Complimentary Role of CT/MRI in the Assessment of Aortic Stenosis


1. CMR angiography: Aortic root morphology including ectasia, aneurysm, coarctation, and potentially planning access for transaortic TAVR

2. Cine MRI

 (a) Planimetry of aortic valve geometric area

 (b) Native valve morphology

  (i) Leaflet/cusp anatomy

  (ii) Endocarditis

   1. Vegetations

   2. Septic aneurysms

 (c) Prosthetic valve morphology

 (d) Visualization of stenotic outflow jet direction and pattern

 (e) Visualization of associated regurgitation flow pattern and volume

 (f) Chamber function and morphology

  (i) Stroke volume/stroke volume index

  (ii) Ejection fraction

  (iii) Global/regional wall motion

  (iv) Myocardial hypertrophy

  (v) Myocardial mass

  (vi) True LVOT area assessment

 (g) Chamber morphology

  (i) Hypertrophic patterns

  (ii) Septic aneurysms; other acquired disorders

 (h) Congenital anomalies

  (i) Associated chamber/vascular anomalies

3. Tissue characterization

 (a) Delayed contrast enhancement

  (i) Infarction

  (ii) Focal fibrosis

 (b) Tissue T1/T2 mapping

  (i) Diffuse fibrosis

  (ii) Myocardial edema

4. Velocity encoded flow

 (a) Aorta/pulmonary artery

  (i) Stroke volume

  (ii) Shunt flow

  (iii) Aortic regurgitant volume

  (iv) Mitral regurgitant volume

 (b) Trans-aortic valvular gradient

 (c) Congenital anomalies

 (d) Assessment of an effective orifice area (application of the continuity equation)




Table 7.1b
Limitations of cardiac MRI in aortic stenosis



































1. Nephrogenic systemic fibrosis: in patients with renal insufficiency

2. Claustrophobia

3. Cine MRI

 (a) Native valve morphology

  (i) Low spatial/temporal resolution of vegetations, calcification

 (b) Prosthetic valve morphology

  (i) Metal artifacts

4. Tissue characterization

 (e) Delayed contrast enhancement

  (i) Artifacts due to patient noncooperation

  (ii) Difficulty in diffuse fibrosis

 (f) Tissue T1/T2 mapping

  (i) Technically demanding

5. Velocity encoded flow

 (a) Technically demanding for gradient measurement






  • CMR angiography


  • Cine MRI


  • Tissue characterization protocols: Delayed contrast enhancement and tissue T1/T2 mapping


  • Velocity encoded flow measures

Certain facets of CMR examinations are robust and routine, such as valve planimetry, ventricular functional analysis, and measurement of aortic flow [14] (Tables 7.1a and 7.1b). Nevertheless, while in general the data obtained is more complete, the process of acquisition is more technically demanding and time consuming. Thus, echocardiography remains the diagnostic mainstay except in particular circumstances, for example, when poor echocardiographic windows impede adequate visualization, when there is discrepant invasive and non-invasive data, or when there is area/gradient mismatch or discordance.



Indications



Aortic Morphology


The most common indication for referral of patients with severe AS to CMR after echocardiography is to define aortic morphology and to exclude aortic aneurysms in patients with bicuspid aortic valves. This is generally done by CMR angiography, but can be done with non-contrast cine CMR if renal dysfunction is significant. A related indication is the exclusion of additional pathology such as coarctation or aneurysm of the aorta or other vascular pathology, which is easily accomplished using CMR as it provides detailed imaging of all intra-thoracic contents. Body habitus and the presence of intercurrent pathology such as chronic obstructive pulmonary disease do not degrade imaging as long as patients can cooperate with breath-holding instructions. A further requirement for cine MRI, is that patients have a stable cardiac rhythm with no frequent ectopy or rapid atrial fibrillation as this degrades image quality; however, this is not essential for aortic evaluation by CMR angiography.


