Aortic stenosis
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《英国医生杂志》
Is common, but often unrecognised
Aortic valve disease is common. In Western populations, about 25% of people aged over 65 have aortic sclerosis, and 3% over 75 have severe stenosis.1 In 2003, 6028 aortic valve operations were done in Britain and Ireland compared with 25 277 for isolated coronary disease.2 Despite this the diagnosis may often be missed. Probably half are still diagnosed at postmortem examination, and 5% of operations are performed at end stage.3 Unrecognised aortic stenosis is an important cause of anaesthetic and obstetric mortality.
The overwhelming cause of aortic valve disease in Europe is calcific degenerative disease, and about 2% of the population have congenitally bicuspid aortic valves. Rheumatic disease is now rare. Stenosis is differentiated from sclerosis, when a restriction of cusp movement and a raised transaortic peak velocity are seen on echocardiography. Around 16% of patients with sclerosis progress to stenosis in seven years.4 The early lesions of calcific degenerative disease resemble atheroma of the coronary artery. Many of the risk factors for aortic stenosis are common to other atherosclerotic processes, and one would expect treatment with statins to reduce the rate of progression. However, a recent, small, randomised study of atorvastatin was negative.5 6 Aortic valve disease is also a marker for coronary disease and coronary events. The incidence of myocardial infarction is 6.0% over five years in septuagenarians with normal aortic valves, 8.6% with aortic sclerosis, and 11.3% with aortic stenosis.7 Current randomised trials, including the simvastatin and ezetimibe in aortic stenosis (SEAS) study will test the effect of lipid lowering on both cardiovascular events and the progression of aortic stenosis.
One reason for failing to make a diagnosis is that the clinical signs can be difficult to interpret. Although recommended indications for echocardiography exclude soft systolic flow murmurs,8 the perceived grade of the murmur may not always reflect the severity of the disease.9 All typical textbook guides are of limited value, particularly when the examiner is inexperienced or does not have specialist training in cardiology.9 A normal or high blood pressure with a normal pulse pressure is often used to dismiss the possibility of severe aortic stenosis. However, only 7% of patients referred for surgery have a pulse pressure of less than 35 mm Hg, and the second sound and carotid upstroke may also be normal.9 The signs of aortic stenosis were originally described in young patients when the dominant cause was rheumatic disease. Calcific degenerative disease in older people is often associated with systemic hypertension, coronary disease, and arteriosclerosis, all of which can confound the effects of aortic stenosis on the circulation and therefore modify the clinical signs.
Another reason for failing to recognise aortic stenosis is that most patients have a long asymptomatic period and may therefore not seek medical attention. During this period, the mortality is low. Guidelines recommend surgery when symptoms develop since mortality then rises sharply. The median survival is 4.5 years with exertional chest pain, 2.6 years with exertional dizziness, and one year with overt heart failure.10 Around 10-15% of patients die soon after the onset of symptoms, giving little time to make the diagnosis and organise surgery.
The aim should therefore be to make the diagnosis while the patient is still apparently asymptomatic. For those who are truly asymptomatic, echocardiography is increasingly being used to predict the likely onset of symptoms so as to plan elective surgery. The use of blood testing for brain natriuretic peptide is also being explored. Most patients should also have a treadmill exercise test because unexpected symptoms will show up in up to half of them.11 Symptoms may not be apparent in daily life because the patient may be sedentary or may limit exercise to avoid symptoms. In many centres, aortic stenosis is still regarded as a contraindication rather than an indication for exercise testing.
In view of the frequency and clinical importance of silent aortic stenosis, we should consider national screening strategies and ways of ensuring that patients with noteworthy murmurs have echocardiography. We need also to develop specialist clinical experience in aortic but also other types of valve disease since diagnostic formulations, treatment plans, and surgery may often be difficult. Aortic valve disease is under-recognised politically as well as clinically. It is not yet covered properly a national strategy document from the National Institute for Clinical Excellence (NICE) or any other organisation. As our population ages, the prevalence of aortic stenosis inevitably rises. By 2020, about 3.5 million of a total population of 54 million in England can be expected to have aortic sclerosis and 150 000 to have severe aortic stenosis.12 We should prepare for this epidemic now.
