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Journal of the Korean Society of Radiology logoLink to Journal of the Korean Society of Radiology
. 2026 Mar 30;87(2):247–267. doi: 10.3348/jksr.2025.0130

Interpreting a Thick Myocardium on Cardiac MR: A Practical Guide for Radiologists

심장 자기공명영상을 이용한 두꺼운 심근의 감별: 영상의학과 의사를 위한 실용 가이드

Moon Young Kim 1,2, Hyun Jung Koo 3, Eun Ju Chun 2,4, Whal Lee 2,5,✉
PMCID: PMC13062393  PMID: 41971104

Abstract

Cardiac MR (CMR) imaging plays a central role in the differential diagnosis of a thick myocardium by enabling a comprehensive assessment of myocardial morphology and tissue characteristics. Cine imaging is useful for assessing the distribution and symmetry of hypertrophy, ventricular cavity size, and focal morphological abnormalities. T1/T2 mapping and extracellular volume measurement provide a quantitative assessment of myocardial fibrosis, inflammation, and infiltration, whereas late gadolinium enhancement patterns offer qualitative visualization of disease-specific tissue injury. Strain analyses provide complementary information on early functional impairment. In this review, we propose a practical CMR-based approach for interpreting increased myocardial wall thickness using increased wall thickness as the initial imaging finding. We systematically distinguish true pathological hypertrophy from pressure-related or physiological hypertrophy, and pseudothickening. Hypertrophic cardiomyopathy, metabolic and systemic diseases, including cardiac amyloidosis, Fabry disease, uremic cardiomyopathy, and acute inflammatory phases of sarcoidosis and myocarditis, along with hypertensive heart disease, aortic stenosis, and athlete’s heart, are reviewed with emphasis on their pathophysiology and characteristic CMR features. Common diagnostic pitfalls and a stepwise diagnostic algorithm applicable in routine clinical practice are also discussed.

Keywords: Hypertrophy, Hypertrophic Cardiomyopathy, Amyloidosis, Sarcoidosis, Fabry Disease, Athletes

INTRODUCTION

A thickened myocardium is a relatively common finding on cardiac MR (CMR) imaging, although the interpretation of this finding cannot be resolved using wall thickness measurements alone. An identical increase in wall thickness may represent true structural hypertrophy related to intrinsic myocardial disease or pseudothickening arising from technical factors during image acquisition. Diagnostic implications differ fundamentally depending on this distinction.

In clinical practice, hypertrophic cardiomyopathy (HCM) is often the first consideration when left ventricular hypertrophy (LVH) occurs. This anchoring tendency may lead to underrecognition of infiltrative or storage diseases, pressure overload hypertrophy, or overestimation of the apparent thickening caused by imaging artifacts.

In this context, CMR is the most powerful noninvasive modality for evaluating both myocardial morphology and tissue characteristics. Three complementary approaches are critical for the assessment of a thick myocardium:

1. Cine imaging: Evaluation of hypertrophy distribution (symmetric vs. asymmetric), left ventricular cavity size, myocardial mass, global systolic function, and hemodynamic features such as left ventricular outflow tract (LVOT) obstruction or valvular jet flow.

2. T1/T2 mapping: Quantitative assessment of myocardial fibrosis, inflammation, and infiltration.

3. Late gadolinium enhancement (LGE): Characterization of abnormal signal distribution patterns that suggest specific etiologies (location: subendocardial, midwall, subepicardial; pattern: patchy, linear, transmural).

This review proposes a practical CMR-centered approach that begins with the single imaging finding of a “thick myocardium” and systematically differentiates true pathologic hypertrophy, physiologic or pressure-related hypertrophy, and pseudothickening. We outline the essential imaging findings to be assessed by CMR and provide a structured interpretive strategy applicable to routine clinical practice.

TRUE PATHOLOGICAL THICKENING

The first step in evaluating a thick myocardium is to determine whether the observed hypertrophy reflects true structural changes related to intrinsic myocardial disease. Pathological hypertrophy can be broadly categorized into HCM, systemic/metabolic diseases, acute inflammatory conditions, and structural remodeling owing to pressure overload or physiological adaptation. This section reviews the representative causes of pathologic hypertrophy, emphasizing characteristic CMR patterns and key diagnostic considerations.

HYPERTROPHIC CARDIOMYOPATHY

HCM is one of the most prevalent causes of pathological myocardial hypertrophy worldwide, with an estimated prevalence of up to 1:200. Advances in diagnostic and therapeutic strategies have substantially reduced morbidity and mortality, with CMR playing a central role in the diagnosis, phenotypic classification, risk stratification, and therapeutic planning (1).

