Arterial-Phase Enhancement Patterns of Hepatocellular Carcinoma: From Pathologic Background to Prognostication and Treatment Response

Jun Gu Kang; Ja Kyung Yoon; Hyungjin Rhee

doi:10.52668/kjar.2026.00031

Korean J Abdom Radiol > Volume 9(1); 2026 > Article

Kang, Yoon, and Rhee: Arterial-Phase Enhancement Patterns of Hepatocellular Carcinoma: From Pathologic Background to Prognostication and Treatment Response

Review Article

Korean Journal of Abdominal Radiology 2026;9(1):14-31.

Published online: June 30, 2026

DOI: https://doi.org/10.52668/kjar.2026.00031

Arterial-Phase Enhancement Patterns of Hepatocellular Carcinoma: From Pathologic Background to Prognostication and Treatment Response

Jun Gu Kang¹

, Ja Kyung Yoon¹

, Hyungjin Rhee^1,²

¹Department of Radiology, Severance Hospital, Research Institute of Radiological Sciences, and Center for Clinical Imaging Data Science, Yonsei University College of Medicine, Seoul, Republic of Korea

²Yonsei Institute for Digital Health, Yonsei University, Seoul, Republic of Korea

Correspondence: Hyungjin Rhee, MD, PhD Department of Radiology, Severance Hospital, Yonsei University College of Medicine, Seoul, Republic of Korea 50-1 Yonsei-ro, Seodaemun-gu, Seoul 03722, Republic of Korea
Tel: +82-2-2228-2353 Fax: +82-2-2227-8337 E-mail: hjinrhee@yuhs.ac

Received April 26, 2026 Accepted May 10, 2026

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Arterial-phase hyperenhancement (APHE), which reflects the hemodynamic shift toward an unpaired arterial supply during hepatocarcinogenesis, is one of the most important imaging features for noninvasive diagnosis of hepatocellular carcinoma (HCC). Although the classic non-rim APHE remains the cornerstone of diagnosis, various enhancement patterns have emerged as critical biomarkers for tumor biology and prognosis. This review provides a comprehensive overview of APHE, tracing its historical development alongside technical advancements in angiography, computed tomography, and magnetic resonance imaging, and explores the pathological and genetic backgrounds of APHE. We categorized distinct enhancement phenotypes, including rim APHE, Kawamura classification, arterial-phase hypoenhancing component, intratumoral artery, and arterial-phase peritumoral enhancement. These patterns serve as imaging surrogates for aggressive clinicopathological traits, such as microvascular invasion, the macrotrabecular-massive subtype, the vessels encapsulating tumor cluster pattern, and TP53 mutation. Furthermore, we discuss how these arterial enhancement patterns guide treatment strategies and predict outcomes of surgical resection, locoregional therapies, and contemporary systemic treatments. Understanding the relationship between diverse enhancement patterns and HCC biology is vital for optimizing therapeutic decision-making.

Keywords: Hepatocellular carcinoma; Arterial phase hyperenhancement; Magnetic resonance imaging; Microvascular invasion; Prognosis

Introduction

Arterial-phase hyperenhancement (APHE) has long been the cornerstone of noninvasive diagnosis of hepatocellular carcinoma (HCC) in high-risk patients. Current guidelines for HCC rely on APHE as the primary diagnostic hallmark [1-3]. APHE reflects the characteristic vascular supply established during early hepatocarcinogenesis, where the tumor transitions from the portal venous system to a predominantly arterial supply through unpaired arteries [4].

With the evolving understanding of the molecular and pathological heterogeneity of HCC, a binary classification of APHE, based solely on its presence or absence, is increasingly being recognized as insufficient for comprehensive tumor characterization. Over the past few decades, various APHE patterns have been described, many of which have been reported to correlate with aggressive histologic subtypes or molecular features, such as the macrotrabecularmassive (MTM) subtype, the scirrhous subtype, and TP53 mutations [5, 6]. Furthermore, specific APHE patterns have been shown to be significantly associated with treatment responses to targeted therapies and overall patient prognosis [7].