John Chambers, consultant cardiologist
Guy's and St Thomas' Hospitals, London SE1 7EH (jboydchambers@aol.com)
Competing interests: None declared.
References
Lindroos M, Kupari M, Heikkala J, Tilvis R. Prevalence of aortic valve abnormalities in the elderly: an echocardiographic study of a random population sample. J Am Coll Cardiol 1993;21: 1220-5.
Keogh BE, Kinsman R. Fifth national adult cardiac surgical database report. London: Society of Cardiothoracic Surgeons of Great Britain and Ireland, 2003.
Connolly HM, Oh JK, Orszulak TA, Osborn SL, Roger VL, Hodge DO, et al. Aortic valve replacement for aortic stenosis with severe left ventricular dysfunction. Prognostic indicators. Circulation 1997;95: 2395-400.
Cosmi JE, Tunick PA, Rosenzweig BP, Freedberg RS, Katz ES. The risk of development of aortic stenosis in patients with `benign' aortic valve thickening. Arch Int Med 2002;162: 2345-7.
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.
Cowell SJ, Newby DE, White A, Burton J, Reid J, Northridge DB, et al. Intensive lipid-lowering therapy does not halt the progression of calcific aortic stenosis. Circulation 2004 ()
Otto CM, Lind BK, Klitzman 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.
Cheitlin MD, Alpert JS, Armstrong WF, Aurigemma JP, Beller GA, Bierman FZ, et al. ACC/AHA guidelines for the clinical application of echocardiography: executive summary. J Am Coll Cardiol 1997;29: 862-79.
Das P, Pocock C, Chambers J. The patient with a systolic murmur: severe aortic stenosis may be missed during cardiovascular examination. Quart J Med 2000;93: 685-8.
Horstkotte D, Loogen F. The natural history of aortic valve stenosis. Eur Heart J 1988;9(suppl E): 57-64.
Carabello BA. Aortic stenosis. N Engl J Med 2002;346: 677-82.
Government Actuary's Department. 2003 figures. www.gad.gov.uk/Population/index.asp (accessed 4 Mar 05).
Aortic valve disease is common. In Western populations, about 25% of people aged over 65 have aortic sclerosis, and 3% over 75 have severe stenosis.1 In 2003, 6028 aortic valve operations were done in Britain and Ireland compared with 25 277 for isolated coronary disease.2 Despite this the diagnosis may often be missed. Probably half are still diagnosed at postmortem examination, and 5% of operations are performed at end stage.3 Unrecognised aortic stenosis is an important cause of anaesthetic and obstetric mortality.
The overwhelming cause of aortic valve disease in Europe is calcific degenerative disease, and about 2% of the population have congenitally bicuspid aortic valves. Rheumatic disease is now rare. Stenosis is differentiated from sclerosis, when a restriction of cusp movement and a raised transaortic peak velocity are seen on echocardiography. Around 16% of patients with sclerosis progress to stenosis in seven years.4 The early lesions of calcific degenerative disease resemble atheroma of the coronary artery. Many of the risk factors for aortic stenosis are common to other atherosclerotic processes, and one would expect treatment with statins to reduce the rate of progression. However, a recent, small, randomised study of atorvastatin was negative.5 6 Aortic valve disease is also a marker for coronary disease and coronary events. The incidence of myocardial infarction is 6.0% over five years in septuagenarians with normal aortic valves, 8.6% with aortic sclerosis, and 11.3% with aortic stenosis.7 Current randomised trials, including the simvastatin and ezetimibe in aortic stenosis (SEAS) study will test the effect of lipid lowering on both cardiovascular events and the progression of aortic stenosis.
One reason for failing to make a diagnosis is that the clinical signs can be difficult to interpret. Although recommended indications for echocardiography exclude soft systolic flow murmurs,8 the perceived grade of the murmur may not always reflect the severity of the disease.9 All typical textbook guides are of limited value, particularly when the examiner is inexperienced or does not have specialist training in cardiology.9 A normal or high blood pressure with a normal pulse pressure is often used to dismiss the possibility of severe aortic stenosis. However, only 7% of patients referred for surgery have a pulse pressure of less than 35 mm Hg, and the second sound and carotid upstroke may also be normal.9 The signs of aortic stenosis were originally described in young patients when the dominant cause was rheumatic disease. Calcific degenerative disease in older people is often associated with systemic hypertension, coronary disease, and arteriosclerosis, all of which can confound the effects of aortic stenosis on the circulation and therefore modify the clinical signs.
