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Article

Cardiovascular Risk Assessments and Ultrasound-Assisted Re-Stratification in Patients with Inflammatory Bowel Disease (IBD) †

by
Giuseppe Blando
1,*,‡,
Arianna Toscano
2,‡,
Anna Viola
1,
Laura Patanè
1,3,
Sabrina Verachtert
2,
Carmela Morace
2,
Giovanni Squadrito
2,
Giuseppe Mandraffino
2,
Angela Alibrandi
4,
Walter Fries
1 and
Giuseppe Costantino
1
1
IBD-Unit, Department of Clinical and Experimental Medicine, University of Messina, 98122 Messina, Italy
2
Division of Internal Medicine, Department of Clinical and Experimental Medicine, University of Messina, 98125 Messina, Italy
3
Gastroenterology and Hepatology Unit, Department of Health Promotion, Mother & Child Care, Internal Medicine & Medical Specialties (PROMISE), University of Palermo, 90133 Palermo, Italy
4
Unit of Statistical and Mathematical Sciences, Department of Economics, University of Messina “Gaetano Barresi”, 98124 Messina, Italy
*
Author to whom correspondence should be addressed.
†
This study was awarded the best poster presentation at the Spring Meeting of the Young Researchers of SID: SIGG, SIIA, SIMI, SIPREC, SISA. Rimini 6–8 April 2025; Italy.
‡
These authors contributed equally to this work.
Gastrointest. Disord. 2025, 7(4), 59; https://doi.org/10.3390/gidisord7040059
Submission received: 30 June 2025 / Revised: 13 September 2025 / Accepted: 23 September 2025 / Published: 24 September 2025
Versions Notes

Abstract

Background: Patients with ulcerative colitis (UC) and Crohn’s disease (CD) have an increased cardiovascular risk (CVR). The aim of the present study was to stratify the CVR of patients with UC and CD according to the most recent guidelines via carotid ultrasound (US) to detect subclinical atherosclerotic disease. Methods: Demographic and disease-related data of consecutive patients with IBD were prospectively collected along with information on blood pressure, body mass index, lipid profile, and concomitant medications. CVR was stratified at inclusion according to the most recent version of Systematic Coronary Risk Evaluation 2 (SCORE2) and re-stratified after carotid US when subclinical atherosclerotic disease was detected. Results: A total of 166 patients aged ≥ 40 years with IBD were included. Before carotid US evaluation, 43.4% of patients with IBD were at moderate risk, 40.3% at high risk, and 16.3% at very high risk. With carotid US, subclinical atherosclerosis was diagnosed in 48% of patients, leading to CVR re-stratification from moderate to high in 18% of patients and from high to very high in 4% of patients. The only predictive factor for re-stratification was failure with more than two biologics (p = 0.047; OR 2.187, 95% CI: 1.004–4.741). Conclusions: CVR is considerably prevalent in patients with IBD. Carotid US may help to re-classify CVR and should be considered as a risk modifier in patients at intermediate risk. Screening for CVD risk factors should be recommended in IBD.

