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Aortic Stenosis: What Long-Term Care Providers Need to Know
Affiliations:
Duke Division of Cardiology, Duke Clinical Research Institute, Durham, NC
Acknowledgements:
This article was supported by Grant Number T32GM086330 from the National Institute of General Medical Sciences. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institute of General Medical Sciences or the National Institutes of Health.
Abstract: Aortic stenosis (AS) can be congenital or degenerative, with the latter resulting from calcification of the aortic valve over time. Degenerative calcific AS is the most common form of AS among older adults in the United States. As the population continues to age, AS will be encountered more frequently in the long-term care (LTC) setting. Patients may or may not have symptoms, but once symptoms manifest, AS has poor outcomes when left untreated. This review article summarizes the presentation and diagnosis of AS and outlines current management options, including surgical aortic valve replacement, and transcatheter aortic valve replacement. It also describes the outcomes of these therapies from an LTC perspective.
Key words: Aortic stenosis, degenerative calcific aortic stenosis, cardiovascular disease, symptomatic aortic stenosis, surgical aortic valve replacement, transcatheter aortic valve replacement.
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Aortic stenosis (AS) is the most common valvular disease in older adults.1,2 Although congenitally bicuspid valve with calcification is the most common form of AS overall,3 degenerative calcific AS of the trileaflet valve is the most common form observed in persons aged 70 years and older.4 Degenerative calcific AS is a disease with a spectrum that ranges from mild aortic valve thickening without valve obstruction, called aortic valve sclerosis, to severe valve obstruction or stenosis.5,6 Only 10% of patients with calcific AS progress to severe AS, with most patients remaining with less severe disease.6 Older age and male sex are associated with progression,5,7 but the rate of progression varies substantially between patients.8
As the population continues to age, AS will become more prevalent. It is estimated that the burden of AS will double within the next 50 years.4 Because AS can cause functional limitations, particularly once it becomes symptomatic, patients may require long-term care (LTC) services, particularly if they have other comorbidities. LTC providers are uniquely situated to make meaningful observations regarding residents at risk of calcific AS in the context of their overall clinical and health status. In this article, we review the signs and symptoms of AS, its natural progression, and its current management options, including surgical interventions, and describe how LTC providers can optimize the care of these patients.
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Considering the Signs and Symptoms of Aortic Stenosis
Symptoms of AS in older adults may be difficult to identify because multimorbidity is so common in this population. Chronic obstructive pulmonary disease, anemia, uncontrolled hypertension, and deconditioning, among other conditions, can cause symptoms similar to those observed with AS. The presence of these conditions should be considered and treated concurrently when AS symptom severity is being assessed. Dyspnea upon exertion is the most common symptom of hemodynamically significant AS, and it is often the result of diastolic dysfunction in the setting of fixed cardiac output due to valve obstruction. Hemodynamically severe AS presents as syncope, progressive angina, or heart failure. Syncope can result from decreased cerebral perfusion (usually with a transient tachyarrhythmia), or from obstruction with fixed cardiac output upon exertion. Angina can result from increased cardiac demand in the setting of prolonged systolic ejection time, which is not necessarily associated with coronary artery disease (CAD), despite CAD being common in this population. Heart failure often results from left ventricular systolic failure in the setting of chronically elevated outflow pressures.
Diagnosing Aortic Stenosis
On physical examination, prolonged duration and late peaking of a systolic murmur on auscultation accompanied by a prolonged carotid upstroke visible on physical examination is characteristic of moderate to severe AS (vs no stenosis or mild stenosis). The S2 heart sounds may be obliterated (with the A2 and P2 valve components being superimposed, or the A2 valve component being soft or absent) or paradoxically split from vigorous left atrial contraction. Affected patients may also have a narrow pulse pressure (ie, <25% of systolic blood pressure).
Transthoracic echocardiography remains the way to objectively determine the severity of AS. According to the American College of Cardiology/American Heart Association 2008 guidelines,9 severe AS is defined by a transthoracic echocardiogram showing an aortic valve area (AVA) <1.0 cm2 and a mean gradient >40 mm Hg. Peak velocity >4.0 m/s is also generally considered severe.5 In contrast, mild AS is characterized by an AVA <1.5 cm2 and a mean gradient <25 mm Hg with a peak velocity <3.0 m/s, and a moderate AS is characterized by an AVA, mean gradient, and peak velocity between that of mild and severe AS (eg, AVA, 1.0-1.5 cm2; mean gradient, 25-40 mm Hg; peak velocity, 3.0-4.0 m/s). Assessments of AS severity can also be underestimated in the setting of impaired left ventricular ejection fraction, so additional testing may be needed in low EF patients to determine AS severity.
