The occurrence of ischemic heart disease (IHD), atrial fibrillation, and flutter demonstrates certain associations with inflammatory bowel disease (IBD), warranting further exploration at the genetic architecture level. This study focused on genome-wide association study (GWAS) data of IHD, atrial fibrillation and flutter, and IBD, analyzing from two dimensions: genetic correlation and shared locus identification. Initially, linkage disequilibrium score regression and genetic covariance analyzer were utilized to assess the overall genetic correlations. Subsequently, the association patterns of local genomic regions were determined using Local Ancestry Variance Association (LAVA) analysis. Mendelian randomization (MR) was employed to assess causal effects. The genetic overlap among different traits was analyzed based on the statistical framework of conditional/conjunctional false discovery rate (cond/conjFDR). Finally, shared loci across these traits were identified by integrating conjFDR analysis with GWAS multi-trait analysis (MTAG). At the genomic level, significant overall correlations were observed among IHD, atrial fibrillation and flutter, and IBD and Crohn's disease (CD), while associations with ulcerative colitis appeared less pronounced. At the local level, IHD and IBD (including subtypes) showed significant associations in multiple regions. However, atrial fibrillation and flutter exhibited local associations only in the context of CD. Through conjFDR analysis, the genetic overlap across these diseases was validated. Additionally, several shared genetic loci were identified by integrating conjFDR and MTAG analyses, with genes confirmed in both IHD and IBD (including subtypes), such as SMAD3, PLCG2, ZNF831, PTPN22, RP11-136O12.2, and RP11-449I17.5. Moreover, six common genes were identified in the analysis between atrial fibrillation and flutter and IBD (including subtypes), such as ZMIZ1, MTHFS, ERAP2, GNA12, and RP1-15D23.2. This study offers empirical evidence of the genetic association between IHD, atrial fibrillation and flutter, and IBD comorbidity, providing new insights for cases where IBD co-occurs with IHD or atrial fibrillation and flutter.

Although inflammatory bowel disease (IBD) has been linked to cardiovascular disease in a growing body of literature, the relationship between IBD and arrhythmia remains unclear. To investigate the causal relationship between inflammatory bowel disease and arrhythmia, we conducted this Mendelian randomization (MR) analysis. We identified single nucleotide polymorphisms (SNP) associated with IBD as instruments, including IBD, ulcerative colitis (UC), and Crohn's disease (CD). SNPs of two arrhythmia phenotypes as outcome data, namely atrioventricular block (AVB), and paroxysmal tachycardia (PTA). The inverse variance weighting method was used to analyze the two-sample Mendelian randomization with four other methods, including MR Egger, Weighted median, Simple mode, and Weighted mode. Sensitivity analysis involves different methods to detect and adjust for bias in results, including heterogeneity analysis, pleiotropy analysis, and leave-one-out sensitivity analysis. To ensure the rigor of the analysis results, we selected another set of exposure data sets and conducted the MR verification analysis using the same method. Results suggested UC is significantly associated with an increased risk of AVB (odds ratio, OR 1.178, 95% CI 1.070-1.297, P = 0.000828), the verification analysis results are consistent with this (OR 1.048, 95% CI 1.007-1.091, P = 0.022947). Our study suggests a potential risk increase of atrioventricular block in patients with UC. These results also provide further evidence that inflammatory bowel disease may increase the risk of developing arrhythmia.

We aimed to characterise the association between inflammatory bowel disease (IBD) and IBD medications and risk of cardiac arrhythmia.

In a retrospective population-based study using the University of Manitoba IBD Epidemiology Database (Manitoba, Canada) from 1984 to 2018, we identified 10 992 IBD cases and 102 875 matched controls.

Arrhythmia risk in IBD was adjusted for the presence of comorbidities of the Charlson Comorbidity Index. The effect of IBD medications on the development of arrhythmia was assessed in a nested cohort study of individuals with IBD. Cases were censored at the date of first database identification of a diagnosis of heart failure or myocardial infarction.

The cohort was 48.5% Crohn's disease and 51.5% ulcerative colitis, and 80.5% were incident cases. The median age of incident cases at IBD diagnosis was 35 (IQR, 25 to 49). The median age at arrhythmia diagnosis for persons with IBD was 69 years (IQR, 59 to 77) and for controls 69 years (IQR, 59 to 78). Persons diagnosed with IBD were more likely than controls (HR 1.51; 95% CI, 1.30 to 1.76) to develop arrhythmia. Persons within their sixth decade or younger had increased risk of arrhythmia. When controlling for comorbidities, the significant association between IBD and arrhythmia remains. Medications including 5-aminosalicylates, thiopurines and tumour necrosis factor-α inhibitors were not associated with arrhythmia.

Persons with IBD have a higher risk of arrhythmia prior to a diagnosis with heart disease. Use of IBD medications was not associated with risk of arrhