9: Hemodynamics of transcatheter and surgical aortic valve replacement

CHAPTER 9
Hemodynamics of transcatheter and surgical aortic valve replacement


John P. Vavalle, Michael Yeung, Thomas G. Caranasos and Cassandra J. Ramm


Aortic valve replacement is the only definitive therapy for the treatment of severe aortic valve stenosis (AS). With the proportion of the US population over the age of 65 growing at the fastest rate, the prevalence of degenerative calcific aortic stenosis is growing rapidly [1]. The 2014 American College of Cardiology/American Heart Association (ACC/AHA) Guidelines list aortic valve replacement (AVR) as a class I therapy for the treatment of severe symptomatic aortic stenosis [2]. Indeed, AVR in patients with progressive symptoms, such as heart failure, angina, syncope, or left ventricular dysfunction, can not only dramatically improve a patient’s quality of life, but is also a life‐saving procedure. Contemporary data demonstrate the ineffectiveness of medical treatment of severe symptomatic AS with an average life expectancy of approximately one year for patients with heart failure due to severe AS in the absence of valve replacement [3].


For decades, the only option for AVR was open‐heart surgery, usually through a median sternotomy incision requiring cardiopulmonary bypass. Unfortunately, many of the patients with severe AS are older and frail, with multiple comorbidities that make them high or even prohibitive risk for surgical AVR (SAVR). Thankfully, over the last decade a new therapeutic option, minimally invasive transcatheter aortic valve replacement (TAVR), has emerged as a viable alternative for these patients. Data from large randomized controlled trials comparing TAVR to SAVR demonstrated 1‐year mortality rates with TAVR that are comparable to, or even lower than, those seen with surgery [4,5]. The uptake of TAVR as a treatment option for severe AS has been brisk due to favorable outcomes in patients who are at high risk or prohibitive risk for surgery. Currently, ongoing studies are looking at TAVR in the intermediate risk surgical population, and it is anticipated that the use of TAVR will eventually expand to this risk cohort as well.


Selection of appropriate patients


A successful outcome with TAVR starts with appropriate patient selection. The TAVR devices currently approved for use in the USA are designed to treat calcific AS and are less well suited to treating other forms of aortic valve disease. In particular, pure aortic valve insufficiency, bicuspid aortic valves, and disrupted aortic valves from ascending aortic aneurysms or dissections are best treated surgically, albeit with some exceptions.


In general, patients who are candidates for AVR are those who have symptoms attributable to AS and meet the criteria for severe AS, defined as having an aortic valve area (AVA) of <1.0 cm2 and either a mean aortic valve gradient above 40 mm Hg or jet velocity across the aortic valve of at least 4.0 m/s. The severity of AS can be determined by measuring simultaneous left ventricular and aortic pressure or by echocardiography, which uses Doppler to determine jet velocity across the stenotic valve as well as mean and peak aortic valve gradients.Further details on the hemodynamic assessment of AS are provided in Chapter 8.


Low flow–low‐gradient aortic stenosis


An increasingly recognized form of AS is low‐flow–low‐gradient (LFLG) severe AS. This condition is characterized by a depressed left ventricular ejection fraction (LVEF), an aortic valve area <1.0 cm2, and a mean aortic gradient <40 mm Hg. Because the transvalvular aortic pressure gradient is dependent on flow across the valve squared, a low flow state (e.g., as seen in heart failure) can significantly diminish the pressure gradient despite the presence of severe AS. These patients often have a dilated left ventricle secondary to the aortic valve pathology and they represent approximately 5–10% of the total patients evaluated with severe AS [6]. A more comprehensive assessment of the severity of AS in these patients can be obtained by measuring pressure gradients during dobutamine administration, which results in increased cardiac output.


More recently, a “paradoxical” LFLG severe AS entity has been described, whereby patients have an aortic valve area <1.0 cm2 and a low transvalvular aortic gradient (<40 mm Hg), but normal left ventricular ejection fraction. These patients are analogous to their heart failure counterparts who have persistent symptoms despite a preserved LVEF, and are characterized by a small, restrictive LV cavity along with impaired diastolic filling. The criteria proposed to define this condition are a cardiac index <3.0 L/min/m2 or a stroke volume index <35 mL/m2. Currently, the most widely used measurement is the stroke volume index, since it is readily obtained by echocardiogram by taking stroke volume (SV) in mL divided by the body surface area (BSA) in m2. This condition is often seen in elderly women with small body size [7]. It is estimated that up to 10–25% of patients undergoing severe AS may fall into this category [7].


Pseudo severe AS is a condition where there is minimal aortic valve disease in the setting of severe cardiomyopathy. Echocardiographic assessment reveals poor aortic valve leaflet mobility, which is primarily due to the myocardial disease and low flow state rather than inherent calcific aortic pathology. The decrease in aortic valve excursion is a function of the overall depressed cardiac state and is not due to AS.


Patients presenting with pseudo severe AS can be differentiated from LFLG severe AS by performing a dobutamine challenge during either echocardiography or cardiac catheterization. This is important, because patients with LFLG severe AS will generally benefit from AVR, whereas patients with pseudo severe AS will not. For those with truly severe AS, a dobutamine challenge will result in an increase in cardiac index and an increase in mean gradient across the aortic valve, with little to no change in the aortic valve area (AVA). A dobutamine challenge in a patient with pseudo severe AS will result in an increase in AVA with relatively no change in the transvalvular mean gradient.


A dobutamine challenge is also useful in order to assess for contractility and/or flow reserve. This is defined as an increase in stroke volume by at least 20% from baseline. Contractile reserve has important prognostic implications, since its absence portends a poor prognosis regardless of valve replacement. However, this should not be used as a reason to withhold valve replacement therapy, since patients with no LV contractile reserve who undergo AVR still have a better survival rate compared to those managed medically, despite a higher perioperative risk.


Using hemodynamics to avoid pitfalls during TAVR


Increasingly, TAVR is the treatment of choice for severe AS when patients are at high risk or prohibitive risk for surgical intervention. TAVR requires a multidisciplinary heart team approach to achieve optimal outcomes. Invasive hemodynamics are an essential component of periprocedural patient monitoring as they help identify potential complications that may occur.


In the early stages of the TAVR procedure, a pigtail catheter is inserted into the left ventricle across the stenotic aortic valve. Simultaneous LV and aortic pressures are taken to confirm the severity of the aortic stenosis, but other hemodynamic parameters should also be assessed and noted (Figure 9.1). Left ventricular end diastolic pressure (LVEDP) and aortic diastolic pressure should be recorded. Often, these patients have stiffened calcified peripheral vessels and a low diastolic blood pressure is not an unusual finding. Noting this at the start of the procedure is helpful, because a significant reduction in diastolic blood pressure following valve deployment can be a sign of severe aortic valve insufficiency and/or paravalvular leak. An elevated LVEDP is also a common finding given the longstanding pressure overload of the ventricle from the stenotic aortic valve.

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Apr 25, 2017 | Posted by in CARDIOLOGY | Comments Off on 9: Hemodynamics of transcatheter and surgical aortic valve replacement

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