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==Systolic Dysfunction==
==Systolic Dysfunction==
Later in the course of aortic stenosis, left ventricular dysfunction may develop due to a variety of pathophysiology processes.  Systolic dysfunction is associated with a poor prognosis, and often does not partially or fully reverse following operative repair<ref name="pmid">{{cite journal |author=Carabello BA, Green LH, Grossman W, Cohn LH, Koster JK, Collins JJ |title= |journal=[[]] |volume= |issue= |pages=42–8 |year=1980 |month=July |pmid= |doi= |url=http://circ.ahajournals.org/cgi/pmidlookup?view=long&pmid=7379284 |accessdate=2012-04-10}}</ref> .
Later in the course of aortic stenosis, left ventricular dysfunction may develop due to a variety of pathophysiological processes.  Systolic dysfunction is associated with a poor prognosis and it often does not partially or fully reverse following operative repair<ref name="pmid">{{cite journal |author=Carabello BA, Green LH, Grossman W, Cohn LH, Koster JK, Collins JJ |title= |journal=[[]] |volume= |issue= |pages=42–8 |year=1980 |month=July |pmid= |doi= |url=http://circ.ahajournals.org/cgi/pmidlookup?view=long&pmid=7379284 |accessdate=2012-04-10}}</ref> .


===Excess Hypertrophy Causes Systolic Dysfunction===
===Excess Hypertrophy Causes Systolic Dysfunction===
Although, this massive concentric hypertrophy characterized by a reduced diastolic radius-to-wall thickness ratio has shown to initially counter balance the increased systolic left ventricular pressure, if this process continues, an inverse relationship has been observed such that [[ejection fraction]] eventually goes down as left ventricular mass increases beyond a certain point.<ref name="pmid2969811">{{cite journal |author=Krayenbuehl HP, Hess OM, Ritter M, Monrad ES, Hoppeler H |title=Left ventricular systolic function in aortic stenosis |journal=[[European Heart Journal]] |volume=9 Suppl E |issue= |pages=19–23 |year=1988 |month=April |pmid=2969811 |doi= |url=http://eurheartj.oxfordjournals.org/cgi/pmidlookup?view=long&pmid=2969811 |accessdate=2012-04-10}}</ref><ref name="pmid">{{cite journal |author=Ross J |title=Afterload mismatch and preload reserve: a conceptual framework for the analysis of ventricular function |journal=[[Progress in Cardiovascular Diseases]] |volume=18 |issue=4 |pages=255–64 |year=1976 |pmid= |doi= |url=http://linkinghub.elsevier.com/retrieve/pii/0033-0620(76)90021-9 |accessdate=2012-04-10}}</ref><ref name="pmid154367">{{cite journal |author=Gunther S, Grossman W |title=Determinants of ventricular function in pressure-overload hypertrophy in man |journal=[[Circulation]] |volume=59 |issue=4 |pages=679–88 |year=1979 |month=April |pmid=154367 |doi= |url=http://circ.ahajournals.org/cgi/pmidlookup?view=long&pmid=154367 |accessdate=2012-04-10}}</ref><ref name="pmid7237709">{{cite journal |author=Huber D, Grimm J, Koch R, Krayenbuehl HP |title=Determinants of ejection performance in aortic stenosis |journal=[[Circulation]] |volume=64 |issue=1 |pages=126–34 |year=1981 |month=July |pmid=7237709 |doi= |url=http://circ.ahajournals.org/cgi/pmidlookup?view=long&pmid=7237709 |accessdate=2012-04-10}}</ref>.
The massive concentric hypertrophy, characterized by a reduced diastolic radius-to-wall thickness ratio, has shown to initially counter balance the increased systolic left ventricular pressure; nevertheless, if this process continues, an inverse relationship has been observed such that the [[ejection fraction]] eventually goes down as the left ventricular mass increases beyond a certain point.<ref name="pmid2969811">{{cite journal |author=Krayenbuehl HP, Hess OM, Ritter M, Monrad ES, Hoppeler H |title=Left ventricular systolic function in aortic stenosis |journal=[[European Heart Journal]] |volume=9 Suppl E |issue= |pages=19–23 |year=1988 |month=April |pmid=2969811 |doi= |url=http://eurheartj.oxfordjournals.org/cgi/pmidlookup?view=long&pmid=2969811 |accessdate=2012-04-10}}</ref><ref name="pmid">{{cite journal |author=Ross J |title=Afterload mismatch and preload reserve: a conceptual framework for the analysis of ventricular function |journal=[[Progress in Cardiovascular Diseases]] |volume=18 |issue=4 |pages=255–64 |year=1976 |pmid= |doi= |url=http://linkinghub.elsevier.com/retrieve/pii/0033-0620(76)90021-9 |accessdate=2012-04-10}}</ref><ref name="pmid154367">{{cite journal |author=Gunther S, Grossman W |title=Determinants of ventricular function in pressure-overload hypertrophy in man |journal=[[Circulation]] |volume=59 |issue=4 |pages=679–88 |year=1979 |month=April |pmid=154367 |doi= |url=http://circ.ahajournals.org/cgi/pmidlookup?view=long&pmid=154367 |accessdate=2012-04-10}}</ref><ref name="pmid7237709">{{cite journal |author=Huber D, Grimm J, Koch R, Krayenbuehl HP |title=Determinants of ejection performance in aortic stenosis |journal=[[Circulation]] |volume=64 |issue=1 |pages=126–34 |year=1981 |month=July |pmid=7237709 |doi= |url=http://circ.ahajournals.org/cgi/pmidlookup?view=long&pmid=7237709 |accessdate=2012-04-10}}</ref>.