The diagnostic criterion for HCM is a maximal left ventricular wall thickness ≥15 mm in the absence of abnormal loading conditions (e.g., chronic severe hypertension or severe aortic stenosis). In individuals with a family history of or confirmed pathogenic sarcomeric mutations, a wall thickness of 13–14 mm may be sufficient for a diagnosis (2). Hypertrophy is typically asymmetrical and commonly manifests as a septal, apical, or midventricular phenotype. The septal phenotype is frequently associated with LVOT obstruction (Fig. 1). The apical phenotype demonstrates the characteristic “apical spade” configuration (Fig. 2). The midventricular phenotype may cause midcavity obstruction and may be accompanied by apical aneurysm (3,4). CMR provides superior spatial resolution compared to echocardiography, particularly in cases with equivocal findings, atypical hypertrophy distribution, associated apical aneurysm, or papillary muscle hypertrophy (5).

Fig. 1. Cardiac MRI findings of septal hypertrophic cardiomyopathy.

Fig. 1

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A. On the short-axis cine image at end-diastole, the mid-anteroseptal wall (arrow) is markedly thickened, measuring 21 mm.

B. Late gadolinium enhancement imaging reveals patchy enhancement (arrow) at the midwall of the thickened myocardium and at the anterior and inferior right ventricle insertion points.

C-E. The native and post-contrast T1 maps and ECV map show high native T1 (up to 1,328 ms), low post-contrast T1 values, and high ECV values (29.2%) respectively, within the thickened myocardium (arrows) on 3T MRI.

F. T2 mapping shows no significant T2 elevation, with values up to 42 ms on 3T MRI.

ECV = extracellular volume fraction

Fig. 2. Cardiac MRI findings of apical hypertrophic cardiomyopathy.

Fig. 2

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A, B. The three-chamber and short-axis cine images at end-diastole reveal a spade-shaped left ventricular cavity due to apical wall thickening (arrows), measuring 17 mm.

C. No significant late gadolinium enhancement is observed in the thickened apical myocardium (arrows).

D, E. The native and post-contrast T1 maps show higher native T1 values (up to 1,317 ms) and lower post T1 values, respectively, at the thickened myocardium on 3T MRI.

F. The T2 map shows T2 values of the thickened myocardium within the normal range, measuring up to 40 ms on 3T MRI.

In HCM, focal or diffuse fibrosis commonly results in LGE patterns at the right ventricular insertion sites and within patchy midwall regions. A greater extent of patchy midwall LGE has been associated with adverse prognosis (6,7), and the LGE burden tends to increase with increasing wall thickness (8). However, because approximately half of patients with HCM do not present LGE, T1/T2 mapping is particularly useful in early or mild disease when hypertrophy is subtle or LGE is not evident. Increased native T1 and extracellular volume fraction (ECV) reflect interstitial fibrosis, whereas T2 elevation may be observed in cases of focal myocardial edema. Recent studies have reported that native T1 and ECV are independent prognostic markers of heart failure–related hospitalization and mortality (9). Furthermore, segmental T1/T2 abnormalities and radiomics-based analyses have been proposed as potential tools for genotype correlation, disease staging, and arrhythmic risk stratification (10,11,12).

Global longitudinal strain (GLS) may be mildly to moderately reduced in patients with HCM, and strain reduction does not necessarily correspond to the distribution of hypertrophy, often demonstrating regional heterogeneity. Importantly, strain impairment may precede overt wall thickening and may serve as an early marker of myocardial remodeling or fibrosis. Reduced GLS is associated with increased LGE burden, progressive fibrosis, and increased risk of ventricular arrhythmia (8).

Diffuse concentric HCM may mimic the hearts of athletes (Fig. 3). Physiological hypertrophy in trained athletes is typically accompanied by an increased left ventricular cavity size and relatively preserved strain function, whereas HCM often demonstrates a smaller cavity size and disproportionate wall thickening. In younger patients with isolated wall thickening without LGE, HCM may be over-diagnosed if the clinical context is not carefully considered. Accordingly, the integration of training history, family history, and functional parameters is essential for an accurate interpretation.

Fig. 3. Cardiac MRI findings of concentric hypertrophic cardiomyopathy.

