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| REVIEW ARTICLE |
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| Year : 2022 | Volume
: 23
| Issue : 1 | Page : 22-32 |
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Multimodality imaging in aortic stenosis
Sabir Abdul Karim1, Sherif Mahmoud Helmy2
1 Department of Adult Cardiology, Heart Hospital, Hamad Medical Corporation, Doha, Qatar
2 Department of Non-Invasive Cardiology, Heart Hospital, Hamad Medical Corporation, Doha, Qatar
| Date of Submission | 28-Feb-2022 |
| Date of Acceptance | 03-Apr-2022 |
| Date of Web Publication | 16-May-2022 |
Correspondence Address:
Dr. Sherif Mahmoud Helmy
Non-Invasive Cardiology, Heart Hospital, Hamad Medical Corporation, P. O. Box 3050, Doha
Qatar
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/heartviews.heartviews_32_22
 Abstract | | |
Aortic stenosis (AS) is the most common cardiac valve lesion in the adult population, with an incidence increasing as the population ages. Accurate assessment of AS severity is necessary for clinical decision-making. Echocardiography is currently the diagnostic method of choice for assessing and managing AS. Transthoracic echocardiography is usually sufficient in most situations. Transesophageal echocardiography and stress echocardiography may also be utilized when there is inadequate image quality and/or discordance in the results and the clinical presentation. There is a role for other imaging modalities such as cardiac computed tomography, magnetic resonance imaging, and catheterization in selected cases. The following describes in some detail the role of these modalities in the diagnosis and assessment of AS.
Keywords: Aortic stenosis, cardiac computed tomography, cardiac magnetic resonance imaging, echocardiography, valvular heart disease
How to cite this article:
Karim SA, Helmy SM. Multimodality imaging in aortic stenosis. Heart Views 2022;23:22-32 |
| Introduction | |  |
Transthoracic echocardiography (TTE) is the main standard for the diagnosis of aortic stenosis (AS). Moreover, transesophageal echocardiography (TEE) may be used in technically difficult cases or to obtain detailed information prior to transaortic aortic valve implantation (TAVI). Exercise stress echocardiography also has a role when there is a discordance between the clinical findings and the degree of stenosis, as in severe asymptomatic AS or moderate symptomatic AS. Dobutamine stress echocardiography is utilized in low flow-low gradient severe AS to differentiate between true and pseudo severe AS. Cardiac computed tomography (CT) and cardiac magnetic resonance (CMR) imaging are noninvasive techniques that may also be used to characterize valvular heart disease in patients with inconclusive findings on echocardiography.
Among the different echocardiographic parameters, the following are their different levels of recommendations according to the current guidelines.[1]
| Standard Clinical Practice Measurements | | |
The primary hemodynamic parameters recommended for clinical evaluation of AS severity are:
- AS peak jet velocity
- Mean transvalvular pressure gradient
- Aortic valve area (AVA) by continuity equation.
| Alternative Measurements of Stenosis Severity | | |
These are reasonable parameters to be obtained in selected patients when additional information is needed:
- Simplified continuity equation to measure AVA
- Velocity ratio and velocity-time integral (VTI) ratio (dimensionless index [DI])
- AVA planimetry.
| Experimental Measurements of Stenosis Severity | | |
These parameters are not recommended for routine clinical use.