Discrepant Diagnostic Data on Severity of Aortic Stenosis and Morphology of the Aortic Valve


The next most common indication is the broad category of discrepant diagnostic information from echocardiography, physical examination and/or cardiac catheterization. In particular, direct planimetry of aortic valve area (AVA), and complete morphologic visualization of aortic valve geometry in multiple oblique planes can resolve many clinical issues. In this context, CMR has become the gold standard for quantitative evaluation of chamber morphology and myocardial function, allowing very accurate assessment of stroke volume as long as mitral regurgitation is not a significant coincident problem [510]. Even in such cases, velocity encoded CMR (VENC) imaging, which provides analogous information to Doppler echocardiography and cardiac catheterization [11], can provide estimates of aortic or mitral regurgitant volume when needed to help determine the net forward cardiac output. Evaluation of the relatively laminar flow in the aorta and left ventricular outflow tract is very reliable in quantifying stroke volume and regurgitant volume [79]. However, determination of valve gradients is generally extremely technically demanding in comparison to echocardiography, for two reasons. First, very small changes in the direction of evaluation are easily accomplished by an experienced echocardiographer with a hand held probe, while each change in VENC imaging requires a separate breath-hold imaging sequence which can be very time consuming, on the order of 1–2 min of additional time per sequence acquisition [2, 3]. In addition, turbulent flow induces magnetic currents that change the velocity encoded flow rate. Thus, CMR gradient measurements are generally not robust enough to be decisive. Additional valuable information about the direction and pattern of high velocity outflow into the aorta downstream from the valve can be defined from cine CMR and velocity encoded imaging. Recent publications have confirmed the influence of angulated jets in affecting the degree of pressure recovery [1214]. Based on in-vitro experiments and a limited number of patient studies, recent publications explain the discrepancy between relatively large geometric valve area and high gradients frequently seen in bicuspid aortic valves (reverse area gradient mismatch), and have provided quantitative formulas to calculate pressure recovery from aortic size and flow angulation in the proximal aorta [1216].


Assessment of Ventricular Function


Further relevant information from chamber morphology and function is often useful in patients with area/gradient mismatch as low-flow low-gradient physiology with normal or reduced ejection fraction (EF). The volume of the left ventricle and stroke volume is vital in assessing the hemodynamics of these patients and recent studies affirm the valuable accuracy CMR can provide in such cases. Further evidence that may be helpful in decision-making includes the degree of hypertrophy, fibrosis and elevated left ventricle mass that may confirm evidence of elevated left ventricular hemodynamic load, and chronic severe resistance to left ventricular outflow which portends a worse prognosis longer term for such patients [1719]. Specific techniques such as delayed gadolinium contrast enhancement may reveal prior infarction or focal myocardial fibrosis that may mediate previously confusing symptomatology. In some cases the new technique of T1 or T2 quantitative mapping provide evidence of diffuse fibrosis that is not clearly revealed by traditional delayed enhancement. At this point a limited number of specialized centers have access to such technology but this is rapidly becoming a routine method. In LF/LG and NF/LG patients, MRI demonstrates larger AVA, less LVH, and similar focal fibrosis to LF/HG AS. This challenges the notion of the more advanced disease of the LF/LG AS patients.


Assessment of Paravalvular Obstruction, Associated Aortic Regurgitation, and Congenital Anomalies


Secondary causes of elevated left ventricular pressure such as intra-ventricular gradients from hypertrophic cardiomyopathy or subvalvular membranes that were missed on echocardiography may be revealed by CMR. In certain cases associated congenital anomalies that are occult or difficult to diagnose without access to thoracic angiography also may be revealed. MRI has become an integral part of evaluation of patients with HOCM for diagnostic, prognostic, and therapeutic considerations. It also can provide quantitative methods for assessment of concomitant aortic valve regurgitation as regurgitant volumes and ratios.



Cardiac Computed Tomography in Aortic Stenosis


CT coronary angiography is the most commonly used advanced imaging technique in patients with chest pain presenting to the emergency room. It has also become an integral part of standard pre-operative and pre-trans catheter valve replacement evaluation.


Indications



Assessment of Coronary Anatomy and Coronary Artery Disease


In native aortic stenosis, it frequently may obviate the need for preoperative invasive coronary angiography, particularly in younger patients with the congenital form of valvular aortic stenosis, bicuspid or unicuspid aortic valves, and subvalvular membrane. However, patients over 65 years old with calcific aortic stenosis or patients who have known prior infarction, and prior coronary bypass grafting or intracoronary stenting are unlikely to benefit from coronary CTA and will require invasive coronary angiography.


Pre SAVR and Pre-TAVR Evaluation by CT Aortography


CT is the state-of-art test for pre surgical and pre transcutaneous evaluation for aortic valve replacement. End-systolic measurement of the aortic annulus dimension and determination of calcification in the aortic valve, aortic root, LVOT, and ascending aorta calcification is also standard for potential TAVR patients, as is measurement of coronary height above the annulus. For potential trans-femoral TAVR patients, analysis of the distal aorto-iliac system and common femoral arteries is a required for size, tortuosity, and calcification. Lastly, assessment of the chest wall morphology, rib site access for transaortic and trans-apical TAVR patients and prior to minimally invasive SAVR is also possible by CT. This will be discussed later in a separate chapter in more detail.


Aortic Morphology


Similar to MRI and MRA, CT and CTA can provide further assessment of the ascending aorta morphology for coarctation, aneurysm, and other vascular pathologies. Septic aneurysm visualization is equally accurate compared with CMR and trans-esophageal echocardiography and superior to TTE.


Discrepant Diagnostic Data on Severity of Aortic Stenosis and Aortic Valve Morphology


Evaluation of aortic valve leaflet and cusp morphology is very accurate with CT; however, detection of vegetations is much less sensitive than with trans-esophageal echocardiography. Interestingly, CTA may have clinical utility in patients with prosthetic heart valves in aiding to detect valvular vegetations when transthoracic echocardiography (TTE) and transesophageal echocardiography (TEE) were unsuccessful [20].

Planimetry of aortic valve area at mid-systole can provide confirmation of geometric valve area (GOA) [2123]. By contrast, CT does not provide effective orifice valve area, as velocity measurements are not possible with current CT methods. Direct measurement of the LVOT area by CT scan and substituting that into the Doppler continuity equation has been proposed and provides a “hybrid” EOA with a cutoff of 1.2 cm2 as severe.

A specifically acquired non-contrast CT can generate an aortic valve calcium score (AVCS), which has gained traction for in use for asymptomatic patients with aortic stenosis. In a study by Utsunomiya et al. [24], the aortic valve calcium score among patients with severe asymptomatic AS was found to be an independent predictor of aortic valve events and long term mortality, specifically when a threshold median value of 723 Agatston Units (AU) was used. Thus obtaining a baseline aortic calcium score in this patient and following serially may aid in decision-making and be used as a marker for serial follow up. In patients with low flow/low gradient AS, the use of AVCS may assist with differentiating patient with severe AS versus moderate AS. An AVCS >1,650 was shown to correlate with severe AS. Measurements of the ascending aorta from CT aortography in cases with discordant echocardiographic and catheterization data also allows for calculation of pressure recovery.


Assessment of Paravalvular Obstruction and Congenital Anomalies


CT angiography also provides detailed coincident data on chamber size and configuration, which can exclude coexisting pathology such as hypertrophic cardiomyopathy, subvalvar membranes, supravalvular stenosis, or other congenital anomalies.


Assessment of Ventricular Function


Cine CT reliably provides access to regional and global wall motion, although it should be restricted to selected cases as it generally doubles radiation exposure [25]. Calculation of ejection fraction (EF) and estimates of stroke volume is also possible without cine CT if static left ventricular images are acquired at both end-diastolic and end-systolic cardiac phases [26]. Additionally, to some extent, CT may reveal the presence of prior infarction by wall thinning, myocardial hypo-enhancement and/or delayed hyper-enhancement.


Multimodality Imaging for Aortic Stenosis: Clinical Application and Case Examples


Though these advanced imaging techniques are novel and exciting, the use of multi-modality imaging is not necessary for every patient with aortic stenosis, except in patients referred to TAVR. Multimodality imaging must be considered on a case-by-case basis, and used only in cases where the added testing provides truly incremental information about the patient’s AS. The next section will highlight cases of aortic stenosis where traditional echocardiography may have reached its limits, and where CT and CMR can be useful adjuncts to help fully diagnose the patient and help drive decision-making. Pre-TAVR procedure planning is discussed elsewhere in the book.


