Role of Cardiac CT in the Evaluation of Valvular Heart Disease

Abstract

Cardiac CT has become an essential imaging modality in the diagnostic and therapeutic workflow for valvular heart disease (VHD), particularly in the era of transcatheter and minimally invasive valve therapies. The existing guidelines emphasize cardiac CT infrastructure and expertise as core requirements for both primary and comprehensive valve centers. Advances in CT acquisition and image reconstruction allow precise evaluation of valvular morphology, motion, and calcification, supporting accurate disease-severity grading and procedural planning. In comparison with echocardiography, cardiac CT provides superior spatial resolution and is less affected by acoustic shadowing from heavy calcification or prosthetic materials, making it especially valuable in complex or inconclusive cases. This review summarizes the CT scanning protocols and reconstruction strategies for valvular assessment and discusses CT-based evaluations of native-valve stenosis and regurgitation, prosthetic-valve dysfunction—including structural degeneration, thrombosis, and pannus—and infective endocarditis, highlighting the complementary role of CT alongside echocardiography in comprehensive VHD management.

INTRODUCTION

Valvular heart disease (VHD) is an increasingly prevalent condition, particularly in aging populations. A population-based study reported an overall prevalence of approximately 2.5% in the United States, with a marked increase from less than 1% in younger adults to nearly 12% among individuals aged ≥75 years (1). With the growing incidence of degenerative valvular disease and an increasing life expectancy, the clinical impact of VHD is expected to continue increasing, highlighting the need for accurate imaging-based diagnosis and treatment planning.

Although echocardiography remains the first-line imaging modality for VHD, cardiac CT has emerged as a key complementary tool in contemporary VHD management. The existing clinical guidelines emphasize the importance of cardiac CT facilities and expertise as essential components of both primary and comprehensive valve centers (2,3,4,5). Owing to its high spatial resolution and 3D imaging capability, cardiac CT allows precise assessment of valvular morphology and calcification and is less affected by acoustic shadowing from heavy calcification or prosthetic materials. CT plays an important role in the evaluation of native-valve diseases, including aortic stenosis (AS), aortic regurgitation (AR), mitral stenosis (MS), and mitral regurgitation (MR), as well as in the assessment of prosthetic-valve dysfunction and infective endocarditis (IE), particularly when echocardiographic findings are inconclusive (6,7,8,9,10,11).

In addition, cardiac CT has become integral to preoperative and pre-interventional workflows, providing comprehensive anatomical information relevant to surgical and transcatheter valve therapies, including evaluation of the thoracic aorta, coronary artery origins, vascular access, and preoperative risk (12,13). As its clinical applications continue to expand, a comprehensive understanding of CT-acquisition techniques and disease-specific imaging findings is required for radiologists and cardiovascular imaging specialists. This review summarizes cardiac CT scanning and image-reconstruction strategies for valvular assessment, with a focus on CT evaluation of native VHD, prosthetic-valve disease, and IE.

CT ACQUISITION AND IMAGE RECONSTRUCTION FOR CARDIAC-VALVE ASSESSMENT

Cardiac CT protocols for valvular assessment are generally based on coronary CT angiography but often require modification of scan coverage on the basis of the underlying valvular pathology and clinical purpose (2,3). Evaluation of the ascending aorta is essential in patients with suspected or known aortic-valve disease, particularly in those with aortopathy (2,3). For preoperative or preprocedural planning, most notably before transcatheter aortic-valve replacement (TAVR) or redo cardiac surgery, scan coverage may have to be extended to include the thoracic and abdominal aorta, aortic arch branches, and iliofemoral access vessels, in accordance with a comprehensive TAVR CT protocol (12,13). In such settings, a combination of electrocardiogram (ECG)–synchronized cardiac CT (including the aortic root) and non-ECG-synchronized CT angiography of the aortoiliac vasculature is commonly performed.

Because the assessment of valvular morphology and motion often requires both systolic and diastolic imaging, ECG-synchronized CT acquisition is essential for cardiac-valve evaluation. In CT systems with limited detector coverage, spiral or helical acquisition with retrospective ECG-gated reconstruction is typically preferred, allowing flexible multiphase reconstruction throughout the cardiac cycle. ECG-based tube-current modulation with a full tube current during the mid–R-R interval and a reduced current during the remaining phases can be applied to reduce radiation exposure. In contrast, CT systems with wide detector coverage that enable whole-heart imaging may employ prospective ECG-triggered axial one-beat acquisition, which offers excellent temporal resolution and a substantially lower radiation dose (5,12). Regardless of the acquisition mode, scan parameters should adhere to the “as low as reasonably achievable” principle, including the use of low tube potential when appropriate.

Intravenous contrast administration generally follows institutional coronary CT angiography protocols; however, additional considerations may be required depending on the valve of interest. Although standard biphasic injection protocols are usually sufficient for evaluation of the aortic and mitral valves, homogeneous enhancement of the right atrium and right ventricle is crucial for optimal assessment of the tricuspid and pulmonary valves. In such cases, a triphasic injection protocol consisting of an initial contrast bolus, followed by a saline–contrast mixture and saline chaser, may improve right-sided chamber opacification and overall image quality (14).

Cardiac CT image reconstruction plays a central role in translating volumetric data into clinically meaningful information for diagnosis and surgical planning (8,9,10). Multiphase cine display, flexible manipulation of imaging planes, and multiple display techniques, including thin- and thick-slab multiplanar reformatted and volume-rendered images, allow detailed evaluation of valvular anatomy and motion. A key advantage of cardiac CT over echocardiography is its ability to freeze the cardiac cycle at a specific phase and freely adjust the imaging planes to examine complex valvular structures. En face views of the aortic and mitral valves are routinely generated, and additional profile views perpendicular to individual leaflets or cusps can further delineate the lesion morphology. Thin-slice reconstructions (1–2 mm) are useful for detailed anatomic assessment, whereas thick-slab reformatted images (10–15 mm) can provide an overview of the lesion extent. When surgical repair is planned, reconstruction of CT images in the “surgeon’s view” orientation may facilitate an intuitive understanding of valvular pathology and improve correlation with intraoperative findings. An example of the image-reconstruction and interpretation processes is summarized in Fig. 1.

Fig. 1. Stepwise CT image acquisition and reconstruction for cardiac-valve assessment.

A. Optimal cardiac-phase selection for valve imaging with ECG-synchronized CT. End-systolic phases (approximately 20%–30% of the R–R interval) are useful for evaluating aortic-valve stenosis and mitral-valve prolapse or regurgitant lesions, whereas mid-diastolic phases (approximately 70%–80% of the R–R interval) are optimal for assessing aortic-valve regurgitation and mitral-valve stenosis.

B. Optimal imaging-plane selection for valve evaluation using multiplanar reformation, allows precise alignment either parallel (en face view) or perpendicular to the valvular plane.