These include hemodynamic measurements of severity such as valve resistance, left ventricle (LV) percentage stroke-work loss, and the energy-loss coefficient are based on different mathematical derivations of the relationship between flow and the trans-valve pressure drop.[2],[3],[4] Correcting for pressure recovery (PR) in the ascending aorta has improved the agreement between invasively and noninvasively derived measurements of the transvalvular pressure gradient. This is most relevant in the presence of a high output state, a moderately narrowed valve orifice, and most importantly, a narrow ascending aorta.[3],[5]
A common limitation of most of these new indices is that long-term longitudinal data from prospective studies are lacking. Consequently, they are seldom used for clinical decision-making.[2]
| Transthoracic Echocardiography and Transesophageal Echocardiography | | |
All modalities are utilized, namely, M-mode, 2-dimensional (2D), pulsed-wave Doppler (PWD), continuous wave Doppler, color flow Doppler, and 3D echocardiography. As shown in [Table 1],[6] different views are recommended by TTE and TEE to visualize the aortic valve (AV). | Table 1: Summarizes the main uses of the different echocardiography modalities
Click here to view |
The AV apparatus is formed of the valve cusps, sinuses of Valsalva, proximal ascending aorta, and left ventricular outflow tract (LVOT). The different views provide detailed 2D and 3D anatomy of the leaflets and annular complex [Table 2].[6] The normal valve consists of three cusps suspended from an associated sinus of Valsalva. Echocardiography examination permits the evaluation of leaflet architecture and the extent of systolic opening and diastolic closure. The AVA can be measured by planimetry. Although this method is simple and rapid, it has poor inter-observer reliability. Overestimation of the valve area occurs when the ultrasound beam intersects the leaflets below the tips. Difficulties may also occur when the AV is calcified, and the orifice of the valve cannot be clearly identified. The success rate of planimetry and accuracy is much better by TEE. | Table 2: Lists the recommended views to visualize the aortic valve by transthoracic echocardiography and transesophageal echocardiography
Click here to view |
| Pathophysiology Aortic Stenosis | | |
The normal AVA in adults is 3–4 cm2. Obstruction can occur at three distinct anatomical sites: valvular, subvalvular, or supravalvular. Valvular obstructions account for most cases of LVOT obstructions. The most common cause of AS is calcific AS in the elderly. Other causes include congenital abnormalities of the AV as bicuspid and less common in the unicuspid or quadricuspid valves [Table 3].[1] | Table 3: The most common causes of aortic stenosis and their main characteristics
Click here to view |
The mechanism of AS in the elderly and congenital cases is distorted flow through a diseased valve, which leads to degenerative changes and progressive calcification. The rate of calcification and stenosis vary widely, although elderly men with associated coronary artery disease, as well as individuals with a history of smoking, hypercholesterolemia, and elevated serum creatinine levels, demonstrate more rapid disease progression.[7],[8],[9] The development of AS is not part of routine aging but is an active process involving chronic inflammation fueled by atherosclerotic risk factors.[10] AV disease may also be a part of some autoimmune diseases or secondary to radiotherapy.
| Qualitative Diagnosis of Aortic Stenosis | | |
Qualitative estimation of AS severity is the first step in the diagnosis of AS. These findings should be correlated with quantitative methods. With the development of acquired AS, the cusps become thickened and calcified, and their motion is restricted. The degree of thickening, calcification, and restriction progresses as the severity of AS increases. If leaflet separation is at least 15 mm or if at least one cusp normally moves, critical AS is unlikely.[10]
| Quantitative Doppler Assessment of Severity of Aortic Stenosis | | |
To quantify the severity of AS, a combination of 2D and Doppler echocardiography is required. As mentioned, the standard routine parameters used to quantitate AS include the peak aortic jet velocity, the mean pressure gradient, and the AVA.
| Transaortic Velocities | | |
Transaortic jet velocities are obtained using a continuous-wave (CW) Doppler. Multiple transducer windows are used to obtain the Doppler signal that is aligned most parallel to the direction of the stenotic jet. TTE has the advantage over TEE as in practice the number of windows is unlimited. The standard windows include the apical three- and five-chamber views, the right sternal border, the suprasternal notch, and subxiphoid views. Using a non-imaging CW Doppler probe (so-called Ped off probe or pencil probe) is recommended because it is smaller, easier to manipulate between the ribs. For TEE, this requires either the deep transgastric or transgastric long-axis view. The peak velocity, which is used to grade AS severity, is the highest value obtained and represents a single instantaneous measurement. The entire velocity envelope can be traced to yield a VTI and mean velocity. Compared to transthoracic echo, TEE tends to underestimate aortic jet velocities. Therefore, several separate measurements should be made, utilizing the highest values obtained. A peak gradient can be calculated from the peak velocity using the simplified Bernoulli equation:
ΔP = 4V2
This is a “peak instantaneous” gradient and will be higher than the “peak to peak” gradient obtained in catheterization laboratories. When the proximal or LVOT velocity (VLVOT) exceeds 1.4 m/s, the modified Bernoulli ejection should be used:
ΔP = 4 (AV Velocity2-VLVOT 2)
Nearly all echo machines will calculate a mean gradient when the velocity envelope is traced, but the mean gradient can also be estimated from the formula:
ΔPmean = 2.4(Vmax) 2
It is noted that calculated pressure gradients also depend on (flow stroke volume [SV] and/or cardiac) output and that higher gradients may occur in patients with altered volume flow rates. Increased flow rates may occur in aortic regurgitation (AR), anemia, hyperthyroidism, AV shunts as in dialysis patients and pregnancy. In these situations, higher pressure gradients may be present, although the degree of AS may only be mild. On the other hand, in patients with decrease flow, for example, in significant LV systolic dysfunction, small LVs, high systemic vascular resistance, or mitral regurgitation any left to right intracardiac shunts may lead to a relatively low gradients despite severe AS. In these situations, it is recommended to obtain AV area, which is relatively more constant and less dependent on flow.
