Periodontitis, a major inflammatory disease of the oral cavity that can cause low-grade systemic inflammation, has been suggested to influence the development of comorbidities. Multiple systemic inflammatory mechanisms are common in the development of periodontal disease and atherosclerosis. Observational studies conducted worldwide have reported that periodontal disease may independently influence the progression of atherosclerotic disease. However, there is still insufficient evidence to demonstrate the causal relationship. This review describes the association between periodontal disease and arteriosclerosis-related diseases with the latest findings.

One fifth of the world population live in East Asia comprising Japan, Korea, and China where ischemic heart disease, a major component of atherosclerotic cardiovascular disease (ASCVD), is the second most frequent cause of death. Each of low-density lipoproteins (LDL), remnant lipoproteins, and lipoprotein(a), summarized as non-high-density lipoproteins (non-HDL) or apolipoprotein B (apoB) containing lipoproteins, causes ASCVD. However, a significant proportion of the evidence on lipoproteins and lipoprotein cholesterol with risk of ASCVD came from White people mainly living in Europe and North America and not from people living in East Asia or of East Asian descent. With a unique biological, geohistorical, and social background in this world region, East Asians have distinctive characteristics that might have potential impact on the association of lipoproteins and lipoprotein cholesterol with risk of ASCVD. Considering the movement across national borders in the World, understanding of lipoprotein and lipoprotein cholesterol evidence on ASCVD in East Asia is important for both East Asian and non-East Asian populations wherever they live in the World.

In this review, we introduce the biological features of lipoproteins and lipoprotein cholesterol and the evidence for their association with risk of ASCVD in East Asian and European populations. We also provide an overview of guideline recommendations for prevention of ASCVD in these two different world regions. Finally, specific preventive strategies and future perspectives are touched upon.

Aim: To date, PM_2.5-associated vascular damage in metabolic abnormalities has remained controversial. We knew little about the vascular damage of PM_2.5 constituents. Thus, this study aimed to investigate the relationship between long-term exposure to PM_2.5 and its constituents and vascular damage in metabolic abnormalities.

Methods: A total of 124,387 participants with metabolic abnormalities (defined as at least one metabolic disorder, such as obesity, elevated blood pressure, elevated triglyceride level, elevated fasting glucose level, or low HDL cholesterol level) were recruited in this study from 11 representative centers in China between January 2011 and December 2017. PM_2.5 and its constituents (black carbon [BC], organic matter [OM], sulfate [SO₄²⁻], nitrate [NO₃⁻], and ammonium salts [NH₄^＋]) were extracted. Elevated brachial-ankle pulse wave velocity (baPWV) (≥ 1,400 cm/s) and declined ankle-brachial index (ABI) (＜0.9) indicated vascular damage. Multivariable logistic regression and Quantile g-Computation models were utilized to explore the impact on outcomes.

Results: Of the 124,387 participants (median age, 49 years), 87,870 (70.64%) were men. One-year lag exposure to PM_2.5 and its constituents was significantly associated with vascular damage in single pollutant models. The adjusted odds ratios (OR) for each 1-µg/m³ increase in PM_2.5 was 1.013 (95% CI, 1.012–1.015) and 1.031 (95% CI, 1.025–1.037) for elevated baPWV and decreased ABI, respectively. PM_2.5 constituents were also associated with vascular damage in multi-pollutant models. Among the PM_2.5 constituents, BC (47.17%), SO₄²⁻ (33.59%), and NH₄^＋ (19.23%) have the highest contribution to elevated baPWV and NO₃⁻ (47.89%) and BC (23.50%) to declined ABI.

Conclusion: Chronic exposure to PM_2.5 and PM_2.5 constituents was related to vascular damage in the abnormal metabolic population in China. The heterogeneous contribution of different PM_2.5 constituents to vessel bed damage is worthy of attention when developing targeted strategies.

Aims: Serum phosphate control is crucial for the progression of vascular and valvular calcifications. Strict phosphate control is recently suggested; however, there is a lack of convincing evidence. Therefore, we explored the effects of strict phosphate control on vascular and valvular calcifications in incident patients undergoing hemodialysis.

