Delayed Trastuzumab-induced Cardiotoxicity Leading to Severe Left Ventricular Dysfunction

Figures

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  Figure 1.. Twelve-lead electrocardiograms (ECGs) before (a), 4 years (b), 7 years (c), and 9 years (on admission, d) after continuous trastuzumab therapy. Twelve-lead ECG recordings both before and four years after trastuzumab administration showed normal findings. After seven years, the R wave decreased in leads V1 to V3 and increased in leads V4 to V6 (c). Upon admission, a 12-lead ECG revealed a complete left bundle branch block (d).

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  Figure 2.. Chest radiography reveals a bilateral pleural effusion.

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  Figure 3.. Transthoracic echocardiography performed 9 years before prior to trastuzumab therapy during diastole (a) and systole (b) reveals normal LV wall motion with LV ejection fraction of 69%. LV: left ventricle, RV: right ventricle, LA: left atrium, RA: right atrium

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  Figure 4.. Transthoracic echocardiography on admission during diastole (a) and systole (b) reveals diffuse LV hypokinesis with an ejection fraction of 25%. LV: left ventricle, RV: right ventricle, LA: left atrium, RA: right atrium

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  Figure 5.. Clinical course in this case. Following the administration of furosemide, spironolactone, temocapril, dapagliflozin, and bisoprolol, her blood pressure dropped to 80 mmHg. By adding pimobendan, her blood pressure normalized, and the symptoms disappeared. After she recovered from heart failure and was discharged from our hospital, her symptoms worsened again, and she was re-hospitalized for another month. She then recovered from heart failure again was monitored as an outpatient.

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  Figure 6.. After a month, apical four-chamber imaging during diastole (a) and systole (b) showed that the interventricular septum had become thin, high echogenic, and dyskinetic (arrow). LV: left ventricle, RV: right ventricle, LA: left atrium, RA: right atrium

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  Figure 7.. Apical 2- chamber imaging during diastole (a) and systole (b) showed diffuse left ventricular hypokinesis with an ejection fraction of 19%. LV: left ventricle, LA: left atrium

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  Figure 8.. Global longitudinal strain imaging showed systolic elongation at the left ventricular septum and anterior wall. The global strain value was -6.7%.

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  Figure 9.. Coronary angiography revealed no significant organic stenosis.

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  Figure 10.. Cardiac magnetic resonance imaging during diastole (a) and systole (b) on the 34th day revealed hypokinesis of the interventricular septum (arrows). LV: left ventricle, LA: left atrium

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  Figure 11.. Native T1 map with color scale in four-chamber imaging. The signal intensity was higher at the interventricular septum and the apex than elsewhere, indicating edema or fibrosis in these areas (arrow). LV: left ventricle, RV: right ventricle, LA: left atrium, RA: right atrium

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  Figure 12.. Timeline of left ventricular end-diastlic dimension (LVDd), left ventricular ejection fraction (LVEF), and plasma brain natriuretic peptide (BNP). After half a year, the LVDd had decreased from 51 mm to 35 mm, the LVEF had increased from 25% to 48%, and the BNP level had decreased from 569 pg/mL to 88 pg/mL. These findings were further improved after nine months.