Left ventricular aneurysm overview: Difference between revisions

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== Overview ==
== Overview ==
Left ventricular (LV) aneurysm forms when intraventricular tension stretches the injured heart muscle during each cardiac cycle. It's a complication of myocardial infarct and is categorized to two types of true and false aneurysms based on the the nature of it's wall. It is usually asymptomatic but may present as chest pain and dyspnea and is suspected in patients with sustained ST elevation after MI. Diagnosis is based on echocardigraphic findings.  
Left ventricular (LV) aneurysm forms when [[intraventricular]] tension stretches the injured heart muscle during each cardiac cycle. It is a complication of [[Myocardial infarction|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==
==Historical perspective==
John and William Hunter, Britanian vascular surgeons first described the aneurysm in 1880.<br>
The British vascular surgeons, John and William Hunter, first described the aneurysm in 1880. In 1967, Gorlin and colleagues reported that [[aneurysm]]<nowiki/>s can be strongly suspected in up to 75% of patients with [[myocardial infarction]].<ref name="pmid6024720">{{cite journal |vauthors=Gorlin R, Klein MD, Sullivan JM |title=Prospective correlative study of ventricular aneurysm. Mechanistic concept and clinical recognition |journal=Am. J. Med. |volume=42 |issue=4 |pages=512–31 |year=1967 |pmid=6024720 |doi= |url=}}</ref>
In 1967, Gorlin and colleagues reported that a strong suspicion of aneurysm could be obtained in 75% of patients with myocardial infarction.<ref name="pmid6024720">{{cite journal |vauthors=Gorlin R, Klein MD, Sullivan JM |title=Prospective correlative study of ventricular aneurysm. Mechanistic concept and clinical recognition |journal=Am. J. Med. |volume=42 |issue=4 |pages=512–31 |year=1967 |pmid=6024720 |doi= |url=}}</ref>


