Not all T wave inversions are ischaemic Ravindran Rajendran, 1 Jigar S Patel, 1,2 Vivek Singla, 3 A C Nagamani 1 1 Department of Cardiology, Sri Jayadeva Institute of Cardiovascular Sciences and Research, Bangalore, Karnataka, India 2 Department of Medicine, Baroda Medical College, Baroda, Gujarat, India 3 Sri Jayadeva Institute of Cardiovascular Sciences, Bangalore, Karnataka, India Correspondence to Dr Ravindran R, [email protected] To cite: Rajendran R, Patel JS, Singla V, et al. BMJ Case Reports Published online: [ please include Day Month Year] doi:10.1136/ bcr-2012-008219 DESCRIPTION A 52- year-old man was referred as a case of acute coronary syndrome (ACS) for he had chest pain, vomiting and deep T wave inversions on ECG. Physical examination was normal except for blood pressure of 190/100 mm Hg. ECG ( figure 1) satis- fied voltage criteria for left ventricular hypertrophy along with deep asymmetrical T wave inversions, a prominent U wave and a prolonged corrected QT interval (QT c 560 ms). Echocardiogram confirmed concentric left ventricular hypertrophy but there was no regional wall motion abnormality, serum potassium was low (2.5 mEq/l) and cardiac biomar- kers were normal. Considering accelerated hyper- tension he was treated with oral amlodipine and intravenous nitroglycerine. Before resorting to ACS treatment, in view of headache, vomiting and sig- nificantly prolonged corrected QT interval along with deep T wave inversions, an intracranial bleed was considered. Subsequently, this was confirmed by a CT of the brain, which showed a haemorrhage involving the left temporo-parietal region ( figure 2). Interestingly, there was no focal neuro- logical deficit till 6 h after presentation. After treat- ing the patient with intravenous mannitol the T inversions normalised and the corrected QT also improved to 496 ms ( figure 3). Deep T wave inversions although commonly because of ischaemia and left ventricular hyper- trophy(LVH), a neurogenic T wave has to be suspected when the QT c is significantly prolonged. 1 Although neurogenic T wave inversions are deep and symmetrical, it may be asymmetrical as in this case when associated with LVH. Failures to recog- nise a neurogenic T inversion could be disastrous if anticoagulation were started inadvertently suspect- ing an ACS. Figure 1 ECG in sinus rhythm with deep T wave inversions, prominent U wave in mid precordial leads and prolonged corrected QT interval of 580 ms. Figure 2 Plain CT image of brain showing a left temporo parietal haemorrhage. Rajendran R, et al. BMJ Case Reports 2013. doi:10.1136/bcr-2012-008219 1 Images in … on 17 June 2020 by guest. Protected by copyright. http://casereports.bmj.com/ BMJ Case Reports: first published as 10.1136/bcr-2012-008219 on 23 January 2013. Downloaded from
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Not all T wave inversions are ischaemicRavindran Rajendran,1 Jigar S Patel,1,2 Vivek Singla,3 A C Nagamani1
1Department of Cardiology,Sri Jayadeva Institute ofCardiovascular Sciences andResearch, Bangalore,Karnataka, India2Department of Medicine,Baroda Medical College,Baroda, Gujarat, India3Sri Jayadeva Institute ofCardiovascular Sciences,Bangalore, Karnataka, India
Correspondence toDr Ravindran R,[email protected]
To cite: Rajendran R,Patel JS, Singla V, et al. BMJCase Reports Publishedonline: [please include DayMonth Year] doi:10.1136/bcr-2012-008219
DESCRIPTIONA 52- year-old man was referred as a case of acutecoronary syndrome (ACS) for he had chest pain,vomiting and deep T wave inversions on ECG.Physical examination was normal except for bloodpressure of 190/100 mm Hg. ECG (figure 1) satis-fied voltage criteria for left ventricular hypertrophyalong with deep asymmetrical T wave inversions, aprominent U wave and a prolonged corrected QTinterval (QTc 560 ms). Echocardiogram confirmedconcentric left ventricular hypertrophy but therewas no regional wall motion abnormality, serumpotassium was low (2.5 mEq/l) and cardiac biomar-kers were normal. Considering accelerated hyper-tension he was treated with oral amlodipine andintravenous nitroglycerine. Before resorting to ACStreatment, in view of headache, vomiting and sig-nificantly prolonged corrected QT interval alongwith deep T wave inversions, an intracranial bleedwas considered. Subsequently, this was confirmedby a CTof the brain, which showed a haemorrhageinvolving the left temporo-parietal region(figure 2). Interestingly, there was no focal neuro-logical deficit till 6 h after presentation. After treat-ing the patient with intravenous mannitol the Tinversions normalised and the corrected QT alsoimproved to 496 ms (figure 3).Deep T wave inversions although commonly
because of ischaemia and left ventricular hyper-trophy(LVH), a neurogenic T wave has to be
suspected when the QTc is significantly prolonged.1
Although neurogenic T wave inversions are deepand symmetrical, it may be asymmetrical as in thiscase when associated with LVH. Failures to recog-nise a neurogenic T inversion could be disastrous ifanticoagulation were started inadvertently suspect-ing an ACS.
Figure 1 ECG in sinus rhythm with deep T wave inversions, prominent U wave in mid precordial leads andprolonged corrected QT interval of 580 ms.
Figure 2 Plain CT image of brain showing a lefttemporo parietal haemorrhage.
Rajendran R, et al. BMJ Case Reports 2013. doi:10.1136/bcr-2012-008219 1
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on 17 June 2020 by guest. Protected by copyright.
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ase Reports: first published as 10.1136/bcr-2012-008219 on 23 January 2013. D
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Learning points
▸ Not all T wave inversions are ischaemic.▸ Symmetric T wave inversions with prolonged QTc though
seen in ischaemia; a cerebral cause has to be ruled outaccording to the clinical profile.
▸ Cerebral T inversion can be asymmetric when there isassociated left ventricular hypertrophy as in our case.
Competing interests None.
Patient consent Obtained.
Provenance and peer review Not commissioned, externally peer reviewed.
REFERENCE1 Oppenheimer S. Neurothanatology-clinical significance of cerebrally induced cardiac
changes. Postgrad Med J 1990;66:591–4.
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Figure 3 ECG after 12 h showing normalisation of T wave inversions and improvement in QTc (496 ms).
2 Rajendran R, et al. BMJ Case Reports 2013. doi:10.1136/bcr-2012-008219
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on 17 June 2020 by guest. Protected by copyright.
http://casereports.bmj.com
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ase Reports: first published as 10.1136/bcr-2012-008219 on 23 January 2013. D
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