C. En face multiplanar reconstruction of the cardiac valves, provides a surgeon’s view of the leaflet anatomy and commissural orientation.

D. Perpendicular multiplanar reconstruction to the valvular plane, enables detailed assessment of leaflet thickness, motion, and coaptation.

E. Thick-slab multiplanar reconstruction in an en face view, offers an overview of the valve and adjacent structures along with measurement of the valve-opening area.

F. Volume-rendered images demonstrate 3D visualization of valve anatomy, facilitating intuitive understanding of spatial relationships and surgical planning.

ECG = electrocardiogram

Within this technical framework, appropriate selection of imaging modalities on the basis of specific clinical scenarios is essential. Accordingly, Table 1 summarizes the appropriate usage criteria for multimodal imaging in VHD, outlining the situations wherein echocardiography, cardiac CT, and cardiac MRI are recommended or complement each other (15).

Table 1. Summary of the Appropriate Use Criteria for Multimodality Imaging in Valvular Heart Disease.

Clinical Scenario	Echocardiography (TTE/TEE)	Cardiac CT	Cardiac MRI
Initial evaluation of suspected valvular heart disease	TTE: appropriate TEE: rarely appropriate	Rarely appropriate	Rarely appropriate
Routine follow-up of stable, asymptomatic valvular heart disease	TTE: appropriate TEE: rarely appropriate	Rarely appropriate	Rarely appropriate
Native valve evaluation with inadequate TTE	TEE: appropriate	May be Appropriate	May be appropriate
Bicuspid aortic valve with suspected aortopathy	TTE: appropriate TEE: rarely appropriate	Appropriate	Appropriate
Infective endocarditis	Appropriate	May be appropriate	May be appropriate
Prosthetic-valve dysfunction with inconclusive TTE/TEE	-	Appropriate	May be appropriate
Preprocedural assessment before transcatheter valve intervention (e.g., TAVR)	Appropriate	Appropriate	May be appropriate

Table contents are summarized from previously published literature (15).

Appropriate Use Criteria ratings are based on international society guidelines and reflect the expected clinical benefit of each imaging modality in a given scenario. Appropriate indicates that the test is generally acceptable and a reasonable approach; May be appropriate indicates that the test may be acceptable depending on individual clinical circumstances; and Rarely appropriate indicates that the test is unlikely to provide additional clinical value.

TAVR = transcatheter aortic-valve replacement, TEE = transesophageal echocardiography, TTE = transthoracic echocardiography

AORTIC STENOSIS

AS is the most common and clinically significant form of VHD in the elderly population. Among individuals older than 75 years, the prevalence of severe AS has been reported to be approximately 3.4% (1). With the growing life expectancy, the burden of AS has also increased, making accurate diagnosis, severity assessment, and treatment planning increasingly important. The three primary causes of valvular AS are as follows: congenital bicuspid aortic valve (BAV), calcific aortic-valve disease, and rheumatic disease; other rare causes include severe atherosclerosis, rheumatoid involvement, and ochronosis associated with alkaptonuria.

Calcific aortic-valve disease, previously referred to as senile or degenerative valve disease, is the most common cause of AS and can affect both tricuspid aortic valves and congenital BAVs. Beyond mechanical stress on the valve leaflets, active biological processes such as inflammation, lipid infiltration, and osteogenic signaling play central roles in the initiation and progression of valve calcification. Progressive leaflet thickening and calcification restrict cusp motion and valvular obstruction. As the disease advances, chronic pressure overload resulting from AS induces concentric left ventricular (LV) hypertrophy, which is followed by myocardial fibrosis, ventricular dysfunction, and secondary pulmonary and systemic vascular changes.

Congenital BAV is present in approximately 0.5%–2% of the general population and accounts for more than half of the cases involving aortic-valve replacement (16). According to the 2021 International Consensus on BAV Nomenclature and Classification, BAV morphology is categorized into fused, two-sinus, and partial-fusion (forme fruste) BAV (Fig. 2) (17). Fused BAV is the predominant phenotype (approximately 90%–95%) and is defined by the fusion of two cusps within three aortic sinuses, often with a raphe. The right–left (R-L) cusp fusion is the most common (70%–80%) and is associated with AS and coarctation, whereas right non-coronary (R-N) cusp fusion (20%–30%) predicts faster progression of AR (18). Two-sinus BAV is uncommon (approximately 5%–7%) and is characterized by two symmetric cusps formed within two aortic sinuses with 180° commissural angles and no raphe. Partial-fusion BAV resembles a tricuspid valve but shows <50% cusp fusion with a small raphe, and may be associated with abnormal flow patterns and aortopathy. BAV is frequently associated with a spectrum of valvuloaortopathies, with AS being the most common clinical manifestation (Fig. 3), followed by ascending aortic dilatation, AR, mitral valve prolapse (MVP), IE, and aortic dissection (16,17). Therefore, accurate phenotypic characterization of BAV and its associated aortopathies is essential for risk stratification and procedural planning.

Fig. 2. BAV phenotypes based on the international consensus classification.

En face views of the aortic valve demonstrate representative BAV morphologies.

A. Two-sinus BAV characterized by two symmetrical sinuses without a raphe.

B. Fused BAV with R-N cusp fusion and complete raphe.

C. Partial-fusion BAV shows incomplete R-L cusp fusion with a small raphe involving <50% of the cusp margin.

BAV = bicuspid aortic valve, R-L = right–left, R-N = right noncoronary

Fig. 3. BAV with severe AS and associated aortopathy.

A, B. Thick-slab en face multiplanar reconstructions of the aortic valve obtained at systole (A) and diastole (B) demonstrate a two-sinus BAV with markedly restricted systolic valve opening, diffuse leaflet thickening, and calcification. The measured aortic-valve area was 0.851 cm², consistent with severe AS.

C. Multiplanar reconstruction perpendicular to the aortic-valve plane at systole shows dilatation of the ascending aorta, indicating concomitant BAV-related aortopathy.

D. 4D flow MRI at systole demonstrates marked flow acceleration at the aortic-valve level (red) with eccentric systolic jet impingement on the anterior wall of the ascending aorta, which supports altered hemodynamics associated with BAV and aortopathy.

AS = aortic stenosis, BAV = bicuspid aortic valve

Rheumatic AS results from chronic rheumatic inflammation that leads to commissural fusion, cusp thickening, and retraction of the free leaflet margins (19,20). Unlike calcific AS, rheumatic involvement typically affects multiple valves and frequently produces combined stenotic and regurgitant lesions. Although the global incidence of rheumatic heart disease has declined in developed countries, it remains an important cause of AS in certain regions and populations (21).