==Classification==
==Classification==
Based on the wall nature and its components, left ventricular aneurysms are classified as ''true'' or ''false [[aneurysm|aneurysms]]''.<ref name="pmid18809796">{{cite journal |vauthors=Maron MS, Finley JJ, Bos JM, Hauser TH, Manning WJ, Haas TS, Lesser JR, Udelson JE, Ackerman MJ, Maron BJ |title=Prevalence, clinical significance, and natural history of left ventricular apical aneurysms in hypertrophic cardiomyopathy |journal=Circulation |volume=118 |issue=15 |pages=1541–9 |year=2008 |pmid=18809796 |doi=10.1161/CIRCULATIONAHA.108.781401 |url=}}</ref>
Based on the nature of the wall and its components, left ventricular aneurysms are classified as ''true'' or ''false [[aneurysm|aneurysms]]''.<ref name="pmid18809796">{{cite journal |vauthors=Maron MS, Finley JJ, Bos JM, Hauser TH, Manning WJ, Haas TS, Lesser JR, Udelson JE, Ackerman MJ, Maron BJ |title=Prevalence, clinical significance, and natural history of left ventricular apical aneurysms in hypertrophic cardiomyopathy |journal=Circulation |volume=118 |issue=15 |pages=1541–9 |year=2008 |pmid=18809796 |doi=10.1161/CIRCULATIONAHA.108.781401 |url=}}</ref>
===True Left Ventricular Aneurysm===
===True Left Ventricular Aneurysm===
A true left ventricular aneurysm has an aneurysmal sac which contains the [[endocardium]], [[epicardium]], and thinned fibrous tissue ([[scar]]) that is a remnant of the left ventricular muscle.
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===
===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.
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==
==Pathophysiology==
Aneurysm forms when intraventricular tension stretches the noncontracting infarcted heart muscle, producing expansion of the thin layer of necrotic muscle and fibrous tissue that bulges with each cardiac contraction. The wall of a mature aneurysm is a white fibrous scar. It becomes more densely fibrotic as the time passages, but bulges outward with each cardiac contraction and causes some of the left ventricular stroke volume to be ineffective. On microscopic histopathological analysis, hyalinized fibrous tissue is the predominant finding. It usually takes 1 month for fibrous tissue to form. <ref name="pmid6024720">{{cite journal |vauthors=Gorlin R, Klein MD, Sullivan JM |title=Prospective correlative study of ventricular aneurysm. Mechanistic concept and clinical recognition |journal=Am. J. Med. |volume=42 |issue=4 |pages=512–31 |year=1967 |pmid=6024720 |doi= |url=}}</ref><ref name="pmid5842520">{{cite journal |vauthors=Dubnow MH, Burchell HB, Titus JL |title=Postinfarction ventricular aneurysm. A clinicomorphologic and electrocardiographic study of 80 cases |journal=Am. Heart J. |volume=70 |issue=6 |pages=753–60 |year=1965 |pmid=5842520 |doi= |url=}}</ref>   
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.<ref name="pmid6024720">{{cite journal |vauthors=Gorlin R, Klein MD, Sullivan JM |title=Prospective correlative study of ventricular aneurysm. Mechanistic concept and clinical recognition |journal=Am. J. Med. |volume=42 |issue=4 |pages=512–31 |year=1967 |pmid=6024720 |doi= |url=}}</ref><ref name="pmid5842520">{{cite journal |vauthors=Dubnow MH, Burchell HB, Titus JL |title=Postinfarction ventricular aneurysm. A clinicomorphologic and electrocardiographic study of 80 cases |journal=Am. Heart J. |volume=70 |issue=6 |pages=753–60 |year=1965 |pmid=5842520 |doi= |url=}}</ref>   
==Causes==
==Causes==
[[Myocardial infarction]] is the most common cause of Left ventricular (LV) aneurysm formation. Less common causes include [[Hypertrophic cardiomyopathy|HCM]], [[trauma]], and [[idiopathic]] and [[Congenital disorder|congenital abnormalities]].<ref>{{cite book | last = Mann | first = Douglas | title = Braunwald's heart disease : a textbook of cardiovascular medicine | publisher = Elsevier/Saunders | location = Philadelphia, PA | year = 2015 | isbn = 978-1455751341 }}</ref>
[[Myocardial infarction]] is the most common cause of left ventricular (LV) aneurysm formation. Less common causes include [[Hypertrophic cardiomyopathy|HCM]], [[trauma]], [[idiopathic]] and [[Congenital disorder|congenital abnormalities]].<ref>{{cite book | last = Mann | first = Douglas | title = Braunwald's heart disease : a textbook of cardiovascular medicine | publisher = Elsevier/Saunders | location = Philadelphia, PA | year = 2015 | isbn = 978-1455751341 }}</ref><ref name="pmid24674752">{{cite journal |vauthors=Ichida M, Nishimura Y, Kario K |title=Clinical significance of left ventricular apical aneurysms in hypertrophic cardiomyopathy patients: the role of diagnostic electrocardiography |journal=J Cardiol |volume=64 |issue=4 |pages=265–72 |year=2014 |pmid=24674752 |doi=10.1016/j.jjcc.2014.02.011 |url=}}</ref><ref name="pmid18809796">{{cite journal |vauthors=Maron MS, Finley JJ, Bos JM, Hauser TH, Manning WJ, Haas TS, Lesser JR, Udelson JE, Ackerman MJ, Maron BJ |title=Prevalence, clinical significance, and natural history of left ventricular apical aneurysms in hypertrophic cardiomyopathy |journal=Circulation |volume=118 |issue=15 |pages=1541–9 |year=2008 |pmid=18809796 |doi=10.1161/CIRCULATIONAHA.108.781401 |url=}}</ref><ref name="pmid20087451">{{cite journal |vauthors=Xia S, Wu B, Zhang X, Hu X |title=Left ventricular aneurysm in patients with idiopathic dilated cardiomyopathy: clinical analysis of six cases |journal=Neth Heart J |volume=17 |issue=12 |pages=475–80 |year=2009 |pmid=20087451 |pmc=2804080 |doi= |url=}}</ref>
Other less common causes include:<ref name="pmid24674752">{{cite journal |vauthors=Ichida M, Nishimura Y, Kario K |title=Clinical significance of left ventricular apical aneurysms in hypertrophic cardiomyopathy patients: the role of diagnostic electrocardiography |journal=J Cardiol |volume=64 |issue=4 |pages=265–72 |year=2014 |pmid=24674752 |doi=10.1016/j.jjcc.2014.02.011 |url=}}</ref><ref name="pmid18809796">{{cite journal |vauthors=Maron MS, Finley JJ, Bos JM, Hauser TH, Manning WJ, Haas TS, Lesser JR, Udelson JE, Ackerman MJ, Maron BJ |title=Prevalence, clinical significance, and natural history of left ventricular apical aneurysms in hypertrophic cardiomyopathy |journal=Circulation |volume=118 |issue=15 |pages=1541–9 |year=2008 |pmid=18809796 |doi=10.1161/CIRCULATIONAHA.108.781401 |url=}}</ref><ref name="pmid20087451">{{cite journal |vauthors=Xia S, Wu B, Zhang X, Hu X |title=Left ventricular aneurysm in patients with idiopathic dilated cardiomyopathy: clinical analysis of six cases |journal=Neth Heart J |volume=17 |issue=12 |pages=475–80 |year=2009 |pmid=20087451 |pmc=2804080 |doi= |url=}}</ref>
 