Fig. 3

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A. The four-chamber cine image of end-diastole shows diffuse concentric thickening of the global left ventricular wall (end-diastolic volume index: 69.2 mL/m2, left ventricular mass index: 162 g/m2).

B. Diffuse midwall patchy enhancement is noted on the short-axis late gadolinium enhancement image.

C. On the native T1 map, significantly higher T1 values (up to 1,348 ms) are noted.

METABOLIC AND SYSTEMIC DISEASE

Metabolic or systemic cardiomyopathies encompass conditions in which increased wall thickness reflects interstitial expansion secondary to deposition, storage, or metabolic derangement, rather than true myocyte hypertrophy. Cardiac amyloidosis (CA) and Fabry disease are characterized by the myocardial deposition of amyloid and glycosphingolipids, respectively, and demonstrate distinctive CMR features that are critical for the differential diagnosis. In contrast, uremic cardiomyopathy arises from complex systemic metabolic disturbances associated with chronic kidney disease and may present as LVH accompanied by a spectrum of CMR abnormalities.

CARDIAC AMYLOIDOSIS

CA is a prototypical infiltrative cardiomyopathy caused by extracellular deposition of amyloid fibrils within the myocardial interstitium, leading to increased left ventricular wall thickness and diastolic dysfunction. Because deposition occurs predominantly within the extracellular space, the myocardium may appear hypertrophied, although interstitial expansion and protein infiltration represent the primary mechanisms of wall thickening. Depending on the distribution of infiltration, cine imaging may demonstrate symmetric or asymmetric LVH, and the right ventricle and atria may also be involved (Fig. 4).

Fig. 4. Cardiac MRI findings of immunoglobulin light-chain amyloidosis.

Fig. 4

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A. Four-chamber cine image of end-diastolic phase shows diffuse LV, RV, and bi-atrial wall thickening and pericardial and bilateral pleural effusion.

B. The late gadolinium enhancement image reveals diffuse circumferential LV and RV subendocardial hyperenhancement with diffuse enhancement of bi-atrial wall.

C. The native T1 map shows diffusely increased native T1 values (up to 1,482 ms) in the myocardium.

D. The myocardium demonstrates low subendocardial post-T1 values in the LV.

E. The ECV polar map shows increased ECV values in the global LV wall.

F. The T2 map shows diffusely increased T2 values in the myocardium, measuring up to 59 ms.

G. LV radial and circumferential strain polar maps reveal characteristic apical sparing patterns.

ECV = extracellular volume fraction, LV = left ventricle, RV = right ventricle

CA is broadly classified into light chain (AL) and transthyretin (ATTR) subtypes, which differ substantially in their therapeutic strategies and prognoses (13). Although CMR imaging cannot definitively distinguish between these subtypes, several imaging modalities may provide diagnostic clues. ATTR amyloidosis often demonstrates pronounced myocardial thickening, extensive transmural LGE, and greater ECV elevation (14). In contrast, AL amyloidosis may present with relatively less marked wall thickening, early or predominantly subendocardial LGE, and more prominent T2 elevation (15). These features are not absolute discriminators; therefore, a multidisciplinary evaluation incorporating hematological testing and nuclear imaging is essential (16,17).

LGE in CA typically appears as a diffuse or band-like subendocardial enhancement and may extend to patchy or transmural patterns. A characteristic feature is the difficulty in determining the appropriate inversion time, which results in abnormal myocardial nulling, in which the myocardium may appear brighter than the blood pool (17).

Since amyloid deposition markedly expands the myocardial interstitium, native T1 and ECV are substantially elevated. ECV has been associated with disease burden and prognosis and plays an important role in the CMR-based assessment of amyloidosis. Although CA is fundamentally a chronic infiltrative disorder, T2 elevation may also be observed in a significant proportion of patients, reflecting superimposed edema or inflammatory injury (18,19).

Strain analysis frequently demonstrates relative apical sparing, with greater impairment at the basal and midventricular segments, corresponding to the regional amyloid burden (20). Longitudinal strain reduction is typically more pronounced in CA than in HCM or Fabry disease (21).

FABRY DISEASE

Anderson–Fabry disease (Fabry disease; Fig. 5) is an X-linked lysosomal storage disorder caused by deficiency of α-galactosidase A due to mutations in the GLA gene, which results in accumulation of glycosphingolipids within cardiomyocytes and the vascular endothelium (22,23).

Fig. 5. Cardiac MRI findings of Fabry disease.

