Journal of Gerontological Nursing

Clinical Concepts 

Severe Symptomatic Aortic Stenosis in Older Adults: Pathophysiology, Clinical Manifestations, Treatment Guidelines, and Transcatheter Aortic Valve Replacement (TAVR)

Leo A. Yurek, PhD, RN; Karen E. Jakub, PhD, RN; Melissa M. Menacho, ACNP

Abstract

The only effective treatment for symptomatic aortic stenosis in the older adult population is surgical aortic valve replacement. However, more than 30% of candidates are denied surgery due to advanced age and multiple comorbidities. Without surgical intervention, death from symptomatic aortic stenosis approximates 2% per month, with mortality rates of approximately 50% within 2 years of symptom onset. There is no effective medical treatment for severe symptomatic aortic stenosis; care has been limited to palliative remedies and end-of-life decisions. Nascent advances in miniaturization and catheter technologies provide a new and less invasive approach: transcatheter aortic valve replacement (TAVR). The current article summarizes treatment guidelines; pathophysiology; clinical manifestations, progression, and classification of severe symptomatic aortic stenosis; and introduces TAVR and discusses randomized controlled trials involving three patient populations from the United States, with relevant nursing implications. [Journal of Gerontological Nursing, 41(6), 8–13.]

Dr. Yurek is Assistant Professor of Nursing, North Carolina Central University, and Ms. Menacho is Acute Care Nurse Practitioner, Division of Cardiothoracic Surgery, Duke University, Durham, North Carolina; and Dr. Jakub is Assistant Professor of Nursing, Duquesne University, Pittsburgh, Pennsylvania.

The authors have disclosed no potential conflicts of interest, financial or otherwise.

Address correspondence to Leo A. Yurek, PhD, RN, Assistant Professor of Nursing, North Carolina Central University, 7822 Fawnbrook Drive, Hillsborough, NC 27278; e-mail: lyurek@nccu.edu.

Posted Online: April 17, 2015

Abstract

The only effective treatment for symptomatic aortic stenosis in the older adult population is surgical aortic valve replacement. However, more than 30% of candidates are denied surgery due to advanced age and multiple comorbidities. Without surgical intervention, death from symptomatic aortic stenosis approximates 2% per month, with mortality rates of approximately 50% within 2 years of symptom onset. There is no effective medical treatment for severe symptomatic aortic stenosis; care has been limited to palliative remedies and end-of-life decisions. Nascent advances in miniaturization and catheter technologies provide a new and less invasive approach: transcatheter aortic valve replacement (TAVR). The current article summarizes treatment guidelines; pathophysiology; clinical manifestations, progression, and classification of severe symptomatic aortic stenosis; and introduces TAVR and discusses randomized controlled trials involving three patient populations from the United States, with relevant nursing implications. [Journal of Gerontological Nursing, 41(6), 8–13.]

Dr. Yurek is Assistant Professor of Nursing, North Carolina Central University, and Ms. Menacho is Acute Care Nurse Practitioner, Division of Cardiothoracic Surgery, Duke University, Durham, North Carolina; and Dr. Jakub is Assistant Professor of Nursing, Duquesne University, Pittsburgh, Pennsylvania.

The authors have disclosed no potential conflicts of interest, financial or otherwise.

Address correspondence to Leo A. Yurek, PhD, RN, Assistant Professor of Nursing, North Carolina Central University, 7822 Fawnbrook Drive, Hillsborough, NC 27278; e-mail: lyurek@nccu.edu.

Posted Online: April 17, 2015

The recommended treatment for symptomatic aortic stenosis is surgical aortic valve replacement (SAVR). However, more than 30% of older adults with symptomatic aortic stenosis do not undergo lifesaving treatment due to advanced age and multiple comorbidities, whereas others may refuse surgery (Bonow et al., 2008; Holmes et al., 2012; Iung et al., 2005). The advent of transcatheter aortic valve replacement (TAVR) offered improved outcomes over conventional medical management and SAVR (without associated risks of median sternotomy and cardiopulmonary bypass), especially for high-risk candidates otherwise denied surgery and limited to palliative and end-of-life treatment decisions (Adams et al., 2014; Leon et al., 2010; Smith et al., 2011).