Cardiac CT plays an increasingly important role in the comprehensive evaluation of AS, particularly in clinical decision-making, preprocedural assessment, and surgical or transcatheter intervention planning (Table 2, Fig. 4). CT enables accurate assessment of aortic-valve morphology, quantification of valvular calcification, and evaluation of the associated aortic and extracardiac anatomy. In addition, CT-derived aortic-valve calcium scoring has emerged as a valuable adjunct for grading AS severity, particularly in patients with discordant echocardiographic findings. These imaging capabilities allow CT to complement echocardiography across the full spectrum of AS, from early to advanced stages, as defined by structural, hemodynamic, and clinical parameters (Table 3) (2).

Table 2. Comprehensive Assessment of the Valve and Aorta in Patients with AS.

Etiology of AS	Calcific/Bicuspid/Rheumatic/Others
Valve morphology	Tricuspid
	Bicuspid
		• BAV type (fused BAV, 2-sinus BAV, partial-fusion BAV)
		• Raphe and symmetry
	Quadricuspid or unicuspid
Measurement of aortic dimensions	Aortic annulus
	Sinuses of Valsalva
	Sinutubular junction
	Ascending aorta tubular portion (usually at the level of the right pulmonary artery)
Location and extent of valve calcification	Valve calcification
		• To predict the rate of disease progression
		• When the severity of the stenosis is in doubt, particularly in low-flow, low gradient AS
		• For decision making of surgical and interventional AV replacement
Preoperative of preprocedural evaluation	Valve sizing/access route/porcelain aorta
Evaluation of coronary artery	Coronary artery disease
	Coronary artery anomaly (e.g., high take-off, anomalous origin)
Potential obstruction to LVOT	Supravalvular stenosis
	Subvalvular stenosis
	Dynamic subaortic obstruction (e.g., hypertrophic cardiomyopathy)

AS = aortic stenosis, AV = aortic valve, BAV = bicuspid aortic valve, LVOT = left ventricular outflow tract

Fig. 4. Cardiac CT findings in aortic stenosis.

A. An en face view of the aortic valve reconstructed at systole demonstrates marked restriction of valve opening, with diffuse leaflet thickening and calcification. The inset image at the lower right shows the corresponding diastolic phase for comparison, highlighting the limited systolic excursion of the valve leaflets.

B. Multiplanar reconstruction perpendicular to the aortic-valve plane at systole confirms severe limitation of valve opening.

C. Thick-slab en face multiplanar reconstruction at systole allows direct planimetric measurement of the maximal aortic-valve area, which measured 0.774 cm², consistent with severe aortic stenosis.

D. A volume-rendered image acquired at systole provides 3D visualization of restricted valve opening and leaflet thickening, with the calcified components highlighted in white.

LA = left atrium, LCC = left coronary cusp, LV = left ventricle, NCC = noncoronary cusp, RCC = right coronary cusp

Table 3. Stages of Valvular Aortic Stenosis.

Stage	Definition	Valve Hemodynamics
A	At risk of AS	Aortic Vmax <2 m/sec with normal leaflet motion
B	Progressive AS	Mild AS:
			Aortic Vmax 2.0–2.9 m/sec or mean ΔP <20 mmHg
		Moderate AS:
			Aortic Vmax 3.0–3.9 m/sec or mean ΔP 20–39 mmHg
C	Asymptomatic severe AS
C1	Asymptomatic severe AS	Severe AS:
			Aortic Vmax ≥4 m/sec or mean ΔP ≥40 mmHg
			AVA ≤1 cm2 (or AVAi ≤0.6 cm2/m2)
		Very Severe AS:
			Aortic Vmax ≥5 m/sec or mean ΔP ≥60 mmHg
C2	Asymptomatic severe AS with LV systolic dysfunction	Aortic Vmax ≥4 m/sec or mean ΔP ≥40 mmHg
		AVA typically ≤1 cm2 (or AVAi ≤0.6 cm2/m2) but is not required to define severe AS
		LV systolic dysfunction (LVEF <50%)
D	Symptomatic severe AS
	Symptomatic severe high-gradient AS	Severe AS:
			Aortic Vmax ≥4 m/sec or mean ΔP ≥40 mmHg
			AVA ≤1 cm2 (or AVAi ≤0.6 cm2/m2), but may be larger with mixed AS/AR
	Symptomatic severe low-flow, low-gradient AS with reduced LVEF	AVA ≤1 cm2 with resting aortic Vmax <4 m/sec, or mean ΔP <40 mmHg
		Dobutamine stress echo:
			AVA ≤1 cm2 with Aortic Vmax ≥4 m/sec at any flow rate
	Symptomatic severe low-gradient AS with normal LVEF or paradoxical low-flow severe AS	AVA ≤1 cm2 (or AVAi ≤0.6 cm2/m2) with an aortic Vmax <4 m/sec, or mean ΔP <40 mmHg
		AND
		Stroke volume index <35 mL/m2
		Measured when patients are normotensive

Stages are summarized from the 2020 AHA/ACC guideline (2).

AR = aortic regurgitation, AS = aortic stenosis, AVA = aortic valve area, AVAi = indexed aortic valve area, LV = left ventricle, LVEF = left ventricular ejection fraction, V_max = peak aortic jet velocity, ΔP = mean transaortic pressure gradient

AORTIC REGURGITATION

AR results from structural abnormalities in the aortic-valve leaflets or dilatation of the aortic root and ascending aorta, which lead to inadequate leaflet coaptation during diastole. Leaflet-related causes of AR vary according to age and underlying pathology (2,3). In younger adults, particularly those aged 20–40 years, noncalcified BAVs frequently demonstrate incomplete leaflet closure or leaflet prolapse, resulting in AR (22). Calcific aortic-valve disease is a common cause in older patients and may coexist with AS. Additional leaflet abnormalities include IE, trauma-related injury, rheumatic valve disease, myxomatous degeneration, and congenital leaflet variants such as unicuspid, bicuspid, and quadricuspid valves. AR may also be associated with congenital heart disease, including aortic-valve prolapse, in the setting of a subaortic ventricular septal defect (23).

AR may also arise from diseases of the aortic root and ascending aorta, wherein the leaflet structure is relatively preserved, but coaptation is impaired due to annular or root dilatation. Common causes of AR include chronic systemic hypertension, Marfan syndrome, annuloaortic ectasia, and aortic dissection. Less frequent causes include osteogenesis imperfecta, atherosclerotic aneurysm, syphilitic aortitis, and systemic inflammatory disorders, such as giant cell arteritis and Behçet disease (23). From a functional perspective, echocardiographic classification describes three principal mechanisms of AR: type 1, which is characterized by normal cusps with central regurgitation due to aortic root dilatation; type 2, which is caused by cusp prolapse producing an eccentric regurgitant jet; and type 3, which results from leaflet retraction or poor tissue quality with either central or eccentric regurgitation (3,24).