Methods: A total of 64 patients undergoing hemodialysis from our previous randomized controlled trial were included in this study. Coronary artery calcification score (CACS) and cardiac valvular calcification score (CVCS) were evaluated using computed tomography and ultrasound cardiography at baseline and 18 months after the initiation of hemodialysis. The absolute changes in CACS (ΔCACS) and CVCS (ΔCVCS) and the percent change in CACS (%ΔCACS) and CVCS (%ΔCVCS) were calculated. Serum phosphate level was measured at 6, 12, and 18 months after the initiation of hemodialysis. Moreover, phosphate control status was evaluated using the area under the curve (AUC) by the amount of time spent with a serum phosphate level of ≥ 4.5 mg/dL and the extent to which this threshold exceeded over the observation period.

Results: ΔCACS, %ΔCACS, ΔCVCS, and %ΔCVCS were significantly lower in the low AUC group than in the high AUC group. ΔCACS and %ΔCACS were also significantly lower. ΔCVCS and %ΔCVCS tended to be lower in patients whose serum phosphate level never exceeded 4.5 mg/dL than in those whose serum phosphate level continuously exceeded 4.5 mg/dL. AUC significantly correlated with ΔCACS and ΔCVCS.

Conclusion: Consistently strict phosphate control may slow the progression of coronary and valvular calcifications in incident patients undergoing hemodialysis.

Aim: We compared the efficacy and safety of pitavastatin/ezetimibe fixed-dose combination with those of pitavastatin monotherapy in patients with hypercholesterolemia.

Methods: This trial was a multicenter, randomized, double-blind, active-controlled, parallel-group trial. A total of 293 patients were randomly assigned into four groups receiving 2 mg pitavastatin, 4 mg pitavastatin, 2 mg pitavastatin/10 mg ezetimibe (K-924 LD), and 4 mg pitavastatin/10 mg ezetimibe (K-924 HD) once daily for 12 weeks.

Results: The percentage changes in low-density lipoprotein cholesterol (LDL-C), the primary endpoint, were −39.5% for 2 mg pitavastatin, −45.2% for 4 mg pitavastatin, −51.4% for K-924 LD, and −57.8% for K-924 HD. Compared with pitavastatin monotherapy, the pitavastatin/ezetimibe fixed-dose combination significantly reduced LDL-C, total cholesterol, and non-high-density lipoprotein cholesterol. Meanwhile, the cholesterol synthesis marker, lathosterol, was significantly decreased with pitavastatin monotherapy and the pitavastatin/ezetimibe fixed-dose combination, although the decrease was attenuated in the latter. On the other hand, the cholesterol absorption markers, beta-sitosterol and campesterol, were reduced with the fixed-dose combination but not with pitavastatin monotherapy. The incidence of adverse events and adverse drug reactions was not significantly different between the two groups receiving the fixed-dose combination and monotherapy. The mean values of laboratory tests that are related to liver function and myopathy increased but remained within the reference range in all groups.

Conclusions: The pitavastatin/ezetimibe fixed-dose combination showed an excellent LDL-C-reducing effect by the complementary pharmacological action of each component, and its safety profile was similar to that of pitavastatin monotherapy (ClinicalTrials.gov Identifier: NCT04289649).

Aim: To date, no studies representing the Southeast Asian population have validated the Pulmonary Embolism Severity Index (PESI) and 2019 European Society of Cardiology (ESC) risk stratification. Therefore, this study aimed to validate the PESI score, simplified PESI (sPESI), PESI risk classification, and 2019 ESC risk stratification in Southeast Asian patients with acute pulmonary embolism (APE).

Methods: The present study is a 10-year cross-sectional study. Here, risk regressions were conducted to identify the PESI risk classification, sPESI, and 2019 ESC risk stratification as predictors for 30-day all-cause and PE-related mortalities. Receiver operating characteristic (ROC) curves were constructed to determine the diagnostic ability of the PESI score, sPESI score, PESI risk classification, and 2019 ESC risk stratification to predict 30-day mortality.

Results: A total of 696 patients (male, 286; female, 410; mean age, 57.7±15.7 years) were included in this study from 2011 to 2020. The risk of 30-day all-cause mortality progressively increased with the 2019 ESC risk stratification, being approximately 6-fold higher in the high-risk than in the low-risk class [risk ratio: 6.24 (95% confidence interval (CI), 3.12, 12.47), P＜0.001]. The risk of 30-day all-cause mortality with the PESI risk classification also increased with the risk classes, being approximately 6-fold higher in class V than in class I [adjusted risk ratio: 5.91 (95% CI, 2.25, 15.51), P＜0.001]. The highest area under the receiver operating characteristic curve (AuROC) of the predictive model was the PESI score [AuROC=0.733 (95% CI, 0.685, 0.782)].

Conclusion: Our study represents a good validation of the PESI and 2019 ESC risk stratification to predict 30-day mortality after APE diagnosis in the Southeast Asian population.

Aim: Adverse limb events after endovascular therapy (EVT) are a major concern. This study aimed to investigate the relationship between serum malondialdehyde-modified low-density lipoprotein (MDA-LDL) level, a potentially potent indicator of atherosclerosis, and clinical outcomes after EVT in patients with lower extremity arterial disease (LEAD).

Methods: A total of 208 LEAD patients who underwent EVT and MDA-LDL measurements were retrospectively analyzed. Those with chronic limb-threatening ischemia (CLTI) were included in the CLTI subgroup (n=106). Patients were further categorized into the High or Low MDA-LDL groups according to the cut-off value calculated by receiver operating characteristic analysis. Major adverse limb events (MALE), a composite of cardiovascular death, limb-related death, major amputation, and target-limb revascularization, were evaluated.

Results: MALE occurred in 73 (35%) patients. The median follow-up interval was 17.4 months. The MDA-LDL cut-off values were 100.5 U/L (area under the curve [AUC] 0.651) in the overall population and 98.0 U/L (AUC 0.724) in the CLTI subgroup. Overall, the High MDA-LDL group showed significantly higher total cholesterol (189.7±37.5 mg/dL vs. 159.3±32.0 mg/dL, p＜0.01), low-density lipoprotein cholesterol (114.3±29.7 mg/dL vs. 87.3±25.3 mg/dL, p＜0.01), and triglyceride (166.9±91.1 mg/dL vs. 115.8±52.3 mg/dL, p＜0.01) than the Low MDA-LDL group. Multivariate Cox regression analyses revealed that MDA-LDL and C-reactive protein were independent predictors of MALE. In the CLTI subgroup, MDA-LDL was an independent predictor of MALE. The High MDA-LDL group showed worse MALE-free survival rates than the Low MDA-LDL group in overall (p＜0.01) and in the CLTI subgroup (p=0.01).

Conclusions: Serum MDA-LDL level was associated with MALE after EVT.

Aims: The study aimed to investigate low-density lipoprotein cholesterol (LDL-C) goal achievement rates in patients receiving LDL-C-lowering therapy using recent real-world data, following the 2017 revision of the Japan Atherosclerosis Society Guidelines for Prevention of Atherosclerotic Cardiovascular Diseases (JAS GL2017).

Methods: Patients with documented LDL-C test results were extracted from the Medical Data Vision claims database between July 2018 and June 2021 and divided into three groups according to JAS GL2017: primary prevention high risk (Group I, LDL-C goal ＜120 mg/dL), secondary prevention (Group II, LDL-C goal ＜100 mg/dL), and secondary prevention high risk (Group III, LDL-C goal ＜70 mg/dL).

Results: The mean LDL-C value was 108.7 mg/dL (n=125,235), 94.4 mg/dL (n=57,910), and 90.6 mg/dL (n=33,850) in Groups I, II, and III, respectively. Intensive statin monotherapy (pitavastatin, rosuvastatin, or atorvastatin) was the most frequently prescribed lipid-lowering treatment (21.6%, 30.8%, and 42.7% in Groups I, II, and III, respectively), followed by ezetimibe (2.5%, 7.1%, and 8.5% in Groups I, II, and III, respectively). LDL-C goals were achieved by 65.5%, 60.6%, and 25.4% of patients overall in Groups I, II, and III, respectively. Achievement rates were 83.9%, 75.3%, and 29.5% in patients prescribed intensive statin monotherapy and 82.3%, 86.4%, and 46.4% in those prescribed statin and ezetimibe combinations in Groups I, II, and III, respectively. In Group III, the proportion of patients with familial hypercholesterolemia prescribed statin and ezetimibe combinations achieving LDL-C goals was low (32.5%).

Conclusions: The proportion of patients achieving LDL-C goals for secondary prevention in the high-risk group remains low even with statin and ezetimibe combination therapy.

Aim: Chronic inflammation is associated with atherosclerosis development. Chronic kidney disease (CKD) is an independent risk factor for cardiovascular events and is associated with chronic inflammation. We aimed to investigate the influence of C-reactive protein (CRP), an important marker of inflammation, on the clinical outcomes of patients with CKD and stable coronary artery disease (CAD) undergoing percutaneous coronary intervention (PCI).

