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{{Template:Aortic stenosis}}
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{{Aortic stenosis}}
{{CMG}}; '''Associate Editor(s)-In-Chief:''' [[User:Mohammed Sbeih|Mohammed A. Sbeih, M.D.]] [mailto:msbeih@wikidoc.org]; {{LG}}; {{USAMA}} '''Assistant Editor-In-Chief:''' [[Kristin Feeney|Kristin Feeney, B.S.]] [mailto:kfeeney@elon.edu]


'''Associate Editors-In-Chief:''' Claudia P. Hochberg, M.D. [mailto:chochber@bidmc.harvard.edu]; [[User:Abdarabi|Abdul-Rahman Arabi, M.D.]] [mailto:abdarabi@yahoo.com]; [[User:KeriShafer|Keri Shafer, M.D.]] [mailto:kshafer@bidmc.harvard.edu]
==Overview==
The main symptoms of aortic stenosis are [[angina]], [[syncope]], and [[congestive heart failure]].  Left untreated, the average survival is 5 years after the onset of angina, 3 years after the onset of syncope, and 1 year after the onset of congestive heart failure. Other symptoms of aortic stenosis are [[dyspnea on exertion]], [[orthopnea]] and [[paroxysmal nocturnal dyspnea]].


==Symptoms==
==Symptoms==
When [[symptomatic]], aortic stenosis can cause dizziness, [[syncope]], [[Angina pectoris|angina]] and [[congestive heart failure]]. More symptoms indicate a worse prognosis. Treatment requires [[aortic valve replacement|replacement]] of the diseased valve with an [[artificial heart valve]].
===Symptoms by Age Group===
====Symptoms in Adults====
The following symptoms are observed in adults with aortic stenosis.<ref name="pmid20424150">{{cite journal| author=Rajani R, Rimington H, Chambers JB| title=Treadmill exercise in apparently asymptomatic patients with moderate or severe aortic stenosis: relationship between cardiac index and revealed symptoms. | journal=Heart | year= 2010 | volume= 96 | issue= 9 | pages= 689-95 | pmid=20424150 | doi=10.1136/hrt.2009.181644 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20424150  }} </ref><ref name="pmid11559673">{{cite journal| author=Amato MC, Moffa PJ, Werner KE, Ramires JA| title=Treatment decision in asymptomatic aortic valve stenosis: role of exercise testing. | journal=Heart | year= 2001 | volume= 86 | issue= 4 | pages= 381-6 | pmid=11559673 | doi= | pmc=1729928 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11559673  }} </ref><ref name="pmid11029480">{{cite journal| author=Das P, Pocock C, Chambers J| title=The patient with a systolic murmur: severe aortic stenosis may be missed during cardiovascular examination. | journal=QJM | year= 2000 | volume= 93 | issue= 10 | pages= 685-8 | pmid=11029480 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11029480  }} </ref><ref name="pmid23489526">{{cite journal| author=Park SJ, Enriquez-Sarano M, Chang SA, Choi JO, Lee SC, Park SW et al.| title=Hemodynamic patterns for symptomatic presentations of severe aortic stenosis. | journal=JACC Cardiovasc Imaging | year= 2013 | volume= 6 | issue= 2 | pages= 137-46 | pmid=23489526 | doi=10.1016/j.jcmg.2012.10.013 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23489526  }} </ref>


===Congestive Heart Failure===
*[[Breathlessness]] with activity
*[[Chest pain]], which resembles what is known as [[angina]]-type pain
**The pain is crushing, squeezing, pressure or tightness in nature
**The pain increases with exercise, relieved with rest
**The patient feels pain under the chest bone, it may move to other areas
*[[Fainting]], [[weakness]], or [[dizziness]] with activity
*[[Sensation of feeling the heart beat]] ([[palpitations]])
 
====Symptoms in Infants and Children====
The following symptoms were observed in infants and children with [[aortic stenosis]].<ref name="pmid6020739">{{cite journal| author=Mody MR, Nadas AS, Bernhard WF| title=Aortic stenosis in infants. | journal=N Engl J Med | year= 1967 | volume= 276 | issue= 15 | pages= 832-8 | pmid=6020739 | doi=10.1056/NEJM196704132761503 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=6020739  }} </ref><ref name="pmid13505014">{{cite journal| author=ONGLEY PA, NADAS AS, PAUL MH, RUDOLPH AM, STARKEY GW| title=Aortic stenosis in infants and children. | journal=Pediatrics | year= 1958 | volume= 21 | issue= 2 | pages= 207-21 | pmid=13505014 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=13505014  }} </ref><ref name="pmid21829408">{{cite journal| author=Yun SW| title=Congenital heart disease in the newborn requiring early intervention. | journal=Korean J Pediatr | year= 2011 | volume= 54 | issue= 5 | pages= 183-91 | pmid=21829408 | doi=10.3345/kjp.2011.54.5.183 | pmc=3145901 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21829408  }} </ref>


