A New Option for the Treatment of Aortic Stenosis: Percutaneous Aortic Valve Replacement

Percutaneous heart valve implantation offers hope for patients with aortic stenosis.Aortic stenosis is the most prevalent valvular heart disease and the third most common cardiovascular condition after coronary artery disease and hypertension.1 Acquired aortic stenosis primarily affects the elderly and causes debilitating signs and symptoms and decreased quality of life.2 Over time, progressive calcification and immobilization of the valve leaflets cause stiffening and narrowing of the aortic leaflets, scarring, impaired valve opening, reduced cardiac output, and, eventually, heart failure.3 Although patients usually remain asymptomatic for a long time, once the classic triad of angina, syncope, and indications of exertional dyspnea and congestion develop, the prognosis becomes dramatically worse.1Aortic stenosis has been documented in 2% to 4% of patients more than 65 years old; the incidence is higher in men than in women.4 Increasing evidence4–6 indicates that the disease is accelerated by the same factors that affect coronary artery disease, including smoking, hypercholesterolemia, hypertension, and diabetes. Until now, surgical valve replacement, pioneered in the 1960s with mechanical or tissue prostheses, was the only effective treatment available to alleviate signs and symptoms and prolong life in patients with severe aortic stenosis.4,7 Surgical aortic valve replacement improves quality of life and prognosis,8 but the procedure is a high-risk one for patients of advanced age who have multisystem dysfunction and calcific aortic stenosis.9Interventional cardiology is rapidly evolving to include innovative approaches to manage valvular heart disease. In 2002, Cribier et al10 reported the first successful human percutaneous aortic valve implantation done via an antegrade transvenous approach. This procedure was technically complex; the implant valve was guided through an interventricular transseptal puncture, across the mitral valve, and then placed in the native aortic annulus. Complications associated with difficulties in steering and stabilizing the equipment, as well as risks of mitral valve damage and pericardial tamponade, prompted development of the arterial retrograde approach. The cardiac catheterization team at the Heart Centre at St. Paul’s Hospital in Vancouver, British Columbia, under the medical leadership of John Webb, MD, has been involved in the development and early evaluation of a percutaneous heart valve replacement program. Initial findings have been reported,9 and, to date, more than 100 procedures have been successfully performed at St. Paul’s Hospital.Such innovations in clinical practice challenge critical care nurses to adapt rapidly, take a leadership role to guide program development, define the care of patients undergoing new procedures, and meet the learning needs of patients and staff. In this article, we review the pathophysiology and clinical features of aortic stenosis, describe the emerging option of percutaneous aortic valve replacement, and discuss implications for critical care nurses.The aortic valve is a trileaflet semilunar valve located between the left ventricle and the arch of the aorta. The valve opens during systole because of the contractile force of the left ventricle, allowing rapid ventricular ejection and circulation to the arterial system. In adults, the area of the aortic valve is normally 3.0 to 4.0 cm2 when the valve is open.11 The 2 coronary artery ostia are located immediately above the valve, ensuring coronary perfusion during diastole when the aortic valve is closed.The restricted opening of the valve leaflets in aortic stenosis is due to progressive calcific changes of either a normal trileaflet or a congenitally bicuspid valve, or to the effects of rheumatic heart disease.4 Until recently, calcific aortic stenosis was considered a degenerative disease of the elderly. However, new evidence11 suggests that aortic stenosis and coronary artery disease have common features; aortic stenosis is now thought to be an active disease involving deposition of lipoproteins, chronic inflammation, and active calcification of the leaflets.12 For example, recent histopathological studies have shown plaquelike lesions on the leaflets of stenotic valves and evidence of accumulation of low-density lipoproteins, oxidation, inflammatory cell infiltrates, and microscopic calcification. These findings are consistent with the pathophysiology and disease progression of atherosclerosis.12As calcium deposits accumulate, the mobility of the aortic leaflets depends on the capacity of the left ventricle to force open the valve during systole.6 Thickening of valve leaflets and the progressive obstruction of left ventricular outflow impair aortic valve hemodynamics and increase left ventricular afterload, resulting in increased thickness of the wall of the left ventricle, diastolic dysfunction, and, less commonly, decreased systolic performance.4 Even in instances of severe aortic stenosis, the left ventricle can initially maintain normal contractility and adequate stroke volume at rest.4 Progressive pressure overload on the left ventricle leads to concentric hypertrophy. This increased muscle mass is an adaptive response to chronic high left ventricular pressure, enabling the left ventricle to generate enough force to propel blood past the stenotic valve. Such cardiac remodeling also has the deleterious effect of decreasing coronary blood flow reserve, causing both diastolic