Cardiac CT plays an important complementary role in the evaluation of AR, particularly in anatomical assessments relevant to surgical decision-making (Fig. 5). CT is recommended for accurate measurement of the maximal diameter of the aortic root and ascending aorta, which is critical for determining the indication and timing of surgical intervention. According to the current guidelines, ascending aortic surgery should be considered at a diameter of 55 mm in the general population, 50 mm in patients with BAV and additional risk factors, and 45 mm in patients with Marfan syndrome and additional risk factors (3,25). These risk factors include a family history of aortic dissection, severe aortic or MR, planned pregnancy, uncontrolled systemic hypertension, and rapid aortic growth exceeding rates of 3 mm/year. In addition, CT allows detailed evaluation of the aortic-valve cusp anatomy, including leaflet prolapse, perforation, retraction, and calcification, thereby facilitating the assessment of suitability for valve repair.

Fig. 5. Cardiac CT and 4D flow MRI findings in aortic regurgitation.

A, B. En face views of the aortic valve reconstructed at diastole (A) and systole (B) demonstrate a central coaptation defect with leaflet thickening, indicating incomplete valve closure.

C. Thick-slab en face multiplanar reconstruction at diastole allows direct planimetric measurement of the central coaptation defect, which measured 0.307 cm², consistent with significant aortic regurgitation.

D. Volume-rendered image acquired at diastole provides 3D visualization of the central coaptation defect and leaflet thickening, facilitating intuitive assessment of valve morphology.

E. Multiplanar reconstruction perpendicular to the aortic-valve plane at diastole reveals degenerative changes of the aortic valve with a central coaptation defect; the arrows indicate degenerative thickening at the leaflet tips.

F. 4D flow MRI at diastole demonstrates marked regurgitant flow directed toward the LV posterior wall, consistent with significant aortic regurgitation.

LA = left atrium, LCC = left coronary cusp, LV = left ventricle, NCC = noncoronary cusp, RCC = right coronary cusp

The severity and progression of chronic AR were classified into distinct stages based on structural, functional, and clinical parameters (Table 4). By providing precise anatomical information regarding both valvular and aortic pathology, cardiac CT complements echocardiography in defining the disease stage and guiding individualized management strategies for patients with chronic AR.

Table 4. Stages of Chronic Aortic Regurgitation.

Stage	Definition	Valve Hemodynamics
A	At risk of AR	AR severity none or trace
B	Progressive AR	Mild AR:
			Jet width <25% of LVOT
			Vena contracta <0.3 cm
			Regurgitant volume <30 mL/beat
			Regurgitant fraction <30%
			ERO <0.10 cm2
			Angiography grade 1
		Moderate AR:
			Jet width 26%–64% of LVOT
			Vena contracta 0.3–0.6 cm
			Regurgitant volume 30–59 mL/beat
			Regurgitant fraction 30% to 49%
			ERO 0.10–0.29 cm2
			Angiography grade 2
C	Asymptomatic severe AR	Severe AR:
			Jet width ≥65% of LVOT
			Vena contracta ≥0.6 cm
			Holodiastolic flow reversal in the proximal abdominal aorta
			Regurgitant volume ≥60 mL/beat
			Regurgitant fraction ≥50%
			ERO ≥0.3 cm2
			Angiography grade 3 to 4
			In addition, diagnosis of chronic severe AR requires evidence of LV dilation
D	Symptomatic severe AS		Severe AR: same as above

Stages are summarized from the 2020 AHA/ACC guideline (2).

AR = aortic regurgitation, ERO = effective regurgitant orifice area, LV = left ventricle, LVOT = left ventricular outflow tract

MITRAL STENOSIS

MS most commonly involves the mitral valve in patients with rheumatic heart disease and remains a major cause of cardiovascular morbidity in low- and middle-income countries (26). In contrast, degenerative MS is being increasingly encountered in high-income countries and is predominantly associated with mitral annular calcification (MAC). The prevalence of MAC in the general population ranges from approximately 8% to 15% (27), and nearly half of the patients with severe AS undergoing TAVR demonstrate concomitant MAC (28). Advanced MAC may result in MS, MR, or a combination of both, with stenosis being the most frequent functional consequence (29).

Echocardiography remains the primary diagnostic modality for MS, providing hemodynamic assessment and grading of disease severity (2,3). Cardiac CT serves as a valuable complementary imaging tool that provides detailed anatomical and structural information, particularly in complex or equivocal cases (30). CT allows accurate delineation of mitral-valve morphology, clarifies the precise location and extent of MAC, leaflet calcification, myocardial extension of calcification, and reveals the associated changes in the cardiac chambers (30). In addition, CT is useful for detecting left atrial thrombi and identifying caseous calcifications of the mitral annulus, which may mimic other cardiac masses on echocardiography.

Rheumatic MS is characterized by distinct morphological features on CT (Fig. 6). Commissural fusion is the hallmark finding, resulting in the classic “fish-mouth” appearance on en face views (31). Additional findings include doming of the anterior mitral leaflet, often described as a “hockey-stick” configuration, and thickened, matted, and retracted chordae caused by fibrosis and fusion of the subvalvular apparatus (31). Rheumatic valve disease frequently demonstrates multivalvular involvement, which most commonly affects the aortic and mitral valves (32). CT and MRI may be helpful for demonstrating concomitant aortic-valve leaflet thickening, restricted valve opening, and calcification, reflecting shared rheumatic inflammatory and fibrotic processes across multiple valves (Fig. 7).

Fig. 6. Cardiac CT findings in rheumatic mitral stenosis.

A. An en face view of the mitral valve reconstructed at diastole demonstrates leaflet thickening with marked limitation of valve opening.

B. Multiplanar reconstruction perpendicular to the mitral-valve plane at diastole further delineates leaflet thickening and restricted valve opening. The inset image in the lower corner shows the corresponding systolic phase for comparison.

C. Thick-slab en face multiplanar reconstruction at diastole allows direct planimetric measurement of the maximal mitral-valve opening area, measuring 1.00 cm², consistent with significant mitral stenosis.

D. A volume-rendered image acquired at diastole provides 3D visualization of restricted mitral-valve opening and leaflet thickening, facilitating intuitive assessment of valve morphology.

LA = left atrium, LV = left ventricle, RV = right ventricle

Fig. 7. Cardiac CT and 4D flow MRI findings in rheumatic multivalvular heart disease.

A, B. En face views of the aortic valve reconstructed at systole (A) and diastole (B) demonstrate a fused bicuspid aortic valve with R-N cusp fusion, along with diffuse leaflet thickening and marked restriction of valve opening; these findings are consistent with rheumatic aortic-valve involvement.

C, D. Multiplanar reconstructions perpendicular to the mitral-valve plane at systole (C) and diastole (D) further delineate leaflet thickening and restricted mitral-valve opening with doming. The inset image in panel (D) shows the corresponding en face view of the mitral valve, indicating severe limitation of valve opening.

E, F. 4D flow MRI demonstrates abnormal transvalvular hemodynamics, with marked systolic-flow acceleration at the aortic-valve level (E, red circle) and diastolic-flow acceleration at the mitral-valve level (F, red circle); these findings are consistent with combined rheumatic aortic and mitral-valve disease.