[[Congestive heart failure]] (CHF) carries a grave prognosis in patients with AS. Patients with CHF that is attributed to AS have a 2 year mortality rate of 50%, if the aortic valve is not replaced.
*Becoming tired or [[fatigue]]d with exertion more easily than others (in mild cases)
*Serious breathing problems that develop within days or weeks of birth (in severe cases)
*Extreme [[fatigue]]
*[[Sweating]]
*Pale skin
*[[Fast breathing]]
*They may also be [[smaller than other children their age]]
*Children with mild or moderate aortic stenosis may get worse as they get older. They also run the risk of developing an infection of the heart valves ([[bacterial endocarditis]]).


CHF in the setting of AS is due to a combination of systolic dysfunction (a decrease in the [[ejection fraction]]) and [[diastolic dysfunction]] (elevated filling pressure of the LV).
===Angina Pectoris===
The following are a few important aspects about Angina Pectoris in Aortic Stenosis. <ref>{{Cite journal
| author = [[E. L. Fallen]], [[W. C. Elliott]] & [[R. Gorlin]]
| title = Mechanisms of angina in aortic stenosis
| journal = [[Circulation]]
| volume = 36
| issue = 4
| pages = 480–488
| year = 1967
| month = October
| pmid = 6041860
}}</ref> <ref name="pmid6215582">{{cite journal| author=Marcus ML, Doty DB, Hiratzka LF, Wright CB, Eastham CL| title=Decreased coronary reserve: a mechanism for angina pectoris in patients with aortic stenosis and normal coronary arteries. | journal=N Engl J Med | year= 1982 | volume= 307 | issue= 22 | pages= 1362-6 | pmid=6215582 | doi=10.1056/NEJM198211253072202 | pmc= | url= }} </ref><ref name="pmid11870246">{{cite journal| author=Carabello BA| title=Clinical practice. Aortic stenosis. | journal=N Engl J Med | year= 2002 | volume= 346 | issue= 9 | pages= 677-82 | pmid=11870246 | doi=10.1056/NEJMcp010846 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11870246  }} </ref>
*The hypertrophied left ventricle and the prolonged ejection time (the time for the heart to eject blood) result in an increased myocardial oxygen requirements. The elevated diastolic filling pressure also reduces the gradient between the aorta and the right atrium ("the height of the waterfall") which normally drives coronary blood flow. The hypertrophied ventricle may also compress the capillaries. All of the above reasons lead to a reduction in coronary blood flow even in the absence of obstructive epicardial stenoses. This may result in subendocardial [[ischemia]] during stress or exercise.
*Left untreated, the average survival is 5 years after the onset of angina in the patient with aortic stenosis.


===Syncope===
===Syncope===
The mechanism of [[syncope]] secondary to [[aortic stenosis]] remains unclear. Left untreated, the average survival is 3 years after the onset of syncope in the patient with aortic stenosis.
Three theories have been hypothesized to explain the relationship between [[aortic stenosis]] and [[syncope]]:<ref>{{Cite journal
| author = [[S. Frank]], [[A. Johnson]] & [[J. Jr Ross]]
| title = Natural history of valvular aortic stenosis
| journal = [[British heart journal]]
| volume = 35
| issue = 1
| pages = 41–46
| year = 1973
| month = January
| pmid = 4685905
}}</ref>


[[Fainting|Syncope]] in the setting of heart failure increases the risk of death. In patients with syncope, the 3 year mortality rate is 50%, if the aortic valve is not replaced.
*Severe aortic stenosis results in a nearly fixed cardiac output. During exercise, the [[peripheral vascular resistance]] will decrease as the blood vessels dilate to allow the [[skeletal muscles]] to receive more blood. This decrease in peripheral vascular resistance is normally compensated by an increase in the [[cardiac output]]. Since patients with severe [[aortic stenosis]] cannot increase their cardiac output, the blood pressure falls and the patient will develop [[syncope]] due to decreased blood flow to the [[brain]].