Clinical and Economic Impact of Aortic Stenosis
A 5-year clinical and economic outcomes analysis of Medicare claims among elderly patients with medically managed severe AS (n=2150) showed that these individuals have limited long-term survival, with a mortality of 49% at 1 year and 88% at 5 years (mean survival, 1.8 years).10 Of these patients, 52% were admitted to skilled nursing care and 28% were admitted to hospice care. Patients had an average of 4.4 hospital admissions over the 5-year period, often with prolonged stays (11.5 hospital days per patient year). After excluding the index admission, beneficiaries experienced an average of 1.9 hospital admissions per year. These patients’ healthcare needs had a substantial economic impact, with a total 5-year cost of $63,844 per patient and a mean annual follow-up cost (excluding the index quarter) per year alive of $29,278. The healthcare costs in this high-risk population were more than 3.4 times those of the average Medicare beneficiary,10 whereas the expected healthcare costs of those undergoing surgical aortic valve replacement (SAVR) are estimated to be lower at 2.9 times that of the average Medicare beneficiary.11
Managing Aortic Stenosis
Patients without symptoms of AS or who have mild AS can generally be followed without intervention or restriction until symptoms develop or AS progresses in severity. Patients with moderate AS should have regular cardiovascular examinations, which may include repeat echocardiography, to closely monitor for disease progression. Monitoring for classic and atypical symptoms of AS is important because of the high morbidity and mortality rate once symptoms manifest. In addition, although their roles are not fully determined, routine assessment of B-type natriuretic peptide (BNP) and its prohormone (NT-proBNP) can be helpful, as they can reflect myocardial stress.12 In one study that included symptomatic and asymptomatic patients with normal left ventricular function, BNP level was a strong independent predictor for cardiovascular death by multivariable analysis adjusted to age and New York Heart Association (NYHA) functional class.13 A 2012 study also showed that AS patients with metabolic syndrome progress more rapidly than individuals without this condition.14
Currently, no medical therapy can effectively slow AS progression. In the past, there had been enthusiasm for using statins to treat AS. The rationale was that AS and atherosclerosis share the same risk factors and demonstrate the same histopathological pattern with regard to inflammation and lipid infiltration; however, a systematic meta-analysis published in 2011 concluded that the data do not support the benefit of statins in improving outcomes or slowing disease progression in calcific AS.15
The relationship between bone remodeling and AS progression is another area of active research. In a recently published French study where the C-terminal-telopeptide of type-1-collagen to osteocalcin ratio was calculated as a marker of bone remodeling, AS progression was associated with a bone resorptive balance in elderly patients with normal vitamin D levels.16 In elderly AS patients with low vitamin D levels, AS progression was associated with intact parathyroid hormone and secondary hyperparathyroidism.16 In contrast, data from a recently published British study indicate that AS disease activity is determined by local calcific processes within the valve that are distinct from skeletal bone remodeling.17
Once symptoms of AS manifest, the medical management options are limited to treating patients’ comorbidities and offering palliation. The only definitive treatment options for severe AS are valve repair or replacement. These treatments may also be considered for some asymptomatic patients with hemodynamically significant or severe AS, including those with an abnormal exercise test, a high likelihood of rapid progression, and a low surgical risk, as these populations have a lower survival rate than that of persons without AS.18,19 Although controversy remains regarding the timing of interventions for asymptomatic patients with severe AS, current practice guidelines recommend valve replacement when these patients have reduced systolic left ventricular function that cannot be attributed to another condition.9
Until recently, surgical repair or replacement options were limited to balloon valvuloplasty or SAVR. Balloon aortic valvuloplasty is performed infrequently as a destination therapy for AS because there has been a lack of survival benefit associated with the procedure and it has a documented recurrence rate of 80% at 1 year.20 Therefore, the only real treatment option was SAVR; however, due to substantial operative risk, not all AS patients, including those with severe AS, were candidates for this intervention. According to the 2001 Euro Heart Survey, one-third of elderly patients with severe, symptomatic AS did not undergo SAVR for this reason; these patients were often older, had neurological dysfunction, and/or left ventricular dysfunction.21 More recently, transcatheter aortic valve replacement (TAVR) has emerged as a viable therapy for AS, substantially expanding the pool of potentially eligible patients for surgical intervention, but its role in the LTC population is still being defined. What follows is a review of the outcomes observed with SAVR and TAVR.