Fig. 5

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A, B. The three-chamber and basal short-axis late gadolinium enhancement images show focal hyperenhancement in the basal inferolateral LV wall with underlying concentric LV wall thickening (arrows).

C. The native T1 map demonstrates significantly decreased T1 values (943–1,232 ms) at the basal level of the LV wall.

LV = left ventricle

Consistent with this pathophysiology, a reduction in native T1 values is a characteristic feature, particularly useful for early diagnosis (24). LGE typically demonstrates a characteristic distribution localized to the basal inferolateral midwall (24,25). With disease progression, inflammatory changes, followed by fibrosis, may lead to a gradual elevation of native T1 values toward the normal range (pseudonormalization). During the inflammatory phase, T2 may be elevated, whereas in later fibrotic stages, ECV may show a modest increase. In intermediate or advanced stages, overlapping imaging features may reduce specificity and complicate the differentiation from other cardiomyopathies.

Myocardial hypertrophy most commonly presents as concentric LVH. However, papillary muscle hypertrophy may precede overt LV wall thickening and serve as an early diagnostic clue (26). A mild reduction in GLS has been reported even before overt hypertrophy becomes apparent. Loss of the normal base-to-apex circumferential strain gradient has also been described, providing complementary information for early detection and disease characterization when interpreted alongside mapping and LGE findings (27,28).

UREMIC CARDIOMYOPATHY

Uremic cardiomyopathy is observed in patients with chronic kidney disease, particularly in those with end-stage renal disease, and is characterized by LVH, LV dilation, and combined systolic and diastolic dysfunction.

Its pathophysiology is multifactorial, involving the accumulation of uremic toxins, insulin resistance, mineral metabolism abnormalities, anemia, and chronic volume overload, which collectively promote myocardial remodeling and interstitial fibrosis. In some patients, partial reversal of the myocardial structure and function has been reported subsequent to optimized dialysis or renal transplantation, suggesting a spectrum of reversible and irreversible myocardial injuries (29,30).

On CMR imaging, uremic cardiomyopathy commonly presents with concentric LVH accompanied by diffuse elevation of native T1 and ECV, reflecting interstitial expansion. LGE may be absent or appear as a nonspecific midwall patchy enhancement, distinguishing it from the more characteristic LGE patterns observed in infiltrative diseases such as amyloidosis (29). Cine imaging may reveal an increased LV mass with preserved or reduced systolic function. Strain analysis may reveal a reduced GLS even when the left ventricular ejection fraction is preserved, suggesting early functional impairment. However, the degree of strain reduction is reportedly less pronounced than that observed in HCM and hypertensive heart disease (HHD) (31).

TRANSIENT MYOCARDIAL THICKENING IN ACUTE INFLAMMATORY PHASE OF CARDIOMYOPATHY

When evaluating a “thick myocardium,” it is important to consider the possibility of transient inflammatory thickening. Both sarcoidosis and myocarditis may demonstrate wall thickening during the acute phase owing to inflammatory injury and myocardial edema, followed by divergent structural evolution over time. Persistent or recurrent inflammation may progress to chronic fibrosis, resulting in regional or diffuse wall thinning and functional impairment. Conversely, the resolution of inflammation may lead to the normalization of myocardial thickness and function. Accordingly, any interpretation should account for the potential transition from thickening to normalization or thinning.

CARDIAC SARCOIDOSIS

Cardiac sarcoidosis (Fig. 6) is an idiopathic granulomatous disease characterized by focal or diffuse myocardial involvement of non-caseating granulomas and may demonstrate both wall thickening and thinning. Myocardial morphology and signal characteristics may vary dynamically depending on disease activity (32).

Fig. 6. Cardiac MRI findings of acute inflammatory phase of sarcoidosis.

Fig. 6

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A, B. On the short-axis cine image of end-diastole, basal septal wall thickening (arrows, A) is noted, measuring up to 18 mm with midwall or transmural enhancement (arrows, B) on the LGE image.

C, D. The T1 maps show increased native T1 values (up to 1,411 ms) and significantly decreased post T1 values on 3T MRI, corresponding to the LGE area (arrows).

E. The ECV map shows increased ECV values (30.8%, arrows).

F. The T2 map shows heterogeneously increased myocardial T2 values (arrows).

G. The 18F-labeled fluorodeoxyglucose PET-CT suggests active inflammation at the basal to mid-septal LV wall (arrow).

ECV = extracellular volume fraction, LGE = late gadolinium enhancement, LV = left ventricle

During the active phase, segmental myocardial thickening may occur secondary to inflammation and edema, accompanied by T2 elevation and increased native T1 and ECV. LGE typically demonstrates a patchy, multifocal distribution and may appear in subepicardial, midwall, or transmural patterns (33).