==Differential diagnosis==
==Differential diagnosis==
True LV aneurysm must be differentiated from false aneurysms.<ref name="pmid17053370">{{cite journal |vauthors=Cho MN, Mehta SK, Matulevicius S, Weinstein D, Wait MA, McGuire DK |title=Differentiating true versus pseudo left ventricular aneurysm: a case report and review of diagnostic strategies |journal=Cardiol Rev |volume=14 |issue=6 |pages=e27–30 |year=2006 |pmid=17053370 |doi=10.1097/01.crd.0000233756.66532.45 |url=}}</ref> <ref name="pmid21224951">{{cite journal |vauthors=Makkuni P, Kotler MN, Figueredo VM |title=Diverticular and aneurysmal structures of the left ventricle in adults: report of a case within the context of a literature review |journal=Tex Heart Inst J |volume=37 |issue=6 |pages=699–705 |year=2010 |pmid=21224951 |pmc=3014120 |doi= |url=}}</ref>
True LV aneurysm must be differentiated from false aneurysms.<ref name="pmid17053370">{{cite journal |vauthors=Cho MN, Mehta SK, Matulevicius S, Weinstein D, Wait MA, McGuire DK |title=Differentiating true versus pseudo left ventricular aneurysm: a case report and review of diagnostic strategies |journal=Cardiol Rev |volume=14 |issue=6 |pages=e27–30 |year=2006 |pmid=17053370 |doi=10.1097/01.crd.0000233756.66532.45 |url=}}</ref> <ref name="pmid21224951">{{cite journal |vauthors=Makkuni P, Kotler MN, Figueredo VM |title=Diverticular and aneurysmal structures of the left ventricle in adults: report of a case within the context of a literature review |journal=Tex Heart Inst J |volume=37 |issue=6 |pages=699–705 |year=2010 |pmid=21224951 |pmc=3014120 |doi= |url=}}</ref>
==Epidemiology==
==Epidemiology==
It was estimated that LV aneurysm develops in 30%-35% of patients with Q wave MI. But it has been decreased significantly due to introduction of improvements in the management of patients with acute MI.<ref name="pmid8452458">{{cite journal |vauthors=Mills NL, Everson CT, Hockmuth DR |title=Technical advances in the treatment of left ventricular aneurysm |journal=Ann. Thorac. Surg. |volume=55 |issue=3 |pages=792–800 |year=1993 |pmid=8452458 |doi= |url=}}</ref> Currently it is estimated that true left ventricular aneurysms develop in less than 5% of all patients with STEMI.<ref name="pmid19145116">{{cite journal |vauthors=Napodano M, Tarantini G, Ramondo A, Cacciavillani L, Corbetti F, Marra MP, Fraccaro C, Peluso D, Razzolini R, Iliceto S |title=Myocardial abnormalities underlying persistent ST-segment elevation after anterior myocardial infarction |journal=J Cardiovasc Med (Hagerstown) |volume=10 |issue=1 |pages=44–50 |year=2009 |pmid=19145116 |doi=10.2459/JCM.0b013e32831967b2 |url=}}</ref>
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]].<ref name="pmid8452458">{{cite journal |vauthors=Mills NL, Everson CT, Hockmuth DR |title=Technical advances in the treatment of left ventricular aneurysm |journal=Ann. Thorac. Surg. |volume=55 |issue=3 |pages=792–800 |year=1993 |pmid=8452458 |doi= |url=}}</ref> Currently it is estimated that true left ventricular aneurysms develop in less than 5% of all patients with STEMI.<ref name="pmid19145116">{{cite journal |vauthors=Napodano M, Tarantini G, Ramondo A, Cacciavillani L, Corbetti F, Marra MP, Fraccaro C, Peluso D, Razzolini R, Iliceto S |title=Myocardial abnormalities underlying persistent ST-segment elevation after anterior myocardial infarction |journal=J Cardiovasc Med (Hagerstown) |volume=10 |issue=1 |pages=44–50 |year=2009 |pmid=19145116 |doi=10.2459/JCM.0b013e32831967b2 |url=}}</ref>
According to this report, the use of thrombolytic agents has decreased the incidence of LV aneurysm from 18.8% to 7.2%.<ref name="pmid19145116">{{cite journal |vauthors=Napodano M, Tarantini G, Ramondo A, Cacciavillani L, Corbetti F, Marra MP, Fraccaro C, Peluso D, Razzolini R, Iliceto S |title=Myocardial abnormalities underlying persistent ST-segment elevation after anterior myocardial infarction |journal=J Cardiovasc Med (Hagerstown) |volume=10 |issue=1 |pages=44–50 |year=2009 |pmid=19145116 |doi=10.2459/JCM.0b013e32831967b2 |url=}}</ref>
