Aortic stenosis pathophysiology
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Aortic Stenosis Microchapters |
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Diagnosis |
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Treatment |
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Percutaneous Aortic Balloon Valvotomy (PABV) or Aortic Valvuloplasty |
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Transcatheter Aortic Valve Replacement (TAVR) |
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Case Studies |
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Aortic stenosis pathophysiology On the Web |
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American Roentgen Ray Society Images of Aortic stenosis pathophysiology |
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Directions to Hospitals Treating Aortic stenosis pathophysiology |
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Risk calculators and risk factors for Aortic stenosis pathophysiology |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editors-In-Chief: Mohammed A. Sbeih, M.D. [2], Claudia P. Hochberg, M.D. [3], Abdul-Rahman Arabi, M.D. [4], Keri Shafer, M.D. [5], Priyamvada Singh, MBBS [6]; Assistant Editor-In-Chief: Kristin Feeney, B.S. [7]
Overview
The impedance to antegrade blood flow as a result of aortic stenosis results in 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 obviously occur at the level of the aortic valve itself, but can also occur at the subvalvular (below the aortic valve) or supravalvular (above the aortic valve) level as well.
Pathophysiology
When the aortic valve becomes stenosed, it can result in the formation of a pressure gradient between the left ventricle (LV) and the aorta [1]. The more constricted the valve, the bigger the gradient between the LV and the aorta. For instance, with a 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 to 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 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. 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.
Due to the increased pressures generated by the left ventricle, the myocardium (muscle) of the LV undergoes hypertrophy (increase in muscle mass). This is seen as thickening of the walls of the LV. The type of hypertrophy most commonly seen in AS is concentric hypertrophy, meaning that all the walls of the LV are (approximately) equally thickened. As a result of increased left ventricular wall thickness , the volume/mass ratio decreases, the compliance of the chamber also decreases, and LV end-diastolic pressure increases without chamber dilatation [2].
Unfortunately, the adaptation to aortic stenosis by concentric left ventricular hypertrophy often carries adverse consequences. The hypertrophied heart may have reduced coronary blood flow even in the absence of obstructive epicardial stenoses due to compression of the capillary network. This may lead to subendocardial ischemia during stress or exercise, which can contribute to systolic or diastolic dysfunction of the left ventricle [3][4]. If left ventricular systolic dysfunction occurs, this may result in reductions in stroke volume and cardiac output, and eventual heart failure. Another factor that may reduce ventricular function is dyssynchronous contraction, resulting from regional wall motion abnormalities, fibrosis or ischemia [5].
In aortic stenosis, the flow velocity across the stenosed valve is at least 2.6 m/sec. if the left ventricular function and contractility is preserved. 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 or diffuse 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 [6]. [7]]].
Low Flow 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. 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.
Definition
- An aortic valve areas < 1.0 cm2
- A left ventricular ejection fraction < 40%
- A mean pressure difference or gradient across the aortic valve of < 30 mm Hg
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.
Progression of Aortic Stenosis
The rate of progression of aortic stenosis occurs at an average rate of reduction in aortic valve area of 0.1 cm2 in valve area per year [8]. Unfortunately, there is a large interpatient variability in the rate of progression. Furthermore, multiple factors are associated with more rapid progression which include the following:
- Left ventricular function
- Bicuspid aortic valve stenosis
- Initial severity of stenosis
- Risk factors for atherosclerosis, such as age, smoking, hypertension, obesity and diabetes, lipid abnormalities, chronic renal failure and dialysis, and atherosclerotic disease itself, such as concomitant coronary artery disease
Relationship of Hemodynamic Severity to Symptoms of Aortic Stenosis
In general, symptoms in patients with aortic stenosis and normal left ventricular systolic function usually occur when:
- The valve area is <1.0 cm2.
- The jet velocity is over 4.0 m/sec.
- The 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.
Low Flow, Low Ejection Fraction, or Low Gradient Aortic Stenosis
In adults with AS, the obstruction develops gradually usually over decades. During this time, the left ventricle adapts to the systolic pressure overload through a hypertrophic process. However, if the hypertrophic process is inadequate and the wall thickness does not increase in proportion to the pressure, wall stress increases and the high afterload may cause a decrease in ejection fraction [9]. It is difficult to determine the cause of a low ejection fraction in this scenario and whether it is due to depressed contractility or to excessive afterload. Corrective surgery will be more beneficial and will have better outcome when the low ejection fraction is caused by high afterload than when caused by depressed contractility of the myocardium.
ACC/AHA Guidelines- Classification of the Severity of Aortic Stenosis in Adults (DO NOT EDIT) [10]
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.
Sources
- 2008 Focused Update Incorporated Into the ACC/AHA 2006 Guidelines for the Management of Patients With Valvular Heart Disease [10].
References
- ↑ Lilly LS (editor) (2003). Pathophysiology of Heart Disease (3rd ed. ed.). Lippincott Williams & Wilkins. ISBN 0-7817-4027-4.
- ↑ Gaasch WH, Levine HJ, Quinones MA, Alexander JK (1976). "Left ventricular compliance: mechanisms and clinical implications". Am J Cardiol. 38 (5): 645–53. PMID 136186.
- ↑ 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.
- ↑ Carabello BA (2002). "Clinical practice. Aortic stenosis". N Engl J Med. 346 (9): 677–82. doi:10.1056/NEJMcp010846. PMID 11870246.
- ↑ Jin XY, Pepper JR, Gibson DG (1996). "Effects of incoordination on left ventricular force-velocity relation in aortic stenosis". Heart. 76 (6): 495–501. PMC 484601. PMID 9014797.
- ↑ 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.
- ↑ {{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.}}
- ↑ Faggiano P, Aurigemma GP, Rusconi C, Gaasch WH (1996). "Progression of valvular aortic stenosis in adults: literature review and clinical implications". Am Heart J. 132 (2 Pt 1): 408–17. PMID 8701905.
- ↑ Rydén L (1988). "Noninvasive techniques in the evaluation of the arrhythmogenic effects". Eur Heart J. 9 Suppl B: 19–23. PMID 3286263.
- ↑ 10.0 10.1 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.