===Myocardial Ischemia===
===Myocardial Ischemia===
The hypertrophied left ventricle and the prolonged ejection time (the time for the heart to eject blood) results in 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") that drives coronary blood flow.  There may be a relative reduction in the density of the capillary network.  The hypertrophied ventricle may also compress the capillaries. All of the above lead to a reduction in coronary blood flow even in the absence of obstructive epicardial stenoses. This may lead to subendocardial [[ischemia]] during stress or exercise.<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 increase in the  myocardial oxygen requirements.  In addition, the elevated diastolic filling pressure reduces the gradient between the aorta and the right atrium ("the height of the waterfall") which normally drives coronary blood flow.  There may be a relative reduction in the density of the capillary network.  The hypertrophied ventricle may also compress the capillaries. All of the above lead to a reduction in coronary blood flow even in the absence of obstructive epicardial stenosis. This may lead to subendocardial [[ischemia]] during stress or exercise<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>.


===Myocardial Fibrosis===
===Myocardial Fibrosis===
Myocardial scarring or fibrosis may develop with prolonged aortic stenosis, perhaps due to chronic [[subendocardial ischemia]] or increased wall stress.
Myocardial scarring or fibrosis may develop with prolonged aortic stenosis, probably due to chronic [[subendocardial ischemia]] or increased wall stress.


===Dyssynchronous Contraction===
===Dyssynchronous Contraction===
Another factor that may contribute to reduced left ventricular systolic function is [[dyssynchronous contraction]] subsequent to regional wall motion abnormalities, [[fibrosis]] or [[ischemia]].<ref name="pmid9014797">{{cite journal |author=Jin XY, Pepper JR, Gibson DG |title=Effects of incoordination on left ventricular force-velocity relation in aortic stenosis |journal=[[Heart (British Cardiac Society)]]|volume=76 |issue=6 |pages=495–501 |year=1996 |month=December |pmid=9014797|pmc=484601 |doi= |url=http://heart.bmj.com/cgi/pmidlookup?view=long&pmid=9014797|accessdate=2012-04-10}}</ref>
Another factor that may contribute to the reduced left ventricular systolic function is the [[dyssynchronous contraction]] subsequent to regional wall motion abnormalities, [[fibrosis]] or [[ischemia]].<ref name="pmid9014797">{{cite journal |author=Jin XY, Pepper JR, Gibson DG |title=Effects of incoordination on left ventricular force-velocity relation in aortic stenosis |journal=[[Heart (British Cardiac Society)]]|volume=76 |issue=6 |pages=495–501 |year=1996 |month=December |pmid=9014797|pmc=484601 |doi= |url=http://heart.bmj.com/cgi/pmidlookup?view=long&pmid=9014797|accessdate=2012-04-10}}</ref>


==Atrial Fibrillation==
==Atrial Fibrillation==

Revision as of 20:16, 15 October 2012

Aortic Stenosis Microchapters

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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] Assistant Editor-In-Chief: Kristin Feeney, B.S. [4]

Overview

Aortic stenosis causes an impedance to antegrade blood flow which leads to chronic pressure overload of the left ventricle. The most common complication of aortic stenosis is left ventricular hypertrophy. The obstruction of flow in aortic stenosis can occur not only at the level of the aortic valve itself, but also at the subvalvular (below the aortic valve) or supravalvular (above the aortic valve) levels as well.

