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• W1997705909 abstract "This document has been developed as an Expert Consensus Document (ECD) by the American College of Cardiology Foundation (ACCF), American Association for Thoracic Surgery (AATS), Society for Cardiovascular Angiography and Interventions, and The Society of Thoracic Surgeons (STS) in collaboration with the American Heart Association (AHA), American Society of Echocardiography, European Association for Cardio-Thoracic Surgery, Heart Failure Society of America, Society of Cardiovascular Computed Tomography, Society of Cardiac Magnetic Resonance, Society of Cardiovascular Anesthesiologists, and Mended Hearts. ECDs are intended to inform practitioners, payers, and other interested parties of the opinion of ACCF and document cosponsors concerning evolving areas of clinical practice and/or technologies that may be widely available or may be new to the practice community. Topics chosen for coverage by ECDs are so designed because the evidence base, the experience with technology, and/or clinical practice are not considered sufficiently well developed to be evaluated by the formal ACCF/AHA Practice Guidelines process. Often the topic is the subject of considerable ongoing investigation. Thus, the reader should view the ECD as the best attempt of the ACCF and document cosponsors to inform and guide clinical practice in areas where rigorous evidence may not yet be available or evidence to date is not widely applied to clinical practice. When feasible, ECDs include indications or contraindications. Some topics covered by ECDs will be addressed subsequently by the ACCF/AHA Practice Guidelines Committee. To avoid actual, potential, or perceived conflicts of interest that may arise as a result of industry relationships or personal interests among the writing committee, all members of the writing committee, as well as peer reviewers of the document, are asked to disclose all current healthcare-related relationships, including those existing 12 months before initiation of the writing effort. The ACCF Task Force on Clinical Expert Consensus Documents (TF CECD) reviews these disclosures to determine what companies make products (on market or in development) that pertain to the document under development. Based on this information, a writing committee is formed to include a majority of members with no relevant relationships with industry or other entity (RWI), led by a chair with no relevant RWI. Authors with relevant RWI are not permitted to draft or vote on text or recommendations pertaining to their RWI. RWI is reviewed on all conference calls and updated as changes occur. Author and peer reviewer RWI pertinent to this document are disclosed in Appendices 1 and 2, Appendices 1 and 2, respectively. Additionally, to ensure complete transparency, authors' comprehensive healthcare-related disclosure information—including RWI not pertinent to this document—is available online (see Online Appendix). Disclosure information for the ACCF TF CECD is also available online at www.cardiosource.org/ACC/About-ACC/Leadership/Guidelines-and-Documents-Task-Forces.aspx, as well as the ACCF disclosure policy for document development at www.cardiosource.org/Science-And-Quality/Practice-Guidelines-and-Quality-Standards/Relationships-With-Industry-Policy.aspx. The work of the writing committee was supported exclusively by the ACCF without commercial support. Writing committee members volunteered their time to this effort. Conference calls of the writing committee were confidential and attended only by committee members. Robert A. Harrington, MD, FACC Chair, ACCF Task Force on Clinical Expert Consensus Documents The Writing Committee consisted of a broad range of members representing 12 societies and the following areas of expertise: cardiothoracic surgery, interventional cardiology, general cardiology, geriatric cardiology, echocardiography, cardiac anesthesiology, cardiac computed tomography (CT), cardiac magnetic resonance (CMR), cardiac nursing, heart failure, neurology, valvular heart disease, structural heart disease, and the consumer perspective. Geographic distribution of members crossed most U.S. time zones and included international representation. Members