Echocardiographic Progression of Calcific Aortic Valve Disease in Patients with Preexisting Aortic Valve Sclerosis

Objective We aimed to evaluate echocardiographic parameters to predict CAVD progression. Background Calcific aortic valve disease (CAVD) ranges from aortic valve sclerosis (ASc) with no functional impairment of the aortic valve to severe aortic stenosis (AS). It remains uncertain, which patients with ASc are at particular high risk of developing AS. Methods We included a total of 153 patients with visual signs of ASc and peak flow velocity (Vmax.) below 2.5m/s at baseline echocardiography. Progression of CAVD to AS was defined as an increase of the Vmax. >= 2.5m/s with a delta of >= 0.1m/s; stable ASc complied with a Vmax. below 2.5m/s and a delta < 0.1m/s. Finally, we compared clinical and echocardiographic parameters between these two groups. Results The mean age at baseline was 73.5 (+- 8.2) years and 66.7% were of male gender. After a mean follow-up of 1463 days, 57 patients developed AS, while 96 patients remained in the ASc group. The AS group showed significantly more calcification (p < 0.001) and thickening (p < 0.001) of the aortic valve cusps at baseline, although hemodynamics showed no evidence of AS in both groups (ASc group: Vmax. 1.6 +- 0.3 m/s versus AS group: Vmax. 1.9 +- 0.3 m/s; p < 0.001). Advanced calcification (OR (95% CI): 4.8 (1.5-15.9); p = 0.009) and a cusp thickness > 0.26cm (OR (95% CI): 16.6 (5.4-50.7); p < 0.001) were independent predictors for the development of AS. Conclusion The acquisition of simple echocardiographic parameter may help to identify patients at particular high risk of developing AS.

[1]  B. Prendergast,et al.  2021 ESC/EACTS Guidelines for the management of valvular heart disease. , 2021, European heart journal.

[2]  M. Dweck,et al.  Pathophysiology of Aortic Stenosis and Future Perspectives for Medical Therapy. , 2020, Cardiology clinics.

[3]  Eric J Velazquez,et al.  Guidelines for Performing a Comprehensive Transthoracic Echocardiographic Examination in Adults: Recommendations from the American Society of Echocardiography. , 2019, Journal of the American Society of Echocardiography : official publication of the American Society of Echocardiography.

[4]  H. Crijns,et al.  Calcific aortic valve stenosis: hard disease in the heart , 2017, European heart journal.

[5]  D. Rader,et al.  Biomarkers of Calcific Aortic Valve Disease , 2017, Arteriosclerosis, thrombosis, and vascular biology.

[6]  Michael J.A. Williams,et al.  The prevalence, incidence, progression, and risks of aortic valve sclerosis: a systematic review and meta-analysis. , 2014, Journal of the American College of Cardiology.

[7]  B. Iung,et al.  Degenerative calcific aortic stenosis: a natural history , 2012, Heart.

[8]  Jennifer Taylor,et al.  ESC/EACTS Guidelines on the management of valvular heart disease. , 2012, European heart journal.

[9]  K. J. Grande-Allen,et al.  Calcific Aortic Valve Disease : Not Simply a Degenerative Process A Review and Agenda for Research from the National Heart and Lung and Blood Institute Aortic Stenosis Working Group , 2012 .

[10]  R. Sainger,et al.  Insights into the use of biomarkers in calcific aortic valve disease. , 2010, The Journal of heart valve disease.

[11]  K. Teo,et al.  Effect of Lipid Lowering With Rosuvastatin on Progression of Aortic Stenosis: Results of the Aortic Stenosis Progression Observation: Measuring Effects of Rosuvastatin (ASTRONOMER) Trial , 2010, Circulation.

[12]  J. Chambers,et al.  Intensive lipid lowering with simvastatin and ezetimibe in aortic stenosis. , 2008, The New England journal of medicine.

[13]  M. Enriquez-Sarano,et al.  Aortic Valve Calcification: Determinants and Progression in the Population , 2007, Arteriosclerosis, thrombosis, and vascular biology.

[14]  Rosario V. Freeman,et al.  Spectrum of Calcific Aortic Valve Disease: Pathogenesis, Disease Progression, and Treatment Strategies , 2005, Circulation.

[15]  R. Prescott,et al.  A randomized trial of intensive lipid-lowering therapy in calcific aortic stenosis. , 2005, The New England journal of medicine.

[16]  P. Faggiano,et al.  Progression of aortic valve sclerosis to aortic stenosis. , 2003, The American journal of cardiology.

[17]  M. Enriquez-Sarano,et al.  Association of cholesterol levels, hydroxymethylglutaryl coenzyme-A reductase inhibitor treatment, and progression of aortic stenosis in the community. , 2002, Journal of the American College of Cardiology.

[18]  I. Kronzon,et al.  The risk of the development of aortic stenosis in patients with "benign" aortic valve thickening. , 2002, Archives of internal medicine.

[19]  Bonnie K. Lind,et al.  Association of aortic-valve sclerosis with cardiovascular mortality and morbidity in the elderly. , 1999, The New England journal of medicine.

[20]  D. Levy,et al.  Prediction of coronary heart disease using risk factor categories. , 1998, Circulation.

[21]  J. Lodder,et al.  Cardiac valve calcification: characteristics of patients with calcification of the mitral annulus or aortic valve , 1997, Heart.

[22]  Bonnie K. Lind,et al.  Clinical factors associated with calcific aortic valve disease. Cardiovascular Health Study. , 1997, Journal of the American College of Cardiology.

[23]  T. Strandberg,et al.  Factors associated with calcific aortic valve degeneration in the elderly. , 1994, European heart journal.

[24]  C. Otto,et al.  Hemodynamic progression of aortic stenosis in adults assessed by Doppler echocardiography. , 1989, Journal of the American College of Cardiology.

[25]  W. Aronow,et al.  Correlation of serum lipids, calcium, and phosphorus, diabetes mellitus and history of systemic hypertension with presence or absence of calcified or thickened aortic cusps or root in elderly patients. , 1987, The American journal of cardiology.