Latent profile analysis of multidimensional muscle profiles versus traditional sarcopenia metrics for capturing sagittal malalignment in adult spinal deformity: a retrospective study

Article information

Asian Spine J. 2026;20(4):627-643
Publication date (electronic) : 2026 August 6
doi : https://doi.org/10.31616/asj.2026.0116
1Department of Orthopaedic Surgery, Hospital for Special Surgery, New York, NY, USA
2Department of Orthopaedic Surgery, The Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China
3Department of Orthopaedics, China Medical University Hospital, Taichung, Taiwan
4Weill Cornell Medicine, New York, NY, USA
Corresponding author: Francis C. Lovecchio, Department of Orthopaedic Surgery, Hospital for Special Surgery, 535 East 70th Street, New York, NY 10021, USA, Tel: +1-212-224-7930, Fax: +1-917-260-4642, E-mail: lovecchiof@hss.edu
Received 2026 March 20; Revised 2026 June 10; Accepted 2026 June 17.

Abstract

Study Design

Retrospective cohort study.

Purpose

Using latent profile analysis (LPA) to multidimensionally profile trunk muscles, we aimed to identify muscle phenotypes, compare LPA-based classification with sarcopenia definitions for explaining sagittal alignment, and examine malalignment patterns across LPA-derived subtypes.

Overview of Literature

Paraspinal sarcopenia is closely associated with sagittal malalignment in adult spinal deformity (ASD), but traditional single-muscle or single-metric definitions fail to capture heterogeneous muscle degeneration.

Methods

This retrospective cohort study included 145 patients with ASD undergoing long-segment fusion (≥5 levels; upper instrumented vertebra T1–L1) with ≥1-year follow-up. We measured muscle quantity using the psoas vertebral body index (PVBI) and paralumbar vertebral body index (PLVBI), and muscle quality using fatty infiltration (FI) of the psoas and paralumbar (multifidus and erector spinae) muscles. LPA was applied to PVBI, PLVBI, and psoas and paralumbar FI to identify clusters. For comparison, sarcopenia was defined by each metric. We compared LPA with single-metric definitions for predicting sagittal measures and examined clinical, radiographic (pre/post), and surgical outcomes across LPA subtypes.

Results

LPA explained sagittal alignment better than any single measure and revealed four phenotypes: Mild-Deg (high quantity, low FI; n=49), Mod-Deg (moderate; n=39), Seve-Deg (low quantity, high FI; n=34), and Hete-Deg (low quantity, high paralumbar FI but low psoas FI; n=23). Preoperative deformity progressively worsened from Mild-Deg to Seve-Deg, while Hete-Deg also showed pronounced malalignment. Postoperatively, most metrics were similar across groups. At last follow-up, however, Mod-Deg/Seve-Deg had greater pelvic incidence (PI)–lumbar lordosis (LL), and LL in Seve-Deg trended toward progressive worsening from postoperative to follow-up (PI–LL and T4 pelvic angle).

Conclusions

Multidimensional LPA muscle phenotyping outperformed single-metric sarcopenia definitions in explaining sagittal alignment. It also identified a heterogeneous Hete-Deg subtype suggestive of functional compensation despite severe preoperative deformity, whereas Seve-Deg reflected irreversible muscle loss with progressive imbalance.

Graphical Abstract

Introduction

Adult spinal deformity (ASD) is characterized by sagittal and/or coronal spinal malalignment and significantly affects the quality of life. These alignment abnormalities are closely associated with muscle degeneration, commonly referred to as sarcopenia [1,2]. The existing diagnostic criteria for systemic sarcopenia (e.g., Asian Working Group for Sarcopenia guidelines [3]) focus on whole-body muscle loss and have limited applicability to the spinal muscles [4,5]. Thus, many studies have focused on “paraspinal sarcopenia” [4,5] and have used various assessments [6]. For example, some studies have graded fatty infiltration (FI) in the multifidus/erector spinae and defined sarcopenia severity using modified Goutallier grades [7]. Others used muscle quantity metrics, such as the psoas cross-sectional area (CSA), defining sarcopenia as the lowest tertile [8] or quartile [9] in the cohort. Some studies adopted fixed cutoff values normalized by height or sex (e.g., paraspinal index <986.1 mm2/m2 [10] or psoas CSA <12 cm2 in men and <8 cm2 in women [11]).

However, these approaches typically involve a single dimension (quality or quantity) in a single muscle and lack an integrated framework. The spinal muscles degenerate heterogeneously; studies have shown that paralumbar FI does not necessarily correlate with muscle volume in the elderly [12,13], and psoas FI may differ significantly from paralumbar FI in surgical patients [14,15]. Therefore, relying on one muscle or metric may overlook the multifactorial nature of trunk muscle degeneration and its effects on alignment.

In the present study, we aimed to comprehensively assess spinal muscle features by incorporating the qualitative and quantitative parameters of the psoas and paralumbar muscles. Specifically, we sought to identify distinct muscle phenotypes using latent profile analysis (LPA) to determine whether LPA-based classification better explains sagittal alignment than traditional sarcopenia definitions. We also aimed to determine whether the patterns of sagittal malalignment differed across the LPA-derived subtypes. We hypothesized that multidimensional profiling would capture sarcopenia more accurately and reveal novel phenotype-specific differences in ASD sagittal alignment and outcomes in patients with ASD.

Materials and Methods

Ethics statement

This study adhered to the Declaration of Helsinki and was approved by the Hospital for Special Surgery institutional review board (approval number: 2018-1599). The requirement for informed consent was waived owing to the retrospective and observational nature of the study.

Study design

The study was designed as a retrospective cohort study.

Patient sample

This cohort included 145 patients with ASD who underwent fusion at ≥5 levels (upper instrumented vertebra [UIV]: T1–L1) with ≥1-year of follow-up. The exclusion criteria were as follows: (1) deformities secondary to other diseases, (2) missing data, and (3) a history of spinal surgery.

Data collection

We extracted patient demographics from our database and recorded the intraoperative and postoperative details, as described below.

Muscle assessment

Lumbar magnetic resonance imaging (MRI; supine T2-weighted axial images) was used to assess the psoas and paralumbar (multifidus and erector spinae) muscles at L4, as the L4 paralumbar level has been reported to be a relevant and reliable surrogate for evaluating muscle status in degenerative ASD with sagittal imbalance [16,17]. Muscle quality was graded according to the Goutallier classification. The bilateral psoas FI was averaged from the left and right sides, whereas the paralumbar FI was calculated as the mean FI of the bilateral multifidus and erector spinae muscles [18,19].

Muscle quantity was assessed using the psoas vertebral body index (PVBI) and paralumbar vertebral body index (PLVBI), calculated from axial T2-weighted MRI at L4 as the ratio of the bilateral muscle CSA to the vertebral body CSA. Most measurements were performed using the Sectra Workstation software by a single, experienced observer following a standardized protocol, as previously reported by our team [20,21].