According to this report, the use of [[Thrombolysis|thrombolytic]] agents has decreased the incidence of LV aneurysm from 18.8% to 7.2%.<ref name="pmid19145116">{{cite journal |vauthors=Napodano M, Tarantini G, Ramondo A, Cacciavillani L, Corbetti F, Marra MP, Fraccaro C, Peluso D, Razzolini R, Iliceto S |title=Myocardial abnormalities underlying persistent ST-segment elevation after anterior myocardial infarction |journal=J Cardiovasc Med (Hagerstown) |volume=10 |issue=1 |pages=44–50 |year=2009 |pmid=19145116 |doi=10.2459/JCM.0b013e32831967b2 |url=}}</ref>
==Risk Factors==
==Risk Factors==
The most potent risk factor for development of the LV aneurysm is '''[[ST elevation myocardial infarction|ST elevation MI]]'''. Other risk factors include:<ref name="pmid19145116">{{cite journal |vauthors=Napodano M, Tarantini G, Ramondo A, Cacciavillani L, Corbetti F, Marra MP, Fraccaro C, Peluso D, Razzolini R, Iliceto S |title=Myocardial abnormalities underlying persistent ST-segment elevation after anterior myocardial infarction |journal=J Cardiovasc Med (Hagerstown) |volume=10 |issue=1 |pages=44–50 |year=2009 |pmid=19145116 |doi=10.2459/JCM.0b013e32831967b2 |url=}}</ref><ref name="pmid18809796">{{cite journal |vauthors=Maron MS, Finley JJ, Bos JM, Hauser TH, Manning WJ, Haas TS, Lesser JR, Udelson JE, Ackerman MJ, Maron BJ |title=Prevalence, clinical significance, and natural history of left ventricular apical aneurysms in hypertrophic cardiomyopathy |journal=Circulation |volume=118 |issue=15 |pages=1541–9 |year=2008 |pmid=18809796 |doi=10.1161/CIRCULATIONAHA.108.781401 |url=}}</ref><ref name="pmid4812079">{{cite journal |vauthors=Bulkley BH, Roberts WC |title=Steroid therapy during acute myocardial infarction. A cause of delayed healing and of ventricular aneurysm |journal=Am. J. Med. |volume=56 |issue=2 |pages=244–50 |year=1974 |pmid=4812079 |doi= |url=}}</ref><ref name="pmid5659397">{{cite journal |vauthors=Mourdjinis A, Olsen E, Raphael MJ, Mounsey JP |title=Clinical diagnosis and prognosis of ventricular aneurysm |journal=Br Heart J |volume=30 |issue=4 |pages=497–513 |year=1968 |pmid=5659397 |pmc=487659 |doi= |url=}}</ref>
The most potent risk factor for the development of LV aneurysm is '''[[ST elevation myocardial infarction|ST elevation MI]]'''. Other risk factors include:<ref name="pmid19145116">{{cite journal |vauthors=Napodano M, Tarantini G, Ramondo A, Cacciavillani L, Corbetti F, Marra MP, Fraccaro C, Peluso D, Razzolini R, Iliceto S |title=Myocardial abnormalities underlying persistent ST-segment elevation after anterior myocardial infarction |journal=J Cardiovasc Med (Hagerstown) |volume=10 |issue=1 |pages=44–50 |year=2009 |pmid=19145116 |doi=10.2459/JCM.0b013e32831967b2 |url=}}</ref><ref name="pmid18809796">{{cite journal |vauthors=Maron MS, Finley JJ, Bos JM, Hauser TH, Manning WJ, Haas TS, Lesser JR, Udelson JE, Ackerman MJ, Maron BJ |title=Prevalence, clinical significance, and natural history of left ventricular apical aneurysms in hypertrophic cardiomyopathy |journal=Circulation |volume=118 |issue=15 |pages=1541–9 |year=2008 |pmid=18809796 |doi=10.1161/CIRCULATIONAHA.108.781401 |url=}}</ref><ref name="pmid4812079">{{cite journal |vauthors=Bulkley BH, Roberts WC |title=Steroid therapy during acute myocardial infarction. A cause of delayed healing and of ventricular aneurysm |journal=Am. J. Med. |volume=56 |issue=2 |pages=244–50 |year=1974 |pmid=4812079 |doi= |url=}}</ref><ref name="pmid5659397">{{cite journal |vauthors=Mourdjinis A, Olsen E, Raphael MJ, Mounsey JP |title=Clinical diagnosis and prognosis of ventricular aneurysm |journal=Br Heart J |volume=30 |issue=4 |pages=497–513 |year=1968 |pmid=5659397 |pmc=487659 |doi= |url=}}</ref>