Normal Flow-High Gradient (NF/HG) Severe AS, Normal Ejection Fraction Symptomatic Severe AS


In cases where the severity of aortic stenosis is not in question and patients are symptomatic, echocardiography may be the only diagnostic tool needed to proceed to the operating room directly [27].

However, other important questions must be asked prior to surgery. Is coronary artery disease present and if so, what is the severity? Is there a concomitant aortopathy in need of repair at the time of aortic valve replacement? In the past, such questions would inevitably lead to a cardiac catheterization for coronary evaluation prior to surgery, and then lead to a static CT angiogram (CTA) of the chest or possibly a chest magnetic resonance angiogram to evaluate aortic size. Today, surgeons are more likely to accept a CTA for coronary evaluation (Fig. 7.1), and at the same time use that data to gather information about the ascending and descending thoracic aorta, as well as view the entire chest for potential ‘pitfalls’ when proceeding with possible sternotomy. It is now possible to get such accurate imaging of the chest to know if prior chest surgery would even allow for a repeat sternotomy, or when a minimally invasive mini-thoracotomy would be the preferred option. In cases of previous bypass, a CTA can clearly show the left internal mammary artery graft adhesion to the chest wall, or saphenous vein grafts which have become adherent to the chest or sternum, typically the graft to the right coronary artery (RCA) as it runs anterior to the heart and sits behind the sternum (Fig. 7.1). In this case, an MRI/MRA of the heart and chest would be less helpful as coronary and graft anatomy would not be well visualized. However, for patients who are unable to tolerate iodinated contrast, MRA can provide excellent imaging of aortic dimensions and pathology. With the chest and coronary anatomy in hand, the patient can be taken to the OR with a detailed surgical plan in place.

A312748_1_En_7_Fig1_HTML.gif


Fig. 7.1
CTA applications: (Left) CTA of patient with previous CABG showing course of the saphenous vein graft to the right coronary (arrow) as it sits just posterior to the sternum. (Right) CTA showing normal left anterior descending (left), Left circumflex (center) and right coronary artery(right) in a curved planar reconstruction

However, other valuable information can be gleaned from the CT or CMR. Information such as left ventricular outflow tract and aortic annular sizing as is done now for trans-catheter aortic valve replacement (TAVR) cases (see Chap. 9), as well as accurate valve planimetry for CT [2124] and CMR [2834] when compared to both TTE, and CMR. Lastly, CMR and cine CT will allow for a very accurate and reproducible left ventricular (LV) volume and EF [69, 26, 35]. Such information may be available from echocardiography, however in cases where echocardiograms may prove difficult to interpret due to patient body habitus or valvular calcification, CMR or cine CT can be helpful (Fig. 7.2). An overview of these and more applications and limitations of both CMR and CT can be found in Tables 7.1a, 7.1b, 7.2a, and 7.2b.

A312748_1_En_7_Fig2_HTML.gif


Fig. 7.2
(Above) Double oblique image of left ventricle by CTA (left) and short axis (right) showing the calcified aortic valve. The short axis valve area in systole can be accurately planimetered. (Below) Transthoracic echo images from the same patient in long axis (left) and short axis (right). CTA images are less affected by calcium than TTE in this case, resulting in greater ease of planimetry