Another reason for failing to recognise aortic stenosis is that most patients have a long asymptomatic period and may therefore not seek medical attention. During this period, the mortality is low. Guidelines recommend surgery when symptoms develop since mortality then rises sharply. The median survival is 4.5 years with exertional chest pain, 2.6 years with exertional dizziness, and one year with overt heart failure.10 Around 10-15% of patients die soon after the onset of symptoms, giving little time to make the diagnosis and organise surgery.
The aim should therefore be to make the diagnosis while the patient is still apparently asymptomatic. For those who are truly asymptomatic, echocardiography is increasingly being used to predict the likely onset of symptoms so as to plan elective surgery. The use of blood testing for brain natriuretic peptide is also being explored. Most patients should also have a treadmill exercise test because unexpected symptoms will show up in up to half of them.11 Symptoms may not be apparent in daily life because the patient may be sedentary or may limit exercise to avoid symptoms. In many centres, aortic stenosis is still regarded as a contraindication rather than an indication for exercise testing.
In view of the frequency and clinical importance of silent aortic stenosis, we should consider national screening strategies and ways of ensuring that patients with noteworthy murmurs have echocardiography. We need also to develop specialist clinical experience in aortic but also other types of valve disease since diagnostic formulations, treatment plans, and surgery may often be difficult. Aortic valve disease is under-recognised politically as well as clinically. It is not yet covered properly a national strategy document from the National Institute for Clinical Excellence (NICE) or any other organisation. As our population ages, the prevalence of aortic stenosis inevitably rises. By 2020, about 3.5 million of a total population of 54 million in England can be expected to have aortic sclerosis and 150 000 to have severe aortic stenosis.12 We should prepare for this epidemic now.
John Chambers, consultant cardiologist
Guy's and St Thomas' Hospitals, London SE1 7EH (jboydchambers@aol.com)
Competing interests: None declared.
References
Lindroos M, Kupari M, Heikkala J, Tilvis R. Prevalence of aortic valve abnormalities in the elderly: an echocardiographic study of a random population sample. J Am Coll Cardiol 1993;21: 1220-5.
Keogh BE, Kinsman R. Fifth national adult cardiac surgical database report. London: Society of Cardiothoracic Surgeons of Great Britain and Ireland, 2003.
Connolly HM, Oh JK, Orszulak TA, Osborn SL, Roger VL, Hodge DO, et al. Aortic valve replacement for aortic stenosis with severe left ventricular dysfunction. Prognostic indicators. Circulation 1997;95: 2395-400.
Cosmi JE, Tunick PA, Rosenzweig BP, Freedberg RS, Katz ES. The risk of development of aortic stenosis in patients with `benign' aortic valve thickening. Arch Int Med 2002;162: 2345-7.
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.
Cowell SJ, Newby DE, White A, Burton J, Reid J, Northridge DB, et al. Intensive lipid-lowering therapy does not halt the progression of calcific aortic stenosis. Circulation 2004 ()
Otto CM, Lind BK, Klitzman 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.
Cheitlin MD, Alpert JS, Armstrong WF, Aurigemma JP, Beller GA, Bierman FZ, et al. ACC/AHA guidelines for the clinical application of echocardiography: executive summary. J Am Coll Cardiol 1997;29: 862-79.
Das P, Pocock C, Chambers J. The patient with a systolic murmur: severe aortic stenosis may be missed during cardiovascular examination. Quart J Med 2000;93: 685-8.
Horstkotte D, Loogen F. The natural history of aortic valve stenosis. Eur Heart J 1988;9(suppl E): 57-64.
Carabello BA. Aortic stenosis. N Engl J Med 2002;346: 677-82.
Government Actuary's Department. 2003 figures. www.gad.gov.uk/Population/index.asp (accessed 4 Mar 05).