A review of the literature identified the most recent treatment guidelines established by the American College of Cardiology (ACC), American Heart Association (AHA), American Society of Echocardiography (ASE), Society of Thoracic Surgeons (STS), and comparable medical and surgical authorities from the European Union with expertise in the treatment of severe symptomatic aortic stenosis. The purpose of the current article is to (a) summarize current treatment guidelines and limitations for aortic stenosis; (b) review pathophysiology, clinical manifestations, progression, and classification of symptomatic aortic stenosis; (c) introduce TAVR; (d) appraise current evidence from multicenter, randomized controlled trials involving three patient populations from the United States; and (e) discuss relevant implications for nursing practice.

Current Treatment Guidelines and Limitations for Aortic Stenosis

The most common type of valvular heart disease in North America and Europe is aortic stenosis (Bonow et al., 2008; Vahanian et al., 2007). Among older adults, aortic stenosis typically results from a progressive and insidious process of calcification affecting the normal trileaflet or congenital bicuspid aortic valve (Otto, 2006; Rajamannan et al., 2011). However, aortic stenosis associated with fusion of the valve leaflets caused by rheumatic heart disease or congenital malformation presents earlier and less frequently, with less calcification (Bonow et al., 2008; Holmes et al., 2012).

The incidence of calcific aortic stenosis purportedly affects more than 13% of adults ages 75 or older with at least moderate diseases (Nkomo et al., 2006). The prevalence of aortic stenosis increases steadily with age and can be attributed to changing epidemiology of an aging population (Go et al., 2013; Holmes et al., 2012). Aortic stenosis commonly appears in the sixth and seventh decades of life, whereas severe symptomatic aortic stenosis is more prevalent in octogenarians and nonagenarians (Carabello & Paulus, 2009).

The goals of medical treatment for symptomatic aortic stenosis tend to be more palliative than curative because current efforts to delay or prevent disease progression remain unsuccessful. A watchful wait approach is adopted for patients with asymptomatic aortic stenosis because outcomes are similar to those seen in normal age-matched patients without aortic stenosis (Bonow et al., 2008). Because the disease process is similar to atherosclerosis and approximately 50% of patients who undergo aortic valve replacement have concomitant coronary artery disease (CAD), evaluation and management of cardiac risk factors (e.g., smoking cessation, hyperlipidemia, hypertension) is recommended (Bonow et al., 2008; Holmes et al., 2012).

Prudent medical management of comorbid conditions in patients with aortic stenosis minimizes exacerbations and the associated metabolic burdens of concomitant illness. Patients should be educated to promptly report worsening symptoms, such as dyspnea, chest discomfort, and lightheadedness, to effectively manage disease progression and heart failure (HF). Further, patient education should emphasize preventive initiatives, such as monitoring daily weights, restricting sodium intake, and vaccinating against influenza and pneumonia (Holmes et al., 2012).

Conventional medical management for aortic stenosis includes balloon aortic valvuloplasty (BAV). BAV dilates the stenotic aortic valve with a balloon-tipped catheter, which immediately increases the valve opening and relieves symptoms. Although BAV gained acceptance in the 1980s, its current use is limited as a bridge to aortic valve replacement. Early outcomes analyses identified serious adverse events, restenosis within weeks to months following the procedure, and mortality rates of more than 50% and 75% at 1 and 2 years, respectively (Ben-Dor et al., 2010).

Surgical removal of the diseased native valve and replacement with a bioprosthetic aortic valve is the recommended treatment for severe symptomatic aortic stenosis (Bonow et al., 2008; Holmes et al., 2012). However, more than 30% of patients diagnosed with severe aortic stenosis are not suitable candidates for SAVR due to high STS-predicted rates of mortality (>10%), which is common among patients with advanced age and concomitant CAD, left ventricle dysfunction, and multiple comorbidities. Although comorbidities, such as cerebral vascular disease, peripheral vascular disease, and respiratory or renal insufficiency, are not contraindications for SAVR, many are associated with higher 30-day mortality rates after SAVR (Iung et al., 2005; Lancellotti et al., 2013). For this reason, a less invasive percutaneous approach (i.e., TAVR) emerged as a therapeutic option for high-risk surgical candidates with symptomatic aortic stenosis (Adams et al., 2014; Leon et al., 2010; Smith et al., 2011).

Pathophysiological Changes Associated with Aortic Stenosis

The active disease process of aortic stenosis is characterized by accumulation of lipoproteins and chronic inflammation followed by calcification and fibrosis (Freeman & Otto, 2005; Holmes et al., 2012). Eventually, the aortic valve leaflets thicken and lose their flexibility, whereas the aortic valve area or opening narrows from the progressive buildup of calcium, obstructing the outflow of blood from the left ventricle. The spectrum of calcific aortic stenosis ranges from a mild stiffening of the valve leaflets (without diminution of blood flow) to severe calcification of the leaflets (with significant outflow obstruction) (Freeman & Otto, 2005).

The flow of blood across the valve, measured as aortic jet velocity, increases because the pressure in the left ventricle rises to overcome the outflow obstruction caused by the narrowed valve orifice and preserve stroke volume and cardiac output. As a result, pressure is higher on the inferior (i.e., ventricular) surface of the diseased valve than on the superior (i.e., aortic) surface, causing an increase in the mean pressure gradient across the valve. The mean pressure gradient between the left ventricle and aorta is directly related to the degree of valve stenosis, whereas the velocity of blood as it flows across the diseased valve is directly related to the mean pressure gradient across the valve; therefore, the greater the pressure gradient, the greater the velocity of the blood flow across the diseased valve (Otto, 2006). For these reasons, the aortic valve area, aortic jet velocity, and mean pressure gradient across the valve are important criteria used to monitor disease progression.

Normally, the pressure on the ventricular surface of the aortic valve is approximately the same as the pressure on the aortic surface, resulting in a negligible pressure gradient across the valve (Figure). The amount of work required by the left ventricle to eject blood across a normal aortic valve is considerably less than that required across a stenotic aortic valve (Klabunde, 2011). Hence, the narrowed aortic valve impedes the ejection of blood from the left ventricle during systole. Initially, intracavitary pressure increases in the left ventricle to overcome growing resistance caused by the narrowed valve as part of the heart’s adaptive physiology. The left ventricle works harder to contract more forcefully and eventually hypertrophies (Figure); afterload (i.e., the resistance the left ventricle needs to overcome to open the aortic valve) and cardiac output remain within normal limits, preserving systolic function (Bonow et al., 2008; Holmes et al., 2012).

Comparison of a normal heart to a heart with aortic stenosis.Note. LA = left atrium; LV = left ventricle. Reprinted with permission from Richard E. Klabunde, PhD (access http://www.cvphysiology.com).

Figure.

Comparison of a normal heart to a heart with aortic stenosis.

Note. LA = left atrium; LV = left ventricle. Reprinted with permission from Richard E. Klabunde, PhD (access http://www.cvphysiology.com).

Over time, the adaptive hypertrophic processes that preserve systolic function cause structural changes to the heart. For example, as the left ventricle works to contract more forcefully, its wall thickness increases and eventually the shape (i.e., geometry) and volume capacity of myocardial structures and chambers are altered. These changes characterize the process of cardiac remodeling, or concentric left ventricular hypertrophy in the case of aortic stenosis, which is associated with significant alterations in aortic valve gradients, flow, and functional capacity, especially in older adults (e.g., octogenarians, nonagenarians) (Elmariah et al., 2014).

Ultimately, greater workload requirements of the hypertrophied left ventricle during systole result in diminished ventricular compliance, which means the hypertrophied left ventricle loses its elasticity (i.e., its ability to distend and accommodate the volume of blood from the left atrium during diastole). Reduced ventricular compliance requires greater end-diastolic pressures to achieve optimal atrioventricular filling volumes because volume capacity of the left ventricle is diminished. Hence, the volume capacity of the left ventricle is displaced by the increased muscle mass of the hypertrophied ventricle and the left atrium hypertrophies to overcome the greater pressure requirements of a stiffer and less accommodating left ventricle (Figure). Greater end-diastolic pressures lead to diastolic failure and a backflow of blood into the left atrium and pulmonary vasculature. Eventually, right-sided HF ensues (Carabello & Paulus, 2009; Holmes et al., 2012).

Clinical Manifestations of Aortic Stenosis

A detailed history, physical examination, and resting echocardiogram are essential for proper identification and management of aortic stenosis; the presence or absence of symptoms determines the course of treatment (Bonow et al., 2008; Freeman & Otto, 2005). Ordinarily, physical examination alone is insufficient to diagnose aortic stenosis because classic symptoms of angina, syncope, and HF may occur in older adults for myriad reasons (Otto, 2006).

