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The spectrum of aortic stenosis

An article from the e-journal of the ESC Council for Cardiology Practice

The spectrum of aortic stenosis ranges from severe stenosis to aortic sclerosis without haemodynamic implications. Recent studies also show that mild and moderate aortic stenosis are not a benign disease and help to identify high-risk patients.

Valvular Heart Disease


Aortic stenosis is the most frequent valvular heart disease in Europe and in the United States. With the aging population the incidence of calcific aortic valve disease is further increasing. Its spectrum ranges from severe symptomatic stenosis on one side to aortic sclerosis without haemodynamic implications on the other. In between are the asymptomatic patients with severe, moderate and mild aortic stenosis. The incidence of aortic stenosis in the population of advanced age is estimated to be between 2 and 9%, aortic sclerosis is present in up to 25% of patients over 65 years of age (1).

The poor outcome of patients with severe symptomatic aortic stenosis has been well documented in the past (2). After the onset of symptoms, the average survival has been reported to be less than 2 to 3 years. On the other hand, current results of aortic valve replacement for acquired aortic stenosis have been shown to be excellent. Thus, it has generally been accepted that surgery must be strongly recommended for patients with critical aortic stenosis who develop symptoms.

In contrast, the management of asymptomatic patients with severe aortic stenosis remains a matter of controversy. Although it has been shown that it is relatively safe to delay surgery until symptoms develop, there are a number of concerns when following patients with severe aortic stenosis conservatively. The following arguments are in favor of early elective surgery: Risk of sudden cardiac death, risk of death while on the waiting list, risk of developing irreversible myocardial damage, rapid development of symptoms and an increased operative risk in severely symptomatic patients. On the other hand the following arguments argue against such an approach: the risk of surgery, prosthetic valve related long-term morbidity and mortality and the eventual need for reoperation. Thus it is obvious that surgery cannot be generally recommended and that the decisions have to be individualised. In particular an appropriate risk stratification individually selecting those patients who are likely to benefit from early elective surgery is required. The combination of calcification and rapid haemodynamic progression identifies a patient group at high-risk (3). There is also a role for exercise testing in asymptomatic patients with severe aortic stenosis for risk stratification and in unmasking symptoms. These criteria have also been recognised as class IIa indications for aortic valve surgery by the European guidelines for the treatment of patients with valvular heart disease (4). It has to be emphasised that exercise testing is only appropriate in asymptomatic patients but should definitely not be performed in symptomatic patients.  When properly performed, exercise testing in asymptomatic patients with severe aortic stenosis has been shown to be safe(5).

Mild and moderate aortic stenosis have been considered a benign disease by many physicians and current guidelines recommend relatively long term intervals for follow-up visits. Nevertheless, patients with rapid progression and poor outcome have been observed and more recent studies have shown that mild and moderate aortic stenosis are not a benign disease (6,7). Mild and moderate aortic stenosis are associated with substantial mortality which is in part due to noncardiac causes. It has also been shown that progression to severe, haemodynamically significant stenosis is common and may be more rapid than previously assumed. Particularly patients with significantly calcified aortic valves but also those with coronary artery disease, patients older than 50 years and patients with a rapid haemodynamic progression have a poor outcome (7). These parameters identify high-risk patients who require closer follow-up than is currently recommended. There is not yet a consensus with regard the required follow-up intervals: in any case they need to be individualised. The peak aortic jet velocity at entry should be considered as it reflects the stage of disease: patients with moderate aortic stenosis will require earlier control exams than patients with mild aortic stenosis. The above mentioned risk factors (calcified aortic valve, coronary artery disease, rapid haemodynamic progression) allow further risk stratification. Some of these high-risk patients might require yearly control exams. Knowing that a rapid progression to severe aortic stenosis may occur, it is important to instruct even patients with mild and moderate aortic stenosis about the typical symptoms of severe aortic stenosis and the necessity to immediately refer to a physician in case that they appear.
There is a perspective that we might be able to slow aortic stenosis progression. Recent retrospective studies suggest that statins may be beneficial in this regard (8,9). However we will have to wait for confirmation in prospective randomised trials until such a treatment can be generally recommended. In the meantime we must avoid the risks of unnecessary delays in early recognition and appropriate treatment of patients who progress to have haemodynamically significant aortic stenosis.
Finally it has to be noted that even the presence of aortic valve sclerosis without haemodynamic obstruction to blood flow is associated with a significantly increased mortality (1).

The content of this article reflects the personal opinion of the author/s and is not necessarily the official position of the European Society of Cardiology.

References


1. Otto CM, Lind BK, Kitzman DW, Gersh BJ, Siscovick DS. Association of aortic-valve sclerosis with cardiovascular mortality and morbidity in the elderly. N Engl J Med 1999;341:142-7
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=10403851

2. Ross J, Jr., Braunwald E. Aortic stenosis. Circulation 1968;38:61-7.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=4894151

3. Rosenhek R, Binder T, Porenta G, et al. Predictors of outcome in severe, asymptomatic aortic stenosis. N Engl J Med 2000;343:611-7.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=10965007

4. Iung B, Gohlke-Barwolf C, Tornos P, et al. Recommendations on the management of the asymptomatic patient with valvular heart disease. Eur Heart J 2002;23:1252-66.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=12698958

5. Amato MC, Moffa PJ, Werner KE, Ramires JA. Treatment decision in asymptomatic aortic valve stenosis: role of exercise testing. Heart 2001;86:381-6.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=11559673

6. Otto CM, Burwash IG, Legget ME, et al. Prospective study of asymptomatic valvular aortic stenosis. Clinical, echocardiographic, and exercise predictors of outcome. Circulation 1997;95:2262-70.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=9142003

7. Rosenhek R, Klaar U, Schemper M, et al. Mild and moderate aortic stenosis; Natural history and risk stratification by echocardiography. Eur Heart J 2004;25:199-205.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=14972419

8. Bellamy MF, Pellikka PA, Klarich KW, Tajik AJ, Enriquez-Sarano M. Association of cholesterol levels, hydroxymethylglutaryl coenzyme-A reductase inhibitor treatment, and progression of aortic stenosis in the community. J Am Coll Cardiol 2002;40:1723-30.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=12446053

9. Novaro GM, Tiong IY, Pearce GL, Lauer MS, Sprecher DL, Griffin BP. Effect of hydroxymethylglutaryl coenzyme a reductase inhibitors on the progression of calcific aortic stenosis. Circulation 2001;104:2205-9.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=11684632

Notes to editor


Dr. A. R. Rosenhek
Vienna, Austria
Nucleus Member of the ESC Working Group on Valvular Heart Disease

The content of this article reflects the personal opinion of the author/s and is not necessarily the official position of the European Society of Cardiology.