with expertise using this new and emerging technology and those with expertise in their content area, but not in the procedure discussed herein, served on the committee to provide appropriate balance of perspectives. This writing committee met the College's disclosure requirements for relationships with industry as described in the Preamble. Important to note, if an author works in an institution that serves as a TAVR trial site but has no direct relationship with the trial sponsor or other relevant company (that produces [competing] products or services discussed in this document) or institutional relationship as defined by the ACCF Disclosure Policy for Document Development, the trial site information was not deemed relevant to this writing effort and is not included in the table of relevant author disclosures (Appendix 1). For example, if an author works in an institution where TAVR is performed, but he/she: 1) does not personally perform the procedure; or 2) performs the procedure but has no direct relationship to the trial (e.g., principal investigator, investigator, steering committee member, consultant) and does not oversee funds related to the trial, then the relationship is not included in the table of relevant disclosures. In these situations, these relationships do not even need to be disclosed. However, in the spirit of full disclosure, this information is recorded in the online disclosure table containing all author healthcare relationships. The Writing Committee convened by conference call and e-mail to finalize the document outline, develop the initial draft, revise the draft per committee feedback, and ultimately sign off on the document for external peer review. All participating organizations participated in peer review, resulting in 48 reviewers representing 1,087 comments. Comments were reviewed and addressed by the writing committee. A member of the ACCF TF CECD served as lead reviewer to ensure that all comments were addressed adequately. Both the Writing Committee and TF CECD approved the final document to be sent for board review. The ACCF Board of Trustees, AATS Council, SCAI Board of Directors, and STS Board of Directors reviewed the document, including all peer review comments and Writing Committee responses, and approved the document in January 2012. The AHA, ASE, EACTS, HFSA, Mended Hearts, SCA, SCCT, and SCMR endorsed the document in January 2012. This document is considered current until the TF CECD revises or withdraws it from publication. Transcatheter aortic valve replacement (TAVR) offers new and potentially transformational technology for patients with severe aortic valvular stenosis who are either extremely high-risk candidates or inoperable for surgical aortic valve replacement (AVR) or who are inoperable by virtue of associated comorbidities. In the future, this technology may be utilized in lower risk surgical candidates. An estimated 40,000 patients have received TAVR worldwide. Multiple single and multicenter registries, and a single randomized trial, have documented favorable outcomes using a wide spectrum of endpoints, including survival, symptom status, quality of life, and need for repeat hospitalization. The implementation of TAVR into the flow of patient care is complex, involving consideration of several key factors such as clinical site selection, operator and team training and experience, patient selection and evaluation, procedural performance and complication management, and postprocedural care. Collaborative stakeholder involvement is required in the management of this high-risk patient population with extensive coexistent medical conditions. A previously published document by ACCF and STS identified a high-level series of issues to be addressed regarding this technology [1Holmes Jr., D.R. Mack M.J. Transcatheter valve therapy a professional society overview from the American College of Cardiology Foundation and the Society of Thoracic Surgeons.J Am Coll Cardiol. 