Methods: Among patients with stable CAD and CKD who underwent PCI, 516 patients whose CRP levels were available before the PCI procedure were identified. The patients were divided into two groups according to the CRP levels: those with CRP ≥ 2.0 mg/L (high-CRP group) and those with CRP ＜2.0 mg/L (low-CRP group). The primary endpoint of this study was the occurrence of major adverse cardiac events (MACE), defined as a composite of cardiac death, myocardial infarction, and unplanned revascularization.

Results: Overall, the mean age of the patients was 72.5±9.7 years, and 20.7% were female. The median CRP level was 1.43 mg/L (0.6–4.9 mg/L). The median follow-up period was 3.6 years. The occurrence of MACE was significantly higher in the high-CRP group than in the low-CRP group (log-rank p＜0.001). Notably, the incidence rate of cardiac death was significantly higher in the high-CRP group (log-rank p＜0.001). According to the multivariable analysis, CRP level ≥ 2.0 mg/L was found to be a significant predictor of MACE (hazard ratio [HR]: 1.54, 95% confidence interval [CI]: 1.04–2.28, p=0.003), as well as estimated glomerular filtration rate (HR: 0.98, 95% CI: 0.97–0.99, p＜0.01).

Conclusion: High-CRP levels adversely affect long-term cardiac events in patients with stable CAD and CKD.

Aim: Experimental studies report that intermediate-density lipoprotein (IDL), the precursor of low-density lipoprotein, promotes atherosclerotic plaque formation. However, whether IDL is involved in the development of atherosclerosis in humans is still unclear. The aim of this community-based study is to examine the association between IDL particle (IDL-P) concentrations and the 5-year progression of carotid atherosclerosis.

Methods: Baseline IDL-P concentrations were measured using nuclear magnetic resonance spectroscopy in 927 participants aged 45–74 years with no history of cardiovascular disease (CVD) at baseline. To estimate the association between baseline IDL-P concentrations and 5-year progression of carotid atherosclerosis, indicated by atherosclerotic plaque progression and changes in total plaque area (TPA), multivariable-adjusted regression was employed.

Results: During the 5-year follow-up period, 45.8% of participants developed new plaques. Baseline IDL-P concentrations were significantly associated with the progression of carotid atherosclerosis. Participants in the highest quartile of IDL-P concentrations exhibited 1.36-fold (95% confidence interval [CI]: 1.09–1.68) increased progression of carotid plaque and 1.67-fold (95% CI: 1.04–2.69) higher TPA than those in the lowest quartile. These relationships were independent of baseline concentrations of low-density lipoprotein particles and very-low-density lipoprotein particles and their subclasses.

Conclusions: Elevated IDL-P concentrations were independently associated with the progression of carotid atherosclerosis, suggesting that IDL-P is a novel risk factor for the development of atherosclerosis.

Aims: Chronic thromboembolic pulmonary hypertension (CTEPH) is a condition with a poor prognosis in which the pulmonary arteries are occluded by organized thrombi. Pulmonary thromboendarterectomy (PEA) is an effective treatment for CTEPH; however, the literature on its histopathological examination is lacking. This study aimed to investigate the histopathological findings and protein and gene expression in PEA specimens, establish an optimal histopathological evaluation method, and clarify the mechanisms of thrombus organization and disease progression in CTEPH.

Methods: In total, 50 patients with CTEPH who underwent PEA were analyzed. The patients were categorized according to their clinical data into two groups: good and poor postoperative courses. The relationship between their histopathological findings and the clinical course was examined. Immunohistochemical studies confirmed the expression of oxidants, antioxidants, and smooth muscle cell (SMC) differentiation markers and their changes during the progression of thrombus organization. The mRNA expression analysis of 102 samples from 27 cases included oxidants, antioxidants, and vasoconstrictor endothelin-1.

Results: In the PEA specimens, colander-like lesions (aggregations of recanalized blood vessels with well-differentiated SMCs) were significantly more common in the good postoperative course group than in the poor postoperative course group; analysis of proteins and genes proposed that oxidative and antioxidant mechanisms were involved. In the colander-like lesions, there was an increase in endothelin-1 mRNA and protein expression of endothelin receptor A.

Conclusions: Colander-like lesions in PEA specimens must be identified. Additionally, SMC differentiation in recanalized vessels and the expression of vasoconstrictors and their receptors may contribute to the progression of CTEPH.

Aim: Patients with chronic limb-threatening ischemia (CLTI) have a high bleeding risk (HBR) and mortality rate. The 2-year life expectancy is an important factor in deciding the appropriate treatment strategy. This study aimed to assess the influence of HBR on the prognosis of patients with CLTI.