Left Ventricular Hypertrophy

Long-standing aortic stenosis exposes the left ventricle to prolonged pressure overload which leads to concentric hypertrophy.[1][2][3] The left ventricular wall increases in thickness (i.e. concentric hypertrophy occurs) as a result of the parallel replication of the sarcomeres.

Diastolic Dysfunction

During the initial period of concentric hypertrophy, the left ventricle is not dilated and there is preservation of the left ventricular systolic function. Diastolic function, however, may be reduced due to a reduction in diastolic compliance [4][5][5][6].

This diastolic dysfunction may in turn lead to a rise in pulmonary capillary wedge pressure and consequently lead to dyspnea. Cardiac output may also be reduced as a result of diastolic dysfunction and impaired filling of the left ventricle. Early in the course of aortic stenosis, there may be a failure to augment cardiac output during exercise resulting in dyspnea on exertion.

Systolic Dysfunction

Later in the course of aortic stenosis, left ventricular dysfunction may develop due to a variety of pathophysiological processes. Systolic dysfunction is associated with a poor prognosis and it often does not partially or fully reverse following operative repair[5] .

Excess Hypertrophy Causes Systolic Dysfunction

The massive concentric hypertrophy, characterized by a reduced diastolic radius-to-wall thickness ratio, has shown to initially counter balance the increased systolic left ventricular pressure; nevertheless, if this process continues, an inverse relationship has been observed such that the ejection fraction eventually goes down as the left ventricular mass increases beyond a certain point.[7][5][8][9].

Myocardial Ischemia

The hypertrophied left ventricle and the prolonged ejection time (the time for the heart to eject blood) result in an increase in the myocardial oxygen requirements. In addition, the elevated diastolic filling pressure reduces the gradient between the aorta and the right atrium ("the height of the waterfall") which normally drives coronary blood flow. There may be a relative reduction in the density of the capillary network. The hypertrophied ventricle may also compress the capillaries. All of the above lead to a reduction in coronary blood flow even in the absence of obstructive epicardial stenosis. This may lead to subendocardial ischemia during stress or exercise[10][11].

Myocardial Fibrosis

Myocardial scarring or fibrosis may develop with prolonged aortic stenosis, probably due to chronic subendocardial ischemia or increased wall stress.

Dyssynchronous Contraction

Another factor that may contribute to the reduced left ventricular systolic function is the dyssynchronous contraction subsequent to regional wall motion abnormalities, fibrosis or ischemia.[12]

Atrial Fibrillation

The stiff, non-compliant left ventricle can become increasingly dependent upon the left atrium for filling. The development of atrial fibrillation and the loss of atrial contractility can result in reduced left ventricular filling and reduced cardiac output.

Pressure Gradient & Valve Area

When the aortic valve becomes stenosed, it can result in the formation of a pressure gradient between the left ventricle (LV) and the aorta [13]. The more constricted the valve, the bigger the gradient between the LV and the aorta.

For instance, in patient with mild AS, the gradient may be 20 mmHg. This means that, at peak systole, while the LV may generate a pressure of 140 mmHg, the pressure that is transmitted into the aorta will only be 120 mmHg. So, while a blood pressure cuff may measure a normal systolic blood pressure the actual pressure generated by and inside the LV would be considerably higher. As the left ventricle fails, however, it may no longer be able to mount the contractility necessary to generate a large gradient across the aortic valve.

Therefore, absence of a large gradient across the aortic valve does not exclude the presence of critical aortic stenosis. The presence of a low gradient and low ejection results in low flow aortic stenosis. It is for this reason that the best measure of the severity of aortic stenosis is the aortic valve area, not the aortic valve gradient.

