Aortic regurgitation natural history, complications and prognosis: Difference between revisions
Jump to navigation
Jump to search
Hardik Patel (talk | contribs) |
Usama Talib (talk | contribs) No edit summary |
||
| (26 intermediate revisions by 4 users not shown) | |||
| Line 1: | Line 1: | ||
__NOTOC__ | __NOTOC__ | ||
{| class="infobox" style="float:right;" | |||
|- | |||
| [[File:Siren.gif|30px|link=Aortic regurgitation resident survival guide]]|| <br> || <br> | |||
| [[Aortic regurgitation resident survival guide|'''Resident'''<br>'''Survival'''<br>'''Guide''']] | |||
|} | |||
{{Aortic insufficiency}} | {{Aortic insufficiency}} | ||
{{CMG}}; '''Associate Editor-in-Chief:''' [[Varun Kumar]], M.B.B.S.; [[Lakshmi Gopalakrishnan]], M.B.B.S | {{CMG}}; '''Associate Editor-in-Chief:''' [[Varun Kumar]], M.B.B.S.; [[Lakshmi Gopalakrishnan]], M.B.B.S; {{USAMA}} | ||
==Overview== | ==Overview== | ||
In acute aortic insufficiency symptoms of [[heart failure]] often develop acutely. Chronic aortic insufficiency is usually insidious and progressive and the patient may remain asymptomatic for years. Once left ventricular dilation and left ventricular failure occur, [[dyspnea on exertion]] and [[exercise intolerance]] begin to occur. Later symptoms such as [[angina]], [[syncope]], and other symptoms of [[heart failure]] are present. | In acute aortic insufficiency symptoms of [[heart failure]] often develop acutely. Chronic aortic insufficiency is usually insidious and progressive and the patient may remain asymptomatic for years. Once left ventricular dilation and left ventricular failure occur, [[dyspnea on exertion]] and [[exercise intolerance]] begin to occur. Later symptoms such as [[angina]], [[syncope]], and other symptoms of [[heart failure]] are present.<ref name="pmid1914102">{{cite journal| author=Bonow RO, Lakatos E, Maron BJ, Epstein SE| title=Serial long-term assessment of the natural history of asymptomatic patients with chronic aortic regurgitation and normal left ventricular systolic function. | journal=Circulation | year= 1991 | volume= 84 | issue= 4 | pages= 1625-35 | pmid=1914102 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=1914102 }} </ref> | ||
==Natural History== | ==Natural History== | ||
| Line 10: | Line 14: | ||
In acute aortic insufficiency symptoms of [[heart failure]] such as [[pulmonary edema]] often develop acutely. Acute aortic insufficiency is often secondary to either [[trauma]] or [[infective endocarditis]]. While the heart can accommodate the changes of chronic aortic insufficiency over time, the acute changes of acute aortic insufficiency are not well accommodated by the [[left ventricle]]. | In acute aortic insufficiency symptoms of [[heart failure]] such as [[pulmonary edema]] often develop acutely. Acute aortic insufficiency is often secondary to either [[trauma]] or [[infective endocarditis]]. While the heart can accommodate the changes of chronic aortic insufficiency over time, the acute changes of acute aortic insufficiency are not well accommodated by the [[left ventricle]]. | ||
The rapid rise in left ventricular pressure causes the [[mitral valve]] to close earlier during [[diastole]]. This early closure fortunately prevents backwards flow of [[blood]] into the pulmonary vascular bed. The very high left ventricular end diastolic pressure often keeps the aortic diastolic pressure from falling too low and thus there is often not a wide [[pulse pressure]]. Indeed absence of a wide [[pulse pressure]] in the patient with acute aortic insufficiency should alert the clinician to potential failure of the [[left ventricle]]. | The rapid rise in left ventricular pressure causes the [[mitral valve]] to close earlier during [[diastole]]. This early closure fortunately prevents backwards flow of [[blood]] into the pulmonary vascular bed. The very high left ventricular end diastolic pressure often keeps the aortic diastolic pressure from falling too low and thus there is often not a wide [[pulse pressure]]. Indeed absence of a wide [[pulse pressure]] in the patient with acute aortic insufficiency should alert the clinician to potential failure of the [[left ventricle]].