Left ventricular aneurysm overview
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Seyedmahdi Pahlavani, M.D. [2]
Overview
Left ventricular (LV) aneurysm forms when intraventricular tension stretches the injured heart muscle during each cardiac cycle. It is a complication of myocardial infarction (MI) and it is categorized into true and false aneurysms, based on the nature of it's wall. It is usually asymptomatic but may present as chest pain and dyspnea, and it should be suspected in patients with sustained ST elevation after MI. The diagnosis is based on echocardiographic findings.
Historical perspective
The British vascular surgeons, John and William Hunter, first described the aneurysm in 1880. In 1967, Gorlin and colleagues reported that aneurysms can be strongly suspected in up to 75% of patients with myocardial infarction.[1]
Classification
Based on the nature of the wall and its components, left ventricular aneurysms are classified as true or false aneurysms.[2]
True Left Ventricular Aneurysm
A true left ventricular aneurysm has an aneurysmal sac which contains the endocardium, epicardium, and thinned fibrous tissue (scar) which is a remnant of the left ventricular muscle.
False Left Ventricular Aneurysm or Pseudoaneurysm
Unlike a true aneurysm which contains some myocardial elements in its wall, the walls of a false aneurysm are composed of organized hematoma and pericardium and lack any element of the original myocardial wall.
Pathophysiology
Aneurysms form when intraventricular tension stretches the noncontracting, infarcted heart muscle, producing the expansion of the thin layer of necrotic muscle and fibrous tissue, which bulge with each cardiac contraction. The wall of a mature aneurysm is a white fibrous scar which becomes more densely fibrotic with the passage of time. The outward bulge with each cardiac contraction compromises the left ventricular stroke volume. On histopathological analysis, hyalinized fibrous tissue is the predominant finding. It usually takes 1 month for fibrous tissue to form.[1][3]
Causes
Myocardial infarction is the most common cause of left ventricular (LV) aneurysm formation. Less common causes include HCM, trauma, idiopathic and congenital abnormalities.[4][5][2][6]
Differential diagnosis
True LV aneurysm must be differentiated from false aneurysms.[7] [8]
Epidemiology
It was estimated that LV aneurysm develops in 30%-35% of patients with Q wave MI, but this has decreased significantly due to improvements in the management of patients with acute MI.[9] Currently it is estimated that true left ventricular aneurysms develop in less than 5% of all patients with STEMI.[10] According to this report, the use of thrombolytic agents has decreased the incidence of LV aneurysm from 18.8% to 7.2%.[10]
Risk Factors
The most potent risk factor for the development of LV aneurysm is ST elevation MI. Other risk factors include:[10][2][11][12]
- Hypertrophic cardiomyopathy (HCM)
- Dilated cardiomyopathy (DCM)
- Advanced age
- Hypertension
- Use of corticosteroids
Screening
The clue to the diagnosis of LV aneurysm following MI is a persistent ST elevation without chest pain, and there is no recommendation to screen patients for LV aneurysm.
Natural History
If left untreated, it may lead to heart failure and persistent anginal pain. For false aneurysms, rupture and hemodynamic compromise are the usual outcomes if left untreated. Improvements in STEMI management, control of hypertension and avoidance of corticosteroids in STEMI have led to a better prognosis and decreased mortality.[12]
Complications
Mural thrombosis, heart failure, persistent angina, and arrhythmia, are the major complications.
Symptoms
The symptoms of left ventricular aneurysm depends on the size of the aneurysm. Small and medium sized aneurysms are usually asymptomatic but large sized aneurysms may present as persistent chest pain and dyspnea despite the proper treatment of the underlying cardiac condition.
Physical exam
Physical findings on cardiac examination in patients with LV aneurysm include diffuse and displaced apical impulse, S3 and/or S4 heart sounds and mitral regurgitation murmur.
