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| [[File:Siren.gif|30px|link=Aortic stenosis resident survival guide]]|| <br> || <br>
| [[Aortic stenosis resident survival guide|'''Resident'''<br>'''Survival'''<br>'''Guide''']]
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{{Aortic stenosis}}
{{Aortic stenosis}}
{{CMG}}; '''Associate Editor(s)-In-Chief:''' [[User:Mohammed Sbeih|Mohammed A. Sbeih, M.D.]] [mailto:msbeih@perfuse.org]; {{LG}}; '''Assistant Editor-In-Chief:''' [[Kristin Feeney|Kristin Feeney, B.S.]] [mailto:kfeeney@perfuse.org]
{{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]


==Overview==
==Overview==
The main symptoms of aortic stenosis include [[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 <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>.  Other symptoms include [[dyspnea on exertion]], [[orthopnea]] and [[paroxysmal nocturnal dyspnea]].
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]].


==Symptomatic Aortic Stenosis==
==Symptoms==
*[[dyspnea|Exertional dyspnea]]
===Symptoms by Age Group===
*[[Angina pectoris]]
====Symptoms in Adults====
*[[Syncope]]
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>
*[[Dizziness]]


*As the disease progresses, symptoms of decreased cardiac output may appear which include:
*[[Breathlessness]] with activity
:*[[Fatigue|Marked fatigability]]
*[[Chest pain]], which resembles what is known as [[angina]]-type pain
:*[[Weakness]]
**The pain is crushing, squeezing, pressure or tightness in nature
:*[[Peripheral cyanosis]]
**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]])


*Patients exhibiting multiple symptoms often experience a worsened prognosis and overall decrement in quality of life.
====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>


==Aortic Stenosis and Congestive Heart Failure==
*Becoming tired or [[fatigue]]d with exertion more easily than others (in mild cases)
*Presence of [[congestive heart failure]] carries a grave prognosis in patients with aortic stenosis.  
*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]]).


*Among such patients, if the aortic valve is not replaced, they tend to have a 50% 2-year mortality rate.  
===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.


*[[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).  
===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>
 
*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 [[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.
 
*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]].
 
===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>


===Symptoms of left ventricular failure include:===
Symptoms of left ventricular failure include the following:
*[[Dyspnea on exertion]]
*[[Fatigue]]
*[[Orthopnea]]
*[[Orthopnea]]
*[[Paroxysmal nocturnal dyspnea]]
*[[Paroxysmal nocturnal dyspnea]]
*[[Pulmonary edema]]
*[[Pulmonary edema]]
* [[Pulmonary hypertension]] that can lead to:
*[[Pulmonary hypertension]] that can lead to:
:*[[Right ventricular failure]]
:*[[Right ventricular failure]]
:*Systemic venous hypertension
:*[[Hepatomegaly]]
:*[[Hepatomegaly]]
:*[[Atrial fibrillation]]
:*[[Atrial fibrillation]]
:*[[Peripheral edema]]
:*[[Tricuspid regurgitation]]
:*[[Tricuspid regurgitation]]
===Angina pectoris===
*[[Angina pectoris|Angina]] in the setting of [[heart failure]] has shown to increase mortality risk. Among patients with angina, in the absence of intervention, the 5 year mortality rate has shown to be ~50%.
*The occurrence of [[angina]] in the setting of [[aortic stenosis]] is secondary to the [[left ventricular hypertrophy]] ([[LVH]]) which is a consequence of constant production of increased pressure that is required to overcome the pressure gradient created by the stenosed aortic valve. While the [[myocardium|left ventricular myocardium]] gets thicker, the arteries that supply the muscle do not get significantly longer or bigger, which results in an ischemic myocardium. 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 [[Exercise stress testing|stress test with imaging]] may be required which demonstrates ischemic myocardium.
*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.
===Syncope===
The mechanism of [[syncope]] secondary to [[aortic stenosis]] remains unclear. Three theroeis have been hypothesized to explain the relationship between [[aortic stenosis]] and [[syncope]].
'''1.''' ''Severe aortic stenosis produces a nearly fixed cardiac output''
When the patient exercises, their [[peripheral vascular resistance]] will decrease as the blood vessels 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 [[aortic stenosis]] cannot increase their cardiac output, the blood pressure falls and the patient will syncopize due to decreased blood perfusion to the [[brain]].
'''2.''' ''During exercise, high pressures generated by the hypertrophy of the left ventricular can result in a vasodepressor response resulting in secondary peripheral vasodilation and decreased overall blood flow to the brain''
A second explanation as to why [[syncope]] may occur in [[aortic stenosis]] includes that during exercise, the high pressures generated in the [[LVH|hypertrophied left ventricle]] causes a vasodepressor response, which subsequently results in [[vasodilation|peripheral vasodilation]] which in turn causes decreased blood flow to the [[brain]]. Therefore, due to the fixed obstruction to blood flow out from the stenosed aortic valve, it may be impossible for the heart to increase its output to offset peripheral vasodilation.
'''3.''' ''Left ventricular hypertrophy may result in a decrement in the functional integrity of the coronary arteries and blood may be inadequate in supplying the walls of the myocardium resulting in syncope''
A third mechanism may sometimes be operative. Due to the [[LVH|hypertrophy of the left ventricle]] in aortic stenosis, including the consequent inability of the [[coronary arteries]] to adequately supply blood to the [[myocardium]], [[arrhythmias]] may develop which can lead to [[syncope]].
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.
==Associated Conditions==
====Heyde's Syndrome====
*In [[Heyde's syndrome]], [[aortic stenosis]] is associated with [[angiodysplasia]] of the [[colon (anatomy)|colon]].
*Presenting symptoms include: [[hematemesis]], [[melena]]
====Von Willebrand Disease====
*[[Aortic stenosis]] may result in a form of [[von Willebrand disease]] due to an increased turbulence around the stenosed aortic valve WHICH subsequently triggers a break down of [[coagulation]] [[factor VIII]]-associated antigen, ''(also called [[von Willebrand factor]])'' and results in a variant of [[von Willebrand disease]].


==References==
==References==
{{reflist|2}}
{{reflist|2}}
[[es:Estenosis aórtica]]
[[fr:Rétrécissement aortique]]
[[pl:Stenoza Aortalnej]]
[[pt:Estenose aórtica]]
[[ro:Stenoza Aortic?]]
[[tr:Aort darl???]]


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Latest revision as of 17:17, 13 December 2019
Resident
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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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