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. 2016 Sep-Oct;113(5):401–406.

Calcific Aortic Stenosis: New Approaches to an Old Disease

Jerry D Kennett 1,✉, Benjamin Z Galper 2
PMCID: PMC6139823  PMID: 30228508

Abstract

Calcific aortic valve disease affects up to 25% of all adults over 65 years of age, with most only having focal valve thickening called aortic sclerosis. However, up to 5% of older adults have significant aortic stenosis (AS) with some degree of obstruction to left ventricular outflow. 1,3,4,5 Once even mild valve obstruction is present, hemodynamic progression is common, leading to severe symptomatic or asymptomatic AS that eventually requires aortic valve replacement in some fashion. 6,7 With our aging population, an increasing number of patients with AS will be presenting for evaluation and care.

Introduction

Aortic Stenosis is most commonly discovered on the basis of the finding of a systolic murmur on physical exam with echocardiography being the best diagnostic test to confirm aortic valve disease. The standard measures of AS severity are the maximum velocity (Vmax) across the stenotic valve, the mean transaortic pressure gradient (ΔP mean) calculated with the Bernoulli equation, and the functional aortic valve area (AVA) calculated with the continuity equation. Echocardiographic ΔP mean and AVA calculations have been well-validated against invasive measurements and are now the standard of care to diagnose the severity of AS. 1,8,9 Transaortic velocities and gradients vary with volume flow rate and may be misleading in high flow states such as concomitant aortic insufficiency, or low flow rates associated with left ventricular dysfunction, making the aortic valve area a critical measurement in determining the severity of stenosis.

Guidelines

The American College of Cardiology (ACC)/American Heart Association (AHA) have developed guidelines defining the four stages of aortic stenosis.2,10 Stage A defines patients at risk of developing AS such as those with congenital bicuspid valves or those with aortic sclerosis. Stage B is a patient who, by echocardiography, has mild or moderate AS. Stage C refers to a patient who has hemodynamically severe AS without symptoms. Stage D refers to hemodynamically severe AS in a patient with symptoms. Hemodynamically severe AS is defined as a peak aortic jet velocity greater than 400 cm/s or a mean transvalvular pressure gradient greater than 40 mmHg or an aortic valve area (AVA) of less than 1 cm2. The guidelines go on to say that aortic valve replacement for symptomatic, hemodynamically severe aortic stenosis is a Class I recommendation. Aortic valve replacement is a Class IIA recommendation for patients with moderate aortic stenosis (stage B) with an aortic velocity between 300 cm/s and 390 cm/s or a mean pressure gradient between 20 mmHg and 39 mmHg who are undergoing cardiac surgery for other indications.

Asymptomatic hemodynamically severe AS presents a more difficult decision-making process. The ACC/AHA guidelines divide this group into two subcategories. Patients who have asymptomatic severe AS and good left ventricular function with an ejection fraction of greater than 50% are categorized as Group C1 and patients with reduced left ventricular systolic function and hemodynamically severe AS are categorized as Group C2. Group C2 also have a Class I recommendation for aortic valve replacement. For patients with asymptomatic hemodynamically severe AS and normal left ventricular systolic function with an ejection fraction greater than 50%, the stage C1 group, aortic valve replacement should be considered with the Class I recommendation if the patient is scheduled to undergo other cardiac surgery or if symptoms are unmasked by additional testing, such as stress testing. For stage C1 patients who are, indeed, asymptomatic, even after stress testing, a plan of watchful waiting is reasonable with clinical follow-up every 6 to 12 months, including echocardiography at least yearly.3,11,12

The risk of hemodynamically severe AS is well-documented. Studies have demonstrated that up to 50% of patients will die within the three to five years from the date of diagnosis without intervention. Even in those who are asymptomatic, 70 to 80% of patients will develop symptoms requiring intervention within two years.1, 6, 7,13,14 Several predictors of rapid hemodynamic progression of AS include smoking, dyslipidemia, male sex, diabetes mellitus, hypertension, chronic renal disease, and concomitant coronary artery disease.2,15