<ref name="pmid2368680">{{cite journal| author=Rhodes LA, Keane JF, Keane JP, Fellows KE, Jonas RA, Castaneda AR et al.| title=Long follow-up (to 43 years) of ventricular septal defect with audible aortic regurgitation. | journal=Am J Cardiol | year= 1990 | volume= 66 | issue= 3 | pages= 340-5 | pmid=2368680 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2368680 }} </ref> | ||
===Chronic Aortic Insufficiency=== | ===Chronic Aortic Insufficiency=== | ||
Chronic aortic insufficiency is usually insidious and progressive and the patient may remain asymptomatic for years. Once left ventricular dilation and left ventricular failure occur, [[dyspnea on exertion]] and [[exercise intolerance]] begin to occur. Later symptoms such as [[angina]], [[syncope]], and other symptoms of [[heart failure]] are present. The hemodynamic impact of aortic regurgitation causes progressive dilation and [[hypertrophy]] of the [[left ventricle]]. The [[mitral valve]] ring may also dilate which may lead in turn to [[mitral regurgitation]]. The [[left atrium]] may dilate as a result of the [[mitral regurgitation]]. It has been said that '[[aortic regurgitation]] begets [[aortic regurgitation]]'. The high oscillatory shear associated with [[aortic regurgitation]] may lead to further dilation of the [[aorta]], which in turn may lead to further [[aortic regurgitation]]. | Chronic aortic insufficiency is usually insidious and progressive and the patient may remain asymptomatic for years. Once left ventricular dilation and left ventricular failure occur, [[dyspnea on exertion]] and [[exercise intolerance]] begin to occur. Later symptoms such as [[angina]], [[syncope]], and other symptoms of [[heart failure]] are present. The hemodynamic impact of aortic regurgitation causes progressive dilation and [[hypertrophy]] of the [[left ventricle]]. The [[mitral valve]] ring may also dilate which may lead in turn to [[mitral regurgitation]]. The [[left atrium]] may dilate as a result of the [[mitral regurgitation]]. It has been said that '[[aortic regurgitation]] begets [[aortic regurgitation]]'. The high oscillatory shear associated with [[aortic regurgitation]] may lead to further dilation of the [[aorta]], which in turn may lead to further [[aortic regurgitation]].<ref name="pmid1914102">{{cite journal| author=Bonow RO, Lakatos E, Maron BJ, Epstein SE| title=Serial long-term assessment of the natural history of asymptomatic patients with chronic aortic regurgitation and normal left ventricular systolic function. | journal=Circulation | year= 1991 | volume= 84 | issue= 4 | pages= 1625-35 | pmid=1914102 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=1914102 }} </ref> | ||
Volume overload associated with [[aortic regurgitation]] leads to left ventricular [[hypertrophy]]. The [[sarcomere]]s replicate in series and there is elongation of the [[myocyte]]s and myocardial fibrils. As a result of this [[hypertrophy]] the ratio of the ventricular wall thickness to cavity radius remains normal and therefore wall stress is normal. In [[aortic regurgitation]] there is eccentric [[hypertrophy]] where as in [[aortic stenosis]] there is concentric hypertrophy where there is replication of the [[sarcomere]]s in parallel. Once wall thickening fails to keep up with the hemodynamic load, end systolic wall stress rises and at this point the [[left ventricle]] fails. The dramatic enlargement of the [[heart]] that is seen with [[aortic regurgitation]] is called [[cor bovinum]]. Over time the [[left ventricle]] will decompensate and there will be increasing interstitial [[fibrosis]] and a stiffening or a reduction in the compliance of the left