The objective of this review was to provide a comprehensive overview of the diverse arterial-phase (AP) enhancement patterns observed in HCC. We explored the technical evolution of APHE imaging, the pathological and genetic backgrounds underlying the various enhancement patterns, and their clinical implications for different HCC treatment modalities.

History of APHE of HCC Along with Technical Evolution

Recognition of APHE as a pathognomonic feature of HCC dates back to the era of conventional catheter angiography in the 1970s and the 1980s. In 81%-95% of patients with HCC, direct injection of contrast medium into the hepatic artery during angiography revealed a dense and persistent “tumor stain” [8-10]. This phenomenon has been reported to be fundamentally associated with neoangiogenesis driven by vascular endothelial growth factor (VEGF) [11, 12].

In the 1980s and the 1990s, the visualization of APHE in catheter angiography was further enhanced by the integration of computed tomography (CT) [13]. CT during hepatic arteriography (CTHA) and CT during arterial portography (CTAP) demonstrated higher sensitivity for HCC detection than conventional angiography [13, 14]

Additionally, analyses of CTHA and CTAP findings established that HCC is characterized by a dominant arterial blood supply, whereas non-HCC cirrhotic nodules typically maintain a dominant portal blood supply [15]. These hemodynamic observations were pivotal in characterizing the importance of bloodsupply patterns for the differential diagnosis of HCC.

The paradigm shift toward noninvasive diagnosis was primarily catalyzed by technical advancements in CT and magnetic resonance imaging (MRI) during the 1990s. Early investigations using incremental (stepand-shoot) scanners demonstrated that a combination of arterial- and portal-phase imaging could achieve high HCC detection rates [16]. However, incremental CT showed notable limitations owing to its prolonged scan time: it was unable to cover the entire liver volume during the narrow window of peak arterial enhancement, posed substantial challenges in yielding consistent dynamic images, and could not cover the entire liver within a single breath-hold. The subsequent introduction of helical CT addressed these limitations by utilizing continuous gantry rotation through slip-ring technology and simultaneous table translation during scanning [17]. This innovation allowed the entire liver volume to be scanned within a single breath-hold. Noninvasive biphasic helical CT, which includes both the arterial and portal phases, has been reported to show the ability to detect a number of HCCs equivalent to those detected by invasive CTHA and/or CTAP, establishing biphasic CT as the recommended initial diagnostic examination [18-21].

The advent of multidetector-row CT (MDCT) has led to further improvements in spatial and temporal resolutions. By significantly reducing scan times in comparison with earlier helical systems, MDCT enables precise capture of the true AP during its narrow optimal contrast window [22]. This increased temporal resolution, combined with the capability of fast volumetric scanning, allowed for routine implementation of thin-section imaging. These technical refinements dramatically improved the detection rate of small HCCs that were often occult on thicker-slice scanners [23]. With the establishment of fast volumetric scanning capabilities, precise determination of scan timing emerged as a pivotal challenge. The “late AP”, defined by the beginning of contrast opacification in the portal vein, was demonstrated to be optimal for HCC detection because it maximized the attenuation difference between the hypervascular HCC and the surrounding liver parenchyma [24-26].

Parallel to the evolution of CT, MRI has undergone major technical transformations. Before the 1990s, liver MRI relied on conventional spin-echo sequences that required more than 5 min per acquisition; consequently, small lesions were frequently obscured by respiratory-motion artifacts or misregistration during staggered acquisitions. The introduction of T1-weighted spoiled gradient-recalled echo (SPGR) sequences in the 1990s, also known as fast low-angle shot (FLASH) or T1-fast field echo (FFE), revolutionized the field by enabling complete liver coverage within a single breath-hold, thereby making dynamic contrastenhanced imaging feasible [27, 28]. Subsequent refinements led to the development of advanced SPGR derivatives such as volumetric interpolated breath-hold examination (VIBE), liver acquisition volume acceleration (LAVA), and enhanced T1 highresolution isotropic volume excitation (eTHRIVE). These sequences enable isotropic 2-3-mm resolution within a single breath-hold and have become the most important sequences for dynamic liver MRI [29]. Due to its superior soft-tissue contrast, MRI offers notable advantages over CT in dynamic imaging, particularly in achieving higher detection rates for small HCCs [30].