| Valve Area (Anatomical by Planimetry Or Functional by Continuity Equation) | | |
The anatomical area of a stenotic AV can often be obtained directly using planimetry. TEE is usually the standard modality; in the mid esophageal AV short axis view, the probe should be manipulated to make the imaging plane at the level of the leaflet tips. Using 3D cropping is usually useful in this setting. Cutting the valve obliquely will overestimate the valve area. Ideally, all leaflets should appear equal in size, and an equilateral triangle can be traced out. Unfortunately, heavy calcium deposits can create significant shadowing, making it difficult to view the leaflets and impossible to identify the valve orifice. Additional limitations of planimetry for AS are tending to overestimate valve areas of <0.75 cm2 and underestimating the functional severity of stenosis in bicuspid AVs.[11],[12]
Tips to obtain the AVA by planimetry:
- TEE ME AV SAX view
- Low gain to minimize artifacts
- Image plane at the level of leaflet tips (use of 3D if the images are of good quality)
- Maximum orifice during systole
- Trace the inner edge of leaflets
- Limited by the ability to get a good view.
| Three-Dimensional Assessment of the Aortic Valve Area | | |
The cropping plane in the 3D dataset can provide a true en face view aligned exactly to image the smallest stenotic AV orifice for planimetry. Several studies have documented superior accuracy of planimetry by real-time 3D (RT3D) TTE compared with conventional 2D-TTE.[13],[14],[15] Therefore, RT3D TTE can, in some situations, overcome some of the limitations of the continuity equation.
The AVA can be reliably evaluated when valvular AS coexists with hypertrophic obstructive cardiomyopathy, discrete subaortic stenosis, or supravalvular AS. In addition, the evaluation of AS severity by the continuity equation may be enhanced by using an RT3D TTE approach for the measurement of the LVOT diameter or CSA. Fifteen TEE has proven to be of better accuracy and reproducibility.
The functional area of the stenotic AV is usually the standard and avoids some of the limitations of planimetry. Echo Doppler assessment of the severity of AS includes the calculation of AVA using the continuity equation. The continuity principle, based on the conservation of mass, states that the flow volumes (Q) at different sites in a closed system, like the heart, is identical. Thus, the SV proximal to the stenotic AV (the LVOT) must be equal to the SV just distal to the stenotic AV (the ascending aorta).
In practice, the diameter of the LVOT (d) is measured in the parasternal long-axis (zoom) by TTE or ME AV long-axis view by TEE, and the formula used is “CSA=π(d/2) 2,” which simplifies to “CSA = 0.785(d2)” [Table 4]. | Table 4: The different variables and the equation to estimate the aortic valve area by the continuity equation
Click here to view |
The measurement should be taken in mid systole. LVOT VTI is best obtained by PWD placed in the LVOT in the apical 3 or 5 chambers by TTE or using the deep transgastric or transgastric long-axis views by TEE and then tracing the VLVOT profile. An alternative method, if a good double envelope is present, the VTI of the LVOT can be acquired by tracing out the VLVOT profile. As a short-cut, peak velocities of the LVOT and AV can be substituted for their respective VTIs (sometimes called the “simplified continuity equation”) as follows:
AVA = D2 × 0.785 × VLVOT/VAV
However, the latter two methods are not the standard measurements because of their better reproducibility.
Potential sources of error in the Doppler assessment of transaortic gradients include; failure to account for increased subvalvular velocity, measuring the wrong gradient as mitral or tricuspid regurgitation, selection of a post premature beat as a representative velocity, PR in patients with the small aorta (<3.0 cm), measurements during uncontrolled hypertension or altered preload or afterload conditions, or inherent comparison with catheter gradients (peak instantaneous vs. peak to peak).