ventricular wall. At this point the patient will experience a rise in the end diastolic pressure and volume. The first decline is seen with exercise and then the patient begins to have a reduction in forward output at rest. | Volume overload associated with [[aortic regurgitation]] leads to left ventricular [[hypertrophy]]. The [[sarcomere]]s replicate in series and there is elongation of the [[myocyte]]s and myocardial fibrils. As a result of this [[hypertrophy]] the ratio of the ventricular wall thickness to cavity radius remains normal and therefore wall stress is normal. In [[aortic regurgitation]] there is eccentric [[hypertrophy]] where as in [[aortic stenosis]] there is concentric hypertrophy where there is replication of the [[sarcomere]]s in parallel. Once wall thickening fails to keep up with the hemodynamic load, end systolic wall stress rises and at this point the [[left ventricle]] fails. The dramatic enlargement of the [[heart]] that is seen with [[aortic regurgitation]] is called [[cor bovinum]]. Over time the [[left ventricle]] will decompensate and there will be increasing interstitial [[fibrosis]] and a stiffening or a reduction in the compliance of the left ventricular wall. At this point the patient will experience a rise in the end diastolic pressure and volume. The first decline is seen with exercise and then the patient begins to have a reduction in forward output at rest. <ref name="pmid21414568">{{cite journal| author=Olsen NT, Sogaard P, Larsson HB, Goetze JP, Jons C, Mogelvang R et al.| title=Speckle-tracking echocardiography for predicting outcome in chronic aortic regurgitation during conservative management and after surgery. | journal=JACC Cardiovasc Imaging | year= 2011 | volume= 4 | issue= 3 | pages= 223-30 | pmid=21414568 | doi=10.1016/j.jcmg.2010.11.016 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21414568 }} </ref> | ||
Patients with chronic aortic insufficiency may also develop [[myocardial ischemia]]. This is due to the fact that they have an increase in demand due to an increased thickness of the [[LV]] and also a reduction in the supply due to a lower perfusion pressure during [[diastole]]. | Patients with chronic aortic insufficiency may also develop [[myocardial ischemia]]. This is due to the fact that they have an increase in demand due to an increased thickness of the [[LV]] and also a reduction in the supply due to a lower perfusion pressure during [[diastole]].<ref name="pmid21414568">{{cite journal| author=Olsen NT, Sogaard P, Larsson HB, Goetze JP, Jons C, Mogelvang R et al.| title=Speckle-tracking echocardiography for predicting outcome in chronic aortic regurgitation during conservative management and after surgery. | journal=JACC Cardiovasc Imaging | year= 2011 | volume= 4 | issue= 3 | pages= 223-30 | pmid=21414568 | doi=10.1016/j.jcmg.2010.11.016 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21414568 }} </ref> | ||
==Complications== | ==Complications== | ||
===Acute Aortic Insufficiency=== | ===Acute Aortic Insufficiency=== | ||
The complications of Acute Aortic Insufficiency include<ref name="pmid1914102">{{cite journal| author=Bonow RO, Lakatos E, Maron BJ, Epstein SE| title=Serial long-term assessment of the natural history of asymptomatic patients with chronic aortic regurgitation and normal left ventricular systolic function. | journal=Circulation | year= 1991 | volume= 84 | issue= 4 | pages= 1625-35 | pmid=1914102 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=1914102 }} </ref><ref name="pmid18820172">{{cite journal |author=Bonow RO, Carabello BA, Chatterjee K, de Leon AC, Faxon DP, Freed MD, Gaasch WH, Lytle BW, Nishimura RA, O'Gara PT, O'Rourke RA, Otto CM, Shah PM, Shanewise JS |title=2008 Focused update incorporated into the ACC/AHA 2006 guidelines for the management of patients with valvular heart disease: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the 1998 Guidelines for the Management of Patients With Valvular Heart Disease): endorsed by the Society of Cardiovascular Anesthesiologists, Society for Cardiovascular Angiography and Interventions, and Society of Thoracic Surgeons |journal=[[Circulation]] |volume=118 |issue=15 |pages=e523–661 |year=2008 |month=October |pmid=18820172 |doi=10.1161/CIRCULATIONAHA.108.190748 |url=http://circ.ahajournals.org/cgi/pmidlookup?view=long&pmid=18820172 |accessdate=2011-04-19}}</ref> | |||