This technological milestone has transitioned the diagnostic focus from invasive hemodynamic mapping using catheter angiography to the standardized, noninvasive imaging criteria utilized in modern clinical practice.

Changes in Arterial Enhancement In Relation to the Pathologic Evolution of Hepatocarcinogenesis

(1) Early Hepatocarcinogenesis: The Gain of APHE

The vascular evolution of HCC is a multistep process that is tightly associated with the pathological progression from dysplastic nodules to progressed HCC [4]. In early hepatocarcinogenesis, the fundamental driver of vascular change is stromal invasion, wherein malignant cells infiltrate and destroy the internal structures within the lesion, including the hepatic veins, portal tracts, and fibrous septa [31, 32]. This stromal invasion leads to destruction of the physiological vascular architecture, impeding both physiologic vascular supply and drainage [33]. This hemodynamic shift typically manifests during the early stages of HCC, causing the tumor to undergo a hypovascular transition. Consequently, early HCC often appears as an iso- or hypoenhancing lesion relative to the background liver parenchyma during the AP [34]. The hypoxic microenvironment resulting from these changes is frequently associated with diffuse intratumoral fatty metamorphosis [33].

The hypoxic microenvironment of early-stage HCC upregulates angiogenic signaling pathways, most notably VEGF, which triggers neoangiogenesis [35, 36]. This process is characterized by the development of unpaired arteries, which are newly formed arterial branches that lack accompanying portal veins or bile ducts [36, 37]. Concurrently, sinusoidal capillarization occurs, where liver sinusoidal endothelial cells lose their fenestrae and develop a basement membrane [37-39]. The culmination of these processes provides a pathological basis for APHE, which is typically observed in moderately differentiated HCC [40, 41].

(2) Late Hepatocarcinogenesis: The Loss of APHE and Emergence of Heterogeneity

In the advanced stages of HCC, particularly in poorly differentiated HCCs, the characteristic global APHE often diminishes or exhibits significant heterogeneity [7, 42]. This phenomenon is driven by several histopathological factors. First, poorly differentiated HCCs frequently undergo extensive intratumoral fibrosis, necrosis, or peliosis [43]. These nonviable or poorly perfused tissue components inherently reduce the APHE of the tumor. Second, microvascular structural remodeling plays a critical role. The “vessels encapsulating the tumor cluster” (VETC) pattern, a distinct microvascular pattern frequently observed in advanced HCC, is associated with a lower microvascular density in comparison with the capillary pattern microvessels in moderately differentiated HCC, leading to a substantial decrease in the overall APHE [44-46].

Evolution of APHE Terminology in Global HCC Guidelines

The integration of noninvasive diagnostic criteria into clinical guidelines marked a paradigm shift in HCC management. The 2001 European Association for the Study of the Liver (EASL) guidelines first introduced imaging diagnostic criteria, stating that in patients with cirrhosis, a focal lesion larger than 2 cm exhibiting “arterial hypervascularization” could be diagnosed as HCC [47]. In the 2005 American Association for the Study of Liver Diseases (AASLD) guidelines, the terminology was slightly changed to “arterial hypervascularity,” and the coexistence of arterial hypervascularity and washout was established as the diagnostic hallmark of HCC [48].