Evaluation

Patients with hemodynamically severe AS who, on initial questioning, appear to be asymptomatic should be evaluated further to determine if they are truly asymptomatic if, indeed, they are candidates for either a transcutaneous aortic valve replacement, (TAVR) (procedure or surgical aortic valve replacement (SAVR). The most common first symptom of hemodynamically severe AS is unexplained exertional dyspnea. Stress testing is valuable in these patients. An abnormal exercise stress test in these patients is defined as development of angina, severe dyspnea, presyncope, decreased exercise tolerance, or inadequate increase in systolic blood pressure of less than 20 mmHg. If any of these findings are present, it places these patients in a Class IIA category for proceeding with aortic valve intervention.1,16,17 In addition, measuring levels of brain natriuretic peptide (BNP) in asymptomatic patients may help predict symptom onset as well as postoperative survival, functional status, and LV function; although, exact levels are not currently defined.1

Unfortunately, there is no medical therapy that has been proven to be beneficial in hemodynamically severe AS. Multiple studies have been done to determine if statin therapy would slow the progression of aortic valve sclerosis or mild stenosis. To date, the vast majority of these studies do not show a benefit of statin therapy.18,19

Since the development of symptoms with hemodynamically severe AS predicts a poor prognosis with the associated high mortality rate over the next five years, aortic valve replacement or intervention definitely is indicated in this group of patients. Surgery in such patients improves symptoms and increases life expectancy.14,20,21,22,23 Aortic valve replacement currently is the most common operation for valvular heart disease in North America. Bioprosthetic valves are most commonly recommended for patients over the age of 65, but may be used in some younger patients if they have an extremely active lifestyle or if the risk of chronic anticoagulation creates a problem1,20. The mortality associated with aortic valve replacement has decreased markedly over the past several decades. The STS database reveals a 30-day mortality of under 3% for isolated aortic valve replacement and under 5% for combined aortic valve replacement plus coronary artery bypass surgery.25,26

While SAVR is the mainstay of treatment of symptomatic severe AS, it also entails substantial risks for patients with severe comorbidities, and for patients considered at “extreme” risk, surgery may not be appropriate. In others, technical limitations, such as porcelain aorta, prior significant mediastinal radiation, or a patent left internal mammary graft lying beneath the sternum, SAVR may not be possible. Additionally, it is possible that less invasive approaches to aortic valve replacement (AVR) may be equivalent to SAVR for patients at high or even intermediate-risk of complications related to SAVR. As a result, TAVR has been developed for the treatment of patients with severe symptomatic AS who have an unacceptably high estimated surgical risk, or in whom TAVR is preferred due to technical issues with surgery.

TAVR is FDA approved for patients with either severe symptomatic native aortic valve stenosis, or for valve-in-valve treatment of failure of a bioprosthetic aortic valve, who are either considered high risk or extreme risk for surgical AVR. Patients can be considered high-risk if either they have a STS calculated risk of 30-day mortality with SAVR of greater than 8% or if they have an STS risk of less than 8% but have been considered high-risk for SAVR by two cardiac surgeons. The preferred access site for TAVR is via a trans-femoral approach, but for patients with significant peripheral vascular disease that cannot accommodate the large size femoral sheaths alternative access approaches have been used. The two currently available TAVR devices in the United States are the balloon expandable Sapien valve (Edwards Lifesciences) which can be placed via a trans-femoral, trans-subclavian, trans-apical, or direct aortic approach, as well as the self-expanding CoreValve (Medtronic) which can be placed via a trans-femoral, trans-subclavian, or direct aortic approach. (See Figure 1).

Figure 1.

Figure 1

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Placement of a Sapien S3 valve via the transfemoral route.

Panel A – Valve positioning, the valve is crimped on a valvuloplasty balloon and inserted to the aortic annulus over a stiff guide wire that is placed across the aortic valve into the left ventricle.

Panel B – Post-valve deployment. The valve is well deployed with no evidence of coronary obstruction or paravalvular leak.

Outcomes of TAVR to treat native aortic valve stenosis with either of these devices have been evaluated in randomized trials. The Sapien valve was first evaluated as part of the Placement of Aortic Transcatheter Valves (PARTNER) multicenter trial which had two arms, a comparison of TAVR to medical therapy including balloon aortic valvuloplasty for patients at prohibitive surgical risk, and a separate arm that randomized high risk patients to SAVR versus TAVR. For the inoperable arm, the investigators randomly assigned 358 patients with a mean age of 83 years. At one year, the mortality rate was reduced with TAVR compared to standard therapy with a 31% mortality with TAVR and a 51% mortality with SAVR. The benefit of TAVR persisted up to five-years of follow-up. Among survivors at one, two, three, and five years, functional class was better with TAVR versus standard therapy. However, the stroke rate was significantly higher in the TAVR group at 30 days and at three years, but by five-years of follow-up the stroke rates were equivalent.27