#Left ventricular volume overload in a non-compliant [[left ventricle]] with acute [[left ventricular failure]] | #Left ventricular volume overload in a non-compliant [[left ventricle]] with acute [[left ventricular failure]] | ||
#[[Pulmonary edema]] | #[[Pulmonary edema]] | ||
| Line 26: | Line 31: | ||
===Chronic Aortic Insufficiency=== | ===Chronic Aortic Insufficiency=== | ||
The complications of Chronic Aortic Insufficiency include:<ref name="pmid6218741">{{cite journal| author=Pichard AD, Smith H, Holt J, Meller J, Gorlin R| title=Coronary vascular reserve in left ventricular hypertrophy secondary to chronic aortic regurgitation. | journal=Am J Cardiol | year= 1983 | volume= 51 | issue= 2 | pages= 315-20 | pmid=6218741 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=6218741 }} </ref><ref name="pmid804313">{{cite journal| author=Basta LL, Raines D, Najjar S, Kioschos JM| title=Clinical, haemodynamic, and coronary angiographic correlates of angina pectoris in patients with severe aortic valve disease. | journal=Br Heart J | year= 1975 | volume= 37 | issue= 2 | pages= 150-7 | pmid=804313 | doi= | pmc=484095 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=804313 }} </ref><ref name="pmid6478563">{{cite journal| author=Bonow RO, Rosing DR, Maron BJ, McIntosh CL, Jones M, Bacharach SL et al.| title=Reversal of left ventricular dysfunction after aortic valve replacement for chronic aortic regurgitation: influence of duration of preoperative left ventricular dysfunction. | journal=Circulation | year= 1984 | volume= 70 | issue= 4 | pages= 570-9 | pmid=6478563 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=6478563 }} </ref> | |||
#[[Heart failure]] | #[[Heart failure]] | ||
#[[Arrhythmia]] | #[[Arrhythmia]] | ||
| Line 35: | Line 41: | ||
The prognosis and survival of patients with symptomatic aortic regurgitation has improved significantly over the last decade. The five year survival rate for symptomatic patients is now more than 80 percent. | The prognosis and survival of patients with symptomatic aortic regurgitation has improved significantly over the last decade. The five year survival rate for symptomatic patients is now more than 80 percent. | ||
===Acute Aortic Insufficiency=== | ===Acute Aortic Insufficiency=== | ||
The prognosis among patients with aortic insufficiency is poor with a high mortality and morbidity due to the acute onset of [[left ventricular failure]], [[pulmonary edema]], or [[myocardial ischemia]] due to the abrupt rise in [[LV]] wall stress and [[sudden cardiac death]].<ref name="pmid18820172">{{cite journal |author=Bonow RO, Carabello BA, Chatterjee K, de Leon AC, Faxon DP, Freed MD, Gaasch WH, Lytle BW, Nishimura RA, O'Gara PT, O'Rourke RA, Otto CM, Shah PM, Shanewise JS |title=2008 Focused update incorporated into the ACC/AHA 2006 guidelines for the management of patients with valvular heart disease: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the 1998 Guidelines for the Management of Patients With Valvular Heart Disease): endorsed by the Society of Cardiovascular Anesthesiologists, Society for Cardiovascular Angiography and Interventions, and Society of Thoracic Surgeons |journal=[[Circulation]] |volume=118 |issue=15 |pages=e523–661 |year=2008 |month=October |pmid=18820172 |doi=10.1161/CIRCULATIONAHA.108.190748 |url=http://circ.ahajournals.org/cgi/pmidlookup?view=long&pmid=18820172 |accessdate=2011-04-19}}</ref> Early surgical intervention improves the prognosis in these patients. | The prognosis among patients with aortic insufficiency is poor with a high mortality and morbidity due to the acute onset of [[left ventricular failure]], [[pulmonary edema]], or [[myocardial ischemia]] due to the abrupt rise in [[LV]] wall stress and [[sudden cardiac death]].