Until 2017, various international guidelines, including those from AASLD, EASL, Asian Pacific Association for the Study of the Liver, Korean Liver Cancer Association-National Cancer Center, and Japan Society of Hepatology, as well as Liver Imaging Reporting and Data System (LI-RADS) v2011-v2014, described APHE using similar but slightly varied terms, such as “arterial hypervascularity,” “hypervascular in the AP,” or “AP hyperenhancement” [49-52]. An important turning point occurred with the release of LI-RADS v2017, which introduced the qualifier “non-rim” to the definition of APHE (Fig. 1) [53]. This refinement was specifically designed to exclude rim APHE, a feature commonly observed in aggressive HCC and non-HCC malignancies such as intrahepatic cholangiocarcinoma, from the diagnostic criteria for definite HCC [53]. Subsequently, LI-RADS v2018 was formally adopted in the 2018 AASLD practice guidelines [54]. The 2018 EASL guidelines also adapted this standardization by using the expression “APHE according to LI-RADS classification,” while the 2018 KLCA-NCC guidelines aligned with this framework by excluding lesions with targetoid appearances from the scope of the imaging diagnosis [55, 56].

The formal differentiation between non-rim and rim APHE in the current diagnostic criteria highlights that APHE is not a monolithic feature but rather encompasses a spectrum of patterns that mirror the diverse biological nature of hepatic lesions. This distinction indicates that specific enhancement phenotypes can serve as markers of distinct tumor characteristics. The following sections will categorize these diverse APHE patterns and discuss their histopathological, genetic, and clinical significance.

Various AP Enhancement Patterns

(1) Rim APHE

Rim APHE is characterized by irregularly shaped peripheral hyperenhancement in the AP with central hypoenhancing areas (Fig. 2 and 3). In the LI-RADS framework, this is the most prevalent targetoid feature that mandates an LR-M category, indicating a malignancy not specific to HCC [57]. Approximately 9.8% (95% confidence interval [CI], 6.9%-13.6%) of all HCCs exhibit this enhancement pattern [57, 58]. Rim APHE is recognized as a critical imaging feature for aggressive biological behavior, showing a high correlation with the MTM subtype, VETC pattern, and the proliferative subclass of HCC [43, 59, 60]. Rim APHE is frequently associated with pathologic features, including microvascular invasion, extensive tumor necrosis, fibrous stroma, poor differentiation, and the expression of stem/progenitor markers such as keratin 19 [43, 61]. These aggressive histopathological traits form the biological basis for the poor clinical outcomes associated with rim APHE-positive HCC, including higher rates of early recurrence and significantly worse overall survival after resection [43, 62, 63]. Beyond its prognostic implications, rim APHE shows notably high inter-reader reliability among radiologists; a recent meta-analysis reported a pooled kappa value of 0.72 (95% CI, 0.65-0.78), making it one of the most reliable prognostic features [64].

(2) Kawamura Classification

The Kawamura classification is a dynamic CTbased system that categorizes HCC into four types on the basis of AP enhancement and heterogeneity: Type I (homogeneous enhancement pattern with no increase in arterial blood flow), Type II (homogeneous enhancement pattern with increased arterial blood flow), Type III (heterogeneous enhancement pattern with septum-like structure), and Type IV (heterogeneous enhancement pattern with irregular ringlike structures) [61]. This classification serves as a surrogate for pathological progression of HCC: Type I lesions typically correspond to well-differentiated HCC. Types II and III align with moderately differentiated HCC, with Type II characterized by single nodular growth and Type III frequently exhibiting extranodular growth or a confluent multinodular growth pattern [61]. Type IV represents HCC with the previously described rim APHE and is strongly associated with poor histological differentiation [43, 61]. Clinically, Type IV HCC is associated with a significantly higher overall recurrence rate following radiofrequency ablation (RFA) [65, 66]. Furthermore, both types III and IV HCCs show a high incidence of intrasubsegmental recurrence post-RFA, suggesting an aggressive tumor nature [66, 67].

(3) AP Hypoenhancing Component

Hepatocellular carcinomas with aggressive histological features often exhibit poor arterial enhancement [43, 68]. This imaging phenotype is attributed to lower microvascular density and the presence of mixed non-enhancing nonviable components, such as fibrosis and necrosis [43]. While these poorly enhancing elements are frequently located centrally, creating a classic rim APHE pattern, they can also manifest in various topographies across the tumor (Fig. 3). Consequently, the relative proportion of the AP hypoenhancing component, regardless of its topological distribution, serves as a robust imaging surrogate for aggressive HCC [60]. In this context, the AP hypoenhancing component can be considered a generalized imaging feature that encompasses the rim APHE. Since AP hypoenhancing component indicates a hypoxic microenvironment, it is closely linked to tumor necrosis and liquefaction, which are typically identified as high-signal-intensity areas on T2-weighted images, called substantial necrosis [69].

The concept of the AP hypoenhancing component was primarily introduced to define the imaging features of MTM-HCC [60]. In the literature, it has been described using various terms, including “AP hypovascular component,” “AP proportion,” “substantial hypoenhancing component,” or “intratumor hypoenhancement” [59, 60, 70-72]. This feature is defined as an area within the HCC nodule that demonstrates lower enhancement than the surrounding liver parenchyma during the AP [60, 70]. To distinguish these advanced lesions from early HCCs, which are also often entirely hypoenhancing, the definition is typically restricted to lesions that simultaneously demonstrate peripheral or focal hypervascular spots in AP [34, 60]. Most studies define an AP hypoenhancing component using a threshold of >50% of the tumor area, although a 20% threshold is occasionally utilized [60, 72]. This imaging feature serves as a critical marker for aggressive pathologic and genetic subtypes, including MTM-HCC and the proliferation class [59, 60]. Furthermore, the AP hypoenhancing component is a critical imaging biomarker for poor prognosis following hepatic resection. HCCs with an AP hypoenhancing component exhibit frequent early recurrence, poor overall survival, and advanced-stage recurrence characterized by extrahepatic metastasis and gross venous invasion following surgical resection [60, 71].

(4) Intratumoral Artery

Intratumoral or internal artery, which have been described in the literature for several decades, are imaging features characterized by discrete linear or branching hyperattenuating or hyperintense structures within the HCC during the AP (Fig. 3) [73]. In HCC, these structures represent the tumor vasculature arising from neoangiogenesis. Although these vessels are frequently dysmorphic or dilated, the specific histopathological abnormalities underlying these morphological changes remain unclear. This finding is distinct from the “hepatic arterypenetrating sign” observed in large-duct intrahepatic cholangiocarcinoma, which results from the encasement of preexisting portal tracts [74, 75].

Segal et al. conducted a comprehensive radiogenomic analysis to link CT imaging features with the transcriptomic profiles of HCC [73]. Their findings revealed that the presence of “internal arteries” is strongly associated with a gene expression signature for venous invasion. Subsequent research using CT and gadoxetic acid-enhanced MRI validated the presence of intratumoral artery as a reliable imaging surrogate for predicting microvascular invasion (MVI) [76-80]. Furthermore, the presence of intratumoral artery or intralesional aneurysm significantly correlated with poor histological differentiation [81]. Beyond its role in predicting MVI, the intratumoral artery is recognized as a key imaging hallmark of MTMHCC, often co-occurring with AP hypoenhancing component [60, 70, 82]. This feature is also prevalent in VETC-positive and TP53-mutated HCCs, which exhibit substantial biological overlap with the MTMHCC [83-85]. Collectively, the presence of intratumoral arteries serves as a powerful indicator of aggressive biological behavior of HCC.

(5) AP Peritumoral Enhancement

AP peritumoral hyperenhancement refers to a non-mass-like area adjacent to the HCC, with hyperenhancement in the AP that subsequently fades in later phases (Fig. 4) [86]. The morphology of the peritumoral enhancement can vary; however, a broad or circumferential contact pattern along the tumor border is recognized as an indicator of MVI [77, 87-91]. This imaging finding is also significantly associated with aggressive HCC phenotypes, such as the MTM-HCC and VETC patterns [60, 82, 92, 93], and serves as a potent predictor of early recurrence following surgical resection [63, 94-96].

