LV Aneurysm

Images and text Genevieve Carbonatto

A 56 year old man presents to the Emergency  Department with chest pain.

This is his ECG

The ECG shows deep Q waves and ST elevation in his anteroseptal leads

These are his vital signs: BP 120/69 mmHg, HR 89/min, Sats 100% on RA, RR16/min

This is his ECHO


Note the akinesis and the aneurysmal deformity of the apex. The entire apex cannot be viewed in the PLAX view, but it is clear that it appears aneurysmal. There is akinesis of the interventricular septum, while the inferolateral  wall is contracting well

PSAX at the level of the papillary muscles

The anteroseptum, inferoseptum and anterior segments are contracting poorly

PSAX from apex to mitral valve

The apex in the PSAX view is dilated

4 chamber view

The basal segments appear to be contracting , the rest of the LV is either akinetic or poorly contracting. The aneurysm is clearly visible

2 chamber view

Again, the akinetic apex is visible.

Notes from another hospital were obtained and it was revealed that he had had a recent coronary angiogram which showed  100% stenosis in the left anterior descending coronary artery which was treated with a stent and  a 90% stenosis in the right coronary artery which was also treated with a stent.

Revision of the LV segments

From the American and European echocardiography societies publication on cardiac chamber quantification in J Am Soc Echocardiogr 2015


The causes of ST elevation include

  1. Acute myocardial infarction
  2. Coronary vasospasm
  3. Pericarditis
  4. Benign early repolarisation
  5. Brugada syndrome
  6. LV hypertrophy
  7. Aneurysm
  8. Raised intracranial pressure
  9. Ventricular paced rhythm

Aetiology of LV aneuryms :  (1)

  • Most commonly occurs after an acute myocardial infarction
  • Myocardial infarction is usually transmural to cause an  LV aneurysm
  • 50% occur within 48 hours from the onset of pain, the remainder within 2 weeks
  • Angiographically defined LV aneurysms has been reported in 7.6% of patients with coronary artery disease referred for coronary angiogram
  • > 80% of LV aneurysm involve the anterior wall  +/- apex
  • Almost all are due to high-grade stenosis or complete occlusion of the proximal or mid-left anterior descending coronary artery
  • The fact that the apex has only 3 layers of muscle compared to the base which has 4 predisposes to apical aneurysm
  • Once formed LV aneurysms rarely resolve
  • Transient occlusion of a coronary artery may cause reversible dyskinesia (physiologic LV aneurysm)
  • Patients with  ischaemic disease may occasionally show LV aneurysm formation either during the period of acute ischaemia (stunned myocardium) or with chronic ischaemia (hibernating myocardium) that become less prominent when the ischaemia resolves. This is usually in the context of angina with no history of MI, and when the ECG shows no Q waves

Complications :

  • More common in large aneurysms
  • Arrhythmias – VT – poor prognosis
  • CCF – from poor LV systolic function if the LV aneurysm is >20% of the LV and from diastolic dysfunction due to a stiff non compliant LV. Occurs in 29% of patients and is a major cause of death
  • Angina – usually due to ischaemia in a different vascular territory. > 60% of patients with LV aneurysms have triple vessel disease
  • Thromboembolism – 50 % of patients with LV aneurysms will develop mural thrombi, but only 5% of uncoagulated patients with develop thromboembolism
  • Rupture of LVaneurysm  is extremely rare unless there is re infarction which occurs at the border of the LV aneurysm


  1. Clin. Cardiol. 12, 5-13 (1989) Review : Left Ventricular Aneurysm:   A. BA’ALBAKMI., D..s . D. CLEMENTS. J r . . M.D. . F.A.C.C. Department of Medicine, Division of Cardiology, Emory University School of Medicine, Emory University Hospital, Atlanta
  2. LV anatomy : An overview of the general segmental anatomy of the left ventricle and the associated coronary perfusion








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