<ref name="pmid18820172">{{cite journal |author=Bonow RO, Carabello BA, Chatterjee K, de Leon AC, Faxon DP, Freed MD, Gaasch WH, Lytle BW, Nishimura RA, O'Gara PT, O'Rourke RA, Otto CM, Shah PM, Shanewise JS |title=2008 Focused update incorporated into the ACC/AHA 2006 guidelines for the management of patients with valvular heart disease: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the 1998 Guidelines for the Management of Patients With Valvular Heart Disease): endorsed by the Society of Cardiovascular Anesthesiologists, Society for Cardiovascular Angiography and Interventions, and Society of Thoracic Surgeons |journal=[[Circulation]] |volume=118 |issue=15 |pages=e523–661 |year=2008 |month=October |pmid=18820172 |doi=10.1161/CIRCULATIONAHA.108.190748 |url=http://circ.ahajournals.org/cgi/pmidlookup?view=long&pmid=18820172 |accessdate=2011-04-19}}</ref> Early surgical intervention improves the prognosis in these patients.<ref name="pmid2368680">{{cite journal| author=Rhodes LA, Keane JF, Keane JP, Fellows KE, Jonas RA, Castaneda AR et al.| title=Long follow-up (to 43 years) of ventricular septal defect with audible aortic regurgitation. | journal=Am J Cardiol | year= 1990 | volume= 66 | issue= 3 | pages= 340-5 | pmid=2368680 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2368680 }} </ref> | ||
===Chronic Aortic Insufficiency=== | ===Chronic Aortic Insufficiency=== | ||
The prognosis of a patient with Chronic Aortic Insufficiency can be summarised as follows:<ref name="pmid24603191">{{cite journal| author=Nishimura RA, Otto CM, Bonow RO, Carabello BA, Erwin JP, Guyton RA et al.| title=2014 AHA/ACC guideline for the management of patients with valvular heart disease: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. | journal=J Am Coll Cardiol | year= 2014 | volume= 63 | issue= 22 | pages= e57-185 | pmid=24603191 | doi=10.1016/j.jacc.2014.02.536 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24603191 }} </ref> | |||
====Asymptomatic Patients==== | ====Asymptomatic Patients==== | ||
The prognosis of asymptotic patients with Aortic Stenosis can be summarised as follow:<ref name="pmid1914102">{{cite journal| author=Bonow RO, Lakatos E, Maron BJ, Epstein SE| title=Serial long-term assessment of the natural history of asymptomatic patients with chronic aortic regurgitation and normal left ventricular systolic function. | journal=Circulation | year= 1991 | volume= 84 | issue= 4 | pages= 1625-35 | pmid=1914102 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=1914102 }} </ref><ref name="pmid6872164">{{cite journal| author=Bonow RO, Rosing DR, McIntosh CL, Jones M, Maron BJ, Lan KK et al.| title=The natural history of asymptomatic patients with aortic regurgitation and normal left ventricular function. | journal=Circulation | year= 1983 | volume= 68 | issue= 3 | pages= 509-17 | pmid=6872164 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=6872164 }} </ref> | |||
:*Mortality rate ≈ 2.8% per year | :*Mortality rate ≈ 2.8% per year | ||
*Asymptomatic patients with normal [[ejection fraction]]: | *Asymptomatic patients with normal [[ejection fraction]]: | ||
| Line 46: | Line 55: | ||
*Asymptomatic patients with reduced [[ejection fraction]]: | *Asymptomatic patients with reduced [[ejection fraction]]: | ||
:*Rate of progression to symptoms ≥ 25% per year | :*Rate of progression to symptoms ≥ 25% per year | ||
====Symptomatic Patients==== | ====Symptomatic Patients==== | ||
The prognosis of symptomatic Aortic Regurgitation patients includes: | |||
:*Mortality rate ≥ 10% per year | :*Mortality rate ≥ 10% per year | ||
:*[[NYHA class]] I - 3.0% per year | :*[[NYHA class]] I - 3.0% per year | ||
:*[[NYHA class]] II - 6.3% per year | :*[[NYHA class]] II - 6.3% per year | ||
:*[[NYHA class]] III-IV - 24.6% per year | :*[[NYHA class]] III-IV - 24.6% per year | ||
====Chronic Severe Aortic Insufficiency Managed Conservatively<ref name="pmid10199882">{{cite journal |author=Dujardin KS, Enriquez-Sarano M, Schaff HV, Bailey KR, Seward JB, Tajik AJ |title=Mortality and morbidity of aortic regurgitation in clinical practice. A long-term follow-up study |journal=[[Circulation]] |volume=99 |issue=14 |pages=1851–7 |year=1999 |month=April |pmid=10199882 |doi= |url=http://circ.ahajournals.org/cgi/pmidlookup?view=long&pmid=10199882 |accessdate=2011-04-19}}</ref> | |||
====Chronic Severe Aortic Insufficiency Managed Conservatively==== | |||
The prognosis of the conservative management of Chronic Severe Aortic Insufficiency includes:<ref name="pmid10199882">{{cite journal |author=Dujardin KS, Enriquez-Sarano M, Schaff HV, Bailey KR, Seward JB, Tajik AJ |title=Mortality and morbidity of aortic regurgitation in clinical practice. A long-term follow-up study |journal=[[Circulation]] |volume=99 |issue=14 |pages=1851–7 |year=1999 |month=April |pmid=10199882 |doi= |url=http://circ.ahajournals.org/cgi/pmidlookup?view=long&pmid=10199882 |accessdate=2011-04-19}}</ref> | |||
:*Death from any cause - 4.7% per year | :*Death from any cause - 4.7% per year | ||
:*[[Congestive heart failure]] - 6.2% per year | :*[[Congestive heart failure]] - 6.2% per year | ||
| Line 58: | Line 71: | ||
==References== | ==References== | ||
{{reflist|2}} | {{reflist|2}} | ||
{{WH}} | |||
{{WS}} | |||
[[CME Category::Cardiology]] | |||
[[Category:Disease]] | |||
[[Category:Cardiology]] | [[Category:Cardiology]] | ||
[[Category:Valvular heart disease]] | |||
[[Category:Congenital heart disease]] | |||
[[Category:Surgery]] | |||
[[Category:Cardiac surgery]] | |||
[[Category:Emergency medicine]] | [[Category:Emergency medicine]] | ||
[[Category:Intensive care medicine]] | [[Category:Intensive care medicine]] | ||
[[Category:Up-To-Date cardiology]] | |||
[[Category:Up-To-Date]] | |||
Latest revision as of 15:21, 5 January 2017
 |
Resident Survival Guide |
|
Aortic Regurgitation Microchapters |
|
Diagnosis |
|---|
|
Treatment |
|
Acute Aortic regurgitation |
|
Chronic Aortic regurgitation |
|
Special Scenarios |
|
Case Studies |
|
Aortic regurgitation natural history, complications and prognosis On the Web |
|
American Roentgen Ray Society Images of Aortic regurgitation natural history, complications and prognosis |
|
FDA on Aortic regurgitation natural history, complications and prognosis |
|
CDC on Aortic regurgitation natural history, complications and prognosis |
|
Aortic regurgitation natural history, complications and prognosis in the news |
|
Blogs on Aortic regurgitation natural history, complications and prognosis |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor-in-Chief: Varun Kumar, M.B.B.S.; Lakshmi Gopalakrishnan, M.B.B.S; Usama Talib, BSc, MD [2]
Overview
In acute aortic insufficiency symptoms of heart failure often develop acutely. Chronic aortic insufficiency is usually insidious and progressive and the patient may remain asymptomatic for years. Once left ventricular dilation and left ventricular failure occur, dyspnea on exertion and exercise intolerance begin to occur. Later symptoms such as angina, syncope, and other symptoms of heart failure are present.[1]
Natural History
Acute Aortic Insufficiency
In acute aortic insufficiency symptoms of heart failure such as pulmonary edema often develop acutely. Acute aortic insufficiency is often secondary to either trauma or infective endocarditis. While the heart can accommodate the changes of chronic aortic insufficiency over time, the acute changes of acute aortic insufficiency are not well accommodated by the left ventricle.