Calcific symptomatic aortic stenosis manifests with progressive activity intolerance, dyspnea on exertion, and orthopnea (Bonow et al., 2008; Otto, 2006). A detailed history that focuses on activities of daily living (ADLs) by comparing current activity levels with those of the prior 6 to 12 months may identify significant reductions in activity. In particular, asking patients why they are doing less and what prompts them to reduce or stop ADLs may also help identify the onset of symptoms sooner. Patients often unconsciously reduce their activity levels to avoid feeling short of breath; as the disease progresses, patients experience the hallmark of severe symptoms, including angina, congestive heart failure, and syncope (Bonow et al., 2008; Holmes et al., 2012). The onset of symptoms changes survival estimates from near-normal life expectancy (in the absence of symptoms) to a mortality rate of approximately 50% within 2 years of symptom onset (Otto, 2000).

One characteristic physical finding among patients with aortic stenosis is a systolic ejection murmur that results when blood from the left ventricle is forced through a narrowed aortic valve opening during systole. Auscultation of the second intercostal space along the right sternal border (i.e., the aortic area) may reveal a 4/6 crescendo–decrescendo murmur radiating to the neck. The murmur begins with the first heart sound getting louder through mid-systole when it peaks, after which it begins to progressively soften, ending with the second heart sound. Although this systolic murmur is specific to aortic stenosis, it is not sensitive to disease severity, particularly in older adults (Bonow et al., 2008; Holmes et al., 2012). The murmur does not get louder with disease progression, but instead softens in severe aortic stenosis, with failure of the left ventricle and a decline of cardiac output. Palpation of the same area may reveal a systolic thrill (i.e., vibratory sensation).

Monitoring Disease Progression

Disease progression is characterized by the onset of symptoms, such as angina and syncope provoked by exercise. Angina may be due to concomitant CAD or the result of diminished coronary blood flow from adaptive hypertrophic changes occurring in the left ventricle, which reduce cardiac output while increasing myocardial oxygen demands. For example, as the left ventricle works harder and contracts more forcefully, the left ventricle wall thickens, which requires a greater myocardial oxygen supply to meet the rise in demands necessary to nourish a larger, thicker, and more forceful left ventricle (Carabello & Paulus, 2009). Although the actual cause of syncope in aortic stenosis is poorly understood, it may result from a progression of the same adaptive processes compounded by calcific narrowing of the valve opening, resulting in a fixed and insufficient cardiac output to maintain adequate cerebral perfusion (Carabello & Paulus, 2009).

Classification and disease progression is also evaluated by two-dimensional transthoracic echocardiography with doppler interrogation (Bonow et al., 2008; Otto, 2006). The resting echocardiogram facilitates disease staging and progression (Table) with the three physiological indicators relevant to management and choice of treatment for aortic stenosis: (a) the aortic valve area, (b) aortic jet velocity, and (c) mean pressure gradient across the valve (Bonow et al., 2008; Otto, 2006). Following the diagnosis of aortic stenosis, periodic echocardiographical monitoring is recommended to effectively manage this population. Current ACC/AHA/ASE treatment guidelines recommend annual echocardiographical studies in asymptomatic patients with severe aortic stenosis and every 2 and 5 years for moderate and mild aortic stenosis, respectively, unless patient condition warrants more frequent monitoring (Bonow et al., 2008; Holmes et al., 2012). The onset of symptoms, with deterioration of echocardiographic changes indicative of severe aortic stenosis (Table), prompts the need for urgent intervention. However, when history, physical examination, and echocardiographical evidence conflict, further evaluation is needed to assess hemodynamic measurements, disease severity, and coronary circulation, especially for those at risk for CAD (Bonow et al., 2008, Holmes et al., 2012).

Classification of Progressive Aortic Stenosis and Frequency of Echocardiogram Monitoring

Table:

Classification of Progressive Aortic Stenosis and Frequency of Echocardiogram Monitoring

A New Treatment Option

TAVR is based on advances in miniaturization and catheter technologies, and involves an advanced form of BAV, in which the diseased aortic valve is compressed against the native annulus, providing sufficient space to anchor a replacement bioprosthetic valve. The bioprosthetic valve contains porcine or bovine leaflets secured to a stent-like scaffolding, which expands initially with balloon inflation and anchors between the left ventricle and aortic root. The prosthetic valve is held in place by either the frame or mesh stent, depending on the manufacturer (McRae, Rodger, & Bailey, 2009).

