Association of cardiovascular health and educational status in a screening cohort.

INTRODUCTION: The global burden of chronic diseases, including cardiovascular disease, remains a significant public health challenge. The Life's Simple 7 (LS7) score was developed as a tool to evaluate cardiovascular health behaviours and habits and identify high-risk individuals. The present study aimed to assess the distribution of LS7 scores among educational strata. METHODS: The study population consisted of 3,383 asymptomatic individuals screened for colorectal cancer at a single centre in Austria. We split patients into lower (n = 1,055), medium (n = 1,997), and higher (n = 331) education, based on the International Standard Classification of Education (ISCED). Cox regression models were utilized to determine the association between education and mortality over a median follow-up period of 7 years. RESULTS: Individuals with higher educational status had a significantly higher prevalence of ideal cardiovascular health metrics, as defined by the LS7 score, compared to those with medium and lower educational status: n = 94 (28%) vs. n = 347 (17%) and n = 84 (8%), respectively, (p < 0.001). In the Cox regression analysis, both medium (HR = 0.61, 95% CI: 0.43-0.84, p < 0.001) and higher educational status (HR = 0.44, 95% CI: 0.19-1.01, p = 0.06) were associated with all-cause mortality, as was the LS7. CONCLUSION: Our findings highlight a significant association between lower educational status and poorer cardiovascular health, as assessed by LS7, which persisted even after multivariable adjustment. Additionally, both educational status and LS7 were associated with increased mortality, underscoring the significance of our results. These findings have important implications for public health, as screening and prevention strategies may need to be tailored to meet the diverse educational backgrounds of individuals, given the higher prevalence of unhealthy lifestyle behaviours among those with lower educational status.

The Impact of Educational Status on the Occurrence of Colonic Diverticula: Insights from an Austrian Cohort Study.

OBJECTIVE: Education often reflects socioeconomic status. Research indicates that lower socioeconomic status may increase the risk of diverticulosis, and according to data from the USA, diverticular disease is a significant and costly health problem. Our study explores the link between educational level and colonic diverticula occurrence. SUBJECT AND METHODS: We conducted a cohort study on 5,532 asymptomatic Austrian patients who underwent colonoscopy, categorizing them by education level using the updated Generalized International Standard Classification of Education (GISCED). Logistic regression models, adjusting for age, gender, metabolic syndrome, diet, and activity, were used to determine the association between education and diverticulosis. RESULTS: Overall, 39% of the patients had low educational status, while 53% had medium, and 8% had high educational status. Colon diverticula were less frequent in patients with medium (OR 0.73) and high (aOR 0.62) educational status. Medium educational level remained associated with lower rates of diverticulosis after adjustment for age and sex (aOR 0.85) and further metabolic syndrome, dietary habits, and physical activity (aOR 0.84). In higher education status, this phenomenon was only seen by trend. CONCLUSION: Low education correlated with higher colon diverticula risk, while medium education showed lower rates even after adjustments. This trend persisted at higher education levels, highlighting the potential for strategies for cost reduction tailored to socioeconomic conditions.

Insulin resistance and central obesity determine hepatic steatosis and explain cardiovascular risk in steatotic liver disease.