Among 699 high risk patients randomized to either SAVR or TAVR with the Edwards Sapien valve, the mean age was 84 years and the mean STS predicted risk of mortality was 11.7%. Mortality rates in the TAVR and surgical group were similar at 30 days (3.4% and 6.5%), one year (24.3% and 26.8%), and five years (67.8% and 62.4%). Combined strokes and transient ischemic attacks were significantly more frequent after TAVR than after SAVR at 30 days (5.5% versus 2.4%) and at one year (8.7% versus 4.3%, p = 0.04) with no significant difference at five years (15.9% versus 14.7%). More patients undergoing TAVR reported symptom improvement at 30 days, but at one year, symptom improvement was similar in the two groups. TAVR was associated with more frequent major vascular complications while SAVR was associated with more frequent major bleeding and new-onset atrial fibrillation. Moderate or severe paravalvular aortic regurgitation was more frequent after TAVR than after surgery at two years (6.9% versus 0.9%) and the presence of significant paravalvular aortic regurgitation was associated with increased late mortality. The risk of permanent pacemaker placement was equal in the surgical and TAVR arms with a risk of 4.0%.28

In the CoreValve High Risk study 795 patients with severe AS and high surgical risk were randomized to either TAVR with the CoreValve self-expanding valve or SAVR. The mean age was 83.2 years and the mean STS predicted risk was 7.4%. Mortality at one year was significantly lower in the TAVR group than in the surgical group (14.2% versus 19.1%) and this mortality benefit persisted at two years of follow-up. Major vascular complications, cardiac perforation, and permanent pacemaker implantation were more frequent after TAVR. Life-threatening or disabling bleeding, acute kidney injury, and new-onset or worsening atrial fibrillation were more frequent after surgery. Compared to the Sapien valve, the risk of a patient needing a pacemaker post-TAVR was higher in patients treated with CoreValve (with rates greater than 20%)29. It is important to note that in both studies, patients treated with a trans-femoral approach had far better outcomes as compared to patients treated by alternative access routes. Additionally both studies demonstrated equivalent valve performance with similar valve areas and gradients across the valve at long-term follow-up for either TAVR or SAVR. Based on the results of these trials, TAVR was FDA approved for use in patients at either high or extreme risk for surgical aortic valve replacement.

While TAVR has been approved in high-risk patients there is growing evidence of patients at intermediate risk being treated with TAVR. The TVT database which tracks the use of TAVR in the United States demonstrated that the average STS score for patients undergoing TAVR is 5.0% which is far below the threshold for determining high risk which is 8.0%.30 Additionally, recent randomized and observational data of TAVR using newer iterations of the original Sapien valve (Sapien XT and Sapien S3) have demonstrated at least equivalent outcomes of TAVR compared to SAVR in intermediate risk patients. The PARTNER 2A trial randomly assigned 2,032 intermediate-risk patients with severe aortic stenosis to undergo either TAVR or SAVR. The mean STS score was 5.8%. Prior to randomization, patients were separated into two cohorts on the basis of an evaluation of the peripheral arteries: 76% were included in the trans-femoral-access cohort and 24% percent were included in the transthoracic-access (trans-apical or trans-aortic) cohort. The rate of death from any cause or disabling stroke was similar in the TAVR and SAVR groups at two years, with rates of 19.3% in the TAVR group and 21.1% in the SAVR group. In the trans-femoral-access cohort, TAVR resulted in a significantly lower event rate than SAVR with a significantly lower risk of death or the combined outcomes of death and stroke. However, similar to prior studies SAVR resulted in less moderate or severe paravalvular aortic regurgitation (0.6%) as compared to TAVR (3.7%), and there continued to be a higher mortality during two-year follow-up for patients with moderate to severe paravalvular regurgitation.31