Spinal alignment

Standing full-length spine radiographs were used to measure alignment at three time points: preoperative, immediate postoperative, and last follow-up (≥1 year). The following parameters were obtained from standing full-spine radiographs: coronal C7 plumb line, coronal maximum Cobb angle, thoracic kyphosis (T4–T12), lumbar lordosis (LL, L1–S1), sacral slope (SS), pelvic incidence (PI), PI–LL mismatch, pelvic tilt (PT), sagittal vertical axis (SVA), L1 pelvic angle (L1PA), L1PA offset (measured L1PA–the normal value, where normal=0.5×PI−21° [22]), T4 pelvic angle (T4PA), and T4–L1PA mismatch (T4PA–L1PA). Changes in alignment (▲) from the immediate postoperative period to the final follow-up were calculated.

Fixation strategy

The UIV was classified as upper thoracic (T1–T6) or lower thoracic (T7–L1) [23,24], and the lowest instrumented vertebra (LIV) was categorized based on whether pelvic fixation was performed. The UIV anchoring technique (hooks and/or screws) and length of fusion were also collected.

Outcomes

Functional outcomes were assessed at baseline and at the final postoperative follow-up (≥1 year) using the Oswestry Disability Index (ODI), and the ODI change from baseline to final follow-up was calculated. Similarly, back/leg pain (Visual Analog Scale [VAS] scores) was recorded but not included in the analysis because of incomplete data.

The intraoperative data included estimated blood loss, operative duration, intraoperative complications (as per the Adult Symptomatic Lumbar Scoliosis–International Spine Study Group classification [25]), and length of hospital stay. Postoperative outcomes included proximal junctional kyphosis (PJK), proximal junctional failure (PJF), reoperations, and any surgical or medical complications.

Statistical analysis

Continuous variables are presented as mean±standard deviation or median with interquartile range, depending on the data distribution. FI and VAS scores were treated as approximate continuous variables in the statistical analysis. Pearson’s or Spearman’s correlation coefficients (r) were calculated to assess the associations among muscle parameters before LPA.

Clustering of muscle profiles

LPA was performed to identify distinct muscle phenotypes. The variables included in the model were PVBI, PLVBI, and FI of the psoas and paralumbar muscles. Analyses were performed using Mplus ver. 8.3 (Muthén & Muthén, Los Angeles, CA, USA). Model fit was evaluated using standard information criteria and likelihood ratio tests, and classification certainty was assessed using entropy. A radar chart was created to illustrate each muscle profile.

Comparison of LPA-based classification and single-parameter sarcopenia classifications in predicting sagittal alignment

We evaluated the predictive performance of the LPA classification for key sagittal alignment parameters (SVA, L1PA offset, T4–L1PA mismatch, PI–LL, and PT) in comparison with the conventional binary definitions of sarcopenia derived from single muscle metrics using linear regression models.

Before this comparison, conventional binary definitions (non-sarcopenic vs. sarcopenic) were applied separately to each muscle parameter. Two classification strategies were used: (1) the lowest tertile, as reported in prior studies [8], and (2) an optimal cutoff value. To determine the optimal cutoff values, we followed a previously described approach [26], in which binary sarcopenia classification was used to predict the five sagittal parameters based on linear regression models. The average R2 across the five models was calculated for each candidate cutoff value, and the cutoff yielding the highest mean R2 was defined as the optimal threshold. This analysis was conducted in R ver. 4.4.1 (The R Foundation for Statistical Computing, Vienna, Austria) using the readxl package, and the relationship between the cutoff values and R2 performance was visualized using line plots for each muscle metric.

Subsequently, we used univariable linear regression to compare the predictive performance (R2 and p-values) of LPA-based classification with that of binary sarcopenia definitions based on both the lowest tertile and optimal cutoffs (defined as ≤cutoff for sarcopenia; >cutoff for non-sarcopenia). A higher R2 with a p-value <0.05 was interpreted as better predictive accuracy.

Comparison across LPA-derived muscle subtypes

Continuous variables were compared using analysis of variance or Kruskal-Wallis tests, and categorical variables were compared using chi-square or Fisher’s exact tests with appropriate post hoc and multiple-comparison adjustments. For alignment parameters showing significant group differences at the last follow-up, additional multivariate linear regression analyses were performed, adjusting for age, fusion length, UIV category (upper thoracic [T1–T6] vs. lower thoracic [T7–L1]), and LIV category (with vs. without pelvic fixation). The muscle phenotype was entered as a categorical variable, with the Hete-Deg group serving as the reference category. Regression coefficients, standard errors (SEs), and 95% confidence intervals (CIs) were also calculated. Statistical significance was set at p<0.05. Analyses were performed in R ver. 4.4.1.

Results

Baseline characteristics

The baseline characteristics of the 145 patients with ASD (Fig. 1) are summarized in Table 1. No strong collinearity was observed among the four muscle parameters (|r| <0.7), justifying their inclusion in the LPA model (Supplement 1).

Fig. 1

Flowchart of patient selection and analytical framework. UIV, upper instrumented vertebra; LPA, latent profile analysis; PVBI, psoas vertebral body index; PLVBI, paralumbar vertebral body index; FI, fat infiltration; Mild-Deg, mild degeneration group; Mod-Deg, moderate degeneration group; Seve-Deg, severe degeneration group; Hete-Deg, heterogeneous degeneration group.

Clinical characteristics for the 145 patients with adult spinal deformity

LPA-based cluster analysis

LPA model fit indices (the lowest AIC, BIC, and aBIC values, significant LMR and BLRT tests, and high class-specific average posterior probabilities [AvePPs]) consistently supported four muscle phenotypes (Table 2): Mild-Deg (high muscle quantity, low FI; n=49; AvePP=0.935), Mod-Deg (moderate muscle quantity and quality; n=39; AvePP=1.000), Seve-Deg (low muscle quantity, high FI; n=34; AvePP=1.000), and Hete-Deg (low muscle quantity, high paralumbar FI but low psoas FI; n=23; AvePP=0.871) (Fig. 2).

Comparison of fit statistics for LPA models with varying class numbers

Fig. 2

Visualization of intergroup differences across latent profile analysis-defined muscle profiles using standardized means of four muscle metrics: psoas vertebral body index (PVBI), paralumbar vertebral body index (PLVBI), psoas fat infiltration (FI), and paralumbar FI. Mild-Deg, mild degeneration group; Mod-Deg, moderate degeneration group; Seve-Deg, severe degeneration group; Hete-Deg, heterogeneous degeneration group.

LPA vs single-parameter prediction

We determined cutoff values for traditional sarcopenia definitions. The lowest tertile cutoffs for the cohort were approximately PVBI ≤1.44, PLVBI ≤2.68, psoas FI ≤0.00, and paralumbar FI ≤2.00 (Table 3). Using the optimal R2 method, the best cutoffs were PVBI ≤2.05, PLVBI ≤2.61, psoas FI ≤0.50, and paralumbar FI ≤3.25 (Fig. 3, Table 3). Patients were classified as sarcopenic (≤cutoff) or non-sarcopenic (>cutoff), and the group sizes for both cutoff methods are summarized in Table 3.

