomarker findings are essential to make the correct diagnosis. The typical patient with TC is a post-menopausal woman who has experienced severe, unexpected emotional stress. These findings are consistent with our patient. ECG showed ST-segment elevation in leads I, II, III, aVF, and V2–6, but not V1 (Fig. 1A, day 0) suggesting typical ECG pattern for TC. Furthermore, peak CK/CK-MB levels were 746/112 IU/L at admission, but NT-proBNP was elevated to an extremely high level (6370.0 pg/mL) 20 days after the cardiac event indicating typical pattern of TC reported by Frohlich et al. [6]. Moreover, CK/CK-MB and troponin T levels normalized 12 days after the cardiac event (Fig. 2E) suggesting that our patient did not suffer chronic myocardial inflammation including cardiac sarcoidosis. Taken together, we diagnosed her with TC rather than focal myocarditis.

If our patient had a myocardial infarction with non-obstructive coronary artery disease (MINOCA) presenting with myocardial infarction due to multivessel spasm of the left coronary artery or myocardial infarction due to primary coronary artery dissection, she may have had similar findings of a LV mass. However, Fig. 3D shows significant epicardial LGE in the LV wall, indicating either the subendocardium was not affected or this did not correspond to any coronary territory. We, thus, think it unlikely that this patient had suffered a MINOCA.

This case shows a patient with LV apical aneurysm caused by TC. Furthermore, we detected epicardial LGE in the LV apical wall and this finding might indicate nonreversible change in this case. Large-scale studies are required to evaluate the exact prognostic value of LGE for TC.

Funding

This report was supported by Grant-in-Aid for Scientific Research [JSPS KAKENHI Grant Number 20K08433 (K.I.) and 21K16035 (M.H.)].

Consent

Written informed consent was obtained from the patient for publication of this case report including accompanying images.

Declaration of competing interest

The authors have no conflicts of interest.