Lastly, an observational study suggested that TAVR with the balloon-expandable Sapien S3 valve may be superior to SAVR for intermediate-risk patients. The S3 valve is the newest iteration of the Edwards balloon expandable valve and was designed with a particular focus on reducing paravalvular regurgitation by affixing a skirt to the lower portion of the valve to seal the valve annulus and prevent leakage. Additionally it has a lower profile allowing for more patients to be treated via a trans-femoral approach. The study included 1077 patients with symptomatic severe AS with intermediate-risk who underwent TAVR with a SAPIEN 3 valve. TAVR was performed via the trans-femoral route in 88 percent of patients. Outcomes were compared with those for 944 patients in the SAVR arm of the PARTNER 2A randomized trial using a pre-specified propensity score analysis. At one-year follow-up, all-cause mortality for the TAVR group was 7.4%. Complications were incredibly low with a disabling stroke rate of only 2% and moderate or severe paravalvular regurgitation of only 1.5%. The primary composite end point was death from any cause, all strokes, and incidence of moderate or severe aortic regurgitation. TAVR was superior to SAVR for the composite end point as well as for the individual outcomes of death and stroke.32 The results of the Sapien S3 Intermediate Risk study are incredibly encouraging and likely mean that TAVR will soon be approved for the intermediate risk population. The SURTAVI trial of intermediate risk patients using the CoreValve device is almost complete and results should be announced soon. Like the Edwards device newer iterations of the CoreValve have been approved. The newest self-expanding valve the Evolut R valve also has a lower vascular profile and is repositionable and re-capturable which have led to a lower pacemaker rate and paravalvular leak rate than in the original CoreValve in provisional studies. Already it is clear that TAVR will move toward lower risk patients as both Edwards and Medtronic are beginning to enroll patients in studies of TAVR in low-risk patients.

While stroke rates in recent studies comparing TAVR to SAVR have been relatively equivalent, a recent study evaluating patients who underwent TAVR and were then evaluated by 4 D comuted tomography (CT) were found to have the presence of subclincial valve leaflet thrombosis. The presence of sub-clinical leaflet thrombosis was first noted in a randomized control trial of the Portico valve, which led to the study being briefly halted. Thereafter a number of registries were formed to evaluate the presence of sub-clinical leaflet thrombosis of other transcatheter and surgical bioprosthetic aortic valves. The combination of these registries included 132 patients, 105 of which had undergone TAVR and 27 who underwent SAVR. A total of 17 of these patients had reduced leaflet motion of the aortic valve, which represented 14% of the patients who underwent TAVR and 7% of the patients who underwent SAVR. While none of these patients demonstrated an increase in aortic valve gradients, they all had thrombus formation on the valve. Interestingly, patients who were placed on therapeutic anticoagulation with warfarin had resolution of the reduced leaflet motion.33 While further investigation is required to determine the incidence, clinical significance, and appropriate management of subclinical bioprosthetic valve leaflet thrombosis, these findings raise the possibility that leaflet thrombosis could be a cause of an increased stroke risk with TAVR and may necessitate patients being placed on more aggressive anti-platelet or anti-thrombotic regimens post-TAVR in the future.

While outcomes with TAVR have significantly improved over the last few years, appropriate patient selection should be performed to ensure that the risks of complications with TAVR are mitigated. In order to determine candidacy for TAVR, patients should undergo CT angiography of the chest, abdomen, and pelvis with 3D reconstruction of the aortic annulus and peripheral vasculature. The CT study will determine if a patient has adequate ilio-femoral diameters for the preferred trans-femoral access route. Additionally by evaluating the CT the operator can determine the height of the coronary arteries from the aortic annulus as low coronaries place a patient at risk of coronary obstruction with TAVR. CT is useful to demonstrate the presence of significant annular and left-ventricular outflow tract calcium which place a patient at risk for annular rupture and paravalvular regurgitation as the calcium can prevent adequate sealing of the valve. Additionally, specific considerations should be given to patients with low ejection fraction as they may not tolerate the rapid ventricular pacing that is needed to place the Sapien valve or the balloon aortic valvuloplasty performed prior to the insertion of the valve in most TAVR procedures. Additionally, patients should undergo pre-TAVR coronary angiography to determine the need for percutaneous coronary revascularization prior to TAVR.