and systolic left ventricular dysfunction and producing the signs and symptoms of congestive heart failure.11Hemodynamically, disturbances become evident only after the valve area has been reduced from the normal area of 3 to 4 cm2 to less than 2 cm2. The additional reduction from half its normal size to 1 cm2 produces severe obstruction to ejection of stroke volume and contributes to progressive pressure on the left ventricle. The increasing pressure gradient between the left ventricle and the aorta and the reduced cross-sectional area of valve opening indicate worsening disease severity11 (Table 1). Figure 1 shows hemodynamic tracings associated with measurement of the pressure gradient in normal cardiac function and in severe aortic stenosis.The rate of progression of aortic stenosis varies among patients, and predictors of outcomes are not well established.6,12 Nevertheless, it is known that mild aortic stenosis can progress to critical disease within a few years. The mean transaortic pressure gradient increases 7 mm Hg/y, and the stenotic valve area decreases 0.1 cm2/y.4,6 Progressively, these changes impair the capacity of the left ventricle to supply an appropriate increase in cardiac output during exercise or in other situations that trigger increased oxygen demand.4Increasing severity of aortic stenosis is poorly correlated with the development of signs and symptoms: the absence of signs and symptoms does not rule out reduction in valve area or development of ventricular systolic dysfunction.6 Many patients initially have decreased exercise tolerance and other vague signs and symptoms. These may be misinterpreted by patients and care providers as the inevitable results of aging.4 A thorough assessment may reveal one or more of the classic manifestations of progressive aortic stenosis: angina, syncope, and heart failure. The development of symptomatic aortic stenosis gravely affects life span; in the absence of aortic valve replacement, half of patients with angina will die within 3 to 5 years. Likewise, the mean survival of patients with severe aortic stenosis is 3 years for those who experience syncope and 2 years for those who have dyspnea.11,14 Sudden death may occur in 3% to 5% of patients with asymptomatic aortic stenosis.6 Figure 2 shows the relationship between the onset of signs and symptoms and mortality in treated and untreated severe aortic stenosis.Dyspnea is usually the result of diastolic dysfunction caused by chronic and severely increased after-load and left ventricular filling pressures. Angina is a manifestation of increased oxygen demand caused by the hypertrophied left ventricle and reduced supply due to alterations in coronary blood flow. Exertional syncope is caused by the inability of the left ventricle to produce the amount of stroke volume required by the increased demand of exercise. Because the fixed obstructive effect of the stenotic aortic valve causes increased ventricular after-load, peripheral vasodilatation normally associated with exercise leads to hypotension and decreased cerebral perfusion.4 The signs and symptoms associated with severe aortic stenosis are summarized in Table 2.Echocardiography is the standard means of evaluation of aortic stenosis. Leaflet anatomy and restriction of cusp movement, severity of calcification and stenosis, mean pressure gradient, thickness of the wall of the left ventricle, systolic and diastolic volume, ejection fraction, and diastolic function are measures of the severity of disease progression. In combination, this information helps guide management.4,12 The transaortic pressure gradient is calculated from Doppler velocity by using standard echocardiographic techniques. In addition, size of the left atrium, pulmonary pressures, and right ventricular function are also assessed, because chronically elevated left ventricular diastolic pressures may result in pulmonary hypertension and right ventricular dysfunction.4Cardiac catheterization may be used to supplement the diagnostic information provided by echocardiography by providing measurements of pressure gradient and valve area. In addition, coronary angiography is routinely performed because of the high prevalence of coronary artery disease among patients who have aortic stenosis.4 High-resolution computed tomography and cardiac magnetic resonance imaging may be future options for the diagnosis of aortic stenosis.4,6 Because of the hemodynamic implications of severe aortic stenosis, exercise stress testing is unwarranted and dangerous, although it may have a role in diagnosis of milder forms of the disease.11Because of its innovative nature, little specific evidence supports valvular interventional cardiology. In order to facilitate communication, coordination of roles, and sequencing of activities within the multidisciplinary team involved in the care of patients undergoing percutaneous heart valve (PHV) implantation, a clinical care map based on existing evidence and best practice has been developed (Table 3). The objective of the care map is to improve the quality of care, reduce risks, increase patients’ satisfaction, and optimize resource utilization.15Before PHV implantation, patients undergo rigorous diagnostic testing to evaluate their suitability for the procedure, including ileofemoral contrast vascular angiography to assess arterial vascular access size and patency and coronary angiography with percutaneous coronary intervention, if appropriate, to optimize cardiac perfusion. Renal function is evaluated (serum levels of urea and creatinine, glomerular