1. Introduction

IBDs, including Crohn’s disease (CD) and ulcerative colitis (UC), are chronic relapsing and remitting diseases that affect the gastrointestinal tract. While incidence has stabilized in Western countries, newly industrialized regions such as Asia, the Middle East, South America, Eastern Europe, and Africa are experiencing a sharp rise, with over 10 million cases projected by 2050 [1].
There is a growing body of evidence that patients with IBD have an increased risk for cardiovascular disease (CVD), with some differences between Crohn’s disease and ulcerative colitis in terms of myocardial infarction (MI), ischemic heart disease (IHD), cerebrovascular accident (CVA), major cardiovascular event (MACE), atrial fibrillation, and premature coronary artery disease frequency. Also, ulcerative colitis is associated with an increased risk of heart failure [2,3,4,5].
An increased incidence of acute arterial events, including peripheral artery disease, was reported, especially in younger patients with severe intestinal disease activity [6]. Reports on mortality in patients with IBD due to CVD are controversial, with some identifying CVD as an important factor [7,8], while others disagree [9].
Among the mechanisms involved in the development of atherosclerosis, systemic inflammation is predominant and promotes atherogenesis, thereby contributing to atheromatous plaque progression and ultimately favoring thrombotic complications [10,11]. Studies on the association between IBD and cardiovascular disease have shown that the risk of ischemic heart disease is more prominent in females and in younger patients (<50 years). Further contributing factors for CVR include obesity, steroid use, dyslipidemia, smoking and diet [5], which is similarly seen in other immune-mediated inflammatory disorders (IMIDs), e.g., psoriatic arthritis [12], rheumatoid arthritis [13], ankylosing spondylitis [14], and systemic lupus erythematosus [15].
A major problem was prompted by the black-box warning by regulatory agencies on Janus kinase inhibitors (JAKis) [16]. JAKis are small molecules that target pro-inflammatory cytokine signaling through the JAK-STAT pathway, and they are approved for treating moderate-to-severe ulcerative colitis and, more recently, Crohn’s disease. A growing body of evidence indicated that JAKis were associated with increased risks of MACEs and venous thromboembolism events. This warning was based on the results of the ORAL surveillance study [17], a comparison study which reported an increased risk of MACEs, among other adverse events, with anti-TNF use in patients aged over 50 years with rheumatoid arthritis and at least one cardiovascular risk (CVR)-factor treated with JAKis. This finding was also subsequently confirmed for thrombosis risk in patients with rheumatoid arthritis [18].
Similar findings, i.e., an excess risk induced by JAkis compared to other therapies such as anti-TNFs or anti-IL23 antibodies, however, were not replicated in patients with IBD [19,20]. Our study aimed to stratify the cardiovascular risk (CVR) of patients with IBD using the most recent scores developed by the European Society of Cardiology (ESC) (SCORE2 [21], SCORE2-Older People (SCORE2-OP), and SCORE2-Diabetes [22]) together with carotid ultrasonography (US) to detect subclinical atherosclerosis and, consequently, to re-classify CVD risk. Similar approaches have been applied in patients with rheumatological diseases [23,24,25].

2. Results

2.1. Baseline Assessment

A total of 166 patients were included (92 with UC and 74 with CD), with 48% being female, and the median age was 59 years (IQR 51–66). The enrolled patients’ baseline characteristics are summarized in Table 1.
Patients with CD and UC differed in terms of their cardiometabolic profiles: CD patients had a higher smoking rate (32% vs. 16%, p < 0.001) and lower median levels of total cholesterol (186 mg/dL vs. 213 mg/dL in UC patients, p < 0.001), as well as lower LDL-C levels (153,5 mg/dL in UC vs. 130 mg/dL in UCD, p < 0.001), and no statistically significant differences were found in terms of triglyceride levels. Comparable results were observed between the two groups regarding diabetes, chronic kidney disease prevalence, and hypertension. Previous myocardial infarction was reported in three UC patients, while four patients (one UC and three CD) had undergone coronary revascularization. Previous stroke or TIA episodes were found in eight patients (three UC and five CD), and three patients (two UC and one CD) had acute arterial events.
As expected, patients with CD had a higher rate of previous surgery (p < 0.001).
Overall, most patients were in clinical remission, with only 22% reporting active disease, and no differences were found between UC and CD. Treatment at baseline included steroids (systemic or low-bioavailability steroids) in 15% of patients and biological therapy in 67% of patients (mostly anti-TNFs with no differences among CD and UC).

2.2. Re-Stratification After Carotid Sonography

Following SCORE risk chart stratification at baseline, patients with moderate, high, and very high cardiovascular risks had values of 43%, 40%, and 16%, respectively. All enrolled patients were from Italy, which is classified as a moderate-risk area, and none of the patients could achieve a score corresponding to a low cardiovascular risk at the inclusion date [21,26].
After carotid US subclinical atherosclerosis detection in 48% of patients, patients with carotid stenosis (>50%) were allocated in the very high-risk category (4%), whereas patients with milder lumen restrictions were moved to the next higher category (48%). A total of 36 out of 166 patients (22%) were re-stratified, as shown in Table 2. CVR increased from moderate to high in 18% of patients and from high to very high in 4% of the overall population. No differences were observed between CD and UC.

2.3. Risk Factors for CVR Re-Stratification

Risk factors for CVR re-classification were assessed with the following variables using stepwise logistic regression: the type of IBD, disease duration, active disease, previous IBD surgery, conventional treatment, steroid use at baseline, biologic therapy at baseline, failure of more than two biologics, and the presence of spondyloarthritis. The only predictive factor for the outcome was failure of more than two biologics (p = 0.047; OR 2.187, 95% CI: 1.004–4.741).