Pathophysiologically, AP peritumoral hyperenhancement can arise from two distinct hemodynamic mechanisms. The first mechanism involves compensatory arterial hyperperfusion occurring during the early AP [97]. This phenomenon is thought to represent a response to decreased portal venous flow caused by obstruction of peritumoral portal vein branches by microscopic tumor thrombi, indicating MVI. Therefore, this type of peritumoral hyperenhancement represents a direct imaging sign of MVI. The second mechanism, specifically termed “corona enhancement,” involves venous drainage of the tumor and is typically observed during the late arterial to early portal phase [98, 99]. During early hepatocarcinogenesis, stromal invasion leads to the destruction of internal hepatic vein branches within the lesion. Consequently, intranodular sinusoids establish connections with the portal veins of the surrounding liver parenchyma to facilitate venous drainage in moderately differentiated HCCs [98, 99]. This drainage-related enhancement marks peritumoral regions with a high risk for MVI and satellitosis. [100]

Treatment-Response Prediction and Tailoring Strategies Based on AP Enhancement

Because specific AP enhancement patterns are closely linked to aggressive clinicopathological traits, including poor differentiation and aggressive pathological and genetic subtypes, they serve as useful biomarkers for predicting treatment response and clinical outcomes.

(1) Surgical Resection and Transplantation

In patients undergoing hepatic resection, rim APHE and AP peritumoral enhancement have been recognized as robust predictors of early recurrence within 2 years [63, 87]. These features also correlate strongly with MVI, which remains the most critical pathological risk factor for postoperative recurrence. Other imaging features associated with poor surgical outcomes include large tumor size (>5 cm), multifocality, peritumoral hypointensity in the hepatobiliary phase, non-smooth tumor margin, and hypointensity on T1-weighted images [87, 91]. The imaging diagnosis criteria for MTM-HCC, which include AP hypoenhancing components, intratumoral arteries, AP peritumoral enhancement, and nonsmooth margins, are significantly associated with early recurrence, frequent extrahepatic metastasis, and unfavorable overall survival [60, 70]. Furthermore, the AP hypoenhancing component itself is a critical independent predictor for advanced-stage recurrence, and is characterized by recurrence with macrovascular invasion and extrahepatic spread [71].

The LR-M category within the LI-RADS framework is frequently assigned to aggressive HCC subtypes in addition to non-HCC malignancies. Consequently, HCCs classified as LR-M are associated with a poor prognosis in patients undergoing either surgical resection or transplantation [58, 101-103]. Among the imaging features defining LR-M, rim APHE is the most prevalent and demonstrates high inter-reader reliability [58, 64, 104]. Notably, it also carries the strongest prognostic weight; one study suggested that HCCs categorized as LR-M but lacking the rim APHE feature may have a prognosis comparable to that of non-LR-M HCCs, underscoring the clinical significance of this specific pattern [58].

(2) Locoregional Therapies

AP enhancement patterns also provide critical prognostic information for patients undergoing locoregional treatment. In RFA, the presence of rim APHE or a Kawamura Type III/IV pattern is associated with a higher incidence of intrasubsegmental recurrence, a finding that is suggestive of local recurrence [65, 66, 105]. Recent evidence suggests that “no-touch” ablation techniques may effectively reduce these local recurrences in Type III and IV tumors, potentially offering survival benefits similar to surgical resection [66, 67].

For transarterial therapies that rely on arterial supply as the primary drug delivery route, such as transarterial chemoembolization (TACE) and transarterial radioembolization (TARE), the degree of pretreatment AP enhancement is a predictive factor for treatment response (Fig. 5). A higher degree of APHE on baseline CT is positively correlated with achieving a complete response after TACE [106]. Similarly, an enhanced tumor volume ratio on pretreatment MRI is a predictor of successful tumor devascularization after TARE [107]. Additionally, identification of dysmorphic intratumoral arteries on pretreatment CT is a known risk factor for a high lung shunt fraction (>20%) in patients undergoing planning arteriography for TARE [108].