Aortic valve area

Aortic valve area calculation

Subvalvular Gradients in AS in the Absence of Anatomic Obstruction

Fluid dynamic mediated subvalvular pressure gradients are often present in patients with severe aortic stenosis in the absence of an anatomic subvalvular obstruction and constitute ~50% of the total measured transvalvular gradient. The extent of increase in cardiac output during exercise is inversely related to the magnitude of subvalvular gradient.[14]

Flow Velocity

If the left ventricular function and contractility is preserved, a flow velocity across the stenosed valve of at least 2.6 m/sec is deemed consistent with aortic stenosis. This is based upon echocardiographic estimation of the aortic jet velocity, aortic valve area and the mean transvalvular gradient. In aortic valve sclerosis (not stenosis); the aortic valve becomes calcified but the aortic jet velocity is ≤ 2.5 m/sec (without a significant gradient). Aortic valve sclerosis is commonly defined as a focal thickening of the aortic cusps with calcific nodules generally at the base of leaflets and transvalvular velocity at Doppler still in the normal range (Vmax <2 m/s). Until few years ago, it was considered a physiologic process related to aging without clinical relevance. However, aortic valve sclerosis is not observed in about 50% of people over 80 years old. Furthermore, several experimental and clinical studies have demonstrated that it could represent an active phenomenon, significantly related to risk factors for atherosclerosis and cardiovascular morbidity and mortality [15]. [16].

Low Flow, Low Gradient, Low Ejection Fraction Aortic Stenosis

If there is a decline in left ventricular function due to systolic dysfunction, there may be only a moderate transvalvular gradient or low flow aortic stenosis. If there is fibrosis of the left ventricle, there may be incomplete recovery after aortic valve replacement[5] . This scenario can also occur among patients in whom there is a history of myocardial infarction: there is insufficient contractility to mount an aortic gradient. It may also occur if there is development of myocardial fibrosis due to longstanding aortic stenosis.

Definition

  1. An aortic valve areas < 1.0 cm2
  2. A left ventricular ejection fraction < 40%
  3. A mean pressure difference or gradient across the aortic valve of < 30 mm Hg

Assessment

  • With a dobutamine infusion, the aortic valve area should increase to > 1.2 cm2, and the mean pressure gradient should rise above 30 mm Hg. If there is a failure to acheive these improvements, early surgical mortality is 32-33%, but it is only 5–7% in those patients who can augment their contractility and gradient. Survival at five years was 88% after surgery if the patient can augment their contractility, but only 10–25% if the patient cannot augment their contractility.

ACC/AHA Guidelines- Recommendation [17]

“

Class IIa

1. Dobutamine stress echocardiography is reasonable to evaluate patients with low-flow/low-gradient aortic stenosis and left ventricular dysfunction. (Level of Evidence: B)

2. Cardiac catheterization for hemodynamic measurements with infusion of dobutamine can be useful for evaluation of patients with low-flow/low-gradient aortic stenosis and left ventricular dysfunction. (Level of Evidence: C)

”

Relationship of Hemodynamic Severity to Symptoms of Aortic Stenosis

  • In general, aortic stenosis patients with normal left ventricular systolic function become symptomatic, usually when:
  • Valve area is less than 1.0 cm2.
  • Jet velocity is over 4.0 m/sec.
  • Mean transvalvular pressure gradient exceeds 40 mm Hg.
  • However, many patients develop symptoms only when more severe valve obstruction is present, other patients become symptomatic at less severe degree of stenosis, particularly if there is coexisting aortic regurgitation.

ACC/AHA Guidelines- Severity Classification [17]

Indicator Mild Moderate Severe
Jet velocity (m per s) Less than 3.0 3.0–4.0 Greater than 4.0
Mean gradient (mm Hg)† Less than 25 25–40 Greater than 40
Valve area (cm2) Greater than 1.5 1.0–1.5 Less than 1.0
Valve area index (cm2 per m2) Less than 0.6

† Valve gradients are flow dependent and when used as estimates of severity of valve stenosis should be assessed with knowledge of cardiac output or forward flow across the valve.