It is unclear why aortic stenosis causes [[syncope]]. One popular theory is that severe AS produces a nearly fixed [[cardiac output]]. When the patient exercises, their [[peripheral vascular resistance]] will decrease as the blood vesels of the [[skeletal muscles]] dilate to allow the muscles to receive more blood to allow them to do more work.  This decrease in peripheral vascular resistance is normally compensated for by an increase in the cardiac output. Since patients with severe AS cannot increase their cardiac output, the blood pressure falls and the patient will syncopize due to decreased blood perfusion to the [[brain]].
*During exercise, the high pressures generated in the [[LVH|hypertrophied left ventricle]] may cause a vasodepressor response, which subsequently results in [[vasodilation|peripheral vasodilation]]. As a consequence, the blood flow to the [[brain]] may decrease. Therefore, due to the fixed outwards blood flow obstruction at the level of the stenosed aortic valve, it may be impossible for the heart to increase its output to offset the peripheral vasodilation.


A second theory as to why syncope may occur in AS is that during exercise, the high pressures generated in the hypertrophied LV cause a vasodepressor response, which causes a secondary peripheral [[vasodilation]] which in turn causes decreased blood flow to the [[brain]]. Indeed, in aortic stenosis, because of the fixed obstruction to bloodflow out from the heart, it may be impossible for the heart to increase its output to offset peripheral vasodilation.
*Syncope can occur in patients with aortic stenosis secondary to [[myocardial ischemia]]. Myocardial ischemia can develop in patients with aortic stenosis due to the [[LVH|hypertrophy of the left ventricle]] and the subsequent inability of the [[coronary arteries]] to adequately supply blood to the [[myocardium]].


A third mechanism may sometimes be operative. Due to the hypertrophy of the [[left ventricle]] in aortic stenosis, including the consequent inability of the [[coronary arteries]] to adequately supply blood to the [[myocardium]] (see "Angina" below), [[arrhythmias]] may develop. These can lead to [[syncope]].
===Congestive Heart Failure===
 
[[CHF]] in the setting of [[aortic stenosis]] is due to a combination of [[systolic dysfunction]] (a decrease in the [[ejection fraction]]) and [[diastolic dysfunction]] (elevated filling pressure of the left ventricle). Left untreated, the average survival is 5 years after the onset of angina, 3 years after the onset of syncope, and 1 year after the onset of congestive heart failure. <ref name="pmid4894151">{{cite journal| author=Ross J, Braunwald E| title=Aortic stenosis. | journal=Circulation | year= 1968 | volume= 38 | issue= 1 Suppl | pages= 61-7 | pmid=4894151 | doi= | pmc= | url= }} </ref><ref name="pmid3337000">{{cite journal| author=Kelly TA, Rothbart RM, Cooper CM, Kaiser DL, Smucker ML, Gibson RS| title=Comparison of outcome of asymptomatic to symptomatic patients older than 20 years of age with valvular aortic stenosis. | journal=Am J Cardiol | year= 1988 | volume= 61 | issue= 1 | pages= 123-30 | pmid=3337000 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=3337000 }} </ref><ref name="pmid8712130">{{cite journal| author=Iivanainen AM, Lindroos M, Tilvis R, Heikkilä J, Kupari M| title=Natural history of aortic valve stenosis of varying severity in the elderly. | journal=Am J Cardiol | year= 1996 | volume= 78 | issue= 1 | pages= 97-101 | pmid=8712130 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8712130 }} </ref>
Finally, in calcific aortic stenosis at least, the calcification in and around the aortic valve can progress and extend to involve the [[electrical conduction system of the heart]]. If that occurs, the result may be [[heart block]] - a potentially lethal condition of which syncope may be a symptom.
 
===Angina===
 
[[Angina pectoris|Angina]] in the setting of heart failure also increases the risk of death.  In patients with angina, the 5 year mortality rate is 50%, if the aortic valve is not replaced.
 
Angina in the setting of AS is secondary to the [[left ventricular hypertrophy]] (LVH) that is caused by the constant production of increased pressure required to overcome the pressure gradient caused by the AS. While the [[myocardium]] (i.e. heart muscle) of the LV gets thicker, the arteries that supply the muscle do not get significantly longer or bigger, so the muscle may become ischemic (i.e. doesn't receive an adequate blood supply).  The [[ischemia]] may first be evident during exercise, when the heart muscle requires increased blood supply to compensate for the increased workload. The individual may complain of exertional angina. At this stage, a [[stress test]] with imaging may be suggestive of ischemia.
 