(3) Systemic Therapies

The reciprocal interaction between the immune and angiogenic microenvironments in HCC has led to the classification of tumors based on immunovascular phenotypes [109]. Thus, AP enhancement patterns can act as imaging surrogates for predicting responses to contemporary first-line systemic treatments, such as atezolizumab plus bevacizumab (Atezo-Bev). While initial reports on the relationship between rim APHE and Atezo-Bev response have been mixed, recent studies have indicated that the presence of an AP hypoenhancing component, along with an infiltrative appearance and tumor-in-vein, is associated with a poor response to this combination therapy [110-112].

In contrast, patients with HCCs exhibiting the heterogeneous enhancement typical of Kawamura Type III and IV patterns have shown significantly higher objective response rates to lenvatinib than those with Type I or II tumors [113, 114]. However, because Type III and IV HCCs are biologically aggressive, they often exhibit a paradoxical clinical course; while they respond well initially, the prognosis can become extremely poor once progression occurs. In such cases, implementing subsequent TACE may be essential for improving overall survival [113].

Conclusions and Future Perspectives

In conclusion, AP enhancement patterns in HCC have evolved from basic diagnostic hallmarks to multifaceted imaging biomarkers that reflect the underlying pathological, genetic, and prognostic landscape of HCC. AP enhancement patterns, such as rim APHE, intratumoral artery, and AP hypoenhancing component, provide noninvasive insights into tumor differentiation, MVI, and the presence of aggressive pathomolecular phenotypes like the MTM, VETC, and TP53 mutations. The integration of these patterns into radiological assessments will facilitate more refined risk stratification and tailoring of treatment strategies, ranging from surgical planning to the selection of firstline systemic agents in the era of precision oncology.

However, several challenges have to be addressed to ensure the routine clinical utility of these patterns. In current clinical practice, the interpretation of these AP phenotypes relies heavily on qualitative visual assessments, which are inherently limited by reader subjectivity and suboptimal inter-reader reliability [115, 116]. A paradigm shift is currently underway from qualitative pattern recognition to quantitative, data-driven analyses. The emergence of radiomics- and deep learning-based models promises to extract high-dimensional features beyond human perception, allowing standardized and automated tumor characterization [117]. Furthermore, most of the existing evidence is derived from retrospective cohort studies, highlighting the critical need for largescale, multi-center, randomized trials to establish standardized evidence for clinical decision-making. This transition toward objective AP enhancement pattern analysis is essential for advancing personalized patient care and optimizing therapeutic outcomes for patients with HCC.

Notes

Author Contributions

● Conceptualization: Hyungjin Rhee

● Funding acquisition: Hyungjin Rhee

● Supervision: Hyngjin Rhee

● Writing—original draft: Jun Gu Kang, Ja Kyung Yoon, and Hyungjin Rhee

● Writing—review & editing: Jun Gu Kang, Ja Kyung Yoon, and Hyungjin Rhee

● Approval of final manuscript: Jun Gu Kang, Ja Kyung Yoon, and Hyungjin Rhee

Conflicts of Interest

None

Funding Statement

This study was supported by a grant from the National Research Foundation of Korea (NRF) funded by the Korean government (MSIT) (No. RS-2023-00208307).

Acknowledgments

The corresponding author, Hyungjin Rhee, serves as the Editor-in-Chief of the Korean Journal of Abdominal Radiology. To avoid any potential conflict of interest, he was recused from the editorial process for this submission. The entire peer review and all subsequent editorial decisions were independently managed by Associate Editor Seung-seob Kim, in accordance with the journal's standard policies.

Fig. 1.