Electrocardiography
A persistent ST elevation is suggestive of LV aneurysm.[12]
Chest X ray
A bulge of the silhouette of the left ventricle on chest x-ray is the characteristic finding for LV aneurysm. [12]
CT scan
Chest CT scan with or without contrast may reveal the size and the location of LV aneurysm, it can also show the presence of calcifications in it.
MRI
Cardiac MRI is helpful for the diagnosis of LV aneurysm and it may be emerging as the preferred noninvasive technique for the preoperative assessment of LV shape, thinning, and resectability.[13]
Echocardiography
- Echocardiography is the modality of choice for the diagnosis of LV aneurysm. [14][15]
- It can measure the size and location of the aneurysm, and it is helpful for distinguishing true from false aneurysms based on the mouth size.
- Echocardiography is useful to diagnose dyskinesia or akinesia during systole.
- Echocardiography is helpful to diagnose mural thrombosis in aneurysm sac.
- Color flow echocardiography is helpful to establish the diagnosis based on in and out flow in the aneurysm.
Medical Therapy
Medical therapy is indicated for small and medium-sized LV aneurysms. Medical therapy is targeted at decreasing the cardiac work load (afterload reduction), anti ischemic therapy for chest pain and anti coagulation if mural thrombosis exist.[16]
- Afterload reduction:
- ACE inhibitors are the drug of choice for decreasing the afterload.
- Anti ischemic therapy:
- Many medications are used for treating underlying ischemic event and decreasing ischemic burden. The medications include:[16]
- Nitrates | Beta Blockers | Calcium Channel Blockers | Potassium Channel Openers | Newer Anti-anginal Agents
Surgery
- Surgical aneurysmectomy is recommended for large symptomatic aneurysms that cause angina pectoris or heart failure. Appropriate CABG is indicated at the time of aneurysmectomy.[17]
- Another indication for surgical intervention is in patients who can not tolerate long term anticoagulation therapy.[18]
References
- ↑ 1.0 1.1 Gorlin R, Klein MD, Sullivan JM (1967). "Prospective correlative study of ventricular aneurysm. Mechanistic concept and clinical recognition". Am. J. Med. 42 (4): 512–31. PMID 6024720.
- ↑ 2.0 2.1 2.2 Maron MS, Finley JJ, Bos JM, Hauser TH, Manning WJ, Haas TS, Lesser JR, Udelson JE, Ackerman MJ, Maron BJ (2008). "Prevalence, clinical significance, and natural history of left ventricular apical aneurysms in hypertrophic cardiomyopathy". Circulation. 118 (15): 1541–9. doi:10.1161/CIRCULATIONAHA.108.781401. PMID 18809796.
- ↑ Dubnow MH, Burchell HB, Titus JL (1965). "Postinfarction ventricular aneurysm. A clinicomorphologic and electrocardiographic study of 80 cases". Am. Heart J. 70 (6): 753–60. PMID 5842520.
- ↑ Mann, Douglas (2015). Braunwald's heart disease : a textbook of cardiovascular medicine. Philadelphia, PA: Elsevier/Saunders. ISBN 978-1455751341.
- ↑ Ichida M, Nishimura Y, Kario K (2014). "Clinical significance of left ventricular apical aneurysms in hypertrophic cardiomyopathy patients: the role of diagnostic electrocardiography". J Cardiol. 64 (4): 265–72. doi:10.1016/j.jjcc.2014.02.011. PMID 24674752.
- ↑ Xia S, Wu B, Zhang X, Hu X (2009). "Left ventricular aneurysm in patients with idiopathic dilated cardiomyopathy: clinical analysis of six cases". Neth Heart J. 17 (12): 475–80. PMC 2804080. PMID 20087451.
- ↑ Cho MN, Mehta SK, Matulevicius S, Weinstein D, Wait MA, McGuire DK (2006). "Differentiating true versus pseudo left ventricular aneurysm: a case report and review of diagnostic strategies". Cardiol Rev. 14 (6): e27–30. doi:10.1097/01.crd.0000233756.66532.45. PMID 17053370.