Preliminary studies indicate TAVR is superior to standard therapy (i.e., only BAV) in patients deemed unsuitable for SAVR (Leon et al., 2010). In a clinical trial with 358 patients (mean age = 83.1 [SD = 8.6] years), Leon et al. (2010) found that the 1-year, all-causes mortality rate for TAVR was significantly lower when compared to standard therapy. Using the New York Heart Association classification system, significant improvements in cardiac symptoms were documented for TAVR patients at 3-, 6-, and 12-month follow up. However, TAVR patients also experienced a significantly higher incidence of bleeding, vascular complications, and transient ischemic attack (TIA) or cerebrovascular attack (CVA) at 30 days and 1 year (Leon et al., 2010).

In a second study, Smith et al. (2011) compared clinical outcomes for 699 high-risk candidates (mean age = 83.6 [SD = 6.8] years) with severe aortic stenosis randomly assigned to TAVR or SAVR treatment groups. Although the mortality rate did not vary significantly between treatment groups, TAVR outcomes were neither inferior nor superior to those of SAVR. Patients in the TAVR group demonstrated higher 30-day and 1-year rates for TIA/CVA and vascular complications. However, patients in the SAVR group demonstrated a significantly higher 30-day all-causes mortality rate and higher rates for major bleeding and new-onset atrial fibrillation.

A third study, by Adams et al. (2014), compared clinical outcomes of 795 candidates (mean age = 83.2 [SD = 7.1] years) with severe aortic stenosis at increased surgical risk, who were randomly assigned to either TAVR or SAVR treatment groups. The investigators found TAVR to be superior to SAVR. The incidence of bleeding, acute kidney injury, and new-onset/worsening atrial fibrillation was reportedly higher in the SAVR group, whereas rates for major vascular complications and permanent pacemaker implantation were higher in the TAVR group.

An important distinction between these three studies was the type of bioprosthetic valve implanted. In the studies conducted by Leon et al. (2010) and Smith et al. (2011), the Edwards Lifesciences Sapien™ was used with the TAVR groups, whereas Adams et al. (2014) used the Medtronic CoreValve®. Structural heart programs affiliated with academic research centers across the United States, Canada, and Europe now offer TAVR as an alternative to SAVR for high-risk candidates otherwise denied surgery.

Nursing Implications

Advance practice nurses (APNs) and RNs should have a clear understanding regarding the classification of calcific aortic stenosis from aortic sclerosis. Teaching patients with aortic stenosis to recognize and immediately report symptoms associated with disease progression, such as activity intolerance, angina, dyspnea on exertion, lightheadedness, and syncope, can reduce subjective denial of symptoms, time to treatment, and mortality.

HF accompanies severe symptomatic aortic stenosis prior to valve replacement. Disease management education by nurses improves patient/family understanding of aortic stenosis and HF, adherence to medication regimens and dietary restrictions, and outcomes through follow up to monitor disease progression (Bonow et al., 2008; Carabello & Paulus, 2009; Holmes et al., 2012).

TAVR patients often return to nonacademic, community, and rural hospitals from valvular heart disease referral centers following implantation. Although most TAVR patients will be monitored annually to maintain registry data by implantation team members, they will also be managed by their primary care physicians and APNs, who are not likely members of the implantation team. Hence, nurses also need to be informed of the traditional plan of care after TAVR.

First and foremost, after TAVR, patients are recovering from debilitating HF while managing stressors related to recent hospitalization, implantation of a foreign device in the heart, and metabolic burdens of concomitant disease, such as chronic atrial fibrillation, hypertension, diabetes, and renal and respiratory insufficiency. Therefore, traditional management of comorbidities continues after TAVR and requires prudent monitoring.

TAVR is associated with a higher incidence of TIA/CVA compared to conventional medical therapy and SAVR (Adams et al., 2014; Leon et al., 2010; Smith et al., 2011). Dual antiplatelet therapy with aspirin and clopidogrel (Plavix®) daily for 3 to 6 months following implantation is common to reduce the risk of thrombotic or thromboembolic events following TAVR (Rodés-Cabau et al., 2013). However, concomitant atrial fibrillation frequently results in withdrawal of clopidogrel and the addition of warfarin (Coumadin®), with the duration of therapy extending indefinitely. Therefore, patients should be informed of the need for regular monitoring to evaluate for unusual bruising, thrombocytopenia, anemia, neutropenia, and bleeding, particularly from the gastrointestinal and genitourinary tracts.