*[[Hypertrophic cardiomyopathy]] (HCM)
*[[Hypertrophic cardiomyopathy]] (HCM)
*[[Dilated cardiomyopathy]] (DCM)
*[[Dilated cardiomyopathy]] (DCM)
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*Use of [[corticosteroids]]
*Use of [[corticosteroids]]
==Screening==
==Screening==
Clue for diagnosis LV aneurysm after MI is, persistant ST elevation without chest pain and there is no recommendation to screen patients for LV aneurysm.
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==
==Natural History==
If left untreated it may lead to heart failure and persistent anginal pain. For false aneurysms rupture and hemodynamic compromise are the outcomes if left untreated. Improvements in STEMI management, control of hypertension and avoidance of corticosteroids in STEMI have led to better prognosis and decreased mortality.<ref name="pmid5659397">{{cite journal |vauthors=Mourdjinis A, Olsen E, Raphael MJ, Mounsey JP |title=Clinical diagnosis and prognosis of ventricular aneurysm |journal=Br Heart J |volume=30 |issue=4 |pages=497–513 |year=1968 |pmid=5659397 |pmc=487659 |doi= |url=}}</ref>
If left untreated, it may lead to [[heart failure]] and persistent [[anginal]] pain. For false aneurysms, rupture and [[Hemodynamics|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.<ref name="pmid5659397">{{cite journal |vauthors=Mourdjinis A, Olsen E, Raphael MJ, Mounsey JP |title=Clinical diagnosis and prognosis of ventricular aneurysm |journal=Br Heart J |volume=30 |issue=4 |pages=497–513 |year=1968 |pmid=5659397 |pmc=487659 |doi= |url=}}</ref>
==Complications==
==Complications==
Mural thrombosis, heart failure, persistent angina and arrhythmia are it's major complications.
Mural [[thrombosis]], [[heart failure]], persistent [[angina]], and [[Arrhythmias|arrhythmia]], are the major complications.
==Symptoms==
==Symptoms==
Symptoms of aneurysm depend on it's size. Small and medium sized are usually asymptomatic but large size aneurysms may present as persistent chest pain and dyspnea despite the proper treatment of underlying cardiac condition.
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 exam==  
Physical findings on cardiac examination in patients with LV aneurysms include diffuse displaced apical impulse, S3 and/or S4 heart sounds and mitral regurgitation murmur.
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==
==Electrocardiography==
Persistent ST elevation is suggestive finding for LV aneurysm.<ref name="pmid5659397">{{cite journal |vauthors=Mourdjinis A, Olsen E, Raphael MJ, Mounsey JP |title=Clinical diagnosis and prognosis of ventricular aneurysm |journal=Br Heart J |volume=30 |issue=4 |pages=497–513 |year=1968 |pmid=5659397 |pmc=487659 |doi= |url=}}</ref>
A persistent [[ST elevation]] is suggestive of LV aneurysm.<ref name="pmid5659397">{{cite journal |vauthors=Mourdjinis A, Olsen E, Raphael MJ, Mounsey JP |title=Clinical diagnosis and prognosis of ventricular aneurysm |journal=Br Heart J |volume=30 |issue=4 |pages=497–513 |year=1968 |pmid=5659397 |pmc=487659 |doi= |url=}}</ref>
==Chest X ray==
==Chest X ray==
A bulge of the silhouette of the left ventricle on chest x-ray is the characteristic finding for LV aneurysm. <ref name="pmid5659397">{{cite journal |vauthors=Mourdjinis A, Olsen E, Raphael MJ, Mounsey JP |title=Clinical diagnosis and prognosis of ventricular aneurysm |journal=Br Heart J |volume=30 |issue=4 |pages=497–513 |year=1968 |pmid=5659397 |pmc=487659 |doi= |url=}}</ref>
A bulge of the silhouette of the left ventricle on chest x-ray is the characteristic finding for LV aneurysm. <ref name="pmid5659397">{{cite journal |vauthors=Mourdjinis A, Olsen E, Raphael MJ, Mounsey JP |title=Clinical diagnosis and prognosis of ventricular aneurysm |journal=Br Heart J |volume=30 |issue=4 |pages=497–513 |year=1968 |pmid=5659397 |pmc=487659 |doi= |url=}}</ref>
==CT scan==
==CT scan==