The rapid rise in left ventricular pressure causes the mitral valve to close earlier during diastole. This early closure fortunately prevents backwards flow of blood into the pulmonary vascular bed. The very high left ventricular end diastolic pressure often keeps the aortic diastolic pressure from falling too low and thus there is often not a wide pulse pressure. Indeed absence of a wide pulse pressure in the patient with acute aortic insufficiency should alert the clinician to potential failure of the left ventricle.[2]
Chronic Aortic Insufficiency
Chronic aortic insufficiency is usually insidious and progressive and the patient may remain asymptomatic for years. Once left ventricular dilation and left ventricular failure occur, dyspnea on exertion and exercise intolerance begin to occur. Later symptoms such as angina, syncope, and other symptoms of heart failure are present. The hemodynamic impact of aortic regurgitation causes progressive dilation and hypertrophy of the left ventricle. The mitral valve ring may also dilate which may lead in turn to mitral regurgitation. The left atrium may dilate as a result of the mitral regurgitation. It has been said that 'aortic regurgitation begets aortic regurgitation'. The high oscillatory shear associated with aortic regurgitation may lead to further dilation of the aorta, which in turn may lead to further aortic regurgitation.[1]
Volume overload associated with aortic regurgitation leads to left ventricular hypertrophy. The sarcomeres replicate in series and there is elongation of the myocytes and myocardial fibrils. As a result of this hypertrophy the ratio of the ventricular wall thickness to cavity radius remains normal and therefore wall stress is normal. In aortic regurgitation there is eccentric hypertrophy where as in aortic stenosis there is concentric hypertrophy where there is replication of the sarcomeres in parallel. Once wall thickening fails to keep up with the hemodynamic load, end systolic wall stress rises and at this point the left ventricle fails. The dramatic enlargement of the heart that is seen with aortic regurgitation is called cor bovinum. Over time the left ventricle will decompensate and there will be increasing interstitial fibrosis and a stiffening or a reduction in the compliance of the left ventricular wall. At this point the patient will experience a rise in the end diastolic pressure and volume. The first decline is seen with exercise and then the patient begins to have a reduction in forward output at rest. [3]
Patients with chronic aortic insufficiency may also develop myocardial ischemia. This is due to the fact that they have an increase in demand due to an increased thickness of the LV and also a reduction in the supply due to a lower perfusion pressure during diastole.[3]
Complications
Acute Aortic Insufficiency
The complications of Acute Aortic Insufficiency include[1][4]
- Left ventricular volume overload in a non-compliant left ventricle with acute left ventricular failure
- Pulmonary edema
- Sudden cardiac death
Chronic Aortic Insufficiency
The complications of Chronic Aortic Insufficiency include:[5][6][7]
- Heart failure
- Arrhythmia
- Myocardial ischemia
- Aortic dissection in patients with bicuspid aortic valve
- Infective endocarditis
Prognosis
The prognosis and survival of patients with symptomatic aortic regurgitation has improved significantly over the last decade. The five year survival rate for symptomatic patients is now more than 80 percent.
Acute Aortic Insufficiency
The prognosis among patients with aortic insufficiency is poor with a high mortality and morbidity due to the acute onset of left ventricular failure, pulmonary edema, or myocardial ischemia due to the abrupt rise in LV wall stress and sudden cardiac death.[4] Early surgical intervention improves the prognosis in these patients.[2]
Chronic Aortic Insufficiency
The prognosis of a patient with Chronic Aortic Insufficiency can be summarised as follows:[8]
Asymptomatic Patients
The prognosis of asymptotic patients with Aortic Stenosis can be summarised as follow:[1][9]
- Mortality rate ≈ 2.8% per year
- Asymptomatic patients with normal ejection fraction:
- Rate of progression to symptoms or left ventricular dysfunction ≤ 6% per year
- Rate of progression to asymptomatic left ventricular dysfunction ≤ 3.5% per year
- Rate of sudden death ≤ 0.2% per year
- Asymptomatic patients with reduced ejection fraction:
- Rate of progression to symptoms ≥ 25% per year
Symptomatic Patients
The prognosis of symptomatic Aortic Regurgitation patients includes:
- Mortality rate ≥ 10% per year
- NYHA class I - 3.0% per year
- NYHA class II - 6.3% per year
- NYHA class III-IV - 24.6% per year
Chronic Severe Aortic Insufficiency Managed Conservatively
The prognosis of the conservative management of Chronic Severe Aortic Insufficiency includes:[10]
- Death from any cause - 4.7% per year
- Congestive heart failure - 6.2% per year
- Aortic valve surgery - 14.6% per year
References
- ↑ 1.0 1.1 1.2 1.3 Bonow RO, Lakatos E, Maron BJ, Epstein SE (1991). "Serial long-term assessment of the natural history of asymptomatic patients with chronic aortic regurgitation and normal left ventricular systolic function". Circulation. 84 (4): 1625–35. PMID 1914102.