With chronic progression, granulomatous inflammation may be replaced by fibrosis, resulting in regional wall thinning and the corresponding wall motion abnormalities. Therefore, it is important to recognize the potential transition from thickening to thinning. Assessment of disease activity and systemic involvement is ideally performed in conjunction with fluorodeoxyglucose (FDG)-PET imaging. Increased FDG uptake reflects active inflammation, whereas CMR characterizes myocardial edema, fibrosis, and established structural injury (34).

ACUTE MYOCARDITIS

Myocarditis is characterized by myocardial inflammation and edema resulting from infectious (most commonly viral) or immune-mediated mechanisms. Acute myocarditis (Fig. 7) refers to onset within four weeks and may present with chest pain, dyspnea, palpitations, syncope, or heart failure. Fulminant myocarditis may be associated with rapid hemodynamic deterioration and malignant arrhythmia, necessitating prompt and accurate imaging.

Fig. 7. Cardiac MRI findings of acute myocarditis.

Fig. 7

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A. The basal short-axis T2-weighted image shows linear subepicardial T2 high-signal intensity at the mildly thickened inferior and inferolateral walls (arrows).

B. The late gadolinium-enhanced image shows hyperenhancement in the corresponding area (arrows).

Diagnosis is based on the integration of clinical findings, myocardial injury biomarkers, electrocardiography, and echocardiography. CMR provides a noninvasive assessment of inflammation and tissue injury and plays an important role in diagnosis. According to the updated Lake Louise criteria (2018), a combination of T2-based markers of edema and T1-based markers of nonischemic myocardial injury is used for diagnostic evaluation (35,36).

On CMR, acute myocarditis demonstrates regional or diffuse T2 elevation on T2 mapping or T2-weighted imaging, which reflects myocardial edema. Increased native T1 and ECV values indicate interstitial expansion and inflammatory injury, respectively. Cine imaging may reveal regional wall motion abnormalities, pericardial effusion, and reversible wall thickening related to edema. Such findings should be interpreted in conjunction with mapping parameters and LGE to avoid the misclassification of structural hypertrophy.

LGE typically appears in a subepicardial or midwall distribution, most commonly involving the inferolateral wall, although its distribution may vary. In early or atypical cases, LGE may be subtle or absent; therefore, quantitative T1/T2/ECV parameters and clinical context should be integrated when establishing a diagnosis or assessing the therapeutic response (37).

Strain analysis, particularly the GLS, may be reduced even when the left ventricular ejection fraction is preserved. Regional strain impairment, which corresponds to the distribution of inflammation, may serve as a useful adjunctive functional marker (38).

PRESSURE-RELATED OR PHYSIOLOGIC THICKENING

Physiological or pressure-related myocardial hypertrophy primarily reflects hypertrophic remodeling of cardiomyocytes and is pathophysiologically distinct from the interstitial expansion observed in infiltrative or inflammatory cardiomyopathies. In this category, wall thickness typically increases gradually, whereas intrinsic myocardial tissue characteristics remain relatively preserved, although morphological variations may occur depending on the underlying condition. On CMR, differentiation from pathological hypertrophy is achieved through an integrated evaluation of wall thickness magnitude, left ventricular cavity size, LGE distribution, and preservation of mapping parameters.

HYPERTENSIVE HEART DISEASE

HHD (Fig. 8) represents structural remodeling in response to chronic pressure overload caused by sustained systemic hypertension. The predominant morphological feature is concentric LVH (39). Myocyte hypertrophy accompanied by mild interstitial fibrosis results in gradual wall thickening. Although the maximal wall thickness is typically <15 mm, values ≥15 mm may occur, thereby making differentiation from HCM challenging (40).

Fig. 8. Cardiac MRI findings of hypertensive heart disease.

Fig. 8

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A. The basal short-axis cine image at end-diastole shows diffuse concentric thickening of the left ventricular wall (end-diastolic volume index: 83.0 mL/m2, left ventricular mass index: 132 g/m2).

B. An ill-defined midwall and subepicardial patchy enhancement near the inferior right ventricle insertion site (arrow) is noted on the short-axis late gadolinium enhancement image.