3. Discussion

The present study showed that using the SCORE2 algorithm, implemented using SCORE-OP and SCORE-Diabetes, 16.3% of patients aged ≥ 40 years with IBD were allocated in the very high-risk CVR group and that, after carotid US, this figure increased to 20%. Our data differ from those of a former Spanish study indicating the need for re-stratification into the very high-risk category in 36% of patients with IBD [27]. In the Spanish study using the previous algorithm, the SCORE algorithm [28], the authors compared a mixed IBD population versus a healthy control group with the exclusion of diabetic patients. A significantly higher frequency of re-classification was found in patients with IBD compared to the controls (35% vs. 24%, p = 0.030). According to contemporary epidemiological data, Spain and Italy were considered as low-CVR countries during the development of the risk charts (SCORE, 2016) when European countries were divided into low- and high-risk countries, whereas Italy was then re-classified into a moderate-risk country in 2021 (SCORE2) when European countries were divided into four categories (low-, moderate-, high-, and very high-risk) [29]; considering these premises, in that study, the majority of Spanish patients before carotid US were classified in the low-risk category but reached the very high-risk category after re-stratification. In the present paper, only patients with significant carotid lumen stenosis were allocated in the very high-risk category, whereas patients with milder alterations on carotid US advanced to the next unfavorable category. Finally, a Brazilian study using the Framingham risk score in a small sample of patients with IBD did not find statistically significant differences for overall CVR between patients with IBD and the controls despite numerically differences of 30.8% vs. 13.5%, respectively [30].
SCORE2 provides a risk estimate by considering fatal and non-fatal cardiovascular events, whilst SCORE considers only cardiovascular mortality. Moreover, SCORE2 has been updated continuously using cardiovascular event rates, whereas SCORE was based on data collected before 1986. SCORE2 is superior in estimating the total burden of cardiovascular diseases, particularly in younger subjects (although the minimum age for the estimates is 40 years old). Ultimately, SCORE2 considers the impact of competitive risks, i.e., non-cardiovascular mortality. Defined according to different levels of CVR, SCORE2′s recalibration in four distinct European regions avoids the use of low-quality data drawn from cohort studies or those from national surveys [21]. Only one risk factor for re-stratification was identified in the present study, i.e., having failed two or more advanced therapies, which may indicate a more aggressive disease and probably the need for more prolonged steroid use and longer periods with systemic inflammation. In our cohort, at enrollment in the study, around 80% of patients were in clinical remission, while 16% of patients were concurrently on steroids. Systemic inflammatory activity and steroid use are hypothesized to be major drivers for CVR [31,32] in the short and long terms, but the transversal character of the present study, which measures the sum of antecedent events potentially leading to atherosclerosis at an arbitrary timepoint, makes it unlikely that the momentary states of disease activity may have influenced the results.
From a clinical perspective, after the CVR assessment, the next step should be to undertake measures to prevent atherosclerosis onset or progression and to consider treatment options in terms of safety and effectiveness [1,33].
Of course, interventions on modifiable risk factors, e.g., tobacco use, diet, obesity, and sedentary lifestyle, should be considered, as well as the pharmacologic treatment of dyslipidemia [34] when carotid plaques are presence. In the present study, the median total and LDL cholesterol values for both CD and UC patients were found to be increased, but compared to UC, CD patients had higher total cholesterol and HDL cholesterol values; conversely, UC patients exhibited a higher LDL cholesterol value and were more frequently on lipid-lowering therapy, underscoring the need of widening blood biochemistry beyond routine intestinal disease-specific markers.
Interestingly, in a recent study from the Swedish National Patients Register, cardiovascular disease, when present before a diagnosis of IBD, represented a risk factor for developing IBD later [35]. Thus, the occurrence of CVD after IBD diagnosis is not necessarily considered an effect of gut inflammation. This finding is reminiscent of an old hypothesis stating that vascular injury and occlusion are involved in CD pathogenesis [36].
Finally, identifying methods for managing and minimizing CVR in patients with IBD via therapy represents a key clinical challenge. In a recent study on a very large database on patients with IBD on or without advanced biologic therapy, matched with propensity score analysis according to gender and comorbidities such as hypertension, diabetes, and dyslipidemia, together with the use of tobacco, aspirin, and lipid-lowering agents, cardiovascular events were lower in patients treated with advanced therapies [37]. In a recent meta-analysis, JAkis were associated with a risk reduction for MACEs, whereas vedolizumab was associated with an increased risk, possibly due to the less systemic action of the latter [2]. Conversely, in a network meta-analysis including different IMIDs, an increased risk of MACEs was identified for anti-IL 12/23, anti-TNFs, and Jakis, with Odds ratios ranging from 2.49 to 3.15, with the only exclusion being mirikizumab [38]. Vedolizumab was not included in this analysis because the authors concentrated on therapies equally indicated for all IMIDs. In view of these controversial data, it is difficult to determine the appropriate drug to offer to our patients. Excluding certain drug categories seems to represent the safest choice, but this hinders access to highly efficacious therapies. Some attempts to overcome this dilemma have been published in a very small number of studies, which showed that case-by-case evaluations in at-risk patients may effectively avoid major adverse events [39], in line with the current strategies in rheumatological patients [40].
The present study has several limitations. First, being a single-center study conducted in Italy, its generalizability to geographic regions with different baseline cardiovascular risk thresholds may be limited. The sample size, although adequate for a monocenter design, may not fully capture the heterogeneity of the IBD population, and the cross-sectional nature of the analysis precludes any assessment of causality or temporal changes.
Furthermore, this study only included patients aged ≥40 years. This age cut-off was set because the ESC CV risk stratification tools (SCORE-2, SCORE-2 OP, and SCORE-2 Diabetes) are designed for middle-aged and older adults. While methodologically appropriate, this may overlook early subclinical atherosclerosis in younger patients with IBD, limiting applicability to the broader IBD population. Finally, only carotid atherosclerosis was evaluated as a marker of subclinical cardiovascular disease. Other manifestations of subclinical atherosclerosis, such as coronary artery calcifications or peripheral arterial disease of the limbs, were not assessed, limiting our understanding of the total atherosclerotic burden in patients with IBD. This, however, represents a relative limitation of this study, as including these additional markers of subclinical atherosclerosis would likely have further reinforced the conclusions or unveiled an even higher overall cardiovascular risk in this patient population.
Despite the limitations, this study also has notable strengths. Foremost, it addresses the clinically relevant issue of elevated cardiovascular risk in IBD using real-world data from a representative IBD cohort with a substantial and well-balanced number of patients affected by both Crohn’s disease and ulcerative colitis. The cross-sectional design and consecutive patient inclusion enhance the robustness of the findings. Using updated ESC guidelines and standardized carotid ultrasound further supports the validity of the results. These findings offer practical guidance for cardiovascular screening in patients with IBD and are particularly timely in the current therapeutic landscape, especially considering the EMA warning regarding Jakis.

