|Year : 2007 | Volume
| Issue : 1 | Page : 24-26
Left ventricular aneurysm presenting as cerebrovascular accident
Wafer Dabdoob, Sayed Abdou
Cardiology and Cardiovascular Surgery Department, Hamad Medical Corporation, Doha, Qatar
|Date of Web Publication||17-Jun-2010|
Cardiology and Cardiovascular Surgery Department, Hamad Medical Corporation, Doha
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Dabdoob W, Abdou S. Left ventricular aneurysm presenting as cerebrovascular accident. Heart Views 2007;8:24-6
| Introduction|| |
A 48 years old male, not known to have any chronic illness, was admitted because of cerebrovascular accident. He presented to our Accident and Emergency Department with dizziness and numbness of the left side of the body of 30 minutes duration. Several months prior to admission, he experienced chest discomfort and tightness and was diagnosed and treated as chest infection by A general practitioner.
In the Emergency Department, thorough neurological examination revealed that the patient was fully conscious, well oriented and there was no neurological deficit. The rest of the physical examination was unremarkable. The 12-lead electrocardiogram (ECG) showed sinus bradycardia and poor R wave progression in leads V 2 -V 3 [Figure 1]. Chest radiography (CXR) was normal. Laboratory evaluation including blood sugar, creatinine, electrolytes and cardiac specific enzymes were normal. Computerized Tomographic scan of the brain in the emergency department revealed an old right occipital lobe infarction and a new onset right frontal lobe infarction.
The patient was admitted to the medical floor as a case of cerebro-vascular accident (CVA). Echocardiography revealed akinesia of the inferoposterior wall, hypokinesia of the lateral wall and large basal posteroinferior aneurysm of the left ventricle [Figure 2] with ejection fraction (EF) of 30%. Carotid Doppler showed a tiny calcified plaque at the origin of left internal carotid artery without significant stenosis. MRI scan of the brain with non-contrast MRA of the intracranial vessels revealed infarction with hemorrhagic foci of the right thalamus, right parieto-occipital region and the right frontal lobe.
As per cardiology staff recommendation, the patient was started on beta blocker, angiotensin converting enzyme inhibitor (ACEI) and statin. The patient was discharged from the hospital without anticoagulation as per the advice of the neurology team.
One week after discharge, follow-up echocardiography showed a large fresh thrombus moving freely inside the left ventricular basal aneurysm [Figure 3]. The patient was re-admitted to the cardiac ward for anticoagulation. ECG was unchanged compared to the previous ECG during his hospitalization. Laboratory data revealed normal blood sugar, creatinine, electrolytes, cardiac specific enzymes, fibrinogen, PTT, PT and INR.
The patient was started on low molecular weight heparin and the warfarin was postponed for one week as per neurology team's advice. Four days after admission, repeat echocardiography showed disappearance of the thrombus. Cardiac MRI showed regional hypokinesia of the apex and infero-septal wall, and late enhancement at the inferior wall, suggesting myocardial scarring in the right coronary artery territories with large aneurysm in the basal inferior wall and no thrombus was detected. The patient was discharged from the hospital on beta blocker, ACEI and statin. No anticoagulation was given. The patient was asymptomatic when he showed up in the outpatient cardiology clinic after one month.
| Discussion|| |
True left ventricular (LV) aneurysm formation develops in less than 5% of patients with ST elevation myocardial infarction and somewhat more frequently in transmural infarction, especially of the anterior wall  . LV aneurysm occurs when intraventricular tension stretches the non-contracting infarcted myocardium, thin layer of necrotic muscles, and fibrous tissue. Most aneurysms are located anterolaterally, or near the LV apex and are often associated with total occlusion of the left anterior descending (LAD) coronary artery with poor collateral supply. Only 5-10% of aneurysms are located posteriorly, and is rarer in the inferior wall  .
The clinical features of LV aneurysm include symptoms of heart failure with or without angina in 50% of patients, severe angina alone was observed in one-third of the patients, and symptomatic ventricular arrhythmias in approximately 15%  . The ventricular arrhythmia may be refractory to treatment and life threatening , . In our case, there was no classical history of angina except one episode of chest discomfort and tightness several months before presentation and also no arrhythmia was observed.
Mural thrombus formation occurs in approximately 40% of anterior myocardial infarction patients who do not receive systemic anticoagulation. Approximately 60% of the thrombi are located in the apex of the left ventricle. The use of systemic anticoagulation during the acute and post-anterior myocardial infarction period has reduced the incidence of mural thrombus formation and embolization  .
The clues for the diagnosis of LV aneurysm include the presence of a persistent ST segment elevation on resting ECG  and a characteristic bulge and calcified LV silhouette on CXR. ECG and CXR have limited sensitivity and low specificity. These findings, however, were also absent in our case. The exact diagnosis of LV aneurysms is best made non-invasively by two-dimension echocardiography (2DE) study. 2DE is also helpful in distinguishing between a true and false aneurysm based on the demonstration of a narrow neck in relation to cavity size  . Left ventriculography is another diagnostic tool; however, it is an invasive method in detecting an abnormal bulge or dyskinetic wall motion in the LV contour during systole. Recently, MRI has emerged as a preferred non-invasive technique for pre-operative assessment of LV shape, the degree of aneurysm thinning, and its respectability  . In our case, the infarcted and scar area with delayed enhancement in the aneurysm was shown on MRI and these findings were compatible with echocardiographic findings.
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[Figure 1], [Figure 2], [Figure 3]