Methods: A total of 259 patients with CLTI who underwent endovascular therapy (EVT) (mean age, 76.2 years; male, 62.9%) between January 2018 and December 2019 were evaluated. The Academic Research Consortium for HBR (ARC-HBR) criteria were applied to each patient, and the ARC-HBR scores were calculated. The cut-off score for predicting all-cause mortality within two years was derived using a survival classification and regression tree (CART) model. Causes of death and the association between ARC-HBR scores and major bleeding events within two years were also investigated.

Results: Based on the CART model, patients were divided into three groups (low HBR score 0–1.0, 48 patients; moderate HBR score 1.5–3.0, 176 patients; and high HBR score ≥ 3.5, 35 patients). During the study period, 82 patients (39.6%) died due to cardiac (n=23) and non-cardiac causes (n=59). All-cause mortality increased significantly with increasing ARC-HBR scores. Cox multivariate analysis revealed a significant association between high ARC-HBR scores and the risk of all-cause mortality within two years. Major bleeding events increased significantly with increasing ARC-HBR scores.

Conclusions: The ARC-HBR score could predict 2-year mortality in patients with CLTI who underwent EVT. Thus, this score can help determine the best revascularization strategy for patients with CLTI.

Aims: Eicosapentaenoic acid (EPA) has shown beneficial effects on coronary plaque stabilization. Based on our previous study, we speculated that EPA might be associated with the development of healed plaques and might limit thrombus size. This study aimed to elucidate the association between EPA and arachidonic acid (AA) ratios and various plaque characteristics in patients with plaque rupture.

Methods: A total of 95 patients with acute coronary syndrome (ACS) caused by plaque rupture who did not take lipid-lowering drugs and underwent percutaneous coronary intervention using optical coherence tomography (OCT) were included. Clinical characteristics, lipid profiles, and OCT findings were compared between patients with lower and higher EPA/AA ratios (0.41) according to the levels in the Japanese general population.

Results: In the high EPA/AA (n=29, 30.5%) and low EPA/AA (n=66, 69.5 %) groups, the high EPA/AA group was significantly older (76.1 vs. 66.1 years, P＜0.01) and had lower peak creatine kinase (556 vs. 1651 U/L, P=0.03) than those with low EPA/AA. Similarly, patients with high EPA/AA had higher prevalence of layered and calcified plaque (75.9 vs. 39.4 %, P＜0.01; 79.3 vs. 50.0 %, P＜0.01, respectively) than low EPA/AA group. Multivariate logistic regression analysis demonstrated that a high EPA/AA ratio was an independent factor in determining the development of layered and calcified plaques.

Conclusion: A high EPA/AA ratio may be associated with the development of layered and calcified plaques in patients with plaque rupture.

Aim: Studies investigating the relationship between pulse pressure (PP) and prognosis in acute ischemic stroke remain limited. Thus, in this study, we aim to determine whether changes in PP in the early phase of ischemic stroke are associated with neurological deterioration or stroke recurrence.

Methods: Patients who participated in the Acute Aspirin Plus Cilostazol Dual Therapy for Non-cardiogenic Stroke Patients Within 48 Hours of Symptom Onset (ADS) trial were included in this study. We then divided the patients into four groups (low-low, low-high, high-low, high-high) according to low or high PP both on admission and 24 h after admission. The threshold PP calculated by receiver operating characteristic curve analysis of PP on admission for neurological deterioration within 14 days and recurrent ischemic stroke/transient ischemic attack (TIA) within 3 months was 69 mmHg.

Results: Neurological deterioration within 14 days was observed in 118 patients (10.6%), whereas recurrent ischemic stroke/TIA within 3 months was noted in 34 patients (3.2%). Among these four groups, both neurological deterioration within 14 days (odds ratio [OR] 2.09, 95% confidence interval [CI] 1.12–3.91; p=0.0209) and recurrent ischemic stroke/TIA within 3 months (OR 4.80; 95% CI 1.62–14.86; p=0.0064) were significantly more frequent in the high-high group than in the low-low group as per the results of our multivariate analysis. In addition, neurological deterioration within 14 days was significantly higher in the high-low group than that in the low-low group (OR 2.70; 95% CI 1.44–5.05; p=0.0019).

Conclusions: High PP during the acute phase of ischemic stroke appears to be associated with ischemic stroke recurrence and neurological deterioration, particularly if PP is elevated both on admission and 24 h later after admission.