C. The ECV map demonstrates mildly increased ECV (27.7%) in the corresponding region (arrow).

ECV = extracellular volume fraction

On CMR, native T1 and ECV may be mildly elevated, but generally do not demonstrate the marked increase observed in infiltrative cardiomyopathies (41). LGE is often absent or limited to focal fibrosis in the basal segments or right ventricular insertion sites, unlike the heterogeneous and more extensive patchy LGE commonly observed in HCM (39,42). T2 values are usually within the normal range, and overt myocardial edema is uncommon (43). Strain analysis typically demonstrates relatively preserved global function. When reduction is present, it is generally mild compared with that observed in HCM or infiltrative cardiomyopathy (44,45). Accordingly, HHD may be distinguished by its underlying pathophysiological basis of pressure overload, concentric hypertrophy, modest mapping abnormalities, and limited LGE distribution (46).

AORTIC STENOSIS–RELATED PRESSURE OVERLOAD

Myocardial hypertrophy associated with aortic stenosis represents a structural adaptation to sustained pressure overload and is characterized by increased myocardial mass and symmetric hypertrophy (47,48). On CMR, wall thickening is often relatively uniform, and the left ventricular cavity size may be normal or reduced, resembling hypertensive remodeling. In older patients, concomitant conditions such as transthyretin amyloidosis may coexist, necessitating careful assessment of mapping parameters and LGE distribution to evaluate potential overlapping pathologies (49). Although concentric remodeling predominates, asymmetric hypertrophy or remodeling (Fig. 9) is common in CMR cohorts. When focal wall thickening is pronounced, differentiation from HCM may be required (50).

Fig. 9. Cardiac MRI findings of aortic stenosis-related pressure overload.

Fig. 9

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A-C. The four-chamber and short-axis cine images of the end-diastole demonstrate basal to mid-septal wall thickening (arrows, A and B) with focal enhancement at anterior RV insertion site (arrow) on the late gadolinium enhancement image (C).

D, E. On the native T1 and ECV maps, focal increases in T1 and ECV values are noted at the anterior RV insertion site (arrows) at the mid-level of the LV wall.

F. The three-chamber cine image at the systolic phase shows aortic valve jet flow (arrows) suggesting aortic stenosis.

ECV = extracellular volume fraction, RV = right ventricle

LGE is not consistently present. When observed, it typically appears as focal patchy enhancement in the basal segments or near the right ventricular insertion sites, reflecting replacement fibrosis (51). Native T1 and ECV may increase in proportion to the severity of pressure overload, particularly in the presence of advanced fibrosis (52). An elevated ECV has been associated with fibrosis burden and adverse long-term outcomes in aortic stenosis (53,54).

Strain analysis has demonstrated reduced longitudinal strain compared with controls and an association with long-term prognosis, whereas radial and circumferential strain findings have varied across studies (55,56).

BASAL SEPTAL BULGE (SIGMOID SEPTUM)

In older individuals or patients with long-standing pressure overload, focal thickening of the basal interventricular septum, referred to as the basal septal bulge or sigmoid septum, can be observed. This represents a localized morphologic variant confined to the basal segment, with no generalized increase in myocardial mass or mid-to-apical hypertrophy, and does not typically indicate primary structural cardiomyopathy.

On CMR, LGE is absent or minimal, and mapping parameters, such as native T1 and ECV, are generally within normal limits, supporting differentiation from pathologic hypertrophy (57). However, because early HCM may also present with focal septal thickening, careful assessment of the hypertrophy distribution, mid-to-apical morphology, and tissue characterization is warranted.

ATHLETE’S HEART

The athlete’s heart undergoes physiological remodeling in response to sustained high-intensity training and is distinguished from pathological hypertrophy by balanced increases in the cavity size and wall thickness (58). The left ventricular volume is often at the upper limit of normal or is enlarged, whereas wall thickening is typically mild. These changes may partially regress with detraining, further differentiating the physiological adaptations from cardiomyopathy (59).

LGE is rarely observed on CMR. Histologically, increased myocyte mass accompanied by a relative reduction in ECV results in lower native T1 and ECV values compared with controls (60). The T2 values generally remain within the normal range. Strain analysis typically demonstrates preserved or near-normal deformation, and asymmetric strain reduction or loss of the base-to-apex gradient, features more characteristic of pathological hypertrophy, are uncommon (61).