Pathology Findings

Gross Pathology

Microscopic Pathology

Guideline Resources

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[17]

References

  1. ↑ Sasayama S, Ross J, Franklin D, Bloor CM, Bishop S, Dilley RB (1976). "Adaptations of the left ventricle to chronic pressure overload". Circulation Research. 38 (3): 172–8. PMID 129304. Retrieved 2012-04-10. Unknown parameter |month= ignored (help)
  2. ↑ Gaasch WH (1979). "Left ventricular radius to wall thickness ratio". The American Journal of Cardiology. 43 (6): 1189–94. PMID 155986. Unknown parameter |month= ignored (help); |access-date= requires |url= (help)
  3. ↑ Spann JF, Bove AA, Natarajan G, Kreulen T (1980). "Ventricular performance, pump function and compensatory mechanisms in patients with aortic stenosis". Circulation. 62 (3): 576–82. PMID 6446989. Retrieved 2012-04-10. Unknown parameter |month= ignored (help)
  4. ↑ Gaasch WH, Levine HJ, Quinones MA, Alexander JK (1976). "Left ventricular compliance: mechanisms and clinical implications". The American Journal of Cardiology. 38 (5): 645–53. PMID 136186. Unknown parameter |month= ignored (help); |access-date= requires |url= (help)
  5. ↑ 5.0 5.1 5.2 5.3 5.4 Murakami T, Hess OM, Gage JE, Grimm J, Krayenbuehl HP. [[]] http://circ.ahajournals.org/cgi/pmidlookup?view=long&pmid=2938847. Retrieved 2012-04-10. Unknown parameter |month= ignored (help); Missing or empty |title= (help)
  6. ↑ Gaasch WH (1994). "Diagnosis and treatment of heart failure based on left ventricular systolic or diastolic dysfunction". JAMA : the Journal of the American Medical Association. 271 (16): 1276–80. PMID 8151903. Unknown parameter |month= ignored (help); |access-date= requires |url= (help)
  7. ↑ Krayenbuehl HP, Hess OM, Ritter M, Monrad ES, Hoppeler H (1988). "Left ventricular systolic function in aortic stenosis". European Heart Journal. 9 Suppl E: 19–23. PMID 2969811. Retrieved 2012-04-10. Unknown parameter |month= ignored (help)
  8. ↑ Gunther S, Grossman W (1979). "Determinants of ventricular function in pressure-overload hypertrophy in man". Circulation. 59 (4): 679–88. PMID 154367. Retrieved 2012-04-10. Unknown parameter |month= ignored (help)
  9. ↑ Huber D, Grimm J, Koch R, Krayenbuehl HP (1981). "Determinants of ejection performance in aortic stenosis". Circulation. 64 (1): 126–34. PMID 7237709. Retrieved 2012-04-10. Unknown parameter |month= ignored (help)
  10. ↑ 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.
  11. ↑ Carabello BA (2002). "Clinical practice. Aortic stenosis". N Engl J Med. 346 (9): 677–82. doi:10.1056/NEJMcp010846. PMID 11870246.
  12. ↑ Jin XY, Pepper JR, Gibson DG (1996). "Effects of incoordination on left ventricular force-velocity relation in aortic stenosis". Heart (British Cardiac Society). 76 (6): 495–501. PMC 484601. PMID 9014797. Retrieved 2012-04-10. Unknown parameter |month= ignored (help)
  13. ↑ Lilly LS (editor) (2003). Pathophysiology of Heart Disease (3rd ed. ed.). Lippincott Williams & Wilkins. ISBN 0-7817-4027-4.
  14. ↑ Laskey WK, Kussmaul WG (2001). "Subvalvular gradients in patients with valvular aortic stenosis: prevalence, magnitude, and physiological importance". Circulation. 104 (9): 1019–22. PMID 11524395. Retrieved 2012-04-12. Unknown parameter |month= ignored (help)
  15. ↑ Branch KR, O'Brien KD, Otto CM (2002). "Aortic valve sclerosis as a marker of active atherosclerosis". Curr Cardiol Rep. 4 (2): 111–7. PMID 11827633.
  16. ↑ {{Faggiano P, D'Aloia A, Antonini-Canterin F, Pinamonti B, DiLenarda A, Brentana L, Metra M, Nodari S, Dei Cas L. Usefulness of cardiac calcification on two-dimensional echocardiography for distinguishing ischemic from nonischemic dilated cardiomyopathy: a preliminary report. J Cardiovasc Med. 2006.}}
  17. ↑ 17.0 17.1 17.2 Bonow RO, Carabello BA, Chatterjee K, de Leon AC, Faxon DP, Freed MD; et al. (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". J Am Coll Cardiol. 52 (13): e1–142. doi:10.1016/j.jacc.2008.05.007. PMID 18848134.

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