Using the above standard measurements, the echocardiographic grading of AS will be possible according to the recommendations of the European Association of Cardiovascular Imaging and the American Society of Echocardiography[1] [Table 5].[6]
It is noted that Doppler measurement of gradients may be limited by TEE because of the difficulty in aligning the echo beam parallel to the aortic jet from the standard transesophageal views. However, in most cases, the deep transgastric view can be used to obtain accurate maximal velocities and gradients. A second useful view can be obtained by slight clockwise rotation of the TEE probe from a standard gastric longitudinal view of the LV.
3D imaging techniques have demonstrated that the LVOT is often elliptical rather than circular. The anteroposterior diameter (sagittal) as obtained from the transthoracic echocardiographic (TTE) PLAX view is smaller than the larger medial-lateral (coronal) diameter.
| Velocity Ratio and VTI Ratio (Dimensionless Index) | | |
When accurate measurement of the LVOT is not possible, the DI, or velocity ratio, may be used as an alternative to the AVA. This simplified parameter avoids the measure of the LVOT and is independent of cardiac output. This Doppler only method uses the following equation:
DI = LVOT V/AV V or
DI = LVOT VTI/AV VTI
A DI <0.25 is consistent with severe AS [Table 5]. The accuracy of DI in assessing AS severity may be affected by extremes in LVOT size.[4],[16]
Given the potential therapeutic and prognostic importance of these echocardiographic parameters, they should only be reported when there is a high level of confidence in their accuracy. Other diagnostic modalities may be considered to further assess the morphology and hemodynamics of the stenotic AV. These may include TEE, magnetic resonance imaging (MRI), and, rarely, cardiac catheterization as outlined in the ASE/EACVI guidelines.[17],[18],[19]
| Associated Echocardiography Findings | | |
The left ventricular hypertrophy is a common compensatory mechanism in AS patients. This also leads to a decrease in LV compliance and coronary perfusion. Poststenotic aortic dilatation is present in about ¼ of AS patients, affecting mainly the sinotubular junction, eight although the proximal ascending aorta is frequently involved as well. The amount of AR should be evaluated in all patients with AS. Calcified, stiff cusps that fail to properly open can also fail to properly close. The degree of regurgitation can influence cardioprotection and cannulation strategies.
| Other Methods of Measuring Aortic Stenosis Severity | | |
Several additional echocardiographic parameters have been proposed to better define the severity of AS and its risk. Those include valve resistance,[20],[21] the energy loss index,[22] stroke work loss,[23] PR,[24] and valvulo-arterial impedance.[25] However, their utility and prognostic significance remain to be proven in large-scale prospective trials, and their clinical relevance has not yet been established.
CT and Cardiac magnetic resonance imaging (CMRI) have also been used to evaluate selected cases of AS and the measurement of AVA in selected patients. These will be discussed in the following sections.
After utilizing the above methodology, exclusion of all possible technical errors, and establishing concordance with clinical variables, we may reach one of the following scenarios:
- Severe AS with AVA <1.0 cm2, mean systolic gradient >40 mmHg (true severe AS)
- Severe AS with AVA <1.0 cm2 but mean gradient <40 mmHg and normal flow (LVOT SV >35 ml/m2) (severe AS with low gradient and normal flow)
- Severe AS with AVA <1.0 cm2 but mean gradient <40 mmHg and low flow (LVOT SV <35 ml/m2) (low flow-low gradient severe AS) with low EF (EF < 50)
- Severe AS with AVA <1.0 cm2 but mean gradient <40 mmHg and PV <4 m/s and low flow (low flow low-gradient severe AS) with preserved EF.
A step-wise approach is recommended to differentiate between such groups to reach the final diagnosis, which is essential because of the different prognostic and management pathways.[1] These steps approach will be discussed in more detail in the following sections.
| Other Imaging Modalities | | |
Echocardiography is the primary imaging modality used to evaluate the cardiac valves. However, with the limitations of the acoustic window in obese and patients with chronic obstructive pulmonary disease, TTE may be inadequate for the examination of the valves. Although TEE overcomes this to some extent, it is slightly invasive and thus subject to complications.