Aim: This study aimed to clarify whether cholesterol crystals (CCs) are the main trigger of innate inflammation in human spontaneously ruptured aortic plaques (SRAPs).

Methods: This study included 260 SRAPs collected during nonobstructive general angioscopy (NOGA) from 126 patients with confirmed or suspected coronary artery disease. Interleukin (IL)-6 levels in SRAPs were measured. IL-6 levels in the Valsalva sinus and femoral or brachial arteries were measured. IL-6 ratios (the IL-6 level in SRAPs and arteries divided by the IL-6 level at the Valsalva sinus at the beginning of the aorta) were calculated. Quantitative analysis of CCs was performed from SRAPs. The correlation between the count of CCs and IL-6 levels in SRAPs and that between the counts of CCs and IL-6 ratios in SRAPs were analyzed.

Results: The IL-6 levels in SRAPs were 3.4 [2.1, 7.2] pg/mL, and the IL-6 ratio (median [interquartile range]) in SRAPs was 1.10 [1.00, 1.26]. CCs were detected in 94 of 260 SRAPs (36%). The count of CCs was 11,590 (95% confidence interval, 2,386–30,113) per 10 mL in CC-positive samples. There was a moderate correlation between the counts of CCs and IL-6 ratios in SRAPs (r=0.49, r＜0.0001), whereas there was no correlation between the count of CCs and IL-6 levels in SRAPs. The IL-6 ratios of the brachial and femoral arteries were 1.06 (95% CI, 0.99–1.20) and 1.11 (95% CI, 1.04–1.20), respectively.

Conclusions: CC is the main trigger of IL-6 production through innate inflammatory response in human SRAPs in situ.

Aims: It is known that there are sex differences in vascular endothelial function and the development of chronic kidney diseases; however, it remains unclear whether sex differences influence the association between vascular endothelial function and renal prognosis.

Methods: To clarify the relationship between vascular endothelial function and longitudinal eGFR changes in male and female patients with cardiovascular risk factors, we retrospectively evaluated 341 patients (176 males and 165 females) with cardiovascular risk factors in whom vascular function was assessed by flow-mediated dilation (FMD) and brachial-ankle pulse wave velocity (baPWV) and in whom 24-month longitudinal eGFR values were recorded after the vascular function examinations. Associations of values of FMD and baPWV with values of eGFR slope were statistically analyzed.

Results: Simple regression analysis showed that the value of FMD was positively associated with eGFR slope in females (p=0.001) and non-smoking males (p=0.033) but not in smoking males. Multiple regression analysis showed that the value of FMD remains a positive contributor for eGFR slope in females (p=0.001) and non-smoking males (p=0.045) but not in smoking males. In contrast, values of baPWV had no significant association with eGFR slope regardless of sex and cigarette smoking.

Conclusions: In individuals with cardiovascular risk factors, evaluation of vascular endothelial function enables prediction of renal prognosis in females and non-smoking males.

Aim: Increasing evidences suggest that HALP is an independent predictor of prognosis in patients with inflammation. However, the relationship between HALP and prognosis in patients with cerebral venous sinus thrombosis (CVST) has not been studied. In this study, we aimed to evaluate the prognosis values of HALP in acute or subacute CVST and explore the new prognostic model for CVST.

Methods: Consecutive patients who were diagnosed as having acute and subacute CVST were retrospectively investigated. We determined the patients’ functional outcomes by modified Rankin Scale (mRS). Multivariate logistic regression analysis was used to assess the relationship between factors and poor functional outcomes. The area under the ROC curve (AUC) was estimated to evaluate the ability of markers and models in predicting clinical prognosis. The prognostic model was presented as nomogram. In addition, the decision curve analysis (DCA) was used to analyze the benefit of this model. Furthermore, survival curves were described by the Kaplan-Meier analysis.

Results: A total of 270 patients were included of which 31 had poor outcome. Multivariable logistic regression analysis demonstrated HALP (OR=0.978, 95%CI: 0.958-0.999, P=0.039) was a protective predictor of outcome. The AUC of HALP was 0.749 (95% CI: 0.633-0.865, P=0.044). DCA demonstrated that this model significantly improved risk prediction at threshold probabilities of CVST at 0 to 85% compared to ISCVT-RS scores. Patients with higher HALP (P=0.006) presented higher overall survival rates.

Conclusion: HALP may be a potential protective marker in acute and subacute CVST patients. The new prognostic model with HALP had potentially better value for acute and subacute CVST patients.