Optimal R2-based and conventional tertile cutoffs for muscle metrics with patient stratification

Fig. 3

Change in mean R2 with different cutoff values of the psoas vertebral body index (PVBI) (A), the paralumbar vertebral body index (PLVBI) (B), psoas fat infiltration (FI) (C), and paralumbar FI (D): identifying optimal cutoffs for single muscle metric. At each cutoff of muscle metric, patients were dichotomized, and the resulting binary variable was used as the predictor in univariate linear regressions, with sagittal vertical axis, L1 pelvic angle (L1PA) offset, T4–L1PA mismatch, pelvic incidence–lumbar lordosis, and pelvic tilt used sequentially as the dependent variables. For each cutoff, the mean R2 across the five models was calculated and plotted. The curve illustrates how the predictive power (mean R2) changes with different cutoffs, with the peak identifying the optimal cutoff for predicting sagittal malalignment.

Using these binary sarcopenia definitions, we performed linear regression for each key sagittal metric. The LPA-based classification achieved the highest R2 values for T4–L1PA mismatch (0.155), PI–LL (0.160), and PT (0.139), and the second highest for SVA (0.116), outperforming all single-metric definitions (Table 4).

Linear regression models of muscle metrics predicting key sagittal spinal alignment parameters

Clinical and radiographic comparisons by LPA group

Table 5 summarizes the results of group comparisons. PVBI, PLVBI, and FI values differed significantly among the groups (p<0.001), further confirming the validity of the classification. Patient age increased significantly from Mild- through Seve-Deg (median, 51, 66, and 68 years; p<0.001), and the prevalence of hypertension, coronary artery disease, and higher Charlson comorbidity index (CCI) also increased with more severe muscle degeneration.

Comparative analysis of clinical characteristics and surgical outcomes across LPA-derived muscle profiles

Preoperative sagittal alignment deteriorated across Mild to Seve-Deg; PI–LL, PT, SVA, L1PA offset, and T4–L1PA mismatch all worsened progressively (p<0.001). Notably, the Hete-Deg group had one of the worst alignments (mean PI–LL, 24.0°; median SVA, 88.1 mm; and median T4–L1PA mismatch, 12.0°), with the second-largest L1PA offset (4.8°).

In the fixation/intraoperative data, the Mild-Deg group had fewer patients with pelvic fixation (p=0.013). The Hete-Deg group tended to have longer fusions (median, 11; p=0.019) and operative times (median, 314 minutes; p=0.011).

Postoperative alignment was largely comparable between the groups. Only PI–LL (p=0.005) and T4–L1PA mismatch (p=0.042) were slightly higher in the Mod-Deg/Seve-Deg groups than in the Mild-Deg/Hete-Deg groups. At the last follow-up, patients in the Mod-Deg and Seve-Deg groups had significantly greater malalignment; PI–LL (p=0.002), T4–L1PA mismatch (p=0.005), T4PA (p=0.017), SS (p=0.006), and LL (p<0.001) were all larger than in the Mild-Deg/Hete-Deg group. In additional multivariable linear regression adjusting for age, fixation strategy (UIV/LIV), and fusion length, the association of muscle phenotype with PI–LL (overall p=0.027) and LL (overall p=0.003) remained significant. Using the Hete-Deg group as the reference category, the Mod-Deg (β=8.90, SE=3.96; 95% CI, 1.06–16.75; p=0.026) and Seve-Deg (β=9.04, SE=4.02; 95% CI, 1.08–17.00; p=0.026) groups demonstrated significantly greater PI–LL values. Similarly, the Mod-Deg (β=−10.32, SE=3.83; 95% CI, −17.90 to −2.74; p=0.008) and Seve-Deg (β= −9.71, SE=3.88; 95% CI, −17.39 to −2.02; p=0.014) groups exhibited significantly lower LL values than the Hete-Deg group. In contrast, the associations for T4–L1PA mismatch (overall p=0.399), T4PA (overall p=0.423), and SS (overall p=0.497) were no longer significant, suggesting that some radiographic differences may be partially confounded by surgical factors. There was a trend toward larger changes in PI–LL and T4PA (postoperative → follow-up) in the Seve-Deg group (p=0.065, and 0.086, respectively).

Finally, there were no significant differences in functional recovery (ODI scores) or complication rates (PJK, PJF, etc.) among the four groups.

Discussion

Summary of findings

Paraspinal sarcopenia is closely associated with sagittal malalignment in ASD; however, traditional definitions based on a single muscle or metric fail to capture the complex and heterogeneous nature of trunk muscle degeneration in patients with ASD. By applying multidimensional muscle profiling with LPA, we identified four distinct muscle phenotypes with varying combinations of quantity and quality in the psoas and paralumbar muscles. Compared with conventional single-metric sarcopenia definitions, LPA-based classification more accurately predicted key sagittal alignment parameters, highlighting its superiority in characterizing sagittal alignment. Importantly, the LPA method effectively identified the distinct Hete-Deg subtype, which is characterized by functional compensation failure rather than structural degeneration. Despite marked preoperative sagittal deformity, patients with Hete-Deg were able to maintain long-term alignment. In contrast, the Seve-Deg subtypes exhibited structural muscle damage associated with both severe preoperative deformity and progressive postoperative imbalance. These findings highlight the value of LPA-based classification not only in phenotypic resolution but also in capturing clinical differences in postoperative alignment stability and progression.

Multidimensional muscle profiling enhances malalignment prediction

Compared to traditional sarcopenia definitions based on single muscle measures, our LPA-based classification better predicted sagittal imbalance by capturing muscle health multidimensionally. This is particularly important given the notable heterogeneity in degeneration between the paralumbar and psoas muscles [14,15] and between muscle quality and quantity within the same muscle group [12,13]. Consistently, our data showed only weak-to-moderate correlations among the four muscle parameters, indicating the need for multidimensional profiling. Conventional criteria often focus on a single metric at a single site, resulting in inconsistent definitions and limited sensitivity to localized changes. However, our LPA model integrates both quantitative (CSA) and qualitative (FI) features across multiple muscle groups, offering a more comprehensive assessment aligned with recent expert recommendations favoring machine learning–based imaging analysis [27]. Such an approach may better reflect the complex, multisite nature of sarcopenia, provide a person-centered framework to identify clinically meaningful phenotypes beyond isolated muscle parameters, and offer a novel framework for future investigations of muscle degeneration and its clinical relevance. Although the sample size was modest and one latent profile was relatively small, methodological studies suggest that reliable latent profile solutions may still be obtained when supported by adequate indicator quality and class separation [28,29]. Consistent with this, the high entropy and favorable fit indices in our model support the stability of the identified profiles, although validation in larger cohorts is warranted (Table 2).