Summary

In summary, TAVR should be the treatment of choice for patients at extreme risk for SAVR with severe symptomatic AS and is considered equivalent if not superior to SAVR in patients who are at high risk for complications with SAVR and who can undergo trans-femoral TAVR. Data is emerging that TAVR may be a reasonable approach for intermediate risk patients and may provide equivalent results as compared to SAVR in this population. While newer iterations of currently available TAVR devices have been designed to reduce the incidence of vascular complications, permanent pacemaker placement, and paravalvular aortic regurgitation, considerations to further mitigate these complications should be taken as TAVR moves toward lower risk populations. The optimal medical management of patients post-TAVR is still being determined and may be altered if the prevalence of sub-clinical valve leaflet thrombosis is more common than originally anticipated. Finally, pre-TAVR imaging and patient selection should be performed to ensure that the procedure can be performed with the lowest possible risk of complication. The dissemination of TAVR into the broader AS population has been rapid and will likely continue, it is important that we continue to move cautiously to ensure the lowest possible complication rate and the highest rate of success and long-term benefit for our patients.

Biography

Jerry D. Kennett, MD, MACC, MSMA member since 1980 and Missouri Medicine Editorial Board member for Cardiology, is an interventional cardiologist with Missouri Heart Center, Columbia. Benjamin Z. Galper, MD, MPH, is Director of the Advanced Valvular and Structural Heart Disease Program at Kaiser Mid-Atlantic Permanente Medical Group, Washington, DC.

Contact: jdkennett@moheartcenter.com

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Footnotes

Disclosure

None reported.

References

  • 1.Lindaman BR, Bonow RO, Otto CM. Current management of calcific aortic stenosis. Circ Res. 2013;113(2):223–37. doi: 10.1161/CIRCRESAHA.111.300084. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 2.Genereux P, Stone GW, O’Gara PT, Marquis-Gravel G, Redfors B, Giustino G, et al. Natural History, Diagnostic Approaches, and Therapeutic Strategies for Patients With Asymptomatic Severe Aortic Stenosis. J Am Coll Cardiol. 2016;67(19):2263–88. doi: 10.1016/j.jacc.2016.02.057. [DOI] [PubMed] [Google Scholar]
  • 3.Stewart BF, Siscovick D, Lind BK, Gardin JM, Gottdiener JS, Smith VE, Kitzman DW, Otto CM. Clinical factors associated with calcific aortic valve disease. Cardiovascular Health Study. J Am Coll Cardiol. 1997;29:630–634. doi: 10.1016/s0735-1097(96)00563-3. [DOI] [PubMed] [Google Scholar]
  • 4.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;341:142–147. doi: 10.1056/NEJM199907153410302. [DOI] [PubMed] [Google Scholar]
  • 5.Nkomo VT, Gardin JM, Skelton TN, Gottdiener JS, Scott CG, Enriquez-Sarano M. Burden of valvular heart diseases: a population-based study. Lancet. 2006;368:1005–1011. doi: 10.1016/S0140-6736(06)69208-8. [DOI] [PubMed] [Google Scholar]
  • 6.Otto CM, Burwash IG, Legget ME, Munt BI, Fujioka M, Healy NL, Kraft CD, Miyake-Hull CY, Schwaegler RG. Prospective study of asymptomatic valvular aortic stenosis. Clinical, echocardiographic, and exercise predictors of outcome. Circulation. 1997;95:2262–2270. doi: 10.1161/01.cir.95.9.2262. [DOI] [PubMed] [Google Scholar]
  • 7.Rosenhek R, Klaar U, Schemper M, Scholten C, Heger M, Gabriel H, Binder T, Maurer G, Baumgartner H. Mild and moderate aortic stenosis. Natural history and risk stratification by echocardiography. Eur Heart J. 2004;25:199–205. doi: 10.1016/j.ehj.2003.12.002. [DOI] [PubMed] [Google Scholar]
  • 8.Rosenhek R. Aortic stenosis: disease severity, progression, timing of intervention, and role in monitoring transcatheter valve implantation. In: Otto CM, editor. The Practice of Clinical Echocardiography. 4th. Elsevier/Saunders; 2012. pp. 425–449. [Google Scholar]
  • 9.Baumgartner H, Hung J, Bermejo J, Chambers JB, Evangelista A, Griffin BP, Lung B, Otto CM, Pellikka PA, Quinones M. Echocardiographic assessment of valve stenosis: EAE/ASE recommendations for clinical practice. Eur J Echocardiogr. 2009;10:1–25. doi: 10.1093/ejechocard/jen303. [DOI] [PubMed] [Google Scholar]
  • 10.Nishimura RA, Otto CM, Bonow RO, et al. 2014 AHA/ACC guideline for the management of patients with valvular heart disease: executive summary: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol. 2014;63:2438–2488. doi: 10.1016/j.jacc.2014.02.537. [DOI] [PubMed] [Google Scholar]
  • 11.Vahanian A, Alfieri O, Andreotti F, et al. Joint Task Force on the Management of Valvular Heart Disease of the European Society of Cardiology (ESC)European Association for Cardiothoracic Surgery (EACTS) Guidelines on the management of valvular heart disease (version 2012) Eur Heart J. 2012;33:2451–2496. doi: 10.1093/eurheartj/ehs109. [DOI] [PubMed] [Google Scholar]
  • 12.Rosenhek R, Binder T, Porenta G, Lang I, Christ G, Schemper M, Maurer G, Baumgartner H. Predictors of outcome in severe, asymptomatic aortic stenosis. N Engl J Med. 2000;343:611–617. doi: 10.1056/NEJM200008313430903. [DOI] [PubMed] [Google Scholar]
  • 13.Stewart RA, Kerr AJ, Whalley GA, Legget ME, Zeng I, Williams MJ, Lainchbury J, Hamer A, Doughty R, Richards MA, White HD. Left ventricular systolic and diastolic function assessed by tissue Doppler imaging and outcome in asymptomatic aortic stenosis. Eur Heart J. 2010;31:2216–2222. doi: 10.1093/eurheartj/ehq159. [DOI] [PubMed] [Google Scholar]
  • 14.Pellikka PA, Sarano ME, Nishimura RA, Malouf JF, Bailey KR, Scott CG, Barnes ME, Tajik AJ. Outcome of 622 adults with asymptomatic, hemodynamically significant aortic stenosis during prolonged follow-up. Circulation. 2005;111:3290–3295. doi: 10.1161/CIRCULATIONAHA.104.495903. [DOI] [PubMed] [Google Scholar]
  • 15.Kamath AR, Pai RG. Risk factors for progression of calcific aortic stenosis and potential therapeutic targets. Int J Angiol. 2008;17:63–70. doi: 10.1055/s-0031-1278283. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 16.Picano E, Pibarot P, Lancellotti P, Monin JL, Bonow RO. The emerging role of exercise testing and stress echocardiography in valvular heart disease. J Am Coll Cardiol. 2009;54:2251–2260. doi: 10.1016/j.jacc.2009.07.046. [DOI] [PubMed] [Google Scholar]
  • 17.Das P, Rimington H, Chambers J. Exercise testing to stratify risk in aortic stenosis. Eur Heart J. 2005;26:1309–1313. doi: 10.1093/eurheartj/ehi250. [DOI] [PubMed] [Google Scholar]
  • 18.Rossebo AB, Pedersen TR, Boman K, Brudi P, Chambers JB, Egstrup K, Gerdts E, Gohlke-Barwolf C, Holme I, Kesaniemi YA, Malbecq W, Nienaber CA, Ray S, Skjaerpe T, Wachtell K, Willenheimer R. Intensive lipid lowering with simvastatin and ezetimibe in aortic stenosis. N Engl J Med. 2008;359:1343–1356. doi: 10.1056/NEJMoa0804602. [DOI] [PubMed] [Google Scholar]
  • 19.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. doi: 10.1161/CIRCULATIONAHA.109.900027. [DOI] [PubMed] [Google Scholar]
  • 20.Bonow RO, Carabello BA, Kanu C, de Leon AC, Jr, Faxon DP, Freed MD, Gaasch WH, Lytle BW, Nishimura RA, O’Gara PT, O’Rourke RA, Otto CM, Shah PM, Shanewise JS, Smith SC, Jr, Jacobs AK, Adams CD, Anderson JL, Antman EM, Fuster V, Halperin JL, Hiratzka LF, Hunt SA, Nishimura R, Page RL, Riegel B. ACC/AHA 2006 guidelines for the management of patients with valvular heart disease: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (writing committee to revise the 1998 Guidelines for the Management of Patients With Valvular Heart Disease) Circulation. 2006;114:e84–231. doi: 10.1161/CIRCULATIONAHA.106.176857. [DOI] [PubMed] [Google Scholar]
  • 21.Vahanian A, Baumgartner H, Bax J, Butchart E, Dion R, Filippatos G, Flachskampf F, Hall R, Iung B, Kasprzak J, Nataf P, Tornos P, Torracca L, Wenink A. Guidelines on the management of valvular heart disease: The Task Force on the Management of Valvular Heart Disease of the European Society of Cardiology. Eur Heart J. 2007;28:230–268. doi: 10.1093/eurheartj/ehl428. [DOI] [PubMed] [Google Scholar]
  • 22.Kvidal P, Bergstrom R, Horte LG, Stahle E. Observed and relative survival after aortic valve replacement. J Am Coll Cardiol. 2000;35:747–756. doi: 10.1016/s0735-1097(99)00584-7. [DOI] [PubMed] [Google Scholar]
  • 23.Bakaeen FG, Chu D, Ratcliffe M, Gopaldas RR, Blaustein AS, Venkat R, Huh J, LeMaire SA, Coselli JS, Carabello BA. Severe aortic stenosis in a veteran population: treatment considerations and survival. Ann Thorac Surg. 2010;89:453–458. doi: 10.1016/j.athoracsur.2009.10.033. [DOI] [PubMed] [Google Scholar]
  • 24.Brown JM, O’Brien SM, Wu C, Sikora JA, Griffith BP, Gammie JS. Isolated aortic valve replacement in North America comprising 108,687 patients in 10 years: changes in risks, valve types, and outcomes in the Society of Thoracic Surgeons National Database. J Thorac Cardiovasc Surg. 2009;137:82–90. doi: 10.1016/j.jtcvs.2008.08.015. [DOI] [PubMed] [Google Scholar]
  • 25.El-Hamamsy I, Eryigit Z, Stevens LM, Sarang Z, George R, Clark L, Melina G, Takkenberg JJ, Yacoub MH. Long-term outcomes after autograft versus homograft aortic root replacement in adults with aortic valve disease: a randomized controlled trial. Lancet. 2010;376:524–531. doi: 10.1016/S0140-6736(10)60828-8. [DOI] [PubMed] [Google Scholar]
  • 26.Lee R, Li S, Rankin JS, O’Brien SM, Gammie JS, Peterson ED, McCarthy PM, Edwards FH. Fifteen-year outcome trends for valve surgery in North America. Ann Thorac Surg. 2011;91:677–684. doi: 10.1016/j.athoracsur.2010.11.009. [DOI] [PubMed] [Google Scholar]
  • 27.Leon MB, Smith CR, Mack M, et al. Transcatheter aortic-valve implantation for aortic stenosis in patients who cannot undergo surgery. N Engl J Med. 2010;363:1597. doi: 10.1056/NEJMoa1008232. [DOI] [PubMed] [Google Scholar]
  • 28.Smith CR, Leon MB, Mack MJ, et al. Transcatheter versus surgical aortic-valve replacement in high-risk patients. N Engl J Med. 2011;364:2187. doi: 10.1056/NEJMoa1103510. [DOI] [PubMed] [Google Scholar]
  • 29.Adams DH, Popma JJ, Reardon MJ, et al. Transcatheter aortic-valve replacement with a self-expanding prosthesis. N Engl J Med. 2014;370:1790. doi: 10.1056/NEJMoa1400590. [DOI] [PubMed] [Google Scholar]
  • 30.Holmes DR, Nishamura RA, Grover FL. Annual Outcomes With Transcatheter Valve Therapy: From the STS/ACC TVT Registry. Ann Thorac Surg. 2016;101:789. doi: 10.1016/j.athoracsur.2015.10.049. [DOI] [PubMed] [Google Scholar]
  • 31.Leon MB, Smith CR, Mack MJ, et al. Transcatheter or Surgical Aortic-Valve Replacement in Intermediate-Risk Patients. N Engl J Med. 2016;374:1609. doi: 10.1056/NEJMoa1514616. [DOI] [PubMed] [Google Scholar]
  • 32.Thourani VH, Kodali S, Makkar RR, et al. Transcatheter aortic valve replacement versus surgical valve replacement in intermediate-risk patients: a propensity score analysis. Lancet. 2016 doi: 10.1016/S0140-6736(16)30073-3. [DOI] [PubMed] [Google Scholar]
  • 33.Makkar RR, Fontana G, Jilaihawi H, et al. Possible Subclinical Leaflet Thrombosis in Bioprosthetic Aortic Valves. N Engl J Med. 2015;2015;373 doi: 10.1056/NEJMoa1509233. [DOI] [PubMed] [Google Scholar]

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