Hepatocellular carcinoma (HCC) with non-rim arterial phase hyperenhancement (APHE)

In a 73-year-old male with metabolic dysfunction-associated steatotic liver disease (MASLD), gadoxetic acid-enhanced magnetic resonance imaging shows an approximately 3-cm nodule in segment 7 of the liver. The lesion is hypointense on the pre-contrast T1-weighted image (A) and exhibits non-rim APHE in the arterial phase (B), washout and an enhancing capsule in the portal phase (C), and hypointensity in the transitional (D) and hepatobiliary (E) phases. Diffusionweighted image (B = 800 s/mm², F) shows high signal intensity, indicating restricted diffusion. The T2-weighted image (G) shows high signal intensity. The lesion was pathologically confirmed by surgical resection as moderately differentiated HCC.

Fig. 2.

Hepatocellular carcinoma (HCC) with rim arterial phase hyperenhancement (APHE)

In a 60-year-old male with chronic hepatitis B, gadoxetic acid-enhanced magnetic resonance imaging shows an approximately 2-cm nodule in segment 8 of the liver. The lesion is hypointense on the pre-contrast T1-weighted image (A) and exhibits rim APHE in the arterial phase (B), and hypointensity in the portal (C), transitional (D), and hepatobiliary (E) phases. Diffusion-weighted imaging (B= 800 s/mm², F) and T2-weighted imaging (G) show high signal intensity. The lesion was pathologically confirmed by surgical resection as HCC with a vessels encapsulating tumor clusters pattern and microvascular invasion.

Fig. 3.

Hepatocellular carcinoma (HCC) with rim arterial phase hyperenhancement (APHE), arterial phase hypoenhancing component, and intratumoral artery.

In a 65-year-old male with alcoholic liver cirrhosis, computed tomography (CT) images reveal an approximately 7-cm HCC in segment 3. The lesion is slightly hypoattenuating on the pre-contrast image (A) and exhibits rim APHE, an arterial phase hypoenhancing component, and an intratumoral artery in its central portion during the arterial phase (B). The lesion shows peripheral washout in the portal (C) and delayed (D) phases. The diagnosis was pathologically confirmed after surgical resection as HCC with a macrotrabecular pattern, keratin 19 expression, and microvascular invasion. Several months post-resection, local recurrence occurred, along with the simultaneous development of multiple lung metastases (E).

Fig. 4.

Hepatocellular carcinoma (HCC) with arterial phase peritumoral enhancement

In a 58-year-old male with chronic hepatitis B, gadoxetic acid-enhanced magnetic resonance imaging reveals an approximately 3.5-cm mass in segment 8 of the liver. The lesion is hypointense on the pre-contrast T1-weighted image (A) and exhibits non-rim APHE and arterial phase peritumoral enhancement (arrows) in the arterial phase (B). The mass shows hypointensity in the portal (C), transitional (D), and hepatobiliary (E) phases. Diffusion-weighted imaging (B = 800 s/mm², F) and T2-weighted imaging (G) show high signal intensity. The diagnosis was pathologically confirmed after surgical resection as HCC with microvascular invasion.

Fig. 5.

Hepatocellular carcinoma (HCC) with an arterial phase hypoenhancing component

In a 59-year-old male with chronic hepatitis B, gadoxetic acid-enhanced magnetic resonance imaging reveals an approximately 4-cm mass in segments 7 and 8 of the liver. The lesion is hypointense on the pre-contrast T1-weighted image (A) and exhibits a nodule-in-nodule appearance, where the inner nodule manifests as an arterial phase hypoenhancing component (B). The mass shows hypointensity in the portal (C), transitional (D), and hepatobiliary (E) phases. Diffusion-weighted image (B = 800 s/mm², F) and T2-weighted image (G) reveal high signal intensity. The lesion was pathologically diagnosed as macrotrabecular-massive HCC via ultrasonography-guided core needle biopsy. Following two sessions of transarterial chemoembolization, CT reveals partial lipiodol uptake in the lesion (H) and the simultaneous detection of multiple lung metastases (I).

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