Chest CT scan with or without contrast may reveal the size and the location of LV aneurysm also, it can show the presence of calcification on it.
Chest CT scan with or without contrast may reveal the size and the location of LV aneurysm, it can also show the presence of [[calcification]]<nowiki/>s in it.
==MRI==
==MRI==
Cardiac MRI is helpful to diagnose LV aneurysm and may be emerging as the preferred noninvasive technique for the preoperative assessment of LV shape, thinning, and resectability.<ref name="pmid21907357">{{cite journal |vauthors=Hüther J, Doenst T, Nitzsche S, Thiele H, Mohr FW, Gutberlet M |title=Cardiac magnetic resonance imaging for the assessment of ventricular function, geometry, and viability before and after surgical ventricular reconstruction |journal=J. Thorac. Cardiovasc. Surg. |volume=142 |issue=6 |pages=1515–22.e1 |year=2011 |pmid=21907357 |doi=10.1016/j.jtcvs.2011.04.040 |url=}}</ref>
[[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.<ref name="pmid21907357">{{cite journal |vauthors=Hüther J, Doenst T, Nitzsche S, Thiele H, Mohr FW, Gutberlet M |title=Cardiac magnetic resonance imaging for the assessment of ventricular function, geometry, and viability before and after surgical ventricular reconstruction |journal=J. Thorac. Cardiovasc. Surg. |volume=142 |issue=6 |pages=1515–22.e1 |year=2011 |pmid=21907357 |doi=10.1016/j.jtcvs.2011.04.040 |url=}}</ref>
==Echocardiography==
==Echocardiography==
*Echocardiography is the modality of choice for diagnosis LV aneurysm. <ref name="pmid6731299">{{cite journal |vauthors=Arvan S, Varat MA |title=Persistent ST-segment elevation and left ventricular wall abnormalities: a 2-dimensional echocardiographic study |journal=Am. J. Cardiol. |volume=53 |issue=11 |pages=1542–6 |year=1984 |pmid=6731299 |doi= |url=}}</ref><ref name="pmid3159507">{{cite journal |vauthors=Matsumoto M, Watanabe F, Goto A, Hamano Y, Yasui K, Minamino T, Abe H, Kamada T |title=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 |journal=Circulation |volume=72 |issue=2 |pages=280–6 |year=1985 |pmid=3159507 |doi= |url=}}</ref>
*Echocardiography is the modality of choice for the diagnosis of LV aneurysm. <ref name="pmid6731299">{{cite journal |vauthors=Arvan S, Varat MA |title=Persistent ST-segment elevation and left ventricular wall abnormalities: a 2-dimensional echocardiographic study |journal=Am. J. Cardiol. |volume=53 |issue=11 |pages=1542–6 |year=1984 |pmid=6731299 |doi= |url=}}</ref><ref name="pmid3159507">{{cite journal |vauthors=Matsumoto M, Watanabe F, Goto A, Hamano Y, Yasui K, Minamino T, Abe H, Kamada T |title=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 |journal=Circulation |volume=72 |issue=2 |pages=280–6 |year=1985 |pmid=3159507 |doi= |url=}}</ref>
*It can measure size and location of aneurysm however, it is helpful to distinguish true from false aneurysms based on the mouth size.
*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 useful to diagnose [[dyskinesia]] or [[akinesia]] during [[systole]].
*Echocardiography is helpful to diagnose mural thrombosis in aneurysm sac.
*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 aneurysm.
*Color flow echocardiography is helpful to establish the diagnosis based on ''in and out'' flow in the aneurysm.
==Medical Therapy==
==Medical Therapy==
Medical therapy is indicated for small and medium sized LV aneurysms. It is based on decreasing cardiac work load (afterload reduction), anti ischemic therapy for [[chest pain]] and [[Anti coagulation therapy|anti coagulation]] if [[Thrombosis|mural thrombosis]] exist.<ref name="brawn">{{cite book | last = Mann | first = Douglas | title = Braunwald's heart disease : a textbook of cardiovascular medicine | publisher = Elsevier/Saunders | location = Philadelphia, PA | year = 2015 | isbn = 978-1455751341 }}</ref>