LA = left atrium, LV = left ventricle, R-N = right noncoronary

In contrast, degenerative MS associated with MAC demonstrates a different imaging phenotype. Commissural fusion and subvalvular involvement, which are characteristics of rheumatic diseases, are typically absent. Instead, extensive and often asymmetric calcification of the mitral annulus, predominantly involving the posterior annulus, leads to progressive narrowing of the mitral orifice. This annular calcification severely restricts the posterior mitral leaflet, while the anterior leaflet and tips of both leaflets are frequently spared and remain relatively mobile (29). Cardiac CT allows precise assessment of the extent, distribution, and thickness of the MAC as well as its relationship with the mitral leaflets and LV inflow tract, which is critical for distinguishing degenerative MS from rheumatic MS and for evaluating procedural feasibility (Fig. 8). Recognition of these characteristic CT findings is essential for accurate diagnosis, mechanism-based classification, and selection of appropriate therapeutic strategies, particularly in elderly patients and candidates for transcatheter mitral interventions.

Fig. 8. Severe mitral annular calcification.

A, B. Non-contrast CT (A) and contrast-enhanced cardiac CT (B) short-axis views demonstrate severe mitral annular calcification circumferentially encircling the entire mitral annulus with extension into the aortomitral continuity. Extensive annular calcification may restrict the posterior mitral leaflet, resulting in degenerative (calcific) mitral stenosis.

The severity of MS is categorized into stages based on structural, functional, and clinical parameters (Table 5) (2). By providing a comprehensive anatomical assessment beyond hemodynamic measurements, cardiac CT complements echocardiography in characterizing disease mechanisms, identifying procedural challenges, and guiding surgical or transcatheter treatment planning for patients with MS.

Table 5. Stages of Mitral Stenosis.

Stage	Definition	Valve Hemodynamics
A	At risk of MS	Normal transmitral flow velocity
B	Progressive MS	Increased transmitral flow velocities
		Mitral valve area >1.5 cm2
		Diastolic pressure half-time <150 ms
C	Asymptomatic severe MS	Mitral valve area ≤1.5 cm2
		Diastolic pressure half-time ≥150 ms
D	Symptomatic severe MS	Same as above

Stages are summarized from the 2020 AHA/ACC guideline (2).

MS = mitral stenosis

MITRAL REGURGITATION

MR is a heterogeneous disease entity with diverse etiologies involving the mitral-valve leaflets, annulus, chordae tendineae, papillary muscles, and LV geometry (2,3). The major causes of MR include myxomatous degeneration manifesting as MVP or ruptured chordae, rheumatic heart disease, IE, hypertrophic cardiomyopathy, MAC, dilated cardiomyopathy, and ischemic heart disease (33,34). Given its multifactorial nature, accurate identification of the underlying mechanisms is essential for optimal management.

MR is broadly categorized into primary and secondary forms based on the presence or absence of intrinsic mitral-valve pathology. Primary MR results from structural abnormalities in one or more components of the mitral-valve apparatus, including the leaflets, chordae, papillary muscles, and the annulus. Degenerative diseases, which encompass fibroelastic deficiency and Barlow’s disease, are the most common causes of primary MR in Western populations (34). In contrast, secondary MR arises from alterations in the LV and left atrial geometry that disrupt the balance between closing and tethering forces despite the presence of structurally normal valve leaflets and chordae. The two principal mechanisms of secondary MR are annular dilatation, often observed in dilated cardiomyopathy or as an iatrogenic consequence, and leaflet tethering caused by ventricular remodeling, most commonly in ischemic or nonischemic cardiomyopathies (2,3).

From a morphological perspective, MR can be classified on the basis of leaflet mobility using the Carpentier classification (35). Type I MR is characterized by normal leaflet motion with regurgitation caused by annular dilatation, leaflet perforation, or cleft, as seen in ischemic or dilated cardiomyopathy, endocarditis, or congenital anomalies such as mitral-valve cleft. Type II MR results from increased leaflet motion, including prolapse or flailing, and is typically associated with degenerative diseases, rheumatic involvement, endocarditis, trauma, or connective tissue disorders. Type III MR is defined by restricted leaflet motion and is subdivided into type IIIA, which shows restriction during both systole and diastole (e.g., rheumatic heart disease, carcinoid, radiation-induced disease, and MAC-related MR), and type IIIB, which shows systolic restriction related to LV enlargement and papillary muscle displacement, as observed in ischemic or dilated cardiomyopathy.

Echocardiography remains the primary imaging modality for MR assessment; however, cardiac CT provides valuable complementary information by offering precise anatomic delineation of the regurgitant leaflet, annulus, and subvalvular apparatus (36,37). CT is particularly useful for surgical or transcatheter planning, allowing detailed evaluation of leaflet morphology, annular geometry, and the extent of annular calcification. In the setting of transcatheter mitral-valve replacement, CT plays a central role in annular sizing and assessment of procedural feasibility (38). For patients with MVP, a stepwise CT-based approach has been proposed to accurately localize the prolapsed scallop (Fig. 9) (8,39,40). This includes the selection of the optimal cardiac phase, typically during early systole at approximately 20%–40% of the R–R interval, followed by determination of the involved leaflet (anterior vs. posterior) using sagittal views analogous to the echocardiographic three-chamber plane. Subsequent localization of the prolapsed scallop (medial, middle, or lateral) can be achieved on coronal images aligned with the coaptation line by using the left atrial appendage and coronary sinus as anatomical landmarks (8). Finally, thick-slab multiplanar reformatted images or volume-rendered reconstructions in the surgeon’s view can facilitate intuitive visualization of the extent and location of prolapse, enhancing communication with the surgical team (Fig. 9).

Fig. 9. Cardiac CT and 4D flow MRI findings in mitral regurgitation caused by mitral valve prolapse.

A. Multiplanar reconstruction perpendicular to the mitral-valve plane at systole demonstrates a coaptation defect caused by prolapse of the posterior leaflet (P2 scallop).

B. The corresponding perpendicular view at diastole shows restoration of leaflet coaptation, confirming dynamic systolic prolapse.

C. An en face view of the mitral valve reconstructed at systole clearly depicts prolapse of the P2 scallop toward the LA.

D. A volume-rendered image acquired at systole provides 3D visualization of P2 prolapse, facilitating intuitive assessment of valve morphology and its spatial relationships to the adjacent cardiac structures.

E, F. 4D flow MRI at early systole (E) and late systole (F) demonstrates continuous regurgitant flow from the LV to the LA at the mitral-valve level (red circles), consistent with severe mitral regurgitation, with a calculated mitral regurgitant fraction of 53%.

A2 = anterior mitral leaflet middle scallop, LA = left atrium, LAA = left atrial appendage, LV = left ventricle, P2 = posterior mitral leaflet middle scallop

The severity and progression of chronic MR can be categorized into stages based on structural abnormalities, ventricular response, and clinical status (Table 6) (2). By providing comprehensive 3D anatomic information that complements functional assessment, cardiac CT plays an increasingly important role in the mechanism-based classification, procedural planning, and individualized management of patients with MR.