Cardiac arrhythmias are not uncommon after TAVR (Steinberg, Harrison, Frazier-Mills, Hughes, & Piccini, 2012) and occur more frequently following implantation of specific devices. High-grade atrioventricular blocks warrant permanent pacemaker implantation, whereas new-onset atrial fibrillation warrants treatment with antiarrhythmic agents, such as amiodarone (Pacerone®), anticoagulant agents, or both.

After TAVR, octogenarians and nonagenarians have unconsciously limited their activity and associated these limitations to age rather than disease progression (Otto, 2006). Post-procedure reconditioning should continue at home and be augmented with cardiac rehabilitation once cleared by the implantation team and/or primary care provider.

Conclusion

APNs, primary care providers, and general cardiologists (particularly in nonacademic and rural hospitals) may not be aware of recent guidelines established for referrals to valvular heart disease experts or advances in treatment (Bonow et al., 2008; Holmes et al., 2012; Lancellotti et al., 2013). APNs can share this information with team members to improve understanding of disease progression and management and outcomes.

As health care organizations integrate innovations of transcatheter technology into new and existing structural heart programs, APNs and RNs working in critical care, telemetry, and step down will be caring for these patients. In addition, nurses working in nonacademic and rural community hospitals will encounter patients after TAVR while hospitalized for other health care needs. Understanding the pathophysiological changes, clinical manifestations, symptoms associated with disease progression, advanced treatment options, and nursing implications is important as nurses increasingly encounter older adult patients with symptomatic aortic stenosis who may be potential candidates for, or who have already undergone, TAVR.