4. Materials and Methods

4.1. Study Design

The current study is a prospective monocentric study that includes consecutive patients with IBD from the IBD-Unit of AOU Policlinico “G Martino” of Messina.
Data of consecutive patients, both males and females, aged ≥40 years with an established diagnosis of CD and UC according to current guidelines and followed in our unit from August 2024 to December 2024 were included. All data were collected in an electronic database. All patients were able to understand and provide written consent for this study.
Patients with incomplete follow-up or incomplete data on clinical charts were excluded.
The study was approved by the local Ethics Committee under protocol n. 123-24 on 16 July 2024.

4.2. Outcomes

The primary outcome was re-classification of CVD risk after subclinical atherosclerosis identification via carotid ultrasound evaluation and risk factor identification for re-classification.

4.3. Data Collection

At baseline, the following data were collected for all groups: gender, age at date of evaluation, age at diagnosis, BMI, and smoking status. Clinical disease activity at the time of enrolment was assessed using the Harvey–Bradshaw index (HBI) for Crohn’s disease and the partial Mayo score (pMS) for ulcerative colitis. Disease activity was classified as remission, mild, moderate, or severe according to the aforementioned scores. Disease location, phenotype, and the presence of perianal disease, as well as UC disease extension, were registered according to the Montreal classification [41] for CD. Disease duration; previous and current IBD therapies, as well as a previous history of CD-related surgery; and extra-intestinal manifestations were also registered.
Cardiometabolic comorbidities including established atherosclerotic cardiovascular diseases (i.e., previous MI or acute coronary syndrome (ACS), CVA, previous coronary or vascular revascularization, peripheral artery disease (PAD), Type 1 and Type 2 Diabetes Mellitus (DM) with or without organ damage, chronic kidney disease (CKD), arterial hypertension (AH), and familial hypercholesterolemia (FH)) were assessed. Additionally, home medications for cardiometabolic conditions were recorded (antihypertensives, antiplatelet drugs, anticoagulants, lipid-lowering agents, heart rate/rhythm control medications, diuretics, mineralocorticoid receptor antagonists (MRAs), and oral and injectable hypoglycemic agents, including insulin).