Hete-Deg: a distinct phenotype reflecting functional compensation

A particularly novel finding was the Hete-Deg phenotype, characterized by a low overall muscle quantity and markedly high paralumbar FI but near-normal psoas FI. Previous studies have noted that psoas FI can remain low even in patients with ASD [30], and is sometimes comparable to levels observed in healthy individuals [31]. However, the absence of concurrent assessment of paralumbar muscle status in these studies precluded the identification of this distinct “Hete-Deg” pattern in their results. Our Hete-Deg group had some of the most severe preoperative deformities; interestingly, they maintained sagittal alignment after >1 year of follow-up after surgery. We speculate that this pattern reflects functional compensation rather than irreversible atrophy, as their preserved psoas function may have compensated for weak paraspinal muscles to sustain alignment after correction [14].

In contrast, the Mod-Deg and Seve-Deg subtypes (moderate-to-low muscle quantity with high FI) had progressively worse baseline malalignment and poorer maintenance of correction over time. Given that FI in the trunk muscles is largely irreversible [32], these groups may represent irreversible structural muscle damage and substantial loss of functional capacity, which may contribute to the progressive deterioration of postoperative alignment over time.

Paraspinal sarcopenia corresponds with greater comorbidity burden

We also observed that more severe muscle degeneration paralleled poor systemic health. Hypertension, coronary artery disease, and higher CCI were more common in the Mod-Deg and Seve-Deg groups, mirroring the pattern in systemic sarcopenia, in which frailty and comorbidities increase with muscle loss. Population data show that individuals with sarcopenia often have more cardiovascular/metabolic diseases, and sarcopenia can accelerate cardiovascular disease progression [33]. In addition, a higher CCI is negatively correlated with muscle mass in older adults [34].

Radiographic-functional discordance

Although LPA-derived phenotypes differed in long-term alignment behavior, no significant differences in ODI improvement or complication rates were observed. This may be related to the relatively short follow-up period, which may have been insufficient for radiographic differences to translate into measurable functional divergence. Moreover, the modest sample size and low event rates may have limited the statistical power to detect between-group differences, and ODI may have been insufficiently sensitive to capture subtle phenotype-related differences in postoperative function. Prior studies have also suggested that functional outcomes may not fully parallel radiographic differences and that ODI may not capture all dimensions of ASD-related disability [35].

Limitations

First, although we found significant associations between LPA-based phenotypes and sagittal alignment, the retrospective design of this study precludes causal interpretation. Several studies have demonstrated that greater spinal malalignment is associated with poor muscle quality and reduced muscle quantity [30]. Most likely, there is a reciprocal relationship [36]; as muscles weaken or atrophy, mild deformities can progress unchecked, highlighting the importance of an accurate muscle profile in patients with ASD. In addition, the single-center design and highly selected surgical cohort may limit the generalizability of these findings to broader ASD populations, particularly patients with less severe deformities or those treated at other institutions. Moreover, the relatively short follow-up period may not have fully captured longer-term progression or functional divergence across phenotypes. Second, the optimal cutoffs were derived and evaluated within the same dataset, raising the possibility of overfitting. External validation is required to confirm the robustness of the identified phenotype. Third, muscle quality was assessed using the semiquantitative Goutallier grading system, which has not been validated for evaluating lumbar muscles. Similar to prior studies treating ordinal variables (e.g., pain scores) as continuous for LPA [37], we approximated FI grades as continuous, although this remains an approximation. Future studies should explore advanced modalities, such as quantitative MRI [38], to better characterize muscle quality and further strengthen LPA-based profiling. Moreover, muscle parameters were assessed using supine MRI, whereas alignment was measured using standing radiographs, and this positional discrepancy may have influenced the observed associations.

Conclusions

Multidimensional muscle profiling using LPA explained sagittal malalignment in ASD better than traditional single-metric sarcopenia definitions. Compared to single measures, LPA identified a unique Hete-Deg phenotype (low muscle mass with disproportionately high paralumbar FI but low psoas FI), suggestive of functional compensation, compared to the Seve-Deg pattern of structural muscle damage. These insights may help stratify patients based on muscle health beyond conventional sarcopenia. Future prospective multicenter studies are needed to validate the predictive value of LPA-based muscle phenotyping. If confirmed, targeted rehabilitation can be developed for individual muscle profiles to optimize outcomes.

Key Points

  • Latent profile analysis (LPA) identified four distinct trunk muscle phenotypes in patients with adult spinal deformity.

  • LPA-based classification better explained sagittal alignment than single metrics.

  • The novel Hete-Deg phenotype exhibited severe deformity but stable postoperative alignment.

  • Seve-Deg patients had progressive malalignment despite surgical correction.

Notes

Conflict of Interest

No potential conflict of interest relevant to this article was reported.

Funding

No direct funding was received for this study. However, this study used REDCap hosted at Weill Cornell Medicine Clinical and Translational Science Center, which is supported by the National Center for Advancing Translational Science of the National Institute of Health (NIH) under award number: UL1TR002384. This study was approved by the Hospital for Special Surgery internal review board (2018-1599).

Author Contributions

Conceptualization: DH, ZW, MD, MJWC, HJK, FL. Data curation: AB, RU, GD, AD, AP, SOS, LFC, KA, QS, FM, SH, Formal analysis: DH, ZW, MD, MJWC, HJK, FL. Analysis and interpretation of data: MC, HJK, FL, Funding acquisition: none. Methodology: none. Project administration: DH, ZW, MD, MJWC, AB, MC, HJK, FL. Technical or material support: DH, ZW, MD, MJWC, AB, RU, GD, AD, AP, SOS, LFC, KA, QS, FM, SH, MC, HJK, FL. Visualization: none. Writing–original draft: DH, ZW, MD, MJWC. Writing–review & editing: AB, RU, GD, AD, AP, SOS, LFC, KA, QS, FM, SH, MC, HJK, FL. Supervision: MC, HJK, FL. Final approval of the manuscript: all authors.

Supplementary Materials

Supplementary materials can be available from https://doi.org/10.31616/asj.2026.0116.

Supplement 1. Spearman correlation of the four muscle metrics.

asj-2026-0116-Supplement-1.pdf

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Article information Continued

Fig. 1

Flowchart of patient selection and analytical framework. UIV, upper instrumented vertebra; LPA, latent profile analysis; PVBI, psoas vertebral body index; PLVBI, paralumbar vertebral body index; FI, fat infiltration; Mild-Deg, mild degeneration group; Mod-Deg, moderate degeneration group; Seve-Deg, severe degeneration group; Hete-Deg, heterogeneous degeneration group.

Fig. 2

Visualization of intergroup differences across latent profile analysis-defined muscle profiles using standardized means of four muscle metrics: psoas vertebral body index (PVBI), paralumbar vertebral body index (PLVBI), psoas fat infiltration (FI), and paralumbar FI. Mild-Deg, mild degeneration group; Mod-Deg, moderate degeneration group; Seve-Deg, severe degeneration group; Hete-Deg, heterogeneous degeneration group.