2011; 58: 445-455Abstract Full Text Full Text PDF PubMed Google Scholar]. This current collaborative expert consensus document, which involves 12 professional societies, addresses these issues in greater detail with the intent to examine the current state of the evidence, facilitate the integration of this technology into the armamentarium of therapeutic options for patients with aortic valvular stenosis, and to enable responsible adoption and diffusion of this promising technology. This document has focused on published data; it must be remembered that there is only 1 single completed randomized trial, although others are in progress or planned; much of the data in this expert consensus document is based upon information from studies and registries, both surgical and TAVR, which are frequently retrospective and include self-reported clinical events rather than adjudicated events. The most common cause of valvular aortic stenosis (AS) in adults is calcification of a normal trileaflet or congenital bicuspid valve [2Roberts W.C. Ko J.M. Frequency by decades of unicuspid, bicuspid, and tricuspid aortic valves in adults having isolated aortic valve replacement for aortic stenosis, with or without associated aortic regurgitation.Circulation. 2005; 111: 920-925Crossref PubMed Scopus (217) Google Scholar, 3Selzer A. Changing aspects of the natural history of valvular aortic stenosis.N Engl J Med. 1987; 317: 91-98Crossref PubMed Google Scholar, 4Stephan P.J. Henry III, A.C. Hebeler Jr., R.F. et al.Comparison of age, gender, number of aortic valve cusps, concomitant coronary artery bypass grafting, and magnitude of left ventricular-systemic arterial peak systolic gradient in adults having aortic valve replacement for isolated aortic valve stenosis.Am J Cardiol. 1997; 79: 166-172Abstract Full Text Full Text PDF PubMed Google Scholar]. Calcific AS is characterized by lipid accumulation, inflammation, fibrosis, and calcification [5Ghaisas N.K. Foley J.B. O'Briain D.S. et al.Adhesion molecules in nonrheumatic aortic valve disease: endothelial expression, serum levels and effects of valve replacement.J Am Coll Cardiol. 2000; 36: 2257-2262Abstract Full Text Full Text PDF PubMed Scopus (68) Google Scholar, 6Otto C.M. Kuusisto J. Reichenbach D.D. et al.Characterization of the early lesion of 'degenerative' valvular aortic stenosis Histological and immunohistochemical studies.Circulation. 1994; 90: 844-853Crossref PubMed Google Scholar] and is common in the United States. It typically presents in older individuals (i.e., >75 years) in contrast to bicuspid AS, which presents a decade or more earlier. Rheumatic AS, uncommon in the Western world, occurs due to fusion of the commissures with scarring and calcification of the cusps, and retraction of the leaflets resulting in the valve being both regurgitant and stenotic. In adults with valvular AS, the obstruction develops gradually, typically over many years during which the left ventricle (LV) adapts to the systolic pressure overload with progressive concentric hypertrophy that results in diastolic dysfunction [4Stephan P.J. Henry III, A.C. Hebeler Jr., R.F. et al.Comparison of age, gender, number of aortic valve cusps, concomitant coronary artery bypass grafting, and magnitude of left ventricular-systemic arterial peak systolic gradient in adults having aortic valve replacement for isolated aortic valve stenosis.Am J Cardiol. 1997; 79: 166-172Abstract Full Text Full Text PDF PubMed Google Scholar, 7Peterson K.L. Tsuji J. Johnson A. et al.Diastolic left ventricular pressure-volume and stress-strain relations in patients with valvular aortic stenosis and left ventricular hypertrophy.Circulation. 1978; 58: 77-89Crossref PubMed Google Scholar, 8Spann J.F. Bove A.A. Natarajan G. et al.Ventricular performance, pump function and compensatory mechanisms in patients with aortic stenosis.Circulation. 1980; 62: 576-582Crossref PubMed Google Scholar], reduced coronary reserve [9Carabello B.A. Paulus W.J. Aortic stenosis.Lancet. 2009; 373: 956-966Abstract Full Text Full Text PDF PubMed Scopus (113) Google Scholar, 10Marcus M.L. Doty D.B. Hiratzka L.F. et al.Decreased coronary reserve: a mechanism for angina pectoris in patients with aortic stenosis and normal coronary arteries.N Engl J Med. 1982; 307: 1362-1366Crossref PubMed Google Scholar], myocardial ischemia [11Koyanagi S. Eastham C.L. Harrison D.G. et al.Increased size of myocardial infarction in dogs with chronic hypertension and left ventricular hypertrophy.Circ Res. 1982; 50: 55-62Crossref PubMed Google Scholar], and eventually, depressed contractility resulting in LV systolic dysfunction [12Gunther S. Grossman W. Determinants of ventricular function in pressure-overload hypertrophy in man.Circulation. 