This ECG is from a 70 yr old patient with a history of ischaemic heart disease complicated by ischaemic cardiomyopathy (LV ejection fraction of 27%) in has an AICD in situ.
The patient presented with worsening dysponea without chest pain.
His intial serial ECGs are below.
|ECG 1 – Click to enlarge|
- ~90 bpm
- Sinus Rhythm
- Last complex PVC
- PR – Prolonged (220ms)
- QRS – Normal (100ms)
- QT – 320ms (QTc Bazette 380-400 ms)
- ST elevation leads III, V1-5
- ST depression (minor) lead I
- Q wave V1-2
- QS Wave V3-4
- T inversion leads aVR, aVF
- Voltage criteria LVH – aVR ~1.2mV
ECG features stongly suggest an old anteroseptal MI, with Q / QS waves in precordial leads, a lack of significant ST depression, and a pain-free patient with a known previous ischaemic insult.
This patient was admitted and investigated for dysponea further with the following investigations:
Myocardial Perfusion Scan
- Large anteroseptal and apical infarction
- Small area of reversible ischaemia in the mid-to-basal anterior wall
- Severely impaired systolic function
- Large anteroapical aneurysm
- No LV thrombus
- LV ejection fraction 27%
For more on LV aneurysm check out the following papers:
- Smith SW. T/QRS ratio best distinguishes ventricular aneurysm from anterior myocardial infarction.Am J Emerg Med. 2005 May;23(3):279-87.
- Engel J, Brady WJ, Mattu A, Perron AD. Electrocardiographic ST segment elevation: left ventricular aneurysm.Am J Emerg Med. 2002 May;20(3):238-42.
- Dr Smith’s ECG Blog – Left ventricular Aneurysm Morphology Distorted by Right Bundle Branch Block, Mimicking Acute STEMI with RBBB
- Dr Smith’s ECG Blog – Persistent ST elevation after previous MI, otherwise known as “LV aneurysm” morphology
- Dr Smith’s ECG Blog – This ECG is nearly pathognomonic. What is it?
- Dr Smith’s ECG Blog – Prolonged Chest Pain. Is this LV aneurysm or acute anterior STEMI? Acuteness of STEMI and viable myocardium.
|ECG 2 – Click to enlarge
- Mean ventricular rate 60bpm
- Regular atrial activity at ~62 bpm
- Regular pacing spikes @ 60 bpm
- Complexes 1-5 V. paced
- Complexes 6-10 progressive morphology change
- Preceeded by p waves with pr segment progressive lengthening 160-220ms
- PR – Progressively prolongs in relation to QRS complex
- QRS – Complexes 1-6 – Prolonged
- QRS – Complexes 7-10 – Normal
- Discordant ST segment / T wave change
- Complexes 1-5
- Pacing spike occurs withtin QRS for complexes 8-10
- Morpholgy similar to native sinus beats
- Pseudo-fusion beats
- Pacing mode likely VVI 60 bpm
- Single chamber device – hence no atrial sensing
- Isorhythmic sinus & pacing rate
- Both ~60 bpm
- For complexes 8-10 these are sinus conducted and given the near identical pacing and sinus rates the QRS complex has begun to form at the same time the pacing spike is delivered – causing a pseudofusion beat. The QRS complex has not yet been detected by the AICD, remebering the AICD uses local electrogram sensing, so a spike is delivered during the initial portion of the QRS which in effect does nothing.
References / Further Reading
Life in the Fast Lane
- Left Ventricular Aneurysm here
- Chan TC, Brady WJ, Harrigan RA, Ornato JP, Rosen P. ECG in Emergency Medicine and Acute Care. Elsevier Mosby 2005.