Fig. 3

Change in mean R2 with different cutoff values of the psoas vertebral body index (PVBI) (A), the paralumbar vertebral body index (PLVBI) (B), psoas fat infiltration (FI) (C), and paralumbar FI (D): identifying optimal cutoffs for single muscle metric. At each cutoff of muscle metric, patients were dichotomized, and the resulting binary variable was used as the predictor in univariate linear regressions, with sagittal vertical axis, L1 pelvic angle (L1PA) offset, T4–L1PA mismatch, pelvic incidence–lumbar lordosis, and pelvic tilt used sequentially as the dependent variables. For each cutoff, the mean R2 across the five models was calculated and plotted. The curve illustrates how the predictive power (mean R2) changes with different cutoffs, with the peak identifying the optimal cutoff for predicting sagittal malalignment.

Table 1

Clinical characteristics for the 145 patients with adult spinal deformity

Characteristic Value
Muscle metricsa)
 PVBI 1.7±0.6
 PLVBI 3.0±0.9
 Psoas FI 0.4±0.5
 Paraspinal FI 2.4±0.9
Demographic metrics
 Age (yr) 58.5±16.1
 Sex
  Male 36
  Female 109
 Body mass index (kg/m2) 25.7±5.6
 Osteoporosis
  Yes 26
  No 119
 Bisphosphonateb)
  Yes 9
  No 92
 Anabolic agentb)
  Yes 11
  No 91
 Smoker (current or former)
  Yes 35
  No 110
 Diabetes
  Yes 6
  No 139
 Hypertension
  Yes 53
  No 92
 Dyslipidemia
  Yes 13
  No 132
 Coronary artery disease
  Yes 10
  No 135
 Peripheral neuropathy
  Yes 1
  No 144
 Autoimmune
  Yes 1
  No 144
 Decompression
  Yes 17
  No 128
 Anxiety
  Yes 16
  No 129
 CCI with age component 2.0±1.6
Preoperative alignment
 C7PL (mm) 20.2 (11.0 to 47.0)
 Max cobb (°) 47.0 (31.0 to 58.0)
 TK (T4–T12) (°) 30.9±16.6
 LL (L1–S1) (°) 34.9±20.8
 SS (°) 29.1±12.0
 PI (°) 52.5±12.6
 PI–LL (°) 17.6±20.8
 PT (°) 24.0±11.7
 SVA (mm) 58.3±68.7
 L1PA (°) 10.4±9.4
 L1PA offset (°) 5.1±7.6
 T4PA (°) 19.2±13.2
 T4–L1PA mismatch (°) 8.8±8.9
Fixation strategy
 UIV
  Upper 50
  Lower 95
 UIV-hook
  Yes 7
  No 138
 UIV-screw
  Yes 100
  No 45
 LIV
  Pelvic 111
  Non-pelvic 34
 Length of fusion (levels) 9.3±3.1
Postoperative alignment
 Max cobb (°) 24.8±13.9
 TK (T4–T12) (°) 37.2±12.5
 LL (L1–S1) (°) 49.0±13.2
 SS (°) 36.0 (24.0 to 42.0)
 PI (°) 52.1±11.9
 PI–LL (°) 3.0±12.2
 PT (°) 17.9±10.1
 L1PA (°) 7.8±7.1
 L1PA offset (°) 2.8±4.7
 T4PA (°) 10.7±8.5
 T4–L1PA mismatch (°) 2.9±4.7
Last FU alignment
 Max cobb (°) 24.6±11.4
 TK (T4–T12) (°) 41.6±14.1
 LL (L1–S1) (°) 47.8±14.1
 SS (°) 30.8±10.7
 PI (°) 52.4±12.5
 PI–LL (°) 4.6±14.3
 PT (°) 21.8±10.5
 L1PA (°) 8.6±7.4
 L1PA offset (°) 3.4±4.5
 T4PA (°) 13.1±9.6
 T4–1PA mismatch (°) 4.6±5.3
▲Alignment (last FU–postoperative)
 ▲Max cobb (°) 0.0 (−3.0 to 3.0)
 ▲TK (T4–T12) (°) 3.0 (−2.0 to 10.1)
 ▲LL (L1–S1) (°) −0.6±8.2
 ▲SS (°) −2.8±6.9
 ▲PI (°) 0.9 (−1.0 to 3.0)
 ▲PI–LL (°) 1.0 (−2.0 to 5.6)
 ▲PT (°) 3.8 (0.0 to 7.8)
 ▲L1PA (°) 1.0 (−0.8 to 3.0)
 ▲L1PA offset (°) 0.7±3.7
 ▲T4PA (°) 2.8 (0.0 to 6.0)
 ▲T4–L1PA mismatch (°) 1.6 (0.0 to 3.0)
ODIb)
 Baseline 35.8±16.7
 Last FU 16.8±16.9
 Last FU–baseline −18.7±17.6
VAS-backc)
 Baseline 6.5±2.3
 Last FU 1.0 (0.0 to 3.0)
VAS-legc)
 Baseline 4.0 (1.0 to 6.0)
 Last FU 0.0 (0.0 to 3.0)
Intraoperative and hospitalization events
 EBL (mL) 1,120±934
 Operative time (min) 266±103
 Intraoperative complications 5 (3.6)
 Length of hospital stay-total (day) 6.0±3.0
Postoperative complications
 PJK 52 (35.9)
 PJF 7 (4.8)
 Surgery-related complications 13 (9.0)
 Medical complications 19 (13.1)
 Reoperation for any reasons 6 (4.1)

Values are presented as mean±standard deviation for normally distributed continuous variables, number for categorical variables, median (interquartile range) for non-normally distributed continuous variables, or number (%) for categorical variables.

PVBI, psoas vertebral body index; PLVBI, paralumbar vertebral body index; FI, fat infiltration; CCI, Charlson comorbidity index; C7PL, coronal C7 plumb line; Max cobb, coronal maximum Cobb angle; TK, thoracic kyphosis; LL, lumbar lordosis; SS, sacral slope; PI, pelvic incidence; PT, pelvic tilt; SVA, sagittal vertical axis; L1PA, L1 pelvic angle; L1PA offset, calculated as L1PA− (0.5×PI−21°); T4PA, T4 pelvic angle; T4–L1PA mismatch, calculated as T4PA–L1PA; UIV, upper instrumented vertebra; LIV, lower instrumented vertebra; Last FU, last follow-up over 1 year; ODI, Oswestry Disability Index; VAS, Visual Analog Scale; EBL, estimated blood loss; PJK, proximal junctional kyphosis; PJF, proximal junctional failure.

a)

Data was measured at L4 level.

b)

Fewer than 30% of patients had missing data.

c)

Approximately two-thirds of patients had missing data and were therefore excluded from further analysis.