1979; 59: 679-688Crossref PubMed Google Scholar, 13Krayenbuehl H.P. Hess O.M. Ritter M. et al.Left ventricular systolic function in aortic stenosis.Eur Heart J. 1988; 9: 19-23Crossref PubMed Google Scholar, 14Carabello B.A. Green L.H. Grossman W. et al.Hemodynamic determinants of prognosis of aortic valve replacement in critical aortic stenosis and advanced congestive heart failure.Circulation. 1980; 62: 42-48Crossref PubMed Google Scholar]. Ultimately, in some patients, heart failure or sudden death occurs. Typically, patients with AS are free from cardiovascular symptoms (i.e., angina, syncope, and heart failure) until late in the course of the disease. However, once symptoms manifest, the prognosis is poor, with the interval from the onset of symptoms to the time of death being approximately 2 years in patients with heart failure, 3 years in those with syncope, and 5 years in those with angina [15Leon M.B. Smith C.R. Mack M. et al.Transcatheter aortic-valve implantation for aortic stenosis in patients who cannot undergo surgery.N Engl J Med. 2010; 363: 1597-1607Crossref PubMed Scopus (1013) Google Scholar]. Gardin et al. reported that among symptomatic patients with moderate-to-severe AS treated medically, mortality rates after the onset of symptoms were approximately 25% at 1 year and 50% at 2 years [16Gardin J.M. Kaplan K.J. Meyers S.N. et al.Aortic stenosis: can severity be reliably estimated noninvasively?.Chest. 1980; 77: 130-131Crossref PubMed Google Scholar], with approximately 50% of deaths being sudden. In the elderly high-risk patients in the PARTNER (Placement of Aortic Transcatheter Valve) trial who were treated medically (Cohort B), the survival at 1 year was only 50% [15Leon M.B. Smith C.R. Mack M. et al.Transcatheter aortic-valve implantation for aortic stenosis in patients who cannot undergo surgery.N Engl J Med. 2010; 363: 1597-1607Crossref PubMed Scopus (1013) Google Scholar]. The natural history of AS has changed since the publication of the seminal paper by Morrow and colleagues in 1968 [17Morrow A.G. Roberts W.C. Ross Jr., J. et al.Obstruction to left ventricular outflow Current concepts of management and operative treatment.Ann Intern Med. 1968; 69: 1255-1286Crossref PubMed Google Scholar]. The original data were derived largely from patients with rheumatic AS or AS due to a bicuspid aortic valve, with an average age of death of 63 years. On the contrary, patients being considered for TAVR on a trileaflet valve present much later in life, typically in their late 70s or older, and have dominantly fibrocalcific AS. Although now occurring later in life, the onset of symptoms still heralds a rapid decline with medical therapy alone [15Leon M.B. Smith C.R. Mack M. et al.Transcatheter aortic-valve implantation for aortic stenosis in patients who cannot undergo surgery.N Engl J Med. 2010; 363: 1597-1607Crossref PubMed Scopus (1013) Google Scholar]. Assessment of the severity of stenosis does not differ in TAVR patients compared with the general AS population, and decisions should therefore be based upon established guidelines [18Baumgartner H. Hung J. Bermejo J. et al.Echocardiographic assessment of valve stenosis: EAE/ASE recommendations for clinical practice.J Am Soc Echocardiogr. 2009; 22: 1-23Abstract Full Text Full Text PDF PubMed Scopus (236) Google Scholar]. Although invasive cardiac catheterization has historically been the standard for quantification of AS, this function has been largely replaced by echocardiography [19Popovic A.D. Thomas J.D. Neskovic A.N. et al.Time-related trends in the preoperative evaluation of patients with valvular stenosis.Am J Cardiol. 