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 therapy|anti coagulation]] if [[Thrombosis|mural thrombosis]] exist.<ref name="brawn">{{cite book | last = Mann | first = Douglas | title = Braunwald's heart disease : a textbook of cardiovascular medicine | publisher = Elsevier/Saunders | location = Philadelphia, PA | year = 2015 | isbn = 978-1455751341 }}</ref>
*[[Afterload]] reduction:
*[[Afterload]] reduction:
:[[ACE inhibitor|ACE inhibitors]] are the drug of choice for decreasing the [[afterload]].
:[[ACE inhibitor|ACE inhibitors]] are the drug of choice for decreasing the [[afterload]].
*Anti ischemic therapy:
*Anti ischemic therapy:
:Many medications can be used to treat underlying ischemic event as well as decreasing ischemic burden including:<ref name="brawn">{{cite book | last = Mann | first = Douglas | title = Braunwald's heart disease : a textbook of cardiovascular medicine | publisher = Elsevier/Saunders | location = Philadelphia, PA | year = 2015 | isbn = 978-1455751341 }}</ref>
:Many medications are used for treating underlying ischemic event and decreasing ischemic burden. The medications include:<ref name="brawn">{{cite book | last = Mann | first = Douglas | title = Braunwald's heart disease : a textbook of cardiovascular medicine | publisher = Elsevier/Saunders | location = Philadelphia, PA | year = 2015 | isbn = 978-1455751341 }}</ref>
:'''[[Chronic stable angina nitrate therapy|Nitrates]] | [[Chronic stable angina beta blocker therapy|Beta Blockers]] | [[Chronic stable angina treatment calcium channel blockers|Calcium Channel Blockers]] | [[Chronic stable angina treatment potassium channel openers|Potassium Channel Openers]] | [[Chronic stable angina newer antianginal agents|Newer Anti-anginal Agents]]'''
:'''[[Chronic stable angina nitrate therapy|Nitrates]] | [[Chronic stable angina beta blocker therapy|Beta Blockers]] | [[Chronic stable angina treatment calcium channel blockers|Calcium Channel Blockers]] | [[Chronic stable angina treatment potassium channel openers|Potassium Channel Openers]] | [[Chronic stable angina newer antianginal agents|Newer Anti-anginal Agents]]'''
==Surgery==
==Surgery==
*Surgical aneurysmectomy is recommended for large symptomatic aneurysms that caused angina pectoris or heart failure. Appropriate CABG is indicated at the time of aneurysmectomy.<ref>{{cite book | last = Kouchoukos | first = Nicholas | title = Kirklin/Barratt-Boyes cardiac surgery : morphology, diagnostic criteria, natural history, techniques, results, and indications | publisher = Elsevier/Saunders | location = Philadelphia | year = 2013 | isbn = 978-1416063919 }}</ref>
*Surgical aneurysmectomy is recommended for large symptomatic aneurysms that cause [[angina pectoris]] or [[heart failure]]. Appropriate [[CABG]] is indicated at the time of aneurysmectomy.<ref>{{cite book | last = Kouchoukos | first = Nicholas | title = Kirklin/Barratt-Boyes cardiac surgery : morphology, diagnostic criteria, natural history, techniques, results, and indications | publisher = Elsevier/Saunders | location = Philadelphia | year = 2013 | isbn = 978-1416063919 }}</ref>
*Another indication for surgical intervention is in patients who can not tolerate long term anticoagulation therapy.<ref name="pmid15289388">{{cite journal |vauthors=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 |title=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) |journal=Circulation |volume=110 |issue=5 |pages=588–636 |year=2004 |pmid=15289388 |doi=10.1161/01.CIR.0000134791.68010.FA |url=}}</ref>
*Another indication for surgical intervention is in patients who can not tolerate long term anticoagulation therapy.<ref name="pmid15289388">{{cite journal |vauthors=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 |title=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) |journal=Circulation |volume=110 |issue=5 |pages=588–636 |year=2004 |pmid=15289388 |doi=10.1161/01.CIR.0000134791.68010.FA |url=}}</ref>