References

  • Adams, D., Popma, J., Reardon, M., Yakubov, S., Coselli, J., Deeb, G. & Oh, J. (2014). Transcatheter aortic-valve replacement with a self-expanding prosthesis. New England Journal of Medicine, 370, 1790–1798. doi:10.1056/NEJMoa1400590 [CrossRef]
  • Ben-Dor, I., Pichard, A., Satler, L, Goldstein, S., Syed, A., Gaglia, M. & Waksman, R. (2010). Complications and outcome of balloon aortic valvuloplasty in high-risk or inoperable patients. Journal of the American College of Cardiology: Cardiovascular Interventions, 3, 1150–1156. doi:10.1016/j.jcin.2010.08.014 [CrossRef]
  • Bonow, R., Carabello, B., Chatterjee, K., de Leon, A., Faxon, D., Freed, M. & Shanewise, J. (2008). 2008 focused update incorporated into the ACC/AHA 2006 guidelines for the management of patients with valvular heart disease. Journal of the American College of Cardiology, 52, e1–e142. doi:10.1016/j.jacc.2008.05.007 [CrossRef]
  • Carabello, B. & Paulus, W. (2009). Aortic stenosis. The Lancet, 373, 956–966. doi:10.1016/S0140-6736(09)60211-7 [CrossRef]
  • Elmariah, S., Passeri, J., Inglessis, I., Baker, J., Stewart, W., Lindman, B. & Palacios, I. (2014). TCT-686 impact of left ventricular remodeling on clinical outcomes after TAVR: Insights from the PARTNER I trial. Journal of the American College of Cardiology, 64, B200–B201. doi:10.1016/j.jacc.2014.07.758 [CrossRef]
  • Freeman, R. & Otto, C. (2005). Spectrum of calcific aortic valve disease: Pathogenesis, disease progression, and treatment strategies. Circulation, 111, 3316–3326. doi:10.1161/CIRCULATIONAHA.104.486738 [CrossRef]
  • Go, A., Mozaffarian, D., Roger, V., Benjamin, E., Berry, J., Borden, W. & Turner, M. (2013). Heart disease and stroke statistics—2013 update. Circulation, 127, e6–e245. doi:10.1161/CIR.0b013e31828124ad [CrossRef]
  • Holmes, D., Mack, M., Kaul, S., Agnihotri, A., Alexander, K., Bailey, S. & Thomas, J. (2012). 2012 ACCF/AATS/SCAI/STS expert consensus document on transcatheter aortic valve replacement. Journal of the American College of Cardiology, 59, 1200–1254. doi:10.1016/j.jacc.2012.01.001 [CrossRef]
  • Iung, B., Cachier, A., Baron, G., Messika-Zeitoun, D., Delahaye, F., Tornos, P. & Vahanian, A. (2005). Decision-making in elderly patients with severe aortic stenosis: Why are so many denied surgery?European Heart Journal, 26, 2714–2720. doi:10.1093/eurheartj/ehi471 [CrossRef]
  • Klabunde, R.E. (2011). Cardiovascular physiology concepts. Baltimore, MD: Wolters Kluwer Health.
  • Lancellotti, P., Rosenhek, R., Pibarot, P., Iung, B., Otto, C.M., Tornos, P. & Maurer, G. (2013). ESC Working Group on Valvular Heart Disease position paper—Heart valve clinics: Organization, structure, and experiences. European Heart Journal, 34, 1597–1606. doi:10.1093/eurheartj/ehs443 [CrossRef]
  • Leon, M., Smith, C., Mack, M., Miller, D., Moses, J., Svensson, L. & Pocock, S. (2010). Transcatheter aortic-valve implantation for aortic stenosis in patients who cannot undergo surgery. New England Journal of Medicine, 363, 1597–1607. doi:10.1056/NEJMoa1008232 [CrossRef]
  • McRae, M., Rodger, M. & Bailey, B. (2009). Transcatheter and transapical aortic valve replacement. Critical Care Nurse, 29, 22–36. doi:10.4037/ccn2009553 [CrossRef]
  • Nkomo, V.T., Gardin, J.M., Skelton, T.N., Gottdiener, J.S., Scott, C.G. & Enriquez-Sarano, M. (2006). Burden of valvular heart diseases: A population-based study. Lancet, 368, 1005–1011. doi:10.1016/S0140-6736(06)69208-8 [CrossRef]
  • Otto, C.M. (2000). Timing of aortic valve surgery. Heart, 84, 211–218. doi:10.1136/heart.84.2.211 [CrossRef]
  • Otto, C.M. (2006). Valvular aortic stenosis: Disease severity and timing of intervention. Journal of the American College of Cardiology, 47, 2141–2151. doi:10.1016/j.jacc.2006.03.002 [CrossRef]
  • Rajamannan, N.M., Evans, F.J., Aikawa, E., Grande-Allen, K.J., Demer, L.L., Heistad, D.D. & Otto, C.M. (2011). Calcific aortic valve disease: Not simply a degenerative process. Circulation, 124, 1783–1791. doi:10.1161/CIRCULATIONAHA.110.006767 [CrossRef]
  • Rodés-Cabau, J., Dauerman, H.L., Cohen, M.G., Mehran, R., Small, E.M., Smyth, S.S. & Becker, R.C. (2013). Antithrombotic treatment in transcatheter aortic valve implantation: Insights for cerebrovascular and bleeding events. Journal of the American College of Cardiology, 62, 2349–2359. doi:10.1016/j.jacc.2013.03.029 [CrossRef]
  • Smith, C.R., Leon, M.B., Mack, M.J., Miller, D.C., Moses, J.W., Svensson, L.G. & Pocock, S.J. (2011). Transcatheter versus surgical aortic-valve replacement in high-risk patients. New England Journal of Medicine, 364, 2187–2198. doi:10.1056/NEJMoa1103510 [CrossRef]
  • Steinberg, B.A., Harrison, J.K., Frazier-Mills, C., Hughes, G.C. & Piccini, J.P. (2012). Cardiac conduction system disease after transcatheter aortic valve replacement. American Heart Journal, 164, 664–671. doi:10.1016/j.ahj.2012.07.028 [CrossRef]
  • Vahanian, A., Baumgartner, H., Bax, J., Butchart, E., Dion, R., Filippatos, G. & Tamargo, J. (2007). Guidelines on the management of valvular heart disease. European Heart Journal, 28, 230–268. doi:10.1093/eurheartj/ehm095 [CrossRef]

Classification of Progressive Aortic Stenosis and Frequency of Echocardiogram Monitoring

IndicatorMildModerateSevere
Jet velocity (m/s)a<33 to 4>4
Mean gradient (mmHg)b<2525 to 40>40
Valve area (cm2)c>1.51 to 1.5<1
Valve area index (cm2/m2)<0.06
Two-dimensional doppler interval (years)521

10.3928/00989134-20150414-02

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