- ↑ 2.0 2.1 Rhodes LA, Keane JF, Keane JP, Fellows KE, Jonas RA, Castaneda AR; et al. (1990). "Long follow-up (to 43 years) of ventricular septal defect with audible aortic regurgitation". Am J Cardiol. 66 (3): 340–5. PMID 2368680.
- ↑ 3.0 3.1 Olsen NT, Sogaard P, Larsson HB, Goetze JP, Jons C, Mogelvang R; et al. (2011). "Speckle-tracking echocardiography for predicting outcome in chronic aortic regurgitation during conservative management and after surgery". JACC Cardiovasc Imaging. 4 (3): 223–30. doi:10.1016/j.jcmg.2010.11.016. PMID 21414568.
- ↑ 4.0 4.1 Bonow RO, Carabello BA, Chatterjee K, de Leon AC, Faxon DP, Freed MD, Gaasch WH, Lytle BW, Nishimura RA, O'Gara PT, O'Rourke RA, Otto CM, Shah PM, Shanewise JS (2008). "2008 Focused update incorporated into the ACC/AHA 2006 guidelines for the management of patients with valvular heart disease: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the 1998 Guidelines for the Management of Patients With Valvular Heart Disease): endorsed by the Society of Cardiovascular Anesthesiologists, Society for Cardiovascular Angiography and Interventions, and Society of Thoracic Surgeons". Circulation. 118 (15): e523–661. doi:10.1161/CIRCULATIONAHA.108.190748. PMID 18820172. Retrieved 2011-04-19. Unknown parameter
|month=ignored (help) - ↑ Pichard AD, Smith H, Holt J, Meller J, Gorlin R (1983). "Coronary vascular reserve in left ventricular hypertrophy secondary to chronic aortic regurgitation". Am J Cardiol. 51 (2): 315–20. PMID 6218741.
- ↑ Basta LL, Raines D, Najjar S, Kioschos JM (1975). "Clinical, haemodynamic, and coronary angiographic correlates of angina pectoris in patients with severe aortic valve disease". Br Heart J. 37 (2): 150–7. PMC 484095. PMID 804313.
- ↑ Bonow RO, Rosing DR, Maron BJ, McIntosh CL, Jones M, Bacharach SL; et al. (1984). "Reversal of left ventricular dysfunction after aortic valve replacement for chronic aortic regurgitation: influence of duration of preoperative left ventricular dysfunction". Circulation. 70 (4): 570–9. PMID 6478563.
- ↑ Nishimura RA, Otto CM, Bonow RO, Carabello BA, Erwin JP, Guyton RA; et al. (2014). "2014 AHA/ACC guideline for the management of patients with valvular heart disease: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines". J Am Coll Cardiol. 63 (22): e57–185. doi:10.1016/j.jacc.2014.02.536. PMID 24603191.
- ↑ Bonow RO, Rosing DR, McIntosh CL, Jones M, Maron BJ, Lan KK; et al. (1983). "The natural history of asymptomatic patients with aortic regurgitation and normal left ventricular function". Circulation. 68 (3): 509–17. PMID 6872164.
- ↑ Dujardin KS, Enriquez-Sarano M, Schaff HV, Bailey KR, Seward JB, Tajik AJ (1999). "Mortality and morbidity of aortic regurgitation in clinical practice. A long-term follow-up study". Circulation. 99 (14): 1851–7. PMID 10199882. Retrieved 2011-04-19. Unknown parameter
|month=ignored (help)