Background: Metabolic dysfunction-associated steatotic liver disease (MASLD) has recently been proposed to replace non-alcoholic fatty liver disease and focus on patients with progressive disease due to the presence of metabolic dysfunction. However, it is unclear whether the new definition actually identifies patients with hepatic steatosis at increased cardiovascular risk. Methods: A total of 4,286 asymptomatic subjects from the SAKKOPI study aged 45-80 years undergoing screening colonoscopy were analyzed. Steatosis was diagnosed by abdominal ultrasound. MASLD was diagnosed according to the recent expert consensus. Insulin resistance was assessed by homeostasis model assessment-insulin resistance score (HOMA-IR) (cutoff: ≥2.5), subclinical inflammation was estimated by ferritin/CRP/uric acid, and cardiovascular risk was assessed using SCORE2/ASCVD. Results: Mean age was 59.4 ± 8.5 years, 51.6% were male; mean BMI was 27.0 ± 4.5 kg/m², 9.2% had type 2 diabetes mellitus. In total, 1,903 (44.4%) were diagnosed with hepatic steatosis and were characterized by more severe metabolic dysfunction including insulin resistance (47.1% vs. 12.2%, p < 0.001) and central obesity (waist circumference ≥102/88 cm, 71.8% vs. 37.1%, p < 0.001). This translated into higher (subclinical) inflammation (ferritin 153 vs. 95 mg/dL, p < 0.001, uric acid 6.3 mg/dL vs. 5.2 mg/dL, p < 0.001) and 10-year cardiovascular risk (SCORE2 7.8 points vs. 5.1 points, p < 0.001, ASCVD 17.9 points vs. 10.8 points, p < 0.001). 99.0% of subjects with steatosis met the MASLD definition, 95.4% met the MAFLD definition, and 53.6% met the definition of metabolic syndrome, while 95.4% of subjects without steatosis also met the MASLD criteria for metabolic dysfunction compared to 69.0% and 17.4% who met the MAFLD and metabolic syndrome criteria, respectively. Forward stepwise regression indicated that waist circumference, HOMA-IR, and triglycerides were most relevant in explaining the presence of hepatic steatosis across all subgroups of increasing metabolic dysfunction. At the same time, hepatic steatosis was not associated with cardiovascular risk in the overall cohort (SCORE2: B = 0.060, 95% CI: -0.193-0.314, and p = 0.642) and in patients with metabolic dysfunction after adjusting for age, sex, and these three metabolic dysfunction components. Conclusion: Although hepatic steatosis is associated with increased central obesity and insulin resistance, metabolic dysfunction per se rather than hepatic steatosis explains cardiovascular risk in these patients.

Diverticulosis and cardiometabolic risk factors: a systematic literature review.

BACKGROUND: There is a hypothesis of an association between diverticulosis and metabolic syndrome (MS) or its components, but data on this topic are inconsistent, and a systematic review has not been performed. We conducted a systematic review to investigate the possible association between cardiometabolic risk factors and diverticulosis. METHODS: A systematic literature search was conducted via PubMed, Cochrane Library, and Web of Science in December 2022 to collect the necessary data. Studies that examined the association between MS or individual metabolic factors and asymptomatic diverticulosis were included in the review. RESULTS: Of the potentially relevant articles identified via PubMed (477), Cochrane Library (224), and Web of Science (296), 29 articles met the inclusion criteria and were used for this work. These studies were assessed for study quality using GRADE. Overall, 6 studies were rated as "very low," 19 studies as "low," and 4 studies as "moderate." The data suggest an association between arterial hypertension, obesity, and fatty liver disease in younger patients and diverticulosis. Patient age appears to play an important role in diverticular formation. Data on diabetes mellitus is inconclusive and may require further investigation depending on the location of the diverticula. CONCLUSION: Based on the synthesized data, there is an association between arterial hypertension, obesity, and fatty liver disease in younger patients. The formation of diverticula seems to be influenced by age and genetic factors. The study suggests a connection with cardiometabolic risk factors. To gain a better understanding of the role of metabolic risk factors in asymptomatic diverticulosis, targeted studies are necessary based on these findings.

sST2 Levels Show No Association with Helicobacter pylori Infection in Asymptomatic Patients: Implications for Biomarker Research.