Surgical Aortic Valve Replacement
Mortality after SAVR has declined substantially over time among older adults.22 According to a 2012 study by Brennan and colleagues,23 long-term survival after SAVR in the elderly is excellent, although patients with certain comorbidities (eg, severe lung disease, renal failure) and/or a high Society of Thoracic Surgeons (STS) perioperative risk of mortality still have a poor long-term prognosis. The survival of elderly individuals (aged ≥70 years) after SAVR was nearly equivalent to that of their age-matched peers.23
Similarly, Bakeen and associates24 reported that after risk adjustment, older age (age ≥80 years) was not independently associated with higher SAVR-related mortality; however, it was associated with higher morbidity. In addition, some octogenarians have expressed regret in undergoing surgery. Maillet and colleagues25 queried 84 octogenarians with a history of symptomatic AS who underwent SAVR with or without coronary artery bypass graft surgery at 1 year or more following the intervention. When asked if they would accept being operated on again, 39.3% reported that they would not. This finding was significantly related to loss of autonomy, suspected depression, and cardiac symptoms.25 Loss of autonomy is a point that requires particular consideration for persons in LTC living situations, as these individuals could require a higher level of care postoperatively. Less invasive treatments, such as TAVR, may offer distinct advantages over SAVR, particularly when including patient preferences in shared decision-making.
Transthoracic Aortic Valve Replacement
In the past 5 years, TAVR, which is also sometimes referred to as transcatheter aortic valve intervention (TAVI), has dramatically changed the therapeutic options for older adults with symptomatic severe AS. TAVR enables a patient to receive a balloon-expandable stented valve that is inserted transcutaneously, often transfemorally, and inflated once in place within the stenotic valve (Figure26). More than 50,000 TAVR procedures have been performed, with more than 40 countries offering the procedure.27
In the landmark PARTNER (Placement of Aortic Transcatheter Valve Trial), TAVR with the SAPIEN heart valve was superior to medical management in inoperable patients and noninferior to SAVR in high-risk operable patients.28 Among the 358 inoperable patients with AS who underwent TAVR, there was a 30.7% mortality rate at 1 year compared with a 50.7% mortality rate in the medically managed group, representing a 20% absolute risk reduction and a 60% relative risk reduction. The rate of the composite end point of death from any cause or repeat hospitalization was 42.5% with TAVR as compared with 71.6% with medical therapy. In addition, the rate of cardiac symptoms at 1 year was lower among those who had undergone TAVR (25% vs 58% for the medically managed group).
In a follow-up study, patients who had been classified as inoperable in PARTNER and received TAVR showed sustained improvements in mortality and reduced rates of rehospitalization at 2 years, but the authors note that these findings may be limited to patients who do not have extensive coexisting conditions.29 TAVR was also associated with improved functional status at 2 years (P<.001). Finally, although cumulative 1-year costs remained higher for TAVR ($106,076 vs $53,621 for standard medical therapy), Reynolds and associates30 project the incremental cost-effectiveness ratio for TAVR at $50,200 per year of life gained, or $61,889 per quality-adjusted life-year gained.
With regard to high-risk operable patients, PARTNER found a similar 1-year mortality rate between those randomly assigned to TAVR and those assigned to SAVR.26,27 Rates of major stroke were 5.1% in the TAVR group versus 2.4% in the SAVR group at 1 year (P=.07). Predictors of neurological events with TAVR included a prior neurological event, more severe atherosclerotic burden, worse functional disability, smaller valve area, and use of a transapical approach.27 At 30 days, vascular complications were significantly more frequent with TAVR (11.0% vs 3.2%, P<.001), and major bleeding (9.3% vs 19.5%, P<.001) and new-onset atrial fibrillation (8.6% vs 16.0%, P=.006) were more frequent after surgical replacement.26 Improvements in NYHA functional class and heart failure symptoms assessed using the Kansas City Cardiomyopathy Questionnaire have been relatively uniform and substantial across trials and registries assessing TAVR outcomes.
A British study evaluating the use of a different valve for TAVR, known as the CoreValve, showed that health-related quality of life significantly improved at both 30 days and 6 months after the procedure in 102 patients who received this valve; the study made this determination using the 12-item medical outcomes study short form health survey version 2.0 (SF-12v2) and the EuroQol (EQ-5D) survey instrument.31 In addition, a prospective German study of 186 inoperable surgical candidates who underwent TAVR with either a CoreValve or a SAPIEN heart valve demonstrated improvements in quality of life at 1 year when assessed using the 36-item short form health survey (SF-36).32 The authors also found that 85% of patients would undergo TAVR again.33 The Table shows the results of quality of life and symptom assessments in various TAVR registries.33-38
With the PARTNER trials having been published in 2010 and 2011, outcomes past 2 years are still being studied. Nevertheless, a Canadian multicenter trial using the SAPIEN heart valve system in inoperable or high-risk surgical patients found that approximately one-half died at a mean follow-up of 3.5 years.39 Late mortality was due to noncardiac comorbidities in more than one-half of these patients. Predictors of late mortality included chronic obstructive pulmonary disease, chronic kidney disease, chronic atrial fibrillation, and frailty. No clinically significant deterioration in valve function was observed during the 4-year follow-up period. This finding emphasizes the importance of selecting the right patients for valve replacement. Currently, this appears to be symptomatic patients who are at low risk of mortality from other causes. Functional status and a comprehensive assessment of comorbidities, including CAD, history of transient ischemic attack or stroke, chronic kidney disease, and dementia, should be performed when assessing candidacy
for TAVR.40
Geriatric assessments can improve the prediction of mortality and major adverse cardiovascular and cerebral events compared with clinical assessments using the STS score. For example, Stortecky and collegues41 incorporated the Multidimensional Geriatric Assessment (MGA), which assesses cognition, nutrition, mobility, activities of daily living, and frailty index, into global risk scores (STS and EuroScore), and found that the addition of this tool improved risk prediction in 100 TAVR patients. MGA identifies patients with diminished physiological reserves and reduced adaptive capacity in multiple organ systems; thus, it has the potential to differentiate between elderly patients recovering better than expected and those at risk of deteriorating after an intervention.42 Larger studies are needed to optimize geriatric variables in risk-based scores for use in clinical practice
Conclusion
Symptomatic degenerative calcific AS is a costly, debilitating illness in older adults that cannot be treated with medication. Its onset of symptoms and progression vary by individual, with approximately 10% of patients progressing to severe AS. Risk stratification and decision-making is particularly complex in adults with AS and multiple comorbidities. Many of these patients will end up requiring LTC services. LTC providers will be expected to assume a gradually greater role in appropriately referring these patients, particularly now that TAVR has enabled more patients to be treated.
Regardless of whether SAVR or TAVR is performed, in properly selected patients, the result should be improved survival and improvement in the classic symptoms of syncope, angina, and heart failure. Individuals who undergo successful intervention with SAVR or TAVR are also likely to require less intensive nursing care, retain more independence, and have lower costs of care. Further research into TAVR candidacy is needed, particularly for persons residing in LTC facilities.
References
1. Iung B, Baron G, Butchart EG, et al. A prospective survey of patients with valvular heart disease in Europe: The Euro Heart Survey on Valvular Heart Disease. Eur Heart J. 2003;24(13):1231-1243.
2. Iung B. Management of the elderly patient with aortic stenosis. Heart. 2008;94(4):519-524.
3. Roberts WC, Ko JM. Frequency by decades of unicuspid, bicuspid, and tricuspid aortic valves in adults having isolated aortic valve replacement for AS, with or without associated aortic regurgitation. Circulation. 2005;111(7):920-925.
4. Iung B, Vahanian A. Degenerative calcific AS: a natural history. Heart. 2012;98 suppl 4:iv7-13.
5. Vahanian A, Otto CM. Risk stratification of patients with AS. Eur Heart J. 2010;31(4):416-423.
6. Freeman RV, Otto CM. Spectrum of calcific aortic valve disease: pathogenesis, disease progression, and treatment strategies. Circulation. 2005;111(24):3316-3326.