Table 6. Stages of Chronic Mitral Regurgitation.

Stage	Definition	Valve Hemodynamics (Primary MR)	Valve Hemodynamics (Secondary MR)
A	At risk of MR	No MR jet or small central jet area <20% LA on Doppler	No MR jet or small central jet area <20% LA on Doppler
		Small vena contracta <0.3 cm	Small vena contracta <0.3 cm
B	Progressive MR	Central jet MR 20%–40% LA or late systolic eccentric jet MR	Regurgitant volume <60 mL
		Vena contracta <0.7 cm	Regurgitant fraction <50%
		Regurgitant volume <60 mL	ERO <0.40 cm2
		Regurgitant fraction <50%
		ERO <0.40 cm2
		Angiography grade 1+ to 2+
C	Asymptomatic severe MR	Central jet MR >40% LA or holosystolic eccentric jet MR	Regurgitant volume ≥60 mL
		Vena contracta ≥0.7 cm	Regurgitant fraction ≥50%
		Regurgitant volume ≥60 mL	ERO ≥0.40 cm2
		Regurgitant fraction ≥50%
		ERO ≥0.40 cm2
		Angiography grade 3+ to 4+
D	Symptomatic severe MR	Same as above	Same as above

Stages are summarized from the 2020 AHA/ACC guideline (2).

ERO = effective regurgitant orifice area, LA = left atrium, MR = mitral regurgitation

TRICUSPID REGURGITATION

Tricuspid regurgitation (TR) can be broadly classified into primary and secondary types on the basis of its underlying pathophysiology (2,3). Primary TR is caused by intrinsic abnormalities in the tricuspid-valve apparatus and is relatively rare. The causes of primary TR include congenital anomalies, such as the Ebstein anomaly, as well as acquired conditions, including rheumatic heart disease, IE, myxomatous degeneration, carcinoid heart disease, trauma, radiation injury, and leaflet distortion caused by intracardiac devices or pacemaker leads (Fig. 10). Since primary TR directly involves structural valve pathology, it should be distinguished from secondary TR to guide appropriate clinical management.

Fig. 10. Cardiac CT findings in tricuspid regurgitation caused by pacemaker-lead impingement.

A. An en face view of the tricuspid valve at diastole demonstrates significant annular dilatation (maximum diameter, 46 mm). Severe circumferential mitral annular calcification involving the entire mitral annulus is also noted.

B. An en face view at systole shows a central coaptation defect of the tricuspid valve (arrowheads) caused by pacemaker-lead impingement (arrow), resulting in tricuspid regurgitation.

C. Multiplanar reconstruction perpendicular to the tricuspid valve at systole also demonstrates a central coaptation defect (arrowheads) due to pacemaker-lead impingement (arrow).

D. A volume-rendered image at systole provides 3D visualization of the central coaptation defect (arrowheads) associated with pacemaker-lead impingement (arrow), indicating the regurgitation site.

RA = right atrium, RV = right ventricle

Secondary (functional) TR is the most common form of TR and results from geometric and functional alterations of the right ventricle and tricuspid-valve apparatus rather than from primary leaflet disease (41). These changes include tricuspid annular dilatation, leaflet tethering or tenting, and mal-coaptation secondary to right ventricular dilatation or dysfunction. Secondary TR is most frequently associated with left-sided heart disease, pulmonary hypertension, or right ventricular myocardial disease, but it may also occur as isolated TR, particularly in patients with long-standing atrial fibrillation (42). Isolated TR is typically characterized by a preserved LV ejection fraction, normal pulmonary artery pressure, absence of significant left-sided valvular disease, and structurally normal-appearing tricuspid-valve leaflets (43). The stages of TR are summarized in Table 7.

Table 7. Stages of Tricuspid Regurgitation.

Stage	Definition	Valve Hemodynamics
A	At risk of TR	No or trivial TR
		Tricuspid annular dilation
		RA enlargement
		RV dilation or dysfunction
		Conditions predisposing to TR (e.g., atrial fibrillation, pulmonary hypertension, left-sided valve disease, intracardiac leads)
B	Progressive TR	Central jet <50% RA
		Vena contracta <0.7 cm
		ERO <0.40 cm2
		Regurgitant volume <45 mL
C	Asymptomatic severe TR	Central jet ≥50% RA
		Vena contracta ≥0.7 cm
		ERO ≥0.40 cm2
		Regurgitant volume ≥45 mL
		Dense continuous wave signal with a triangular shape
		Hepatic vein systolic flow reversal
D	Symptomatic severe TR	Same as above

Stages are summarized from the 2020 AHA/ACC guideline (2).

ERO = effective regurgitant orifice area, RA = right atrium, RV = right ventricle, TR = tricuspid regurgitation

CT plays a complementary role in the anatomical and functional assessment of TR, particularly in patients undergoing comprehensive cardiac evaluation or preprocedural planning. CT allows detailed visualization of the tricuspid-valve apparatus, including leaflet morphology, annular geometry, and spatial relationships with adjacent structures or intracardiac devices. En face views of the tricuspid valve enable direct assessment of the annular size and shape, which are particularly useful in functional TR, where annular dilatation is a key mechanism. For TR evaluation, multiphase ECG-gated cardiac CT is typically used to assess dynamic annular changes and leaflet coaptation during the cardiac cycle (14). Annular measurements are generally performed at end-diastole by using short-axis or reconstructed en face images (14). For reference, prior echocardiographic studies have reported normal tricuspid annular dimensions on the four-chamber view, including a mean maximum diameter of approximately 3.1 cm, circumference of approximately 11.9 cm, and annular area of roughly 11.3 cm² (44). In functional TR, annular dilatation is commonly defined as a maximum diameter greater than 40 mm (45). Although CT is not routinely used for quantitative grading of TR severity, it provides valuable information regarding the structural mechanisms of regurgitation, device–leaflet interactions, and right-sided chamber remodeling, thereby supporting clinical decision-making and interventional planning.

PROSTHETIC-VALVE DISEASE

Prosthetic-valve dysfunction is a complex clinical entity in which accurate differentiation of the underlying mechanisms is essential for appropriate management. In mechanical prosthetic valves, stenosis commonly results from thrombus formation, pannus ingrowth, or a combination of both. In contrast, bioprosthetic-valve stenosis is typically caused by structural valve degeneration, including leaflet thickening, calcification, and tearing, but may also be associated with thrombosis, IE, or pannus formation (2). Cine cardiac CT enables dynamic assessment of prosthetic-valve leaflet motion, allowing measurement of the opening and closing angles of mechanical valves and detection of abnormal tissue on or adjacent to the valve. The existing guidelines recommend cardiac CT as a key imaging modality for treatment planning when prosthetic-valve stenosis is suspected, particularly when echocardiographic findings are inconclusive (2,3,5,46). In addition, paravalvular leakage (PVL) may occur as a result of suture-line disruption related to technical factors, annular dehiscence, or IE, further contributing to prosthetic-valve dysfunction (10,47).