INTRODUCTION: Helicobacter pylori (H. pylori) is a prevalent stomach bacterium that can cause a range of clinical outcomes, including gastric cancer. In recent years, soluble suppression of tumorigenicity-2 (sST2) has gained attention as a biomarker associated with various diseases, such as gastric cancer. The purpose of this study was to explore the possible connection between H. pylori infection and sST2 levels in patients who do not exhibit symptoms. METHODS: A total of 694 patients from the Salzburg Colon Cancer Prevention Initiative (Sakkopi) were included in the study. The prevalence of H. pylori infection was determined by histology, and sST2 levels were measured in serum samples. Clinical and laboratory parameters, such as age, sex, BMI, smoking status, hypertension, and metabolic syndrome, were also collected. RESULTS: The median sST2 concentration was similar between patients with (9.62; 7.18-13.44 ng/mL; p = 0.66) and without (9.67; 7.08-13.06 ng/mL) H. pylori. Logistic regression analysis did not show any association (OR 1.00; 95%CI 0.97-1.04; p = 0.93) between sST2 levels and H. pylori infection, which remained so (aOR 0.99; 95%CI 0.95-1.03; p = 0.60) after adjustment for age, sex, educational status, and metabolic syndrome. In addition, sensitivity analyses stratified by age, sex, BMI, smoking status, educational status, and the concomitant diagnosis of metabolic syndrome could not show any association between sST2 levels and H. pylori infection. CONCLUSION: The results indicate that sST2 may not serve as a valuable biomarker in the diagnosis and treatment of H. pylori infection. Our findings are of relevance for further research investigating sST2, as we could not find an influence of asymptomatic H. pylori infection on sST2 concentration. WHAT IS ALREADY KNOWN?: Soluble suppression of tumorigenicity-2 (sST2) has gained attention as a biomarker associated with various diseases, such as gastric cancer. WHAT IS NEW IN THIS STUDY?: The median sST2 concentration was similar between patients with (9.62; 7.18-13.44 ng/mL; p = 0.66) and without (9.67; 7.08-13.06 ng/mL) H. pylori. WHAT ARE THE FUTURE CLINICAL AND RESEARCH IMPLICATIONS OF THE STUDY FINDINGS?: The results indicate that sST2 may not serve as a valuable biomarker in the diagnosis and treatment of H. pylori infection.

Helicobacter pylori and cardiovascular risk: Only a dead Helicobacter is a good Helicobacter?

OBJECTIVES: Helicobacter pylori (H. pylori) and cardiovascular (CV) disease share common symptoms and underlie many general medical complaints. Preliminary studies suggest an association between H. pylori positivity and CV risk, and gastroenterological guidelines recommend eradication of H. pylori in patients with manifest atherosclerosis. Therefore, the aim of this study was to examine the reciprocal association of H. pylori positivity and CV risk for their independence of shared risk factors. METHODS: We included 3284 asymptomatic participants of a colorectal cancer screening cohort who were offered and underwent upper gastrointestinal endoscopy. We calculated the 10-year risk for a CV event using the novel SCORE2 for each patient. We evaluated the association between H. pylori positivity and CV risk assessed by SCORE2 using both multilevel logistic and linear regression. We adjusted for age, sex and the concomitant diagnosis of metabolic syndrome. Lastly, we assessed the association between H. pylori status and mortality using proportional hazard Cox regression. RESULTS: In total, 2659 patients were H. pylori negative and 625 H. pylori positive. Helicobacter pylori positivity was associated with SCORE2 and remained so (r = .33; 95% CI 0.09-0.57; p = .006) after adjustment for age, sex, and the diagnosis of metabolic syndrome. Also, SCORE2 was associated with higher odds for H. pylori positivity (aOR 1.03 95% CI 1.01-1.05; p = .02) even after multivariable adjustment. Helicobacter pylori positivity was associated with neither CV (HR 0.60 95% CI 0.14-2.63; p = .50) nor all-cause (HR 1.20 95% CI 0.77-1.87; p = .43) mortality during a median follow-up of 9 years. CONCLUSIONS: In our study, H. pylori positivity and CV risk were independently associated. This did not translate into a dissimilar CV mortality between H. pylori positive and H. pylori negative patients. However, the overwhelming majority of our patients underwent H. pylori eradication. We, therefore, think that H. pylori eradication is at least safe from a cardiovascular perspective and warranted from gastrointestinal standpoint.

Cardiovascular Risk Assessment by SCORE2 Predicts Risk for Colorectal Neoplasia and Tumor-Related Mortality.