1997; 80: 1464-1468Abstract Full Text Full Text PDF PubMed Scopus (10) Google Scholar]. Echocardiographic diagnosis is made by the observation of a calcified valve with restricted leaflet opening by two-dimensional (2D) echocardiography with quantification of the peak and mean AV gradient made by applying the simplified Bernoulli equation (Δp = 4v2) to the maximal velocity recorded through the aortic valve by continuous-wave Doppler. Multiple imaging windows (apical 4-chamber and long-axis, right parasternal, suprasternal notch, and subcostal views) should be obtained to assure acquisition of the maximal velocity and to avoid angle-related errors. Although aortic valve area (AVA) can be measured by planimetry, it is more accurately assessed by application of the continuity equation, using pulsed-wave Doppler in the left ventricular outflow tract (LVOT) and continuous-wave Doppler across the valve. Severe stenosis is defined in the guidelines as a peak velocity >4.0 m/s (corresponding to a peak gradient of 64 mm Hg), a mean gradient >40 mm Hg, OR valve area <1.0 cm2 when LV systolic function is normal. To account for patient size, the valve area is often indexed to body surface area, with 0.6 cm2/m2 considered to be the threshold for severe AS. An important exception is when the gradient suggests less severe stenosis than the valve area, most commonly due to low stroke volume, either in dilated ventricles with low ejection fraction (EF) or small ventricles with normal EF. In this setting, a dobutamine stress study (maximum stress dose 20 mcg/kg/min), may be helpful. If the maximum jet velocity rises over 4 m/s with the dobutamine-induced increase in stroke volume whereas the AVA remains less than 1.0 cm2, then the valve is truly severely stenotic. On the other hand, if stroke volume increases with little rise in gradient (causing valve area to increase substantially), then the AS is only mild to moderate in severity, and the LV dysfunction is due to causes other than AS [20Blais C. Burwash I.G. Mundigler G. et al.Projected valve area at normal flow rate improves the assessment of stenosis severity in patients with low-flow, low-gradient aortic stenosis: the multicenter TOPAS (Truly or Pseudo-Severe Aortic Stenosis) study.Circulation. 2006; 113: 711-721Crossref PubMed Scopus (55) Google Scholar, 21Grayburn P.A. Assessment of low-gradient aortic stenosis with dobutamine.Circulation. 2006; 113: 604-606Crossref PubMed Scopus (18) Google Scholar, 22Monin J.L. Monchi M. Gest V. et al.Aortic stenosis with severe left ventricular dysfunction and low transvalvular pressure gradients: risk stratification by low-dose dobutamine echocardiography.J Am Coll Cardiol. 2001; 37: 2101-2107Abstract Full Text Full Text PDF PubMed Scopus (132) Google Scholar]. Occasionally, the AVA appears larger than the elevated gradient would suggest, usually due to elevated stroke volume from aortic regurgitation (AR), anemia, fever, or hyperthyroidism. Sometimes, though, it reflects a technical error in applying the continuity equation, when the blood accelerates within the LVOT due to an upper septal bulge, which may result in an overestimation of valve area. To avoid this, one can try to measure the LVOT area at the point of maximal velocity, though the geometry is often quite distorted in this region, making estimation of the LVOT area difficult. Alternatively, one can use the LV stroke volume (from 2D or three-dimensional [3D] measurements of the LV, ideally with contrast infusion) or right ventricular (RV) stroke volume (from RV outflow tract) as the input into the continuity equation. Dividing this stroke volume by the time velocity integral of the AV continuous-wave Doppler will also yield the AVA, independent of any distortion in the LVOT. Despite the convenience and wide-spread applicability of transthoracic echocardiography (TTE), there are occasions when invasive measurements are needed, such as in patients with a discrepancy between clinical and echocardiographic assessments. In such cases, catheterization should generally be performed with dual catheters, 1 placed in the LV, the other in the proximal aorta to obtain simultaneous pressure measurements and obtain the most accurate assessment of the gradient. Infusion of dobutamine may allow assessment of low-output, low-gradient AS in the catheterization laboratory [23Nishimura R.A. Grantham J.A. Connolly H.M. et al.Low-output, low-gradient aortic stenosis in patients with depressed left ventricular systolic function: the clinical utility of the dobutamine challenge in the catheterization laboratory.Circulation. 