- ↑ Makkuni P, Kotler MN, Figueredo VM (2010). "Diverticular and aneurysmal structures of the left ventricle in adults: report of a case within the context of a literature review". Tex Heart Inst J. 37 (6): 699–705. PMC 3014120. PMID 21224951.
- ↑ Mills NL, Everson CT, Hockmuth DR (1993). "Technical advances in the treatment of left ventricular aneurysm". Ann. Thorac. Surg. 55 (3): 792–800. PMID 8452458.
- ↑ 10.0 10.1 10.2 Napodano M, Tarantini G, Ramondo A, Cacciavillani L, Corbetti F, Marra MP, Fraccaro C, Peluso D, Razzolini R, Iliceto S (2009). "Myocardial abnormalities underlying persistent ST-segment elevation after anterior myocardial infarction". J Cardiovasc Med (Hagerstown). 10 (1): 44–50. doi:10.2459/JCM.0b013e32831967b2. PMID 19145116.
- ↑ Bulkley BH, Roberts WC (1974). "Steroid therapy during acute myocardial infarction. A cause of delayed healing and of ventricular aneurysm". Am. J. Med. 56 (2): 244–50. PMID 4812079.
- ↑ 12.0 12.1 12.2 12.3 Mourdjinis A, Olsen E, Raphael MJ, Mounsey JP (1968). "Clinical diagnosis and prognosis of ventricular aneurysm". Br Heart J. 30 (4): 497–513. PMC 487659. PMID 5659397.
- ↑ Hüther J, Doenst T, Nitzsche S, Thiele H, Mohr FW, Gutberlet M (2011). "Cardiac magnetic resonance imaging for the assessment of ventricular function, geometry, and viability before and after surgical ventricular reconstruction". J. Thorac. Cardiovasc. Surg. 142 (6): 1515–22.e1. doi:10.1016/j.jtcvs.2011.04.040. PMID 21907357.
- ↑ Arvan S, Varat MA (1984). "Persistent ST-segment elevation and left ventricular wall abnormalities: a 2-dimensional echocardiographic study". Am. J. Cardiol. 53 (11): 1542–6. PMID 6731299.
- ↑ Matsumoto M, Watanabe F, Goto A, Hamano Y, Yasui K, Minamino T, Abe H, Kamada T (1985). "Left ventricular aneurysm and the prediction of left ventricular enlargement studied by two-dimensional echocardiography: quantitative assessment of aneurysm size in relation to clinical course". Circulation. 72 (2): 280–6. PMID 3159507.
- ↑ 16.0 16.1 Mann, Douglas (2015). Braunwald's heart disease : a textbook of cardiovascular medicine. Philadelphia, PA: Elsevier/Saunders. ISBN 978-1455751341.
- ↑ Kouchoukos, Nicholas (2013). Kirklin/Barratt-Boyes cardiac surgery : morphology, diagnostic criteria, natural history, techniques, results, and indications. Philadelphia: Elsevier/Saunders. ISBN 978-1416063919.
- ↑ Antman EM, Anbe DT, Armstrong PW, Bates ER, Green LA, Hand M, Hochman JS, Krumholz HM, Kushner FG, Lamas GA, Mullany CJ, Ornato JP, Pearle DL, Sloan MA, Smith SC, Alpert JS, Anderson JL, Faxon DP, Fuster V, Gibbons RJ, Gregoratos G, Halperin JL, Hiratzka LF, Hunt SA, Jacobs AK (2004). "ACC/AHA guidelines for the management of patients with ST-elevation myocardial infarction--executive summary: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the 1999 Guidelines for the Management of Patients With Acute Myocardial Infarction)". Circulation. 110 (5): 588–636. doi:10.1161/01.CIR.0000134791.68010.FA. PMID 15289388.