filtration rate), and coagulation studies are performed, especially if patients are receiving oral anticoagulants.Because of the advanced age of patients undergoing PHV implantation, anticipating, assessing, and managing clinical issues are especially challenging. A careful review of each patient’s functional status, comorbid conditions, family and community support, and quality of life is essential to meet the patient’s needs during hospitalization and to facilitate the discharge process.The day before admission, patients are seen in the preassessment clinic. Patients are assessed by a nurse practitioner to establish baseline findings and begin discharge planning. Patients must also be assessed by the anesthesia service, because they will require general anesthesia during the implant procedure.Coordination of cardiac echocardiography and vascular surgery services is needed to facilitate transesophageal echocardiography during the procedure and closure of the vascular access site after the procedure. Immediately before the procedure, a nurse administers aspirin, clopidogrel, and a prophylactic intravenous antibiotic.Percutaneous heart valve implantation is performed either in a cardiac catheterization laboratory or in an operating room that has the capacity for hemodynamic monitoring and fluoroscopy imaging. In preparation for a procedure that may take up to 3 hours, patients are positioned carefully and appropriately, according to perioperative nursing standards, including use of padding materials under all bony prominences, tucking techniques to ensure the patients’ safety, and warming equipment to prevent heat loss during the procedure.16 A urinary catheter is inserted to track urine output. Standard equipment is used to monitor heart rate and rhythm, respiratory rate and oxygen saturation, and arterial blood pressure.Patients undergo parenteral induction for general anesthesia, which is then maintained with inhaled agents for the duration of the procedure. Because patients with aortic stenosis usually have vasoconstriction before induction and can easily become hypotensive with the administration of anesthetics, aggressive treatment of hypotension may be started with an α-adrenergic agonist such as phenylephrine. Early intervention decreases the risks of decreased coronary perfusion, myocardial perfusion, ventricular dysfunction, and cardiovascular collapse associated with sudden hypotension in patients with severe aortic stenosis.13Although the actual valve deployment takes less than 20 seconds, the PHV procedure requires careful preparation of the access site, steering of catheters, and placement of the valve apparatus with the aid of fluoroscopic and echocardiographic imaging. The following events occur during the procedure:Our experience has been with the Cribier-Edwards valve (Edwards LifeSciences, Irvine, California), which consists of a large tubular stainless steel stent with an attached bovine pericardial trileaflet valve. The stent-valve is available with a diameter of 23 or 26 mm with a height of 14.5 or 16 mm, respectively (Figures 3 and 4). A deflectable guiding catheter (Edwards LifeSciences) and a valvuloplasty delivery balloon catheter onto which the stent-valve is crimped, are used to steer and deploy the device.In preparation for the implant, aortic balloon valvuloplasty is performed to separate the calcified valve leaflets and improve the pressure gradient between the left ventricle and the aorta. Great care is taken during the advancement of the delivery catheter and the prosthetic valve because vessel tortuosity, peripheral vascular disease, and calcification can be severe. As in routine interventional cardiology procedures, injection of contrast agent and fluoroscopy are used to visualize catheter and stent placement. In addition, information provided by transesophageal echocardiography is used to guide delivery and implantation of the stent-valve.When the position of the stent-valve within the native aortic annulus is confirmed, the device is ready for deployment. Short-term, rapid, right ventricular pacing, which reduces cardiac wall motion, left ventricular blood ejection, and transaortic flow, is used to prevent the stent-valve from slipping from its correct position during balloon inflation. A temporary pacing lead is placed in the right ventricle via the femoral vein and is connected to a temporary pacemaker pulse generator.Coordination and clear communication between the interventional cardiologist and the critical care nurse responsible for initiating and terminating pacing are essential during the rapid sequence of pacing and stent deployment (see Along Side). The cardiologist observes the fluoroscopic image, maintains valve position, and coordinates balloon inflation and stent deployment; the circulating nurse initiates pacing when requested, at a rate of 200 to 220 impulses per minute, and observes for reliable pacemaker capture and desired reduction in arterial pressure (Figure 5). Initiation of pacing resulting in adequately decreased cardiac output is promptly followed by rapid inflation and deflation of the stent-deployment valvuloplasty balloon and termination of pacing with return of normal rhythm and cardiac output. Figures 6 and 7 show placement and deployment of the stent-valve.Once the catheter delivery system is pulled back, the deployed stent-valve should cover the native aortic valve leaflets and be tightly fitted within the aortic valve annulus. This positioning ensures that the coronary ostia, which are situated immediately above the aortic valve, are