2002; 106: 809-813Crossref PubMed Scopus (132) Google Scholar]. Other adjunctive testing used in quantifying AS includes transesophageal echocardiography (TEE) [24Shanewise J.S. Cheung A.T. Aronson S. et al.ASE/SCA guidelines for performing a comprehensive intraoperative multiplane transesophageal echocardiography examination: recommendations of the American Society of Echocardiography Council for Intraoperative Echocardiography and the Society of Cardiovascular Anesthesiologists Task Force for Certification in Perioperative Transesophageal Echocardiography.Anesth Analg. 1999; 89: 870-884PubMed Google Scholar], CT scanning (dynamic or gated during systole) [25Greenland P. Bonow R.O. Brundage B.H. et al.ACCF/AHA 2007 clinical expert consensus document on coronary artery calcium scoring by computed tomography in global cardiovascular risk assessment and in evaluation of patients with chest pain: a report of the American College of Cardiology Foundation Clinical Expert Consensus Task Force (ACCF/AHA Writing Committee to Update the 2000 Expert Consensus Document on Electron Beam Computed Tomography).J Am Coll Cardiol. 2007; 49: 378-402Abstract Full Text Full Text PDF PubMed Scopus (385) Google Scholar], and CMR [26Hundley W.G. Bluemke D.A. Finn J.P. et al.ACCF/ACR/AHA/NASCI/SCMR 2010 expert consensus document on cardiovascular magnetic resonance: a report of the American College of Cardiology Foundation Task Force on Expert Consensus Documents.J Am Coll Cardiol. 2010; 55: 2614-2662Abstract Full Text Full Text PDF PubMed Scopus (92) Google Scholar]. The presence or absence of symptoms should guide the management of AS patients, yet in many cases, this important clinical benchmark is difficult to establish, owing to the subjective nature of the symptoms and comorbid conditions such as chronic lung disease in this patient population. In general, stress testing is contraindicated when symptoms are present because of the potential for complications in these patients. However, in patients with equivocal symptoms, stress testing, and in particular stress echocardiography, can be very helpful [27Lancellotti P. Lebois F. Simon M. et al.Prognostic importance of quantitative exercise Doppler echocardiography in asymptomatic valvular aortic stenosis.Circulation. 2005; 112: I377-I382PubMed Google Scholar]. Simple determination of functional capacity may help show limitations of which a patient may be unaware. Isolated echocardiographic (ECG) changes during the stress test without symptoms or change in blood pressure should not be interpreted as a positive indicator of severe AS. Other potential markers for AS severity include signs of LV dysfunction on exercise echo or a rise in left atrial or right ventricular pressure [28Bonow R.O. Carabello B.A. 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).J Am Coll Cardiol. 2008; 52: e1-e142Abstract Full Text Full Text PDF PubMed Scopus (548) Google Scholar, 29Vahanian A. Baumgartner H. Bax J. et al.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: 230-268PubMed Google Scholar]. With severe, symptomatic, calcific AS, AVR is the only effective treatment that improves symptoms and prolongs survival [30Connolly H.M. Oh J.K. Orszulak T.A. et al.Aortic valve replacement for aortic stenosis with severe left ventricular dysfunction Prognostic indicators.Circulation. 1997; 95: 2395-2400Crossref PubMed Google Scholar, 31Kvidal P. Bergstrom R. Horte L.G. et al.Observed and relative survival after aortic valve replacement.J Am Coll Cardiol. 2000; 35: 747-756Abstract Full Text Full Text PDF PubMed Scopus (207) Google Scholar]. These results are partly dependent on LV function. In the setting of LV dysfunction caused by afterload mismatch, survival is still improved, although improvement in LV function and resolution of symptoms might be incomplete after AVR. Age itself is a risk factor for adverse outcome, but it is not a contraindication to AVR even in the very elderly [32Kolh P. Kerzmann A. Honore C. et al.Aortic valve surgery in octogenarians: predictive factors for operative and long-term results.Eur J Cardiothorac Surg. 2007; 31: 600-606Crossref PubMed Scopus (129) Google Scholar, 33Litmathe J. Feindt P. Kurt M. et al.Aortic valve replacement in octogenarians: outcome and predictors of complications.Hellenic J Cardiol. 