Differentiating between an athlete’s heart and HCM is clinically important. In athlete’s heart, ventricular cavity enlargement is typically present, whereas HCM often demonstrates reduced cavity size (62). Athletes are usually asymptomatic with enhanced exercise tolerance, whereas HCM may be associated with a family history or risk factors for sudden cardiac death. As HCM remains the leading cause of sudden cardiac death in young athletes, appropriate screening and careful differentiation are essential (58).

PSEUDOTHICKENING

Pseudothickening refers to apparent myocardial wall thickening caused by technical factors during image acquisition or interpretation rather than true structural hypertrophy. This category must be considered early to avoid the misclassification of pathological hypertrophy. The most common causes include inaccurate imaging planes, motion-related image degradation, and anatomical optical illusions associated with the apical myocardium.

OFF-AXIS IMAGING

Inaccurate imaging planes are the most frequent cause of pseudothickening. When the prescribed long-axis view does not align with the true long axis of the left ventricle, short-axis images may be obtained obliquely, leading to an overestimation of the wall thickness. Short-axis stacks should be carefully aligned perpendicular to standardized long-axis views, and the basal, midventricular, and apical levels should be matched consistently across sequences to ensure accurate assessment (63).

MOTION ARTIFACTS

Tachycardia, arrhythmia, and inadequate breath-holding may generate motion artifacts that blur myocardial borders and exaggerate the apparent wall thickness through partial volume effects. In patients with arrhythmias, arrhythmia-rejection algorithms may improve image quality. When breath-holding is suboptimal, single-shot techniques or navigator-gated sequences that monitor diaphragmatic motion can be employed. If arrhythmias and respiratory limitations coexist, real-time acquisition may serve as an alternative approach (64).

APICAL THICKENING PITFALLS

The apical myocardium is anatomically thin and tapered, making it particularly susceptible to partial volume effects and minor deviations in imaging planes. Consequently, the apex may appear to be falsely thickened. Apically displaced papillary muscles may mimic apical hypertrophy (Fig. 10), and ambiguous trabeculation in suspected apical noncompaction is another common pitfall (65). Evaluation in at least two orthogonal planes is recommended to confirm true apical myocardial thickening.

Fig. 10. Cardiac MRI findings of apical hypertrophy mimicked by apically displaced papillary muscles.

Fig. 10

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A-C. On the short-axis cine image (A) of the end-diastole, the apical lateral and inferior wall (arrows) is suspicious for abnormal thickening. However, the upper apical short-axis and two-chamber cine images (B, C) demonstrate a preserved apical myocardium, with anterior and posterior papillary muscles (arrows) inserted near left ventricular apex, mimicking apical hypertrophic cardiomyopathy.

D, E. The apical T1 and T2 maps reveal normal T1 (<1,285 ms) and T2 (<43 ms) values at the apical lateral and inferior wall.

ALGORITHMIC APPROACH FOR RADIOLOGISTS

When myocardial thickening is identified on CMR, a structured diagnostic approach that extends beyond simple wall thickness measurement is useful.

1. TRUE HYPERTROPHY VS. PSEUDOTHICKENING

True hypertrophy is generally defined as end-diastolic left ventricular wall thickness ≥12 mm, whereas pseudothickening results from off-axis imaging, motion artifacts, or apical pitfalls.

2. CLINICAL CONTEXT AND COMORBIDITIES

Assessment of age, hypertension, aortic stenosis, athletic training status, and involvement of major organ systems (e.g., pulmonary, renal, and neurological) may be suggestive of metabolic or systemic disease.

3. PATTERN OF HYPERTROPHY

Concentric, asymmetric, or apical distribution.

4. LEFT VENTRICULAR CAVITY SIZE

Cavity reduction favors HCM, whereas cavity enlargement supports physiological adaptation (e.g., athlete’s heart).

5. TISSUE CHARACTERIZATION

Integration of LGE and mapping parameters (native T1, T2, and ECV) for etiological refinement.

The sequential framework proposed in this review may reduce unnecessary overdiagnosis and help avoid overlooking less common etiologies or relevant clinical conditions. Fig. 11 illustrates the diagnostic pathway beginning with the differentiation between true and pseudo-thickening, followed by the integration of the LVH pattern, clinical features, and CMR tissue characterization. Table 1 summarizes the key clinical and CMR features of the major causes of true myocardial hypertrophy. Because T1/T2 mapping values may vary significantly depending on the magnetic field strength, vendor, and sequence parameters, interpretation should be based on institution-specific reference ranges (66).

Fig. 11. Diagnostic approach for a thick myocardium on cardiac MRI.

