Korean Circ J.  2011 Nov;41(11):649-653. 10.4070/kcj.2011.41.11.649.

Predictors of Echocardiographic Progression in Patients With Mild Aortic Stenosis

• Seo JS
• Kang DH
• Kim DH
• Song JM
• Song JK

• KMID: 2225072
• DOI: http://doi.org/10.4070/kcj.2011.41.11.649

Abstract

BACKGROUND AND OBJECTIVES
The factors related to the progression of mild aortic stenosis (AS) remain unknown. We wanted to evaluate the long-term outcomes and predictors of echocardiographic progression in patients with mild AS.
SUBJECTS AND METHODS
We prospectively included 103 consecutive asymptomatic patients (62.1+/-11.9 years, 31 males) with mild AS. Mild AS was defined as aortic valve (AV) thickening accompanied by a peak aortic jet velocity (AV Vmax) > or =2.0 and <3.0 m/sec, and rapid progression of AS was defined as an average annual increase in the AV Vmax > or =0.2 m/sec, and cardiac events were defined as cardiac death or AV replacement.
RESULTS
During a median echocardiographic follow-up time of 6.0 years, the average change in the AV Vmax was 0.08+/-0.10 m/sec per year. The rate of progression was significantly associated with age, moderate-to-severe AV calcification and the baseline AV Vmax, but not with the serum cholesterol level. The baseline AV Vmax (2.6+/-0.3 m/sec vs. 2.2+/-0.3 m/sec, respectively, p<0.001) and the incidence of moderate-to-severe AV calcification (92.9% vs. 36.5%, respectively, p<0.001) were significantly higher in the rapid progression group than in the slow progression group. The 7-year cardiac event-free survival rate was lower in the rapid progression group than in the slow pro-gression group (87.5+/-8.3% vs. 100%, respectively).
CONCLUSION
The progression of AS was slower than expected and it was related to age, the baseline AV Vmax and AV calcification. Because of the marked individual variability in progression, the patients showing rapid progression of AS need closer follow-up.

Keyword

Aortic stenosis; Predictors; Prognosis

MeSH Terms

Aortic Valve
Aortic Valve Stenosis
Cholesterol
Death
Disease-Free Survival
Follow-Up Studies
Humans
Incidence
Prognosis
Prospective Studies
Cholesterol

Figure

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  Fig. 1 Association between the patients' age, the baseline aortic jet velocity and the annual change in the aortic jet velocity.

Reference

1. Olsson M, Dalsgaard CJ, Haegerstrand A, Rosenqvist M, Rydén L, Nilsson J. Accumulation of T lymphocytes and expression of interleukin-2 receptors in nonrheumatic stenotic aortic valves. J Am Coll Cardiol. 1994. 23:1162–1170.

2. Otto CM, Kuusisto J, Reichenbach DD, Gown AM, O'Brien KD. Characterization of the early lesion of degenerative valvular aortic stenosis: histological and immunohistochemical studies. Circulation. 1994. 90:844–853.

3. O'Brien KD, Reichenbach DD, Marcovina SM, Kuusisto J, Alpers CE, Otto CM. Apolipoproteins B, (a), and E accumulate in the morphologically early lesion of 'degenerative' valvular aortic stenosis. Arterioscler Thromb Vasc Biol. 1996. 16:523–532.

4. Olsson M, Thyberg J, Nilsson J. Presence of oxidized low density lipoprotein in nonrheumatic stenotic aortic valves. Arterioscler Thromb Vasc Biol. 1999. 19:1218–1222.

5. Cowell SJ, Newby DE, Prescott RJ, et al. A randomized trial of intensive lipid-lowering therapy in calcific aortic stenosis. N Engl J Med. 2005. 352:2389–2397.

6. Rossebø AB, Pedersen TR, Boman K, et al. Intensive lipid lowering with simvastatin and ezetimibe in aortic stenosis. N Engl J Med. 2008. 359:1343–1356.

7. Chan KL, Teo K, Dumesnil JG, Ni A, Tam J. Effect of lipid lowering with rosuvastatin on progression of aortic stenosis: results of the aortic stenosis progression observation: measuring effects of rosuvastatin (astronomer) trial. Circulation. 2010. 121:306–314.

8. Owens DS, Otto CM. Is it time for a new paradigm in calcific aortic valve disease? JACC Cardiovasc Imaging. 2009. 2:928–930.

9. Ngo DT, Sverdlov AL, Willoughby SR, et al. Determinants of occurrence of aortic sclerosis in an aging population. JACC Cardiovasc Imaging. 2009. 2:919–927.

10. 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.

11. Kang DH, Park SJ, Rim JH, et al. Early surgery versus conventional treatment in asymptomatic very severe aortic stenosis. Circulation. 2010. 121:1502–1509.

12. Otto CM, Burwash IG, Legget ME, et al. Prospective study of asymptomatic valvular aortic stenosis: clinical, echocardiographic, and exercise predictors of outcome. Circulation. 1997. 95:2262–2270.

13. Schiller NB, Shah PM, Crawford M, et al. Recommendations for quantitation of the left ventricle by two-dimensional echocardiography: American society of echocardiography committee on standards, subcommittee on quantitation of two-dimensional echocardiograms. J Am Soc Echocardiogr. 1989. 2:358–367.

14. Devereux RB, Alonso DR, Lutas EM, et al. Echocardiographic assessment of left ventricular hypertrophy: comparison to necropsy findings. Am J Cardiol. 1986. 57:450–458.

15. Skjaerpe T, Hegrenaes L, Hatle L. Noninvasive estimation of valve area in patients with aortic stenosis by Doppler ultrasound and two-dimensional echocardiography. Circulation. 1985. 72:810–818.

16. Rosenhek R, Binder T, Porenta G, et al. Predictors of outcome in severe, asymptomatic aortic stenosis. N Engl J Med. 2000. 343:611–617.

17. Aronow WS, Ahn C, Kronzon I, Goldman ME. Association of coronary risk factors and use of statins with progression of mild valvular aortic stenosis in older persons. Am J Cardiol. 2001. 88:693–695.

18. 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. 104:2205–2209.

19. 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. 40:1723–1730.

20. Rosenhek R, Rader F, Loho N, et al. Statins but not angiotensin-converting enzyme inhibitors delay progression of aortic stenosis. Circulation. 2004. 110:1291–1295.

21. Ryu DR, Park SJ, Han H, et al. Progression rate of aortic valve stenosis in Korean patients. J Cardiovasc Ultrasound. 2010. 18:127–133.

22. Messika-Zeitoun D, Aubry MC, Detaint D, et al. Evaluation and clinical implications of aortic valve calcification measured by electron-beam computed tomography. Circulation. 2004. 110:356–362.

23. Caira FC, Stock SR, Gleason TG, et al. Human degenerative valve disease is associated with up-regulation of low-density lipoprotein receptor-related protein 5 receptor-mediated bone formation. J Am Coll Cardiol. 2006. 47:1707–1712.

24. Mohty D, Pibarot P, Després JP, et al. Association between plasma LDL particle size, valvular accumulation of oxidized LDL, and inflammation in patients with aortic stenosis. Arterioscler Thromb Vasc Biol. 2008. 28:187–193.

25. Deutscher S, Rockette HE, Krishnaswami V. Diabetes and hypercholesterolemia among patients with calcific aortic stenosis. J Chronic Dis. 1984. 37:407–415.