Table 2

Comparison of fit statistics for LPA models with varying class numbers

No. of classes Loglikelihood AIC BIC aBIC Entropy LMR p-value BLRT p-value
2-Class −785.9 1,597.7 1,636.4 1,595.3 0.619 - -
3-Class −760.8 1,557.7 1,611.2 1,554.3 0.804 0.162 0.000
4-Class −714.1 1,474.2 1,542.7 1,469.9 0.920 0.046 0.000
5-Class −738.7 1,533.4 1,616.8 1,528.2 0.799 0.513 1.000

LPA, latent profile analysis; AIC, Akaike information criterion; BIC, Bayesian information criterion; aBIC, sample-size adjusted BIC; LMR, Lo–Mendell–Rubin adjusted likelihood ratio test; BLRT, bootstrapped likelihood ratio test.

Table 3

Optimal R2-based and conventional tertile cutoffs for muscle metrics with patient stratification

Variable Category Optimal cutoff Cutoff closest to the lowest 3rd
PVBI Cutoff 2.05 1.44
Lower 113 49
Upper 32 96
PLVBI Cutoff 2.61 2.68
Lower 45 49
Upper 100 96
Psoas FI Cutoff 0.50 0.00
Lower 111 72
Upper 34 73
Paraspinal FI Cutoff 3.25 2.00
Lower 120 60
Upper 25 85

PVBI, psoas vertebral body index; PLVBI, paralumbar vertebral body index; FI, fat infiltration.

Table 4

Linear regression models of muscle metrics predicting key sagittal spinal alignment parameters

Variable Category R2/p-value SVA L1PA offset T4–L1PA mismatch PI–LL PT
PVBI Optimal cutoff R2 0.051 0.016 0.064 0.060 0.029
p-value 0.006 0.135 0.002 0.003 0.042
Cutoff closest to the lowest 3rd R2 0.038 0.022 0.022 0.014 0.015
p-value 0.019 0.073 0.073 0.160 0.148
PLVBI Optimal cutoff R2 0.092 0.069 0.101 0.063 0.067
p-value 0.000 0.001 0.000 0.002 0.002
Cutoff closest to the lowest 3rd R2 0.075 0.077 0.082 0.057 0.056
p-value 0.001 0.001 0.000 0.004 0.004
Psoas FI Optimal cutoff R2 0.054 0.043 0.029 0.037 0.033
p-value 0.005 0.012 0.040 0.021 0.028
Cutoff closest to the lowest 3rd R2 0.018 0.015 0.031 0.077 0.041
p-value 0.104 0.141 0.034 0.001 0.015
Paraspinal FI Optimal cutoff R2 0.164 0.070 0.100 0.094 0.057
p-value 0.000 0.001 0.000 0.000 0.004
Cutoff closest to the lowest 3rd R2 0.047 0.015 0.085 0.074 0.076
p-value 0.009 0.139 0.000 0.001 0.001
LPA profile R2 0.116 0.047 0.155 0.160 0.139
p-value 0.001 0.079 0.000 0.000 0.000

The deeper the red in the heatmap, the greater the R2 value and the stronger the correlation.

SVA, sagittal vertical axis; L1PA offset, L1 pelvic angle offset; T4–L1PA mismatch, T4 to L1 pelvic angle mismatch; PI–LL, pelvic incidence minus lumbar lordosis; PT, pelvic tilt; PVBI, psoas vertebral body index; PLVBI, paralumbar vertebral body index; FI, fat infiltration; LPA, latent profile analysis.

Table 5

Comparative analysis of clinical characteristics and surgical outcomes across LPA-derived muscle profiles