Cardiac CT and CMR imaging are noninvasive techniques that may be used to characterize valvular heart disease in patients with inconclusive findings on TTE. They also provide additional information on the dimensions and geometry of the aortic root and ascending aorta and the extent of calcification in the AVs. In low-gradient AS, quantification of the valve calcification has become particularly important in assessing the severity of AS.[26],[27] CMR is the gold standard for functional evaluation of the LV and, unlike CT, can identify the pathological effects of the left ventricular remodeling, particularly subendocardial myocardial fibrosis, regardless of the presence of coronary artery disease, which has been implicated in prognosis.[28]
Cardiac computed tomography
Techniques for imaging the AV using cardiac CT have evolved rapidly, and it allows for quantification of AV calcification and characterization of valvular masses and vegetations. Reconstructed multiplanar images analogous to standard TTE images can be obtained in assessing the valve leaflets and performing planimetry.[29] Extending the images to include the ascending aorta, especially when they are dilated, helps clarify aortic diameter and to assess aortic morphology and configuration, which is essential in the planning of surgical AV intervention or TAVI.
Aortic valve calcium score
Although echocardiography remains the first line in the assessment of AV, there exists uncertainty as to the true severity of valvular disease in up to 40% of patients. The most frequent setting this can happen is when the peak aortic velocity (<4 m/s) or the mean gradient falls (<40 mmHg) in the moderate range while the AVA measures as severe stenosis (<1 cm2). AV calcium scoring can be performed using the Agatston method, using electron beam CT scanners, and has since been adapted to modern multidetector scanners. The scan requires ECG-gated specific scan parameter compliance and uses a tube current (mA) varied based on the patient weight.[30] There has been a significant reduction in the dose of radiation for calcium scoring with the use of advanced scanners and acquisition protocols. Improved signal-to-noise ratio with the latest image reconstruction strategies has reduced the tube current without compromising calcium-score accuracy.[31],[32]
Thus, CT-derived AV calcium score has evolved as a complementary marker in questionable severe AS patients, as stated in the 2017 European society of cardiology guidelines for the management of patients with valvular heart diseases.[33] The threshold for identifying true AS was considered as for an AV calcium score ≥1600 AU in women and ≥3000 AU in men (as very likely); ≥1300 AU in women and ≥2000 AU in men (as likely), and if <800 AU in women and <1600 AU in men (unlikely). Parade et al. have recently established the previously considered calcium scoring thresholds from a multicenter study.[34]
The echocardiography estimated AVA with the use of the smaller LVOT dimension tends to give smaller AVA from the continuity equation. AV calcium score quantification from cardiac CT corresponds well with the severity of AV and prognosis as well.[27],[35] The main advantage of such AV calcium scoring is it is independent of the hemodynamic status of the patient and is a faster alternative in a broad number of cases. However, in fibrotic valves, like in the bicuspid valves of young female patients, mindful assessment is required, and in fact, CT measured AV calcium score neglects calcific leaflet thickening that can also contribute to hemodynamic obstruction, which may be the main reason for the valvular stenosis.
Aortic valve planimetry
In CT, it is also possible to measure AVA from direct planimetry by aligning the plane of AV orifice images from the three-dimensional volumetric scan data. This distinct capability of CT is independent of any geometric assumptions.[36] The measurements are acquired during maximum valve opening from the mid-systolic phase and precise orthogonal alignment in the short axis of the valve plane to calculate the minimum orifice area. Halpern et al. had shown that AVA from CT would be the same as echocardiography-derived AVA when LVOT area was obtained from CT images for continuity equation.[37] CT acquisition with ECG gating of the end-diastolic and end-systolic phases also allows for accurate estimation of SV. AV calcification which deposits within the margins of the cusp, does not seem to impede the planimetry assessment of AVA from CT. Multi-slice cardiac CT also offers a highly accurate evaluation of annulus size, annulus to coronary artery distance, and aortic root shape to facilitate planning prior to intervention [Table 6]. | Table 6: Assessment of the severity of aortic stenosis from cardiac CT and cardiac MR
Click here to view |
Cardiac magnetic resonance
Advances in CMR have helped it evolve as an alternative noninvasive imaging modality in the assessment of various cardiac diseases. Although TTE remains to be the clinical reference standard for a safe and quick anatomical and functional evaluation of aortic valvular disease, the considerable high-quality CMR images present as an excellent substitute, especially in difficult and inconclusive severe AS diagnosis. Severe AS is determined by a combination of mean and peak pressure gradients across the valve as well as the effective valve orifice or AVA.