Objectives: The European Society of Cardiology endorsed SCORE2 to assess cardiovascular risk. The aim of this observational, retrospective study was to assess whether SCORE2 is associated with colorectal neoplasia in an asymptomatic screening population. Further, we evaluated if SCORE2 predicts tumor-related mortality. Methods: We included 3408 asymptomatic patients who underwent a screening colonoscopy. We calculated SCORE2 for each participant and stratified patients according to their predicted 10-year risk of cardiovascular disease: SCORE2 0−4.9%, SCORE2 5−9.9%, and SCORE2 ≥ 10%. We assessed the association between SCORE2 as a continuous variable, the presence of colorectal neoplasia using multilevel logistic regression, and SCORE2 and mortality using Cox regression. Results: In total, 1537 patients had a SCORE2 of 0−4.9%, 1235 a SCORE2 of 5−9.9%, and 636 a SCORE2 ≥ 10%. The respective rates of colorectal neoplasia were 20%, 37%, and 44%. SCORE2 was associated with the presence of any (OR 1.11 95%CI 1.09−1.12; p < 0.001) and advanced colorectal neoplasia (OR 1.06 95%CI 1.08−1.13; p < 0.001) in univariate analysis. After multivariable adjustment (age, sex, family history, and metabolic syndrome) a higher SCORE2 remained associated with higher odds for any (aOR 1.04 95%CI 1.02−1.06; p = 0.001) and advanced (aOR 1.06 95%CI 1.03−1.10; p < 0.001) colorectal neoplasia. SCORE2 was associated with both all-cause (HR 1.11 95%CI 1.09−1.14; p < 0.001) and tumor-related mortality (HR 1.10 95%CI 1.05−1.14; p < 0.001). Conclusions: We found that SCORE2 is associated with the presence of colorectal neoplasia. Clinicians could kill two birds with one stone calculating SCORE2. In patients with a high SCORE2, screening colonoscopy aside from cardiovascular risk mitigation could improve outcomes.

Non-alcoholic fatty liver disease is not independently associated with Helicobacter pylori in a central European screening cohort.

BACKGROUND: The association between Helicobacter pylori (Hp) infection and non-alcoholic fatty liver disease (NAFLD) is subject of a contentious debate. Data mainly stem from Asian cohorts whereas European data are scarce. We, therefore, investigated an Austrian colorectal cancer screening cohort for an association between Hp and NAFLD. METHODS: In total, 5338 consecutive participants undergoing screening colonoscopy at a single center in Austria were evaluated in this cross-sectional study. The primary risk factor was being Hp negative or positive. The primary endpoint was the presence of NAFLD defined by ultrasound (NAFLD; primary endpoint). Uni- and multivariable logistic regression models were fitted to obtain odds ratios (OR) and 95% confidence intervals (95%CI). Finally, this association was analyzed in a subgroup of 1128 patients in whom NAFLD was diagnosed by transient elastography (TE, secondary endpoint). RESULTS: NAFLD prevalence defined by ultrasound did not differ between Hp positive (48%) and negative patients (45%, P=0.097). Accordingly, in uni- (OR 1.12 95% CI 0.98-1.29; P=0.098) and multivariable analysis adjusting for different risk factors (aOR 0.96 95%CI 0.82-1.13; P=0.601) no independent association was found. On subgroup analysis, NAFLD diagnosed by TE was more prevalent in the Hp positive compared to the Hp negative group (49% vs. 38%, P=0.004) and these patients also had higher steatosis grades. However, after adjustment for risk factors, no independent association between Hp positivity and NAFLD diagnosed by TE (aOR 1.26 95%CI 0.89-1.78; P=0.194) was confirmed. CONCLUSIONS: In this Central European cohort, Hp-positivity was not associated with the diagnosis of NAFLD. Although Hp positive patients seem to be more likely to have a concomitant NAFLD diagnosis, this association might rather relate to a cardiometabolic risk phenotype than causality.