7. Novaro GM, Katz R, Aviles RJ, et al. Clinical factors, but not C-reactive protein, predict progression of calcific aortic-valve disease: the Cardiovascular Health Study. J Am Coll Cardiol. 2007;50(20):1992-1998.
8. Palta S, Pai AM, Gill KS, Pai RG. New insights into the progression of AS: implications for secondary prevention. Circulation. 2000;101(21):2497-2502.
9. Bonow RO, Carabello BA, Chatterjee K, et al. 2008 focused update incorporated into the 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): endorsed by the Society of Cardiovascular Anesthesiologists, Society for
Cardiovascular Angiography and Interventions, and Society of Thoracic Surgeons. Circulation. 2008;118(15):e523-e661.
10. Clark MA, Arnold SV, Duhav FG, et al. Five-year clinical and economic outcomes among patients with medically managed severe AS: results from a Medicare claims analysis. Circ Cardiovasc Qual Outcomes. 2012;5(5):697-704.
11. Clark MA, Duhav FG, Thompson AK, et al. Clinical and economic outcomes after surgical aortic valve replacement in Medicare patients. Risk Manag Healthc Policy. 2012;5:117-126.
12. Lancellotti P, Magne J, Donal E, et al. Clinical outcome in asymptomatic severe AS: insights from the new proposed AS grading classification. J Am Coll Cardiol. 2012;59(3):235-243.
13. Lim P, Monin JL, Monchi M, et al. Predictors of outcome in patients with severe aortic stenosis and normal left ventricular function: role of B-type natriuretic peptide. Eur Heart J. 2004;25(22):2048-2053.
14. Capoulade R, Clavel MA, Dumesnil JG, et al; ASTRONOMER Investigators. Impact of metabolic syndrome on progression of aortic stenosis: influence of age and statin therapy. J Am Coll Cardiol. 2012;60(3):216-223.
15. Parolari A, Tremoli E, Cavallotti L, et al. Do statins improve outcomes and delay the progression of non-rheumatic calcific AS? Heart. 2011;97(7):523-529.
16. Hekimian G, Boutten A, Flamant M, et al. Progression of aortic valve stenosis is associated with bone remodelling and secondary hyperparathyroidism in elderly patients—the COFRASA study. Eur Heart J. 2013;34(25):1915-1922.
17. Dweck MR, Khaw HJ, Sng GK, et al. Aortic stenosis, atherosclerosis, and skeletal bone: is there a common link with calcification and inflammation? Eur Heart J. 2013;34(21):1567-1574.
18. Pellikka PA, Sarano ME, Nishimura RA, et al. Outcome of 622 adults with asymptomatic, hemodynamically significant AS during prolonged follow-up. Circulation. 2005;111(24):3290-3295.
19. Kaleschke G, Baumgartner H. Asymptomatic aortic stenosis: when to operate? Curr Cardiol Rep. 2011;13(3):220-225.
20. Bohula May EA, Faxon D. Transcatheter aortic valve replacement: history and current status. Trends Cardiovasc Med. 2013.
21. Iung B, Cachier A, Baron G, et al. Decision-making in elderly patients with severe AS: why are so many denied surgery? Eur Heart J. 2005;26(24):2714-2720.
22. 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(1):82-90.
23. Brennan JM, Edwards FH, Zhao Y, et al. Long-term survival after aortic valve replacement among high-risk elderly patients in the United States: insights from the Society of Thoracic Surgeons Adult Cardiac Surgery Database, 1991 to 2007. Circulation. 2012;126(13):1621-1629.
24. Bakaeen FG, Chu D, Huh J, Carabello BA, et al. Is an age of 80 years or greater an important predictor of short-term outcomes of isolated aortic valve replacement in veterans? Ann Thorac Surg. 2010;90(3):769-774.
25. Maillet JM, Somme D, Hennel E, Lessana A, Saint-Jean O, Brodaty D, et al. Frailty after aortic valve replacement (AVR) in octogenarians. Arch Gerontol Geriatr. 2009;48(3):391-396.