2011; 52: 211-215PubMed Google Scholar]. In patients with moderate AS, who are undergoing coronary artery bypass graft surgery (CABG), AVR should be performed at the time of revascularization irrespective of symptoms related to moderate AS [34Pereira J.J. Balaban K. Lauer M.S. et al.Aortic valve replacement in patients with mild or moderate aortic stenosis and coronary bypass surgery.Am J Med. 2005; 118: 735-742Abstract Full Text Full Text PDF PubMed Scopus (29) Google Scholar, 35Smith W.T. Ferguson Jr., T.B. Ryan T. et al.Should coronary artery bypass graft surgery patients with mild or moderate aortic stenosis undergo concomitant aortic valve replacement? A decision analysis approach to the surgical dilemma.J Am Coll Cardiol. 2004; 44: 1241-1247Abstract Full Text Full Text PDF PubMed Scopus (42) Google Scholar]. There are no data to support performing AVR for mild AS at the time of CABG. Patients undergoing surgical AVR with significant stenoses (>50% to 70% stenosis) in major coronary arteries should be treated with concomitant CABG. Options in patients with combined AS and CAD continue to grow with the use of hybrid procedures where PCI is followed by valve surgery. It is possible that such a strategy could be performed in the setting of TAVR [36Adams D.H. Chikwe J. Filsoufi F. et al.The year in cardiovascular surgery.J Am Coll Cardiol. 2011; 57: 1425-1444Abstract Full Text Full Text PDF PubMed Scopus (4) Google Scholar, 37Byrne J.G. Leacche M. Unic D. et al.Staged initial percutaneous coronary intervention followed by valve surgery (“hybrid approach”) for patients with complex coronary and valve disease.J Am Coll Cardiol. 2005; 45: 14-18Abstract Full Text Full Text PDF PubMed Scopus (51) Google Scholar]. Patients with severe AS often have additional associated significant valvular heart disease. Treatment of these lesions in patients undergoing AVR should be undertaken using standard criteria. However, treatment of associated valvular lesions may increase the risk of AVR [38He G.W. Acuff T.E. Ryan W.H. et al.Aortic valve replacement: determinants of operative mortality.Ann Thorac Surg. 1994; 57: 1140-1146Abstract Full Text PDF PubMed Google Scholar]. A special circumstance is that of pulmonary hypertension (PH) either primary or secondary (reactive or related to increased LV end-diastolic pressure). Both conditions may increase the risk of AVR and must be taken into consideration in the risk/benefit ratio. PH can be present in patients with severe AS, either from the transmission of increased LV diastolic and/or left atrial pressures, associated mitral regurgitation (MR), or from a secondary increase in pulmonary vascular tone. The prevalence of PH in patients with AS is undefined, varying widely on the definition used and the population studied [39Pai R.G. Varadarajan P. Kapoor N. et al.Aortic valve replacement improves survival in severe aortic stenosis associated with severe pulmonary hypertension.Ann Thorac Surg. 2007; 84: 80-85Abstract Full Text Full Text PDF PubMed Scopus (23) Google Scholar, 40Kapoor N. Varadarajan P. Pai R.G. Echocardiographic predictors of pulmonary hypertension in patients with severe aortic stenosis.Eur J Echocardiogr. 2008; 9: 31-33PubMed Google Scholar]. Clinically, PH associated with critical AS portends a poor prognosis and is associated with an increased risk of sudden cardiac death [41McHenry M.M. Rice J. Matlof H.J. et al.Pulmonary hypertension and sudden death in aortic stenosis.Br Heart J. 1979; 41: 463-467Crossref PubMed Google Scholar]. Consistent with the surgical valve implant experience, PH after TAVR is a predictive factor for both early (30-day) and late (1-year) mortality, similar in risk to major access site complications and renal insufficiency [39Pai R.G. Varadarajan P. Kapoor N. et al.Aortic valve replacement improves survival in severe aortic stenosis associated with severe pulmonary hypertension.Ann Thorac Surg. 2007; 84: 80-85Abstract Full Text Full Text PDF PubMed Scopus" @default.
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• W1997705909 title "2012 ACCF/AATS/SCAI/STS Expert Consensus Document on Transcatheter Aortic Valve Replacement" @default.
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