4.4. Carotid Plaque Assessment

Carotid ultrasound was performed to determine carotid intima media thickness (IMT) in the common carotid artery and to detect focal plaques. Carotid US was carried out using a commercial scanner “ESAOTE MYLAB TWICE” (Genoa; Italy) equipped with 7–12 MHz linear transducer. The examinations were acquired and evaluated by an experienced operator (A.T. or S.V), and the records were then revised by a blinded supervisor (G.M.). Carotid US Doppler scan was performed as per the standard recommendations recording the IMT bilaterally in the areas of the common carotid (1 cm proximal to the carotid bulb), the carotid bifurcation (1 cm proximal to the flow divider) and the internal carotid artery (1 cm distal to the flow divider). The six measures were then averaged (cIMT) in patients without plaque, as well as the maximum IMT, the presence of carotid plaque, any carotid stenosis >50%, and hemodynamic alterations possibly caused by plaques. The definition of plaque, in accordance with the Mannheim Consensus, was a focal wall thickening of at least 50% compared to the surrounding vessel wall or an IMT ≥1.5 mm with focal protrusion into the vessel lumen [42].

4.5. Cardiovascular Risk Stratification

Cardiovascular risk was stratified according to the latest guidelines of the European Society of Cardiology (ESC)/European Atherosclerosis Society (EAS) [21], based on medical history, comorbidities, and traditional risk factors. Patients with confirmed atherosclerotic cardiovascular disease, familial hypercholesterolemia with evidence of organ damage, diabetes with organ damage, or severe chronic kidney disease (glomerular filtration rate below 30 mL/min) were classified as being at very high cardiovascular risk.
Patients with familial hypercholesterolemia without organ damage, with moderate chronic kidney disease (glomerular filtration rate between 30 and 60 mL/min), or with significantly elevated individual parameters (total cholesterol greater than 310 mg/dL, low-density lipoprotein cholesterol (LDL) over 190 mg/dL, or systolic blood pressure ≥180 mmHg and diastolic blood pressure ≥110 mmHg) were classified as high risk.
Patients with no documented atherosclerotic cardiovascular disease, no diabetes, no moderate-to-severe chronic kidney disease, and no familial hypercholesterolemia with or without organ damage were stratified using the SCORE2, which was implemented by SCORE-OP [21], when appropriate and SCORE2-Diabetes algorithms [22] by means of the “ESC Cardiovascular Disease Risk Calculation App”, which is available on the official ESC website [43].

4.6. Statistical Analysis

Statistical analysis was performed using SPSS (statistical package for the Social Science) version 22. Descriptive statistics included the calculation of mean values with standard deviation (SD) or of median values with interquartile ranges (IQRs) for all continuous variables. Categorical variables were summarized using absolute frequencies and percentages. Univariate and stepwise logistic regression analyses were performed to assess the relation between IBD-related data and the need for CVR re-stratification.
p-Values < 0.05 were considered statistically significant.

5. Conclusions

Carotid US assessments are useful for CV re-classification in patients with IBD, especially in intermediate-risk patients. This practice could reasonably be proposed as part of the routine assessment of patients with IBD to identify potential risk factors for adverse outcomes. Further studies are needed to evaluate the impact of biologic therapies and small molecules on modifying cardiovascular risk.

Author Contributions

G.B., G.M. and W.F.: conceptualization G.C., G.M. and C.M.: supervision G.B. and W.F.: data sampling and writing—original draft. L.P.: data sampling and patients’ supervision. A.V. and A.A.: statistical analysis and critical review of the manuscript. A.V.: administrative supervision. A.T., S.V. and G.M.: carotid ultrasound evaluations. G.S., G.C., G.M. and C.M.: critical review of the manuscript. All authors have read and agreed to the published version of the manuscript.