26. Smith CR, Leon MB, Mack MJ, et al. Transcatheter versus surgical aortic-valve replacement in high-risk patients. N Engl J Med. 2011;364(23):2187-2198.
27. Webb JG, Wood DA. Current status of transcatheter aortic valve replacement. J Am Coll Cardiol. 2012;60(6):483-492.
28. Leon MB, Smith CR, Mack M, et al. Transcatheter aortic-valve implantation for AS in patients who cannot undergo surgery. N Engl J Med. 2010;363(17):1597-1607.
29. Makkar RR, Fontana GP, Jilaihawi H, et al. Transcatheter aortic-valve replacement for inoperable severe AS. N Engl J Med. 2012;366(18):1696-1704.
30. Reynolds MR, Magnuson EA, Wang K, et al. Cost-effectiveness of transcatheter aortic valve replacement compared with standard care among inoperable patients with severe AS: results from the placement of aortic transcatheter valves (PARTNER) trial (Cohort B). Circulation. 2012;125(9):1102-1109.
31. Fairbairn TA, Meads DM, Mather AN, et al. Serial change in health-related quality of life over 1 year after transcatheter aortic valve implantation: predictors of health outcomes. J Am Coll Cardiol. 2012;59(19):1672-1680.
32. Krane M, Deutsch MA, Piazza N, et al. One-year results of health-related quality of life among patients undergoing transcatheter aortic valve implantation. Am J Cardiol. 2012;109(12):1774-1781.
33. Krane M, Deutsch MA, Bleiziffer S, et al. Quality of life among patients undergoing transcatheter aortic valve implantation. Am Heart J. 2010;160(3):451-457.
34. Lefèvre T, Kappetein AP, Wolner E, et al. One year follow-up of the multi-centre European PARTNER transcatheter heart valve study. Eur Heart J. 2011;32(2):148-157.
35. Buellesfeld L, Gerckens U, Schuler G, et al. 2-year follow-up of patients undergoing transcatheter aortic valve implantation using a self-expanding valve prosthesis. J Am Coll Cardiol. 2011;57(16):1650-1657.
36. Ussia GP, Mulè M, Barbanti M, et al. Quality of life assessment after percutaneous aortic valve implantation. Eur Heart J. 2009;30(14)1790-1796.
37. Bekeredjian R, Krumsdorf U, Chorianopoulos E, et al. Usefulness of percutaneous aortic valve implantation to improve quality of life in patients >80 years of age. Am J Cardiol. 2010;106(12):1777-1781.
38. Gotzmann M, Hehen T, Germing A, et al. Short-term effects of transcatheter aortic valve implantation on neurohormonal activation, quality of life and 6-minute walk test in severe and symptomatic AS. Heart. 2010;96(14):1102-1106.
39. Rodés-Cabau J, Webb JG, Cheung A, et al. Long-term outcomes after transcatheter aortic valve implantation: insights on prognostic factors and valve durability from the Canadian multicenter experience. J Am Coll Cardiol. 2012;60(19):1864-1875.
40. Holmes DR Jr, Mack MJ, Kaul S, et al. 2012 ACCF/AATS/SCAI/STS expert consensus document on transcatheter aortic valve replacement: developed in collabration with the American Heart Association, American Society of Echocardiography, European Association for Cardio-Thoracic Surgery, Heart Failure Society of America, Mended Hearts, Society of Cardiovascular Anesthesiologists, Society of Cardiovascular Computed Tomography, and Society for Cardiovascular Magnetic Resonance. J Thorac Cardiovasc Surg. 2012;144(3):e29-e84.
41. Stortecky S, Schoenenberger AW, Moser A, et al. Evaluation of multidimensional geriatric assessment as a predictor of mortality and cardiovascular events after transcatheter aortic valve implantation. JACC Cardiovasc Interv. 2012;5(5):489-496.
42. Spoon DB, Orszulak TA, Edell ES, Li Z, Nishimura RA. Risk of aortic valve replacement in patients with AS and chronic obstructive pulmonary disease. J Heart Valve Dis. 2012;21(3):314-319.
Disclosures: The authors report no relevant financial relationships.
Address correspondence to: Gwen M. Bernacki, MD, MHSA, Duke Clinical Research Institute, 2400 Pratt Street, Durham, NC 27705; gwen.bernacki@dm.duke.edu