unobstructed and patent (Figure 8). Angiography of the right and left coronary arteries is performed to assess coronary blood flow, because any degree of blockage by the newly implanted valve could cause decreased coronary perfusion, leading to myocardial ischemia and impaired cardiac output.Perivalvular leakage and aortic insufficiency are ruled out by using aortic root angiography and trans-esophageal echocardiography. Hemodynamic pressure measurement is used to confirm the extent of improvement in the pressure gradient between the aorta and the left ventricle.In the immediate period after implantation, the focus is on repairing the femoral artery and achieving hemostasis. The removal of a 22F (8 mm) to 24F (9 mm) sheath in an elderly with peripheral vascular disease and calcification be with standard techniques for sheath for a vascular to the procedure team after valve deployment. In addition, nurses from the cardiac catheterization laboratory who have additional and in vascular operating room with the surgical closure of the This has in and accelerated and and early and Early indicates for the development of a vascular closure device to surgical the procedure, patients are to a critical care area by with the of cardiac patients, the focus is from general anesthesia, of adequate and assessment of the vascular standard and is on ensuring in size or movement, or response could indicate an of a calcified valve, aortic and arterial system may result in Because elderly patients experience alterations in of after general anesthesia, it is that nurses and thorough to early and as monitoring is by hemodynamic monitoring of arterial and pressure to early of cardiac or PHV patients are to risks for myocardial including the of the device to the coronary ostia, a high incidence of coronary artery disease, and the for alterations in cardiac output due to the implant procedure. monitoring and after the procedure for early of myocardial may also be impaired by aortic insufficiency and due to the stent-valve is not deployed or does not the native annulus blood may from the aorta the left ventricle through the of In aortic the left ventricle to causing a increase in left and ventricular pressures, congestive heart and pulmonary monitor for vascular access including and the femoral site and and the movement, and in the in the first after to the area and then for the 4 The must be and the of the should be elevated more than for after with maintained for to after the procedure. include a in the arterial and or computed tomography may be required if or ischemia are measures are started after the procedure to and risks associated with including increased myocardial demand and Because intravenous can cause in elderly patients, we and early of large amount of contrast required for a long fluoroscopic procedure is especially in patients with impaired if a patient’s glomerular filtration rate is less than a to prevent is normal is at a rate of per for the of the procedure. levels of and urea and glomerular filtration rate are for the 2 and at the of order to early and return to normal function and to elderly patients’ risks for in and alterations in and and urinary function associated with to a critical care should be to rapidly PHV patients to an care, or the day after the procedure. to rapidly care assessment for is to facilitate discharge and return and hemodynamic monitoring and urinary catheterization are before patients are from the coronary care to facilitate and Patients must as early as the day after the procedure, to prevent and of all including cardiac and is because are not required in the and should be by the patient’s care agent such as is usually for a to prevent within the stent valve. Early with or care nursing services may additional for discharge patients also undergo echocardiography and fluoroscopy to assess and valve These diagnostic are well and not require levels of and and are during the after the implant more than 100 patients have successful percutaneous aortic valve replacement at St. Paul’s The of this new practice has not been to the cardiac catheterization laboratory and the cardiac care for PHV patients has involved not the coronary care and cardiology but also anesthesia, vascular cardiac and operating room nursing and communication, as well as nursing have been essential to successfully the PHV implantation the learning needs of the critical care nurses in interventional and clinical has also been at all nurses in the cardiac program. The of PHV implantation, its innovative and nature, and to ensure of care between the clinical have the program. As experience in the care of PHV patients, advanced age and comorbid at high for nurses are in and and in to optimize are the early in the percutaneous of valvular heart disease. The early results of the PHV implantation program at the Heart Centre at St. Paul’s Hospital are summarized in Table The of and clinical have on critical care and cardiac nursing and a to communication, and PHV implantation, although an offers patients with aortic stenosis the hope of decreasing their signs and providing quality of life in the more advanced years of In the of a who to in to new approaches to valvular heart disease, especially for the care nurses are well positioned to to the and of such new treatment options for and in the cardiac catheterization the coronary care and the cardiology have to the of the innovative PHV implantation program at St. Paul’s also the and to this provided by John Webb,

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