Funding

This research received no external funding.

Informed Consent Statement

Informed consent was obtained from all subjects involved in the study.

Data Availability Statement

The data presented in this study are available upon request from the corresponding author.

Conflicts of Interest

The authors declare no conflicts of interest.

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Table 1. Baseline characteristics of patients. BMI = body mass index; SBP = systolic blood pressure; DBP = diastolic blood pressure; CKD = chronic kidney disease; * Clinical disease activity according to the Harvey–Bradshaw index for CD (HBI) and the partial Mayo score for UC (pMS); anti-TNFs: anti-tumor necrosis factor; ** conventional therapy: mesalazine with or without thiopurines or methotrexate; *** Conventional therapy (add on): mesalazine + steroids or + advanced therapies.
Table 1. Baseline characteristics of patients. BMI = body mass index; SBP = systolic blood pressure; DBP = diastolic blood pressure; CKD = chronic kidney disease; * Clinical disease activity according to the Harvey–Bradshaw index for CD (HBI) and the partial Mayo score for UC (pMS); anti-TNFs: anti-tumor necrosis factor; ** conventional therapy: mesalazine with or without thiopurines or methotrexate; *** Conventional therapy (add on): mesalazine + steroids or + advanced therapies.
Total (166)UC (92)CD (74)p
Gender (female); n (%)79 (47.6)39 (42.4)40 (54)0.170
Median age (range)59 (51–66)59.5 (49.7–66)59 (51–66)0.626
BMI (Kg/m2); median (range)25 (22.8–27.7)25.6 (23.2–27.7)24.6 (22.5–27.1)0.371
Smokers; n (%)48 (28.9)16 (17.4)32 (43.2)<0.001
Blood pressure assessment
 SBP (mmHg) median (range)125 (115–135)125 (120–135)120 (110–135)0.221
 DBP (mmHg) median (range)75 (70–80)77.5 (70–80)72.5 (70–80)0.301
 Hypertension; n (%)59 (35.5)29 (31.5)30 (40.5)0.204
Lipid profile
 Total cholesterol (mg/dL); median (range)203.5 (172–227.7)213.5 (185–234)186 (145.7–214.7)<0.001
 HDL cholesterol (mg/dL); median(range)54 (47–64)58 (48.8–68.2)51 (46–58.5)0.022
 Triglycerides (mg/dL); median (range)109 (82–149.5)103 (80–143.2)120 (89.2–154.5)0.079
 LDL cholesterol (mg/dL) median (range)120 (95.3–146.1)130 (106–150)153.5 (112.9–186)<0.001
 Hypolipidemic therapy n (%)71 (42.8)46 (50)25 (33.8)0.042
Glycemic compensation
 Hb1Ac (%); median (range)5.4 (5–5.9)5.6 (5–5.9)5.3 (5–5.9)0.177
 Diabetes; n (%)20 (12.05)13 (14.1)7 (9.5)0.377
 On pharmacological therapy; n (%)15 (9)10 (10.9)5 (6.8)0.375
Moderate or severe CKD; n (%)6 (3.6)1 (1.1)5 (6.8)0.049
Antiplatelet or anticoagulant therapy; n (%)36 (21.7)19 (20.6)17 (23)0.686
Disease characteristics:
IBD duration (yrs); median (range)11 (6–22)12 (6.7–22.2)10 (5.2–20.7)0.208
Montreal CD;
 L1; n (%)--43 (58.1)-
 L2; n (%)--10 (13.5)-
 L3; n (%)--19 (25.7)-
p; n (%) 2 (2.7)-
Montreal UC; n (%)
 E1; n (%)-4 (4.3)--
 E2; n (%)-62 (67.4)--
 E3; n (%)-26 (28.2)--
Clinical disease activity *:
 Remission; n (%)129 (77)77 (83.7)52 (70.3)0.039
 Mild; n (%)19 (11.5)7 (7.6)12 (16.2)0.084
 Moderate; n (%)13 (7.8)6 (6.5)7 (9.5)0.476
 Severe: n (%)5 (3.0)2 (2.1)3 (4)0.473
Previous surgery for IBD n (%)37 (22.3)4 (4.3)33 (14.1)<0.001
Conventional therapy (only) **; n (%)42 (25.3)27 (29)15 (20)0.184
Conventional therapy (add on) ***; n (%)112 (67.5)88 (95.6)24 (32.4)0.035
Steroids n (%)26 (15.7)13 (14.1)13 (17.6)0.538
Advanced therapies; n (%)111 (66.8)63 (68.5)48 (64.9)<0.001
 Anti-TNFs; n (%)44 (26.5)20 (21.7)24 (32.4)0.121
 Vedolizumab; n (%)10 (6)9 (9.8)1 (1.3)0.022
 Ustekinumab; n (%)22 (13.2)8 (8.7)14 (8.9)0.964
 Risankizumab; n (%)8 (4.8)08 (10.8)0.001
 Mirikizumab; (%)2 (1.2)2 (2.1)0 (0)0.211
 Anti-JAKs; n (%)25 (15)24 (26.1)1 (1.3)<0.001
Failure to 1 advanced therapy n (%)40 (24.1)28 (30.4)12 (16.2)0.033
Failure to 2 advanced therapy n (%)47 (28.3)25 (27.2)22 (29.7)0.723
Spondiloarthritis; n (%)38 (22.9)17 (18.5)21 (28.4)0.120
Table 2. Cardiovascular risk before and after carotid US. CVR = cardiovascular risk; US = ultrasound.
Table 2. Cardiovascular risk before and after carotid US. CVR = cardiovascular risk; US = ultrasound.
TOT (166)UC (92)CD (74)p
Cardiovascular risk at baseline
CVR moderate; n (%)72 (43)43 (47)29 (39)0.302
CVR high; n (%)67 (40)35 (38)32 (43)0.515
CVR very high; n (%)27 (16)14 (15)13 (8)0.167
Carotid US findings
Subclinical atherosclerosis; n (%)79 (48)45 (49)34 (46)0.792
Carotid stenosis > 50%: n (%)6 (4)4 (4)2 (3)0.955
Cardiovascular risk after carotid US
CVR moderate; n (%)42 (25)24 (26)18 (24)0.883
CVR high; n (%)91 (55)50 (54)41 (55)0.924
CVR very high; n (%)33 (20)18 (20)15 (20)1
CVR re-stratification; n (%)36 (22)23 (25)13 (18)0.633
From moderate to high; n (%)30 (18)19 (21)11 (15)0.690
From high to very high; n (%)6 (4)4 (4)2 (3)0.955
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Blando, G.; Toscano, A.; Viola, A.; Patanè, L.; Verachtert, S.; Morace, C.; Squadrito, G.; Mandraffino, G.; Alibrandi, A.; Fries, W.; et al. Cardiovascular Risk Assessments and Ultrasound-Assisted Re-Stratification in Patients with Inflammatory Bowel Disease (IBD). Gastrointest. Disord. 2025, 7, 59. https://doi.org/10.3390/gidisord7040059

AMA Style

Blando G, Toscano A, Viola A, Patanè L, Verachtert S, Morace C, Squadrito G, Mandraffino G, Alibrandi A, Fries W, et al. Cardiovascular Risk Assessments and Ultrasound-Assisted Re-Stratification in Patients with Inflammatory Bowel Disease (IBD). Gastrointestinal Disorders. 2025; 7(4):59. https://doi.org/10.3390/gidisord7040059

Chicago/Turabian Style

Blando, Giuseppe, Arianna Toscano, Anna Viola, Laura Patanè, Sabrina Verachtert, Carmela Morace, Giovanni Squadrito, Giuseppe Mandraffino, Angela Alibrandi, Walter Fries, and et al. 2025. "Cardiovascular Risk Assessments and Ultrasound-Assisted Re-Stratification in Patients with Inflammatory Bowel Disease (IBD)" Gastrointestinal Disorders 7, no. 4: 59. https://doi.org/10.3390/gidisord7040059

APA Style

Blando, G., Toscano, A., Viola, A., Patanè, L., Verachtert, S., Morace, C., Squadrito, G., Mandraffino, G., Alibrandi, A., Fries, W., & Costantino, G. (2025). Cardiovascular Risk Assessments and Ultrasound-Assisted Re-Stratification in Patients with Inflammatory Bowel Disease (IBD). Gastrointestinal Disorders, 7(4), 59. https://doi.org/10.3390/gidisord7040059

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