Differentiating between pannus and thrombus formation is a critical clinical task, since management strategies differ substantially (Fig. 11, Table 8). Pannus formation is typically characterized by a gradual increase in the transvalvular pressure gradient, whereas thrombus formation is often accompanied by acute or subacute hemodynamic deterioration. On CT, the pannus typically appears as a high-attenuation (≥145 Hounsfield unit [HU]) or partially calcified, crescent-shaped fibrous overgrowth arising from the subvalvular inflow side along the sewing ring, whereas the thrombus is seen as a lower-attenuation (<90–145 HU), irregular mass on the valvular or supravalvular outflow side (Fig. 11) (48). Longitudinal CT studies have demonstrated that the extent of pannus formation increases over time and correlates with transvalvular pressure gradients measured using echocardiography (Fig. 12) (9,49,50). This relationship has been further supported by both clinical and experimental investigations, which suggest that subvalvular pannus formation may alter local hemodynamics, such as flow oscillations and reduced leaflet torque, leading to decreased opening angles of mechanical valve leaflets (47,49,50,51). Importantly, when echocardiographic assessment is limited by acoustic shadowing from mechanical prostheses or heavy calcification, CT provides incremental diagnostic value by enabling direct visualization and quantification of the subprosthetic pannus, precise assessment of leaflet opening angles, and accurate delineation of the anatomic mechanism of prosthetic-valve obstruction.

Fig. 11. Differentiation between pannus and thrombus in a prosthetic aortic valve.

A, C. Pannus formation. (A) En face view and (C) multiplanar reconstruction perpendicular to the prosthetic aortic-valve plane at systole demonstrate circumferential subprosthetic partially calcified soft-tissue thickening (arrowheads and arrows) resulting in narrowing of the valve orifice, consistent with pannus formation.

B, D. Prosthetic-valve thrombosis. (B) En face view and (D) multiplanar reconstruction perpendicular to the prosthetic aortic-valve plane at systole show a low-attenuation mass involving the valve leaflets and subprosthetic region (arrowheads and arrows), causing narrowing of the valve orifice, consistent with thrombus (hypoattenuated leaflet thickening).

Table 8. Characteristics of Pannus and Thrombosis in Prosthetic Heart Valves.

	Obstructive Pannus	Obstructive Thrombus
Clinical findings	- All PHV - Adequate prothrombin time - Non-acute presentation	- Mitral/right-sided PHV - Low prothrombin time - Acute presentation
Fluoroscopy	- Leaflet motion restriction is common but may be absent	- Leaflet motion restriction
Echocardiography	- Gradual increase of pressure gradient - Small mass with high echogenicity or absent mass	- Sudden increase of pressure gradient - Large mass (>2 cm) with low echogenicity
Cardiac CT	- Circumferential lesion along valve strut ring - Subvalvular lesion; attachment of lesion to PHV ring/hinge points - May be partially or totally calcified lesion	- Irregularly shaped mass with low attenuation - Mass attached to the leaflet or hinge point - Sub- or supra-valvular mass location

Table contents are summarized from previously published literature (46).

PHV = prosthetic heart valve

Fig. 12. Cardiac CT findings for pannus formation causing mechanical prosthetic aortic-valve stenosis.

A, B. TTE in the parasternal long-axis (A) and short-axis (B) views indicates pannus formation. Serial follow-up echocardiographic assessments demonstrated progressive elevation of aortic-valve peak velocity and mean pressure gradient, although they offered limited visualization of the mechanical prosthetic valve.

C. Multiplanar reconstruction perpendicular to the prosthetic aortic-valve plane at systole demonstrated subprosthetic soft-tissue thickening (arrows) along the sewing ring, resulting in a reduced opening angle of the mechanical valve leaflets.

D. An en face view at systole shows circumferential subprosthetic soft-tissue thickening (arrowheads) encroaching the valve orifice, consistent with pannus formation.

E. Thick-slab en face multiplanar reconstruction at systole further delineates the extent of subprosthetic pannus (arrowheads) and its relationship with the prosthetic-valve leaflets.

F. A volume-rendered image acquired at systole provides 3D visualization of the mechanical prosthetic valve and surrounding pannus tissue, facilitating intuitive assessment of the spatial extent of pannus formation.

LA = left atrium, LV = left ventricle, TTE = transthoracic echocardiography

PVL is another important complication of prosthetic-valve implantation (Fig. 13). Although 2D and 3D echocardiography remain the primary imaging techniques for detecting and grading PVL, cardiac CT provides valuable complementary anatomic information that can guide surgical or transcatheter interventions. CT-based evaluation of the PVL should include precise localization of the defect, accurate measurement of its dimensions, assessment of its orientation relative to the sewing ring and prosthetic occluders or leaflets, and evaluation of the adjacent subvalvular structures (2). Beyond anatomical delineation, cardiac CT can generate reconstructions tailored to the surgeon’s or fluoroscopic view, thereby facilitating communication between imaging specialists and operators and improving procedural planning for PVL closure (10,52).

Fig. 13. Cardiac CT findings of paravalvular leakage caused by mechanical mitral-valve dehiscence.

A. Multiplanar reconstruction perpendicular to the mechanical mitral-valve plane at systole demonstrates focal prosthetic-valve dehiscence along the sewing ring (arrows), consistent with paravalvular leakage.

B. Thick-slab en face multiplanar reconstruction at systole localizes the dehiscence to the 6–7 o’clock position (arrows); the 12 o’clock position corresponds to the aortic side and serves as an anatomic reference.

C. Thick-slab en face multiplanar reconstruction at systole allows direct planimetric measurement of the dehiscence, measuring 0.280 cm².

D. A volume-rendered image of the mechanical mitral valve acquired at systole provides 3D visualization of the paravalvular defect, with the dehiscent region highlighted in red.

AV = aortic valve, LA = left atrium, LV = left ventricle

INFECTIVE ENDOCARDITIS

IE is a life-threatening condition associated with substantial morbidity and mortality despite advances in antimicrobial therapy and surgical management. The reported in-hospital mortality rates for IE range from approximately 15% to 20%, underscoring the importance of early and accurate diagnosis (2,4). The modified Duke criteria, which integrate clinical, microbiological, and imaging findings, remain the current standard diagnostic framework for IE. Two major criteria define definite IE: positive blood cultures for typical microorganisms and evidence of endocardial involvement (2,4).