Table 7.2a
Applications of cardiac CTA in aortic stenosis



























































1. Coronary angiography

 (a) Native vessels

 (b) Coronary bypass grafts

 (c) Stents

2. Aortic valve morphology

 (a) Leaflet/cusp anatomy

 (b) Valve area planimetry

 (c) Valve calcification

3. Aortic morphology

 (a) Sizing/aneurysm/atheroma

 (b) Calcification

 (c) Configuration

4. Myocardial morphology

 (a) Hypertrophy

 (b) Chamber sizing/configuration

 (c) Annular sizing/calcification

 (d) Myocardial perfusion pattern

 (e) Delayed hyper-enhancement

5. Cine CT functional analysis

 (a) Stroke volume/stroke volume index

 (b) Ejection fraction

 (c) Regional wall motion

 (d) True LVOT area assessment

6. Trans aortic valve replacement (TAVR)

 (a) Annulus size dimensions for sizing of TAVR prosthetic size

 (b) Iliac artery dimension to determine candidacy for trans-femoral TAVR

 (c) Ascending aortic CTA to determine candidacy for trans-aortic TAVR



Table 7.2b
Limitations of cardiac CT in aortic stenosis































1. Radiation exposure

2. Contrast nephropathy

3. Coronary angiography

 (a) Coronary/graft calcification

 (b) Stent inaccuracy

 (c) Moderate/severe lesions require ICA

4. Aortic valve morphology

 (a) No effective orifice size

5. Myocardial morphology

 (a) Myocardial perfusion difficult

 (b) Delayed hyperenhancement difficult

6. Cine CT functional analysis

 (a) Marked increase in radiation exposure


Area/Gradient Mismatch: Low Flow/Low Gradient Severe Aortic Stenosis with Reduced Ejection Fraction


A 71-year-old male with H/O CAD and prior myocardial infarctions presents with shortness of breath and fatigue. On auscultation, a single second heart sound, and a loud, harsh, III/VI mid to late peaking systolic ejection murmur which is mid to late peaking at the right upper sternal border.

His echocardiogram reveals a calcified AV with a peak velocity of 3.1 m/s, a mean gradient of 32 mmHg, an AVA of 0.6 cm2, a calculated stroke volume index of 37 ml/m2, and an EF of 38 %.

A dobutamine stress echo shows that the patient’s EF rises to 50 %, the stroke volume rises by 25 %–51 ml/m2, the mean gradient increases to 44 mmHg, and the AVA remains at 0.6 cm2. The patient has a projected AVA of 1.0 cm2. All signs in this case point to a low-flow, low gradient severe aortic stenosis with contractile reserve, which would portend a favorable prognosis [3640] (see Chap. 5). The patient undergoes a cardiac MRI for additional risk stratification prior to aortic valve surgery. This confirms his low ejection fraction of 34.75 %, however notable was a previous infarct in the lateral wall seen on delayed enhancement images (Fig. 7.3). His AVA planimetry reveals confirming the presence of severe AS as well as a low SVI confirming the low flow state. Though patients with poor contractile reserve have a higher mortality than those with reserve, their comparative mortality is much lower with surgery than with medical management [4043]. Independent variables which predict poor surgical outcomes also include patients with previous myocardial infarction, any concomitant CAD (>50 % lesion stenosis) and those with immediate need for circulatory support following surgery (i.e. IABP or inotropes) [44].

A312748_1_En_7_Fig3_HTML.jpg


Fig. 7.3
Late gadolinium enhancement pattern seen in the patient from Case 1 with low flow, low gradient AS. This patient has had a prior MI in the lateral wall depicted by the white, delayed enhancement areas (white arrows), and thinned, darker appearing myocardium. Presence of infarction is an independent risk factor for death and poor long term prognosis, and the presence of any fibrosis is associated with decreased functional recovery post aortic valve replacement

In this setting, CMR is helpful to define the etiology of myocardial dysfunction. In addition to its ability to give accurate and reproducible ejection fraction and LV volumes pre and post operatively in this low flow group [45] the use of delayed hyper-enhancement imaging can describe in detail if a patient has suffered a previous myocardial infarction, another independent preoperative risk factor [1719] or additional etiologies such as inter-current amyloid heart disease. Other prospective studies in patients with LFLG aortic stenosis have shown that cardiac fibrosis in general is an independent risk factor for decreased functional class post aortic valve replacement [45]. Thus, an assessment of myocardial fibrosis with CMR pre-operatively among patients with depressed ejection fraction and confirmed severe aortic stenosis may prove beneficial to understand the level to which a patient’s symptoms may improve.

Another means by which CMR can be helpful in this case would be calculation of valvulo-arterial impedance (Zva), which is calculated as follows:



$$ Zva=\frac{SAP+MPG}{SVI} $$
SAP=systolic arterial pressure in mmHg, MPG= mean pressure gradient in mmHg, and SVI is the stroke volume index in ml/m2 .

Zva has also been validated among symptomatic patients with paradoxical LFLG AS to determine prognosis, with values >4.5 mmHg/ml/m2 portending a much poorer prognosis and higher mortality [4648]. Though TTE is fully capable of calculating this value, CMR has robust capabilities in measuring left ventricular volumes and stroke volume, and via flow mapping, calculation of the MPG can be made [2], or alternatively can be taken from echocardiographic findings. This positions CMR as an alternate method to accurately calculate the Zva. Taking the SAP from the patient’s physical exam, and MPG obtained from the time velocity integral of the trans-aortic flow by echocardiography, the patient’s Zva can be calculated readily. In this patient, we calculate 
$$ {\mathrm{Z}}_{\mathrm{va}}:148\mathrm{mmHg}+32\mathrm{mmHg}/\left(78\mathrm{ml}\right)/2.1{\mathrm{m}}^2\Big) $$
. This would place the patient in a severe range of >4.5 mmHg/ml/m2. This would portend a poor prognosis for this patient, and valve surgery would be recommended [4749].


Indeterminate Severity Aortic Stenosis, Preserved Ejection Fraction


Several times practitioners will face patients who clearly suffer from aortic stenosis with conflicting evidence about disease severity. The difficulties generally arise when there are conflicting test findings or when the patient’s symptoms may be due to intercurrent non-cardiac disease as demonstrated below.


Clinical


A 74-year-old male presents with a recently discovered murmur and shortness of breath on minimal exertion with minimal exertion. He has a previous heavy smoking history with documented moderate range COPD. A grade III/VI mid to late peaking systolic ejection murmur with a single S2 is noted.


TTE


An echocardiogram shows an EF of 55 %, a peak aortic valve velocity of 3.6 m/s, a mean aortic valve gradient of 25 mmHg, and an aortic valve area of 0.82 cm2, with a dimensionless index of 0.29. In addition, there is mild aortic regurgitation and no evidence of pulmonary hypertension.


Catheterization


Despite adequate medical treatment, the patient continues to experience shortness of breath with exertion and a right and left heart catheterization is performed. The right heart catheterization showed a mean right atrial pressure of 10 mmHg, PA pressure of 39/15 mmHg, and a mean PA pressure of 26 mmHg. The pulmonary capillary wedge pressure showed a mean of 17 mmHg without evidence of large V waves. A saturation run showed no evidence of ‘step up’ and the Fick cardiac output was calculated to be 4.7 L/min at rest, with a cardiac index of 2.2 L/min/m2. Simultaneous measure of the central aortic pressure and LV pressure showed a central aortic pressure of 136/97 mmHg and an LV pressure of 167/18 mmHg, with a peak to peak gradient of 31 mmHg, and a calculated mean gradient of 23 mmHg. The calculated aortic valve area was 1.0 cm2. This was felt to represent moderate to severe aortic stenosis. Coronary angiography showed a mid-LAD 40–50 % stenosis. The RCA showed a 90 % proximal segment lesion extending to mid vessel lesion. This was felt to be the lesion causing the patient’s symptoms and was fixed with placement of overlapping drug eluting stents with post high pressure inflation.

The patient is seen in office post coronary stenting, and disappointingly he continues to experience the same level of exertional dyspnea. Though by exam his COPD is not active, the idea that his lung disease is contributing to or causing his symptoms is beginning to register with you. However, his moderate to severe aortic stenosis is still an impediment to your being able to fully place blame on another organ system, which does not outwardly appear to be causing much issue. For that reason, you have him undergo a TEE to assess the valve area by planimetry (Fig. 7.4).

A312748_1_En_7_Fig4_HTML.gif


Fig. 7.4
Short axis images on (a) TTE, (b) TEE and (c) CMR for patient with moderate to severe aortic stenosis. (Left) The TTE aortic valve short axis image is of poor quality, and the valve opening is barely discernable. (Center) The TEE short axis shows a calcified valve (dark arrows) with at least partial opening, however due to shadowing, the valve cannot be accurately planimetered. (Right) The CMR shows a much more visible valve orifice which can be more easily planimetered


TEE


The TEE is performed which confirms a GOA by planimetry of 1.22 cm2, an EF of 55–60 %, and an aortic valve area by TVI of 1.0 cm2. At this time, his valve is downgraded to a moderate level of stenosis. It is felt his continued exertional dyspnea is largely pulmonary in etiology, and he is referred to a pulmonologist for treatment.