Factors Mild-Deg (n=49) Mod-Deg (n=39) Seve-Deg (n=34) Hete-Deg (n=23) p-value
Total Mild vs. Mod Mild vs. Seve Mild vs. Hete Mod vs. Seve Mod vs. Hete Seve vs. Hete
Muscle metricsa)
 PVBI 1.9 (1.6 to 2.2) 1.7 (1.4 to 2.2) 1.4 (1.2 to 1.7) 1.5 (1.1 to 1.7) 0.000b) NS 0.001 0.003 NS NS NS
 PLVBI 3.5±0.7 3.1±0.8 2.7±0.9 2.4±0.6 0.000c) 0.009 0.000 0.000 NS 0.002 NS
 Psoas FI 0.0 (0.0 to 0.0) 0.5 (0.5 to 0.5) 1.0 (1.0 to 1.0) 0.0 (0.0 to 0.0) 0.000b) 0.000 0.000 NS 0.000 0.000 0.000
 Paraspinal FI 1.7±0.7 2.4±0.7 2.9±0.9 3.2±0.6 0.000c) 0.000 0.000 0.000 0.001 0.000 NS
Demographic metrics
 Age (yr) 51.0 (34.0 to 61.0) 66.0 (57.0 to 73.0) 70.0 (61.0 to 73.0) 66.0 (58.0 to 68.0) 0.000b) 0.000 0.000 0.001 NS NS NS
 Sex (M:F) 12:37 10:29 10:24 4:19 0.782d) NS NS NS NS NS NS
 Body mass index (kg/m2) 23.8 (20.4 to 27.5) 24.8 (21.3 to 28.9) 26.2 (21.8 to 30.7) 24.1 (20.6 to 34.0) 0.306b) NS NS NS NS NS NS
 Osteoporosis (yes:no) 6:43 4:35 7:27 9:14 0.020d) NS NS 0.067 NS 0.062 NS
 Bisphosphonate (yes:no)e) 3:35 3:29 1:18 2:10 0.739d) NS NS NS NS NS NS
 Anabolic agent (yes:no)e) 4:34 1:31 3:17 3:9 0.184d) NS NS NS NS NS NS
 Smoker (current or former) (yes:no) 13:36 7:32 10:24 5:18 0.669d) NS NS NS NS NS NS
 Diabetes (yes:no) 0:49 1:38 4:30 1:22 0.061d) NS NS NS NS NS NS
 Hypertension (yes:no) 7:42 16:23 22:12 8:15 0.000d) 0.034 0.000 NS NS NS NS
 Dyslipidemia (yes:no) 5:44 3:36 4:30 1:22 0.778d) NS NS NS NS NS NS
 Coronary artery disease (yes:no) 0:49 4:35 6:28 0:23 0.007d) NS 0.021 NS NS NS NS
Peripheral neuropathy (yes:no) 0:49 1:38 0:34 0:23 0.434d) NS NS NS NS NS NS
 Autoimmune (yes:no) 0:49 1:38 0:34 0:23 0.434d) NS NS NS NS NS NS
 Decompression (yes:no) 4:45 5:34 7:27 1:22 0.218d) NS NS NS NS NS NS
 Anxiety (yes:no) 6:43 4:35 4:30 2:21 0.970d) NS NS NS NS NS NS
 CCI with age component 1.0 (0.0 to 2.0) 2.0 (1.0 to 3.0) 3.0 (2.0 to 4.0) 2.0 (2.0 to 3.0) 0.000b) 0.000 0.000 0.000 NS NS NS
 Preoperative alignment
 C7PL (mm) 16.0 (11.0 to 45.0) 17.0 (11.0 to 40.0) 27.4 (9.3 to 63.0) 29.9 (12.5 to 57.0) 0.379b) NS NS NS NS NS NS
 Max cobb (°) 49.9±22.0 42.4±18.7 43.6±18.6 46.3±22.3 0.332c) NS NS NS NS NS NS
 TK (T4–T12) (°) 32.7±16.3 26.6±14.1 28.1±13.6 38.5±22.2 0.029c) NS NS NS NS 0.006 0.019
 LL (L1–S1) (°) 44.9±19.7 32.8±19.5 26.2±14.7 30.0±25.3 0.000c) 0.005 0.000 0.003 NS NS NS
 SS (°) 34.0 (27.0 to 41.6) 29.0 (22.0 to 34.0) 25.7 (16.8 to 32.1) 26.7 (15.0 to 31.2) 0.001b) NS 0.002 0.029 NS NS NS
 PI (°) 51.1±12.2 54.9±13.2 50.9±11.4 54.0±14.0 0.413c) NS NS NS NS NS NS
 PI–LL (°) 6.1±20.2 22.0±18.4 24.8±16.1 24.0±22.5 0.000c) 0.000 0.000 0.000 NS NS NS
 PT (°) 18.2±11.3 25.0±10.8 27.8±10.5 28.9±11.3 0.000c) 0.004 0.000 0.000 NS NS NS
 SVA (mm) 30.0 (−7.7 to 55.0) 46.0 (10.0 to 84.0) 72.5 (46.8 to 143.0) 88.1 (33.0 to 124.0) 0.000b) NS 0.001 0.010 NS NS NS
 L1PA (°) 8.3±8.9 10.8±10.1 12.5±8.8 11.1±9.9 0.236c) NS 0.050 NS NS NS NS
 L1PA offset (°) 2.1 (−1.4 to 7.5) 4.0 (0.0 to 8.9) 8.5 (4.0 to 12.7) 4.8 (−0.5 to 9.7) 0.013b) NS 0.009 NS NS NS NS
 T4PA (°) 12.6±12.0 20.2±12.4 24.0±12.4 24.7±12.7 0.000c) 0.005 0.000 0.000 NS NS NS
 T4–L1PA mismatch (°) 3.3 (0.0 to 8.8) 9.8 (6.0 to 12.0) 12.1 (7.4 to 17.0) 12.0 (5.4 to 18.3) 0.000b) 0.010 0.000 0.000 NS NS NS
Fixation strategy
 UIV (upper:lower) 23:26 10:29 6:28 11:12 0.013d) NS 0.057 NS NS NS 0.099
 UIV-hook (yes:no) 4:45 2:37 1:33 0:23 0.453d) NS NS NS NS NS NS
 UIV-screw (yes:no) 37:12 31:8 19:15 13:10 0.061d) NS NS NS NS NS NS
 LIV (pelvic:non-pelvic) 25:24 32:7 32:2 22:1 0.000d) 0.013 0.000 0.001 NS NS NS
 Length of fusion (levels) 8.0 (7.0 to 12.0) 8.0 (7.0 to 10.0) 8.0 (7.0 to 9.0) 11.0 (8.0 to 15.0) 0.019b) NS NS NS NS NS 0.015
Postoperative alignment
 Max cobb (°) 21.0 (13.0 to 31.0) 22.7 (15.0 to 30.0) 22.5 (15.0 to 33.0) 25.9 (13.0 to 36.0) 0.809b) NS NS NS NS NS NS
 TK (T4–T12) (°) 37.5±11.8 35.8±11.6 36.0±11.9 40.7±15.8 0.457c) NS NS NS NS NS NS
 LL (L1–S1) (°) 52.5±13.4 45.5±14.4 45.4±11.3 53.1±10.7 0.011c) 0.012 0.015 NS NS 0.026 0.028
 SS (°) 36.1 (28.0 to 43.6) 29.0 (23.0 to 38.3) 32.0 (27.0 to 40.8) 35.0 (28.8 to 44.0) 0.141b) NS NS NS NS NS NS
 PI (°) 51.0 (42.0 to 60.0) 53.0 (45.0 to 59.0) 51.2 (47.8 to 58.0) 50.8 (42.8 to 67.0) 0.930b) NS NS NS NS NS NS
 PI–LL (°) −0.5±12.0 7.2±11.9 5.8±12.4 −0.5±10.0 0.005c) 0.003 0.018 NS NS 0.014 0.049
 PT (°) 16.2±11.5 20.1±8.2 18.7±10.1 16.6±9.9 0.280c) NS NS NS NS NS NS
 L1PA (°) 7.1±7.3 9.0±7.3 7.5±6.0 7.7±8.0 0.654c) NS NS NS NS NS NS
 L1PA offset (°) 2.1±5.1 3.7±4.9 2.9±4.0 2.5±4.4 0.489c) NS NS NS NS NS NS
 T4PA (°) 8.8±8.4 12.6±7.4 11.8±9.4 9.9±8.4 0.151c) 0.037 NS NS NS NS NS
 T4–L1PA mismatch (°) 1.7±4.3 3.6±4.3 4.4±4.7 2.1±5.7 0.042c) NS 0.009 NS NS NS 0.075
Last FU alignment
 Max cobb (°) 21.5 (13.3 to 32.0) 23.0 (15.0 to 30.0) 23.5 (16.0 to 33.0) 22.7 (15.0 to 32.5) 0.913b) NS NS NS NS NS NS
 TK (T4–T12) (°) 42.6±12.9 41.6±14.9 38.6±14.0 43.7±15.8 0.551c) NS NS NS NS NS NS
 LL (L1–S1) (°) 49.8 (44.0 to 58.8) 40.0 (33.0 to 50.0) 45.5 (36.0 to 49.0) 54.9 (44.6 to 63.0) 0.000b) 0.007 NS NS NS 0.003 0.018
 SS (°) 33.0 (26.8 to 40.9) 25.0 (22.0 to 30.0) 28.0 (23.0 to 34.3) 34.0 (29.6 to 40.2) 0.006b) 0.019 NS NS NS 0.031 NS
 PI (°) 52.1±12.6 51.3±13.2 52.2±10.4 54.9±14.5 0.785c) NS NS NS NS NS NS
 PI–LL (˚) −0.4±14.9 9.0±13.0 9.7±14.4 0.0±9.6 0.002c) 0.003 0.002 NS NS 0.021 0.014
 PT (°) 20.5 (12.0 to 27.4) 23.0 (19.0 to 32.0) 21.2 (17.0 to 28.8) 22.1 (15.8 to 28.3) 0.252b) NS NS NS NS NS NS
 L1PA (°) 7.0±7.5 9.5±7.7 9.5±6.6 9.0±7.9 0.389c) NS NS NS NS NS NS
 L1PA offset (°) 3.0 (−1.1 to 5.0) 3.5 (2.0 to 7.1) 3.9 (2.3 to 6.8) 2.2 (−0.5 to 6.5) 0.065b) NS NS NS NS NS NS
 T4PA (°) 9.9±10.3 15.6±8.1 15.8±9.6 11.9±8.6 0.017c) 0.009 0.007 NS NS NS NS
 T4–L1PA mismatch (°) 2.9±5.7 6.2±4.8 6.4±4.5 2.9±5.4 0.005c) 0.007 0.005 NS NS 0.026 0.019
▲Alignment (last FU–postoperative)
 ▲Max cobb (°) 1.0 (−1.0 to 4.0) −1.4 (−5.0 to 3.0) 0.0 (−2.0 to 2.0) 0.5 (−2.5 to 2.5) 0.198b) NS NS NS NS NS NS
 ▲TK (T4–T12) (°) 4.0±10.5 6.3±8.0 3.7±8.3 5.2±7.1 0.618c) NS NS NS NS NS NS
 ▲LL (L1–S1) (°) 0.8 (−5.6 to 6.4) −1.0 (−5.0 to 2.0) −3.3 (−6.7 to 1.9) −0.4 (−4.0 to 6.5) 0.306b) NS NS NS NS NS NS
 ▲SS (°) −1.8±7.1 −3.0±7.0 −3.7±6.4 −3.4±7.1 0.633c) NS NS NS NS NS NS
 ▲PI (°) 1.0 (−1.0 to 3.0) 0.9 (−2.2 to 4.0) 0.3 (−1.0 to 2.7) 0.1 (−1.2 to 1.9) 0.928b) NS NS NS NS NS NS
 ▲PI–LL (°) −1.0(−4.5 to 4.3) 1.0 (−2.6 to 6.1) 4.0 (−0.9 to 7.8) −0.3 (−3.3 to 3.4) 0.065b) NS NS NS NS NS NS
 ▲PT (°) 2.8 (−0.7 to 7.3) 3.2 (−1.0 to 9.6) 5.0 (2.9 to 9.5) 3.0 (0.3 to 6.7) 0.303b) NS NS NS NS NS NS
 ▲L1PA (°) 0.5 (−1.0 to 3.3) 1.0 (−1.6 to 4.0) 2.0 (0.5 to 3.9) 0.5 (−0.6 to 2.3) 0.139b) NS NS NS NS NS NS
 ▲L1PA offset (°) 0.3 (−2.0 to 2.5) 1.5 (−1.1 to 3.0) 1.2 (−1.3 to 2.9) 0.9 (−1.7 to 2.2) 0.591b) NS NS NS NS NS NS
 ▲T4PA (°) 2.0 (−1.3 to 5.5) 3.0 (0.0 to 6.0) 4.2 (1.5 to 6.6) 1.8 (−1.7 to 3.8) 0.086b) NS NS NS NS NS NS
 ▲T4–L1PA mismatch (°) 1.0 (−0.9 to 3.0) 2.0 (1.0 to 3.0) 1.6 (0.5 to 3.5) 0.8 (−0.4 to 3.0) 0.206b) NS NS NS NS NS NS
ODIe)
 Baseline 30.9±17.6 37.1±16.0 39.8±16.1 38.3±15.1 0.070c) 0.079 0.016 0.077 NS NS NS
 Last FU 8.0 (4.0 to 20.0) 14.0 (2.2 to 22.0) 20.0 (6.0 to 40.0) 11.0 (0.0 to 22.0) 0.444b) NS NS NS NS NS NS
 Last FU–baseline −15.4±15.9 −21.5±16.1 −16.6±21.5 −26.5±13.5 0.172c) NS NS 0.043 NS NS 0.077
Intraoperative and hospitalization events
 EBL (mL) 700 (400 to 1,200) 800 (400 to 1,500) 800 (400 to 1,500) 1,450 (600 to 2,000) 0.074b) NS NS NS NS NS NS
 Operative time (min) 215 (183 to 288) 250 (192 to 308) 254 (208 to 308) 314 (245 to 372) 0.011b) NS NS 0.006 NS NS NS
 Intraoperative complications (yes:no) 1:48 2:37 1:33 1:22 0.872d) NS NS NS NS NS NS
 Length of hospital stay-total (day)e) 5.1 (4.3 to 6.3) 5.3 (4.3 to 6.5) 5.4 (4.3 to 6.5) 6.4 (4.4 to 8.8) 0.313b) NS NS NS NS NS NS
Postoperative complications
 PJK (yes:no) 16:33 13:26 15:19 8:15 0.718d) NS NS NS NS NS NS
 PJF (yes:no) 3:46 2:37 0:34 2:21 0.447d) NS NS NS NS NS NS
 Surgery-related complications (yes:no) 4:45 5:34 1:33 3:20 0.435d) NS NS NS NS NS NS
 Medical complications (yes:no) 9:40 8:31 1:33 1:22 0.052d) NS NS NS NS NS NS
 Reoperation for any reasons (yes:no) 2:47 2:37 2:32 0:23 0.717d) NS NS NS NS NS NS