Latest revision as of 10:45, 9 April 2017

Left ventricular aneurysm Microchapters

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Patient Information

Overview

Historical Perspective

Classification

Pathophysiology

Causes

Differentiating Left ventricular aneurysm from other Diseases

Epidemiology and Demographics

Risk Factors

Screening

Natural History, Complications and Prognosis

Diagnosis

History and Symptoms

Physical Examination

Laboratory Findings

Electrocardiogram

Chest X Ray

CT

MRI

Echocardiography or Ultrasound

Other Imaging Findings

Other Diagnostic Studies

Treatment

Medical Therapy

Surgery

Primary Prevention

Secondary Prevention

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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]

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]

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. 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. 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.
  3. 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.
  4. Mann, Douglas (2015). Braunwald's heart disease : a textbook of cardiovascular medicine. Philadelphia, PA: Elsevier/Saunders. ISBN 978-1455751341.
  5. 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.
  6. 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.
  7. 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.
  8. 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.
  9. 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. 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.
  11. 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. 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.
  13. 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.
  14. 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.
  15. 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. 16.0 16.1 Mann, Douglas (2015). Braunwald's heart disease : a textbook of cardiovascular medicine. Philadelphia, PA: Elsevier/Saunders. ISBN 978-1455751341.
  17. Kouchoukos, Nicholas (2013). Kirklin/Barratt-Boyes cardiac surgery : morphology, diagnostic criteria, natural history, techniques, results, and indications. Philadelphia: Elsevier/Saunders. ISBN 978-1416063919.
  18. 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.


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