Fig. 11

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This flowchart illustrates a stepwise diagnostic strategy, beginning with the distinction between true myocardial thickening and pseudothickening. Subsequent differentiation is guided by the characteristic combinations of LVH patterns, clinical context, and CMR tissue characterization, including the mapping of parameters and LGE distribution. This approach guides the differentiation between physiological thickening, hypertrophic cardiomyopathy phenotypes, metabolic/systemic cardiomyopathies, pressure-related thickening, and acute inflammatory conditions. Changes in mapping values are expressed as relative trends rather than absolute cutoff values, acknowledging inter-scanner and inter-vendor variabilities.

AV = aortic valve, CMR = cardiac MR, ECV = extracellular volume fraction, LGE = late gadolinium enhancement, LV = left ventricle, LVH = left ventricular hypertrophy

Table 1. Differential Diagnoses of True Myocardial Thickening.

HCM Amyloidosis Fabry Disease Uremic Cardiomyopathy Sarcoidosis (Acute Phase) Acute Myocarditis Hypertensive Heart Disease Aortic Stenosis Athlete’s Heart
Pathophysiology Myocyte disarray, interstitial fibrosis Amyloid infiltration Lipid deposition Multifactorial (uremic toxin, insulin resistance…) Granuloma infiltration Inflammatory myocardial injury Pressure overload Pressure overload Physiologic adaptation to exercise
LVH pattern Asymmetric > Concentric Concentric > Asymmetric Asymmetric > Concentric Concentric > Asymmetric Concentric > Asymmetric
LGE location pattern Variable (-/+/++) Midwall patchy +++/++
Subendocardial/D5transmural linear		 +
Basal inferolateral midwall patchy		 +/-
Midwall patchy		 ++/+
Midwall/subepicardial patchy		 ++/+
Inferolateral midwall/subepicardial patchy		 +/-
Basal/RV insertion site patchy		 -
T1 ↑↑ ↑↑↑ ↓↓→↔* ↑/↔ ↑↑ ↑↑ ↑/↔ ↑/↔ ↓/↔
ECV ↑↑ ↑↑↑ ↔ → ↑* ↑/↔ ↑↑ ↑↑ ↑/↔ ↑/↔ ↓
T2 ↑/↔ ↑ ↔ (↑: inflammatory phase) ↑/↔ ↑↑ ↑↑↑ ↔ ↔ ↔
Differential keys Family history, decreased LV cavity, systolic LVOT jet flow Systemic involvement (kidney, effusion) Systemic involvement (kidney, nervous system) Chronic renal disease Systemic involvement (lung, lymph nodes) Preceding (viral) infection, acute symptom development, cardiac enzyme elevation Hypertension Aortic stenosis (systolic AV jet flow) Increased LV cavity, after detraining
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*T1 and ECV profile changes in inflammatory and fibrotic phases of Fabry disease.

AV = aortic valve, ECV = extracellular volume fraction, HCM = hypertrophic cardiomyopathy, LGE = late gadolinium enhancement, LV = left ventricle, LVH = left ventricular hypertrophy, LVOT = left ventricular outflow tract, RV = right ventricle

CONCLUSION

Myocardial thickening may arise from diverse pathophysiological mechanisms, and accurate interpretation requires integrated structural and tissue characterization using CMR. When an increase in wall thickness is identified, the initial step involves the differentiation between true hypertrophy and pseudothickening. The subsequent integration of the clinical context with morphological features, mapping parameters, and LGE distribution facilitates the systematic categorization.

This review outlines the principal causes of myocardial thickening encountered in routine CMR practice, emphasizing their pathophysiological background, characteristic imaging findings, and diagnostic pitfalls. This structured approach may provide practical guidance for daily interpretation and differential diagnoses. Nevertheless, atypical presentations may occur, and overlapping pathologies are common in older patients or in those with multiple comorbidities; therefore, careful interpretation within the clinical context remains essential.

Footnotes

Author Contributions:
  • Conceptualization, K.M.Y., L.W.
  • data curation, K.M.Y., L.W.
  • methodology, K.M.Y.
  • project administration, L.W.
  • resources, K.H.J., C.E.J.
  • supervision, L.W.
  • visualization, K.M.Y., K.H.J., C.E.J.
  • writing—original draft, K.M.Y., K.H.J.
  • writing—review & editing, K.M.Y., C.E.J., L.W.

Conflicts of Interest: The authors have no potential conflicts of interest to disclose.

Funding: None

Supplementary Materials

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