Aortic stenosis natural history, complications and prognosis
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editors-In-Chief: Mohammed A. Sbeih, M.D. [2]; Lakshmi Gopalakrishnan, M.B.B.S. [3]
Overview
Left untreated, aortic valve stenosis can lead to angina, syncope, congestive heart failure, atrial fibrillation, endocarditis, and sudden cardiac death. Surgical treatment of aortic stenosis also carries risks and potential complications including vascular complications and mitral valve injury.
Natural History
Degenerative Calcific Aortic Stenosis
Aortic stenosis due to degeneration of a calcified aortic valve has a prolonged latent period during which time symptoms may be minimal or even lacking [1]. The average rate of progression in valvular aortic stenosis, once moderate stenosis is present and symptomatic, is a decrease in valve area of 0.1 cm2 per year [2][1]. Also on average, there is an increase in the jet velocity of 0.3 m / second per year and an increase in the mean pressure gradient of 7 mm Hg per year [3] [4][5]. There is tremendous individual variability in the rate of progression of aortic 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 are associated with more rapid rates of aortic stenosis progression.
Bicuspid Aortic Valve Disease
Bicuspid aortic valve stenosis presents one to two decades earlier. The rate of progression of degenerative aortic stenosis can be faster than in those with congenital or rheumatic disease [6]. Bicuspid aortic valve, during childhood functions without any significant pressure gradient. However, the thickening and calcification of the valves may be detectable pathologically and on echocardiography by second decade[7]. This progresses to aortic stenosis requiring operative correction in approximately 75% of cases.[8][9]
Bicuspid aortic stenosis progressively leads to heart failure, arrythmias, angina and other symptoms which generally manifests between 40 to 60 years of age which is relatively younger to manifestation of aortic stenosis otherwise.[8] However, children who develop early pathologic changes in bicuspid aortic valve are more likely to develop aortic insufficiency than stenosis.
Aortic Sclerosis
Aortic sclerosis (defined as aortic valve thickening without obstruction to ventricular outflow) may progress to narrowing of the aortic valve or aortic stenosis. If the pulse pressure or upstroke of the pulse diminishes in the patient with aortic sclerosis, this can be a sign of progression to aortic stenosis.
Complications
Degenerative Calcific Aortic Stenosis
If left untreated, aortic stenosis may lead to complications such as angina, syncope, or heart failure. A complete list of complications of aortic stenosis includes the following:
- Angina
- Arrhythmias
- Atrial fibrillation
- Bleeding. Impaired platelet function and coagulation abnormalities as decreased levels of Von Willebrand factor can be seen in most patients with severe AS. This resolves after valve replacement procedure. 20% of patients have clinical bleeding, most often epistaxis or ecchymoses [10]
- Congestive heart failure, particularly left-sided heart failure or systolic dysfunction
- Endocarditis
- Fainting or syncope. Since the stenosed aortic valve may limit the heart's output, people with aortic stenosis are at risk of syncope and dangerously low blood pressure should they use any of a number of common medications. Ironically, these same medicines are used to treat a variety of cardiovascular diseases, many of which may co-exist with aortic stenosis. Examples include nitroglycerin, nitrates, ACE inhibitors, terazosin (Hytrin), and hydralazine. Note that all of these substances lead to peripheral vasodilation. Normally, however, in the absence of aortic stenosis, the heart is able to increase its output and thereby offset the effect of the dilated blood vessels. In some cases of aortic stenosis, however, due to the obstruction of blood flow out of the heart caused by the stenosed aortic valve, cardiac output cannot be increased. Low blood pressure or syncope may ensue.
- Left ventricular hypertrophy
- Myocardial infarction
Bicuspid Aortic Valve Disease
Bicuspid aortic valve disease is associated with the following complications:
- Aortic stenosis in the majority (75%) of patients.[8]
- Aortic insufficiency[11][12]
- Endocarditis[13]
- Aortic aneurysm[9]
- Aortic dissection[9]
- Sudden death can occur in children during and immediately after exertion especially among those with pressure gradient > 50 mmHg across the aortic valve.[14]
Prognosis
Asymptomatic Patients
The prognosis of patients with aortic stenosis who do not have symptoms is quite good [15]. The annual mortality rate is < 1% per year in asymptomatic patients. Only 4% of sudden cardiac deaths that occur in patients with aortic stenosis occur in those patients who are asymptomatic.
Symptomatic Patients
Medical treatment of newly diagnosed moderate to severe symptomatic aortic stenosis is associated with a 25% mortality at one year, and a 50% mortality at two years. Half the deaths are due to sudden cardiac death [16] [17].
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 [16][18][19].
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.
It should be noted that left ventricular contractile reserve is a better predictor of surgical outcomes than markers of stenosis. Aortic valve surgery is indicated if there is severe AS along with an increase in the systolic velocity integral by >20% during a dobutamine infusion.
References
- ↑ 1.0 1.1 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.