CMR is particularly beneficial in patients with impaired renal function when iodinated contrast required for CT imaging is contraindicated and provides opportunities for planning pre-TAVI or surgical AV replacement.[38] In addition, gadolinium-enhanced CMR can offer valuable information on anatomy and myocardial scar.[39] The relative safety of nonionic gadolinium contrast relative to iodinated agents, lack of radiation, and the ability to display cross-sectional anatomical, ventricular functional, and flow information enhances the utility of CMR. Unnecessary sedation, as in TEE, is also avoided with CMR. As the most severe AS patients are elderly, with the diminishing GFR values in this patient population, the use of CMR further adds value. Caution is still advocated for such patients with an increased risk of contrast-induced renal injury in the latest guidelines.
However, in severely calcified AS signal void, making the discrimination of the valve leaflet borders difficult and thus lead to inaccurate measurement. The presence of arrhythmias is also a cause of reduction in image quality. It must be understood that while the continuity equation measures the effective valve orifice area, the planimetry measures the anatomic valve orifice area.
Aortic valve planimetry
Woldendorp et al. demonstrated that CMR planimetry measurement of AVA obtained during the maximal opening in systole from the inner valve leaflet edges is similar to measurements obtained by TEE. However, AVA derived by CMR planimetry was significantly larger than TTE by 10.7% (mean difference: +0.14 cm2, 95% confidence interval 0.07–0.21, P < 0.001).[40] AVA planimetry from CMR is not dependent on the observer and is reproducible. However, in severely calcified AS signal void, making discrimination of the valve leaflet borders difficult and thus leads to inaccurate measurement. The presence of arrhythmias is also a cause of reduction in image quality. It must be understood that while the continuity equation measures the effective valve area, the planimetry measures the anatomic valve area, both of which can vary significantly.[41] Certainly, direct planimetry brings a larger AVA and there is no validated threshold for defining the severity of AS using planimetry.
Severe AS is still defined using the continuity equation in the guidelines and can be complemented from the AV calcium score inappropriate scenarios. Hence, an area of the AV below 1 cm2 on planimetry from CMR can only support the argument of inconclusive echocardiographic severe AS.
Good correlation in patients with low-gradient severe AS was noted between CMR and TTE values for measured LVOT and AVA wherein CMR derived values were slightly larger, attributed to incomplete visualization of the nonuniform anatomy of the AV and LVOT dimension.[42] Although not in clinical practice, CMR also allows for hemodynamic measurements of the cardiovascular system. Evidence available hints that there is a good correlation to TTE measured hemodynamics.[43],[44],[45]
Phase-contrast imaging
2D phase-contrast imaging in CMR has demonstrated good concordance with TTE derived data; however, they are time-consuming and require specific sequences. Time-resolved 3D phase-contrast MRI/4D flow MRI is a reasonable alternative to noninvasively measure blood flow velocities as flow dynamic quantification is possible in both great vessels and the heart. This technique is better, especially for eccentric jets for peak velocity assessment, and more accurate in bicuspid AVs.[46]
Assessment of left ventricle
CMR is the imaging modality for the assessment of the impact of AS on the LV. It is well recognized that CMR is the gold standard for LV mass and thickness assessment. The LV adaptation and response to AS are independent of the severity of AS. Adaptation from the prolonged pressure overload on LV and the patterns of remodeling vary. LV hypertrophy is a compensatory mechanism to maintain systolic function by normalizing wall stress. Nevertheless, these adaptive measures from LV are linked to adverse clinical outcomes.[47],[48],[49] Further studies are required using CMR and complementary TTE to understand if early AV replacement may be favorable for these patients with remodeled LV.