Values are presented as median (Q1–Q3 interquartile range), mean±standard deviation, or number ratio unless otherwise stated. Statistically significant results are marked in bold (p<0.05).

LPA, latent profile analysis; Mild-Deg, mild degeneration group; Mod-Deg, moderate degeneration group; Seve-Deg, severe degeneration group; Hete-Deg, heterogeneous degeneration group; PVBI, psoas vertebral body index; PLVBI, paralumbar vertebral body index; FI, fat infiltration; M, male; F, female; NS, no significance; C7PL, coronal C7 plumb line; Max cobb, coronal maximum Cobb angle; TK, thoracic kyphosis; LL, lumbar lordosis; SS, sacral slope; PI, pelvic incidence; PT, pelvic tilt; SVA, sagittal vertical axis; L1PA, L1 pelvic angle; L1PA offset, calculated as L1PA− (0.5×PI−21°); T4PA, T4 pelvic angle; T4–L1PA mismatch, calculated as T4PA–L1PA; UIV, upper instrumented vertebra; LIV, lower instrumented vertebra; Last FU, last follow-up over 1 year; ODI, Oswestry Disability Index; VAS, Visual Analog Scale; EBL, estimated blood loss; PJK, proximal junctional kyphosis; PJF, proximal junctional failure.

a)

Data was measured at L4 level.

b)

By Kruskal-Wallis test.

c)

By one-way analysis of variance.

d)

Overall comparisons were performed using the chi-square test and pairwise comparisons were further conducted using either the chi-square test or Fisher’s exact test, as appropriate, with Holm-Bonferroni adjustment.

e)

Fewer than 30% of patients had missing data.