Evidence of endocardial involvement according to the modified Duke criteria is primarily based on echocardiographic findings or new valvular dysfunction. Echocardiographic features consistent with IE include oscillating intracardiac masses attached to the valves or supporting structures, paravalvular abscesses, and new partial dehiscence of the prosthetic valves. In addition, the development of new valvular regurgitation is considered a major diagnostic criterion reflecting structural valve destruction or leaflet perforation (2). While transthoracic and transesophageal echocardiography remain the first-line imaging modalities, their diagnostic performance may be limited in certain clinical scenarios, particularly in patients with prosthetic valves or extensive calcification.

Cardiac CT has emerged as a valuable complementary imaging modality for evaluating IE, particularly for assessing extracardiac and paravalvular complications. CT is especially useful for detecting the paravalvular extension of infection, including abscess and pseudoaneurysm formation, which may be underestimated or missed on echocardiography (Fig. 14). In cases of right-sided IE, CT provides a whole-thorax evaluation and is effective in identifying septic pulmonary emboli, pulmonary infarcts, or abscesses, which are important determinants of disease severity and treatment strategies (2).

Fig. 14. Cardiac CT findings for infective endocarditis complicated by aortic regurgitation and perivalvular pseudoaneurysm.

A. Multiplanar reconstruction perpendicular to the aortic-valve plane at systole demonstrates a mass-like lesion attached to the RCC (arrow), consistent with vegetation.

B. The corresponding perpendicular view at diastole shows prolapse and perforation of the RCC (arrow) with a focal coaptation defect (arrowheads), resulting in aortic regurgitation.

C. An en face view at systole reveals nodular thickening of the aortic-valve leaflets, which was most pronounced at the RCC (arrows). A contrast-filled outpouching in the periaortic space adjacent to the RCC indicates formation of a perivalvular pseudoaneurysm (arrowheads).

D. A volume-rendered image acquired at diastole demonstrates a central coaptation defect (red circle) caused by RCC prolapse and perforation, providing 3D visualization of the regurgitation mechanism.

LA = left atrium, LCC = left coronary cusp, LV = left ventricle, NCC = noncoronary cusp, RCC = right coronary cusp

Cardiac CT offers distinct advantages over echocardiography in patients with prosthetic heart valves, because it is less susceptible to the acoustic shadowing artifacts caused by prosthetic materials. This allows for improved visualization of paravalvular lesions, prosthetic-valve dehiscence, and infected vegetations or thrombi attached to the prosthetic-valve leaflets (11). By providing detailed anatomical information that complements echocardiographic assessments, cardiac CT plays an increasingly important role in the comprehensive evaluation of IE, particularly in complex cases requiring surgical decision-making or multidisciplinary management (Table 9).

Table 9. Anatomical and Echocardiographic Definitions in Infective Endocarditis.

Term	Surgery/Necropsy (4)	Echocardiography (8)	CT (11)
Vegetation	An infected mass attached to an endocardial structure or on implanted intracardiac material	Oscillating or non-oscillating intracardiac mass on valve or other endocardial structures or on implanted intracardiac material	An irregular-shaped soft tissue lesion that is attached to valves or paravalvular structures and distinct from the endocardium*
Abscess	Perivalvular cavity with necrosis and purulent material not communicating with the cardiovascular lumen	Thickened, a non-homogeneous perivalvular area with echodense or echolucent appearance	A perivalvular fluid collection showing 0–40 HU with a layer of thickened inflammatory enhancing tissue or irregular inhomogeneous paravalvular areas surrounding the fluid
Pseudoaneurysm	Perivalvular cavity communicating with the cardiovascular lumen	Pulsatile perivalvular echo-free space, with color-Doppler flow detected	A space filled with contrast or blood that has communication with cardiac chambers or the aortic root; located near the paravalvular or periannular region, possibly extending to the myocardium or pericardium
Dehiscence of a prosthetic valve	Dehiscence of the prosthesis	Paravalvular regurgitation identified by echocardiography, with or without rocking motion of the prosthesis	Tearing of any part of the stitch site that has formed a hole connecting two different chambers, without or without rocking motion of the prosthesis

Numbers in parentheses indicate reference numbers cited in the reference list: (4) surgical/pathologic definitions, (8) echocardiographic definitions, and (11) cardiac CT definitions.

^*Lesions should be identified in more than two different imaging planes to reduce false-positive findings.

HU = Hounsfield unit

PITFALLS AND LIMITATIONS OF CARDIAC CT IN VALVULAR HEART DISEASE

Despite its expanding role, cardiac CT has several limitations that should be considered when evaluating VHD. Motion artifacts related to inadequate heart rate control or arrhythmia may degrade image quality, particularly at the valvular level, and limit the accurate assessment of leaflet motion and coaptation. In addition, heavy valvular or annular calcification may cause blooming artifacts, leading to overestimation of the calcific burden and potential obscuring adjacent soft-tissue structures. Metal-related artifacts from prosthetic valves, surgical clips, or intracardiac devices may further impair image interpretation, particularly when assessing prosthetic-valve dysfunction. Finally, cardiac CT provides limited direct hemodynamic information in comparison with echocardiography and requires exposure to ionizing radiation and iodinated contrast material. Awareness of these pitfalls and appropriate protocol optimization are essential to maximize the diagnostic value of cardiac CT, while minimizing potential misinterpretation.

CONCLUSIONS

When cardiac CT was first introduced in clinical practice in the early 2,000s, its application in the evaluation of VHD was largely exploratory and case-based. At the time, cardiac CT was regarded as an interesting imaging technique with limited and unproven clinical utility for valve assessment. However, over the past two decades, substantial advances in CT technology, image reconstruction, and 3D visualization, together with paradigm shifts in surgical and transcatheter valve therapies, have fundamentally transformed the role of cardiac CT in VHD.

In contemporary clinical practice, particularly in institutions performing surgical and transcatheter valve interventions, cardiac CT has evolved from an ancillary imaging tool to an essential component of the diagnostic and therapeutic workflow. Cardiac CT provides a high-resolution, comprehensive anatomical assessment of valvular structures, accurate delineation of disease mechanisms, and reliable evaluation of adjacent cardiac and extracardiac anatomies. Importantly, cardiac CT remains robust in scenarios wherein echocardiography is limited by acoustic shadowing from heavy calcifications or prosthetic materials, thereby offering critical problem-solving capabilities.

Similar to the routine use of abdominal CT to confirm and characterize suspicious findings detected on abdominal ultrasonography, cardiac CT is well-positioned to serve as a confirmatory and complementary reference standard for indeterminate or complex findings on echocardiographic assessments. Thus, instead of replacing echocardiography, cardiac CT can extend and strengthen the diagnostic value of echocardiography by providing precise anatomical insights that directly inform clinical decision-making. With the expansion of multidisciplinary valve care, cardiac CT is expected to remain a cornerstone imaging modality, allowing accurate diagnosis, optimized procedural planning, and improved outcomes in patients with VHD.

Supplementary Materials

Korean translation of this article is available with the Online-only Data Supplement at http://doi.org/10.3348/jksr.2026.0002.