Hypertrophy and the increase in myocyte size results in myocyte apoptosis, and following LV, myocardial fibrosis is seen in AS.[50] CMR is the only noninvasive test that detects this myocardial fibrosis. While the cardiac biopsy is the gold standard to evaluate for fibrosis, it is limited by an inability to assess global LV fibrosis and low yield from sampling errors; moreover, the complications associated due to the invasive nature also reduce its clinical application.[51] CMR assesses fibrosis using late gadolinium enhancement imaging and myocardial T1 mapping. T1 mapping allows for diffuse interstitial fibrosis, whereas late gadolinium helps in the evaluation of focal replacement fibrosis. The excessive collagen deposition in the extracellular space leads to a delay in gadolinium washout as it accumulates in these regions, thereby appearing bright compared to normal myocardium.[52],[53]
Myocardial fibrosis in AS takes a mid-wall enhancement pattern and is associated with adverse outcomes. It is a frequent finding that is also attributed to diastolic and systolic dysfunction in these patients. Dweck et al. demonstrated an 8-fold increase in all-cause mortality despite similar severity of AS. The more the fibrosis burden, the worse is the prognosis.[28],[54],[55] Not only preoperatively, even the perioperative risk of 30-day mortality and for major adverse cardiac and cerebrovascular events increases with the presence of myocardial fibrosis in patients undergoing AV replacement. It has also been found to be linked to the failure to recover left ventricular function in post-surgical patients.[56] Musa et al. have demonstrated that from a larger AV replacement group that myocardial fibrosis is associated with 2-fold higher mortality postoperatively.[57]
As per Lee et al., in patients with significant AS, regardless of the presence of late gadolinium enhancement, native T1 mapping values may be an independent predictor of adverse outcomes.[58] Diffuse interstitial fibrosis detected from non-contrast T1 mapping could be a possible target for treatment. Serial assessment of T1 myocardial mapping thus may help assess the progression of the disease.[59],[60]
However, the more frequently found (50%) myocardial fibrosis visualized from late gadolinium imaging seems to be irreversible in AS patients. Post gadolinium estimation of extracellular volume was also noted to be independently related to all-cause and cardiovascular mortality.[61]
Ultimately, such measures of T1 mapping and late gadolinium enhancement could guide treatment strategies by supporting us in comprehending the progression of disease and response to treatment.
Other clinical use of cardiac magnetic resonance
For patients in whom iodinated contrast is inappropriate, noncontrast CMR could be a substitute for inaccurate measurement of the aortic annulus for correct prosthesis sizing and avoiding paravalvular leaks.[62] Dilatation of ascending aorta is also seen in AS, especially in patients with the bicuspid AV.[63] With poor acoustic windows, it may be difficult for TTE to assess the morphology of the AV, particularly with excessive calcification, and CMR imaging can play a vital role.[64]
AR happens commonly with AS, and CMR assessment of AR using phase-contrast velocity encoded flow at the sinotubular junction allows for accurate quantification of the volume and fraction.[65]
The association of transthyretin cardiac amyloidosis with age-related degenerative AS (almost 15%) is well known in multiple studies, and CMR is a very good alternative noninvasive diagnostic modality along with cardiac scintigraphy.[66] Raised native T1 mapping, ECV, difficult nulling of blood pool along with diffuse subendocardial late gadolinium enhancement are the classic findings on CMR in cardiac amyloidosis.[67],[68]
CMR is also capable of diagnosing unknown myocardial infarction, which may be the reason for LV dysfunction in subsets of low-flow low-grade AS [Table 6]. Thus, it is worth realizing that although LV ejection fraction is a powerful predictor in asymptomatic AS patients, there may also be other structural and functional abnormalities of LV which may have a significant impact on the outcome of AS patients.
| Conclusions | | |
The diagnosis and precise assessment of AS severity are necessary for clinical decision-making. This is achieved by a multimodality approach which depends on clinical diagnosis, imaging, hemodynamic studies, and laboratories investigations. Echocardiography is the diagnostic imaging and hemodynamic method of choice which is endorsed by the current guidelines. In most situations, TTE is enough for the assessment of both severity and serial evaluation of AS. Moreover, the prediction of clinical outcomes has been studied mainly by TTE. Standardization of the echocardiography methodology and interpretation is the current goal of all guidelines.
Although quantification of AS severity is possible from different techniques, echocardiography will always remain the safe and rapid gold standard tool; still, other imaging modalities such as CT and CMR prove to be excellent alternatives. Their application is not only limited to difficult echocardiography windows but also as a complementary imaging assessment for confirmation of the findings. The power of CT to estimate the AV calcium score and correlation to the grading of AS severity is very well illustrated. The advantage of CMR lies in the lack of radiation and use in patients in chronic renal insufficiency where iodinated contrast is inappropriate. The assessment of the repercussions on LV from the overload of AS assessed from CMR has the potential for wider utilization in the evaluation of disease progression and in guiding treatment. Although CT-derived AV calcium scoring has been validated well and included in guidelines for assessing the severity of AS, the CMR assessments of AVA or peak velocity have not yet been part of any recommendation.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
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[Table 1], [Table 2], [Table 3], [Table 4], [Table 5], [Table 6]
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