Eventually, however, the muscle will require more blood supply at rest than can be supplied by the coronary artery branches. At this point there may be signs of ''ventricular strain pattern'' on the [[EKG]], suggesting subendocardial ischemia.  The subendocardium is the region that becomes ischemic because it is the most distant from the epicardial coronary arteries.


===Associated Symptoms===
Symptoms of left ventricular failure include the following:
In [[Heyde's syndrome]], aortic stenosis is associated with [[angiodysplasia]] of the [[colon (anatomy)|colon]]. Recent research has shown that the stenosis causes a form of [[von Willebrand disease]] by breaking down its associated [[coagulation]] factor ([[factor VIII]]-associated antigen, also called [[von Willebrand factor]]), due to increased turbulence around the stenosed valve.
*[[Dyspnea on exertion]]
*[[Fatigue]]
*[[Orthopnea]]
*[[Paroxysmal nocturnal dyspnea]]
*[[Pulmonary edema]]
*[[Pulmonary hypertension]] that can lead to:
:*[[Right ventricular failure]]
:*[[Hepatomegaly]]
:*[[Atrial fibrillation]]
:*[[Peripheral edema]]
:*[[Tricuspid regurgitation]]


==References==
==References==
{{reflist|2}}
{{reflist|2}}


{{WH}}
{{WS}}
[[CME Category::Cardiology]]


{{Circulatory system pathology}}
[[Category:Disease]]
{{Congenital malformations and deformations of circulatory system}}
[[Category:DiseaseState]]
[[Category:Signs and symptoms]]
[[Category:Physical Examination]]
[[Category:Valvular heart disease]]
[[Category:Valvular heart disease]]
[[Category:Cardiology]]
[[Category:Cardiology]]
[[Category:Congenital heart disease]]
[[Category:Congenital heart disease]]
[[Category:Pediatrics]]
[[Category:Cardiac surgery]]
 
[[Category:Surgery]]
[[de:Aortenstenose (angeboren)]]
[[es:Estenosis aórtica]]
[[fr:Rétrécissement aortique]]
[[no:Aortastenose]]
[[nn:Aortastenose]]
[[pl:Stenoza Aortalnej]]
[[pt:Estenose aórtica]]
[[ro:Stenoza Aortică]]
[[sv:Aortastenos]]
[[tr:Aort darlığı]]
 
 
{{WH}}
 
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Latest revision as of 17:17, 13 December 2019
Resident
Survival
Guide

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-In-Chief: Mohammed A. Sbeih, M.D. [2]; Lakshmi Gopalakrishnan, M.B.B.S. [3]; Usama Talib, BSc, MD [4] Assistant Editor-In-Chief: Kristin Feeney, B.S. [5]

Overview

The main symptoms of aortic stenosis are angina, syncope, and congestive heart failure. Left untreated, the average survival is 5 years after the onset of angina, 3 years after the onset of syncope, and 1 year after the onset of congestive heart failure. Other symptoms of aortic stenosis are dyspnea on exertion, orthopnea and paroxysmal nocturnal dyspnea.

Symptoms

Symptoms by Age Group

Symptoms in Adults

The following symptoms are observed in adults with aortic stenosis.[1][2][3][4]

Symptoms in Infants and Children

The following symptoms were observed in infants and children with aortic stenosis.[5][6][7]

Angina Pectoris

The following are a few important aspects about Angina Pectoris in Aortic Stenosis. [8] [9][10]

  • The hypertrophied left ventricle and the prolonged ejection time (the time for the heart to eject blood) result in an increased myocardial oxygen requirements. The elevated diastolic filling pressure also reduces the gradient between the aorta and the right atrium ("the height of the waterfall") which normally drives coronary blood flow. The hypertrophied ventricle may also compress the capillaries. All of the above reasons lead to a reduction in coronary blood flow even in the absence of obstructive epicardial stenoses. This may result in subendocardial ischemia during stress or exercise.
  • Left untreated, the average survival is 5 years after the onset of angina in the patient with aortic stenosis.

Syncope

The mechanism of syncope secondary to aortic stenosis remains unclear. Left untreated, the average survival is 3 years after the onset of syncope in the patient with aortic stenosis. Three theories have been hypothesized to explain the relationship between aortic stenosis and syncope:[11]

  • Severe aortic stenosis results in a nearly fixed cardiac output. During exercise, the peripheral vascular resistance will decrease as the blood vessels dilate to allow the skeletal muscles to receive more blood. This decrease in peripheral vascular resistance is normally compensated by an increase in the cardiac output. Since patients with severe aortic stenosis cannot increase their cardiac output, the blood pressure falls and the patient will develop syncope due to decreased blood flow to the brain.
  • During exercise, the high pressures generated in the hypertrophied left ventricle may cause a vasodepressor response, which subsequently results in peripheral vasodilation. As a consequence, the blood flow to the brain may decrease. Therefore, due to the fixed outwards blood flow obstruction at the level of the stenosed aortic valve, it may be impossible for the heart to increase its output to offset the peripheral vasodilation.

Congestive Heart Failure

CHF in the setting of aortic stenosis is due to a combination of systolic dysfunction (a decrease in the ejection fraction) and diastolic dysfunction (elevated filling pressure of the left ventricle). Left untreated, the average survival is 5 years after the onset of angina, 3 years after the onset of syncope, and 1 year after the onset of congestive heart failure. [12][13][14]

Symptoms of left ventricular failure include the following:

References

  1. ↑ Rajani R, Rimington H, Chambers JB (2010). "Treadmill exercise in apparently asymptomatic patients with moderate or severe aortic stenosis: relationship between cardiac index and revealed symptoms". Heart. 96 (9): 689–95. doi:10.1136/hrt.2009.181644. PMID 20424150.
  2. ↑ Amato MC, Moffa PJ, Werner KE, Ramires JA (2001). "Treatment decision in asymptomatic aortic valve stenosis: role of exercise testing". Heart. 86 (4): 381–6. PMC 1729928. PMID 11559673.
  3. ↑ Das P, Pocock C, Chambers J (2000). "The patient with a systolic murmur: severe aortic stenosis may be missed during cardiovascular examination". QJM. 93 (10): 685–8. PMID 11029480.
  4. ↑ Park SJ, Enriquez-Sarano M, Chang SA, Choi JO, Lee SC, Park SW; et al. (2013). "Hemodynamic patterns for symptomatic presentations of severe aortic stenosis". JACC Cardiovasc Imaging. 6 (2): 137–46. doi:10.1016/j.jcmg.2012.10.013. PMID 23489526.
  5. ↑ Mody MR, Nadas AS, Bernhard WF (1967). "Aortic stenosis in infants". N Engl J Med. 276 (15): 832–8. doi:10.1056/NEJM196704132761503. PMID 6020739.
  6. ↑ ONGLEY PA, NADAS AS, PAUL MH, RUDOLPH AM, STARKEY GW (1958). "Aortic stenosis in infants and children". Pediatrics. 21 (2): 207–21. PMID 13505014.
  7. ↑ Yun SW (2011). "Congenital heart disease in the newborn requiring early intervention". Korean J Pediatr. 54 (5): 183–91. doi:10.3345/kjp.2011.54.5.183. PMC 3145901. PMID 21829408.
  8. ↑ E. L. Fallen, W. C. Elliott & R. Gorlin (1967). "Mechanisms of angina in aortic stenosis". Circulation. 36 (4): 480–488. PMID 6041860. Unknown parameter |month= ignored (help)
  9. ↑ Marcus ML, Doty DB, Hiratzka LF, Wright CB, Eastham CL (1982). "Decreased coronary reserve: a mechanism for angina pectoris in patients with aortic stenosis and normal coronary arteries". N Engl J Med. 307 (22): 1362–6. doi:10.1056/NEJM198211253072202. PMID 6215582.
  10. ↑ Carabello BA (2002). "Clinical practice. Aortic stenosis". N Engl J Med. 346 (9): 677–82. doi:10.1056/NEJMcp010846. PMID 11870246.
  11. ↑ S. Frank, A. Johnson & J. Jr Ross (1973). "Natural history of valvular aortic stenosis". British heart journal. 35 (1): 41–46. PMID 4685905. Unknown parameter |month= ignored (help)
  12. ↑ Ross J, Braunwald E (1968). "Aortic stenosis". Circulation. 38 (1 Suppl): 61–7. PMID 4894151.
  13. ↑ Kelly TA, Rothbart RM, Cooper CM, Kaiser DL, Smucker ML, Gibson RS (1988). "Comparison of outcome of asymptomatic to symptomatic patients older than 20 years of age with valvular aortic stenosis". Am J Cardiol. 61 (1): 123–30. PMID 3337000.
  14. ↑ Iivanainen AM, Lindroos M, Tilvis R, Heikkilä J, Kupari M (1996). "Natural history of aortic valve stenosis of varying severity in the elderly". Am J Cardiol. 78 (1): 97–101. PMID 8712130.

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