Mr. L sees his pulmonologist, who performs spirometry and agrees that he has moderate COPD, but it is not active, and unlikely to be contributing to his symptoms. He places him on respiratory inhalers and he returns in 2 weeks to see you. After this consultation and intervention, the patient is still quite hampered with being able to only walk 25–50 ft before becoming dyspneic, and notes no change with the addition of the inhalers. For this reason, you have him undergo a cardiac MRI for better delineation of his aortic valve disease, to determine if the valve is of moderate, moderate to severe or in fact severe range disease.


MRI


The CMR images are also seen in Fig. 7.5. The valve itself is heavily calcified, and when planimetered, the valve area is 1.4 cm2. The myocardial mass derived from the LV wall contours is 1.3× normal at 160 g. The velocity-encoded images show an aortic valve velocity of 350 cm/s (3.5 m/s). There was also noted to be an EF of 46 % calculated from the end diastolic volume of 205.88 ml and end systolic volume of 109.97 ml at a heart rate of 71 beats per minute. Also of note was the presence of at least mild aortic regurgitation. The consensus from the MRI was that the aortic valve was of moderate level of stenosis. However, as the EF was now felt to be mildly depressed for the first time, a dobutamine stress echocardiogram was recommended to help detect for low flow, low gradient severe AS.

A312748_1_En_7_Fig5_HTML.gif


Fig. 7.5
CMR data from Case 2 patient with moderate to severe aortic stenosis. (Top left) The short axis view of the valve used for planimetry gives a planimetered valve area of 1.41 cm2. (Top right) Velocity flow mapping data shows the peak aortic valve velocity to be 325 cm/s. (Bottom left) The LVOT view and the three chamber view (bottom right) shows significant turbulence at the level of the aortic valve


Dobutamine Stress Echo


This dobutamine stress echocardiogram was performed, which confirmed a low EF of 45 %, and with peak dobutamine infusion to 40 mcg/kg/min, the patient’s EF improved to 55 % and the mean gradient remained at 25 mmHg. This was consistent with moderate aortic stenosis.

In this case, the initial echo data suggested that the aortic valve had moderate to severe stenosis, however the exam evidence did not suggest severe stenosis. The subsequent cardiac catheterization demonstrated a moderate to severe level of disease, however the following TEE showed moderate disease, which was confirmed by CMR and subsequent dobutamine stress echocardiogram. So which one is correct?

CMR confirmed that the valve was of moderate range stenosis both by VENC measurements and planimetry, which was re-confirmed by TEE and dobutamine stress echocardiography. There is a wealth of data supporting the accuracy of CMR, CT and TEE aortic valve planimetry as compared to TTE derived Doppler gradients and catheterization gradients [2123, 2835, 50]. In general with CMR, there is not felt to be a need to use the continuity equation with the LVOT and aortic valve velocities as those calculations can introduce error into the system [51, 52] (see Chap. 5). While it is true that CMR and TEE planimetry will tend to slightly overestimate valve area compared to TTE derived calculations and catheterization gradients [29, 30, 33], the overestimation in this case was similar by both, and well above the cutoff of 1.0 cm2. The true difficulty in this case was whether the valvular stenosis valve was causing the patient’s continued symptoms and volume overload. He had exam evidence of mild heart failure; however, his COPD was a confounding factor, possibly contributing to his right heart failure, his pulmonary hypertension and thus his dyspnea. His aortic stenosis has presumably always been in the moderate range, however mildly variable hemodynamic circumstances of volume expansion led in turn to relatively higher LVEDP and central aortic pressures, and thus higher estimated gradients by TTE and catheterization. The patient was likely more volume contracted from his diuretics by the time he underwent TEE and CMR, thus pushing him slightly toward a moderate range AS. Given that the planimetry valve area was never <1.0 cm2, additional testing in this case offered insight and confirmation that the valvular stenosis was not in the severe range.

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May 23, 2017 | Posted by in CARDIOLOGY | Comments Off on Complimentary Role of CT/MRI in the Assessment of Aortic Stenosis

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