PMC5401723_01
Electrocardiogram shows normal sinus rhythm, ST elevation in AVr, ST depression, and T waves inversion in inferior and apicolateral leads with premature ventricular beats.
CRIC2017-6287015.001.jpg
PMC5401723_01_CRIC2017-6287015.001.jpg
fig1
The electrocardiogram showed ST-segment elevation in AVr lead with ST-segment depression in inferior and anteroapical leads (Figure 1).
Transthoracic echocardiography showing apical left ventricular thrombus extending to the anterior and anterolateral walls. (a) Apical four-chamber view; (b) apical three-chamber view; (c) apical two-chamber view; (d) short axis view at the apical level.
CRIC2017-6287015.002.jpg
PMC5401723_01_CRIC2017-6287015.002.jpg
fig2
On the second day of intoxication, a transthoracic echocardiography was performed and objectified global hypokinesia of the left ventricule with an ejection fraction of 20% and an apical left ventricular thrombus extending to the anterior and anterolateral walls measuring 25 x 30 mm (Figure 2).
(a) Global longitudinal strain of the left ventricule at -3.5% suggesting severely reduced left ventricle systolic function. (b) Global longitudinal strain improved to -13.5% after 25 days.
CRIC2017-6287015.003.jpg
PMC5401723_01_CRIC2017-6287015.003.jpg
fig3
The global longitudinal strain of the left ventricule was evaluated at -3.5% (Figure 3(a)). Both the left ventricule ejection fraction and the global longitudinal strain increased, respectively, to 55% and to -13.5% (Figure 3(b)), after 25 days of ALP ingestion.
Transthoracic echocardiography, tissular Doppler showing a preserved function of the right ventricule: (a) TAPSE at 22 mm, (b) tricuspid lateral annular systolic velocity wave (S') at 0.12 m/s.
CRIC2017-6287015.004.jpg
PMC5401723_01_CRIC2017-6287015.004.jpg
fig4
The right ventricule had a preserved systolic function (Figure 4).
Cardiac magnetic resonance imaging: sequences HASTE (short axis) showing a hypersignal in the anterior wall (a) on the 5th day and (b) on the 60th day of aluminium phosphide poisoning.
CRIC2017-6287015.005.jpg
PMC5401723_01_CRIC2017-6287015.005.jpg
fig5
It showed an intramyocardial subepicardial signal anomaly in the anterior, inferoseptal, and anterolateral walls in T2 and in late gadolinium enhancement in T1-weighted images (after 10 min of gadolinium injection) suggesting acute toxic myocarditis (Figures 5(a) and 6). Regression of the intraventricular thrombus, of the hyperintense signal in the anterior wall in T2 (Figure 5(b)), and of late gadolinium enhancement in inferoseptal, anterior, and anterolateral walls in T1-weighted images (Figure 7) was confirmed by CMR control in two months.
Cardiac magnetic resonance imaging showing a decreased thrombus size in two months following ALP poisoning (after anticoagulant therapy). (a) Four-chamber view and (b) two-chamber view show a decrease of thrombus size of 80%; (c) four-chamber view (10 min of late gadolinium enhancement): regression of LGE in inferoseptal and anterolateral walls and in the apex; (d) two-chamber view (10 min of late gadolinium enhancement): regression of LGE in the anterior wall.
CRIC2017-6287015.007.jpg
PMC5401723_01_CRIC2017-6287015.007.jpg
fig7
Regression of the intraventricular thrombus, of the hyperintense signal in the anterior wall in T2 (Figure 5(b)), and of late gadolinium enhancement in inferoseptal, anterior, and anterolateral walls in T1-weighted images (Figure 7) was confirmed by CMR control in two months.