- ↑ Zoghbi WA, Enriquez-Sarano M, Foster E, Grayburn PA, Kraft CD, Levine RA; et al. (2003). "Recommendations for evaluation of the severity of native valvular regurgitation with two-dimensional and Doppler echocardiography". J Am Soc Echocardiogr. 16 (7): 777–802. doi:10.1016/S0894-7317(03)00335-3. PMID 12835667.
- ↑ Cheitlin MD, Gertz EW, Brundage BH, Carlson CJ, Quash JA, Bode RS (1979). "Rate of progression of severity of valvular aortic stenosis in the adult". Am Heart J. 98 (6): 689–700. PMID 495418.
- ↑ Jonasson R, Jonsson B, Nordlander R, Orinius E, Szamosi A (1983). "Rate of progression of severity of valvular aortic stenosis". Acta Med Scand. 213 (1): 51–4. PMID 6829320.
- ↑ Peter M, Hoffmann A, Parker C, Lüscher T, Burckhardt D (1993). "Progression of aortic stenosis. Role of age and concomitant coronary artery disease". Chest. 103 (6): 1715–9. PMID 8404089.
- ↑ Rosenhek R, Binder T, Porenta G, Lang I, Christ G, Schemper M; et al. (2000). "Predictors of outcome in severe, asymptomatic aortic stenosis". N Engl J Med. 343 (9): 611–7. doi:10.1056/NEJM200008313430903. PMID 10965007.
- ↑ Beppu S, Suzuki S, Matsuda H, Ohmori F, Nagata S, Miyatake K (1993). "Rapidity of progression of aortic stenosis in patients with congenital bicuspid aortic valves". The American Journal of Cardiology. 71 (4): 322–7. PMID 8427176. Unknown parameter
|month=ignored (help);|access-date=requires|url=(help) - ↑ 8.0 8.1 8.2 Fenoglio JJ, McAllister HA, DeCastro CM, Davia JE, Cheitlin MD (1977). "Congenital bicuspid aortic valve after age 20". The American Journal of Cardiology. 39 (2): 164–9. PMID 835475. Unknown parameter
|month=ignored (help);|access-date=requires|url=(help) - ↑ 9.0 9.1 9.2 Lewin MB, Otto CM (2005). "The bicuspid aortic valve: adverse outcomes from infancy to old age". Circulation. 111 (7): 832–4. doi:10.1161/01.CIR.0000157137.59691.0B. PMID 15723989. Retrieved 2012-04-10. Unknown parameter
|month=ignored (help) - ↑ Vincentelli A, Susen S, Le Tourneau T, Six I, Fabre O, Juthier F; et al. (2003). "Acquired von Willebrand syndrome in aortic stenosis". N Engl J Med. 349 (4): 343–9. doi:10.1056/NEJMoa022831. PMID 12878741.
- ↑ Keane MG, Wiegers SE, Plappert T, Pochettino A, Bavaria JE, Sutton MG (2000). "Bicuspid aortic valves are associated with aortic dilatation out of proportion to coexistent valvular lesions". Circulation. 102 (19 Suppl 3): III35–9. PMID 11082359. Retrieved 2012-04-10. Unknown parameter
|month=ignored (help) - ↑ Roberts WC, Morrow AG, McIntosh CL, Jones M, Epstein SE (1981). "Congenitally bicuspid aortic valve causing severe, pure aortic regurgitation without superimposed infective endocarditis. Analysis of 13 patients requiring aortic valve replacement". The American Journal of Cardiology. 47 (2): 206–9. PMID 7468467. Unknown parameter
|month=ignored (help);|access-date=requires|url=(help) - ↑ Gersony WM, Hayes CJ, Driscoll DJ, Keane JF, Kidd L, O'Fallon WM, Pieroni DR, Wolfe RR, Weidman WH (1993). "Bacterial endocarditis in patients with aortic stenosis, pulmonary stenosis, or ventricular septal defect". Circulation. 87 (2 Suppl): I121–6. PMID 8425318. Unknown parameter
|month=ignored (help);|access-date=requires|url=(help) - ↑ Keane JF, Driscoll DJ, Gersony WM, Hayes CJ, Kidd L, O'Fallon WM, Pieroni DR, Wolfe RR, Weidman WH (1993). "Second natural history study of congenital heart defects. Results of treatment of patients with aortic valvar stenosis". Circulation. 87 (2 Suppl): I16–27. PMID 8425319. Unknown parameter
|month=ignored (help);|access-date=requires|url=(help) - ↑ Lancellotti P, Magne J, Donal E, et al. Clinical outcome in asymptomatic severe aortic stenosis insights from the new proposed aortic stenosis grading classification. J Am Coll Cardiol. Jan 17 2012;59(3):235-43.
- ↑ 16.0 16.1 Ross J, Braunwald E (1968). "Aortic stenosis". Circulation. 38 (1 Suppl): 61–7. PMID 4894151.
- ↑ Chizner MA, Pearle DL, deLeon AC (1980). "The natural history of aortic stenosis in adults". Am Heart J. 99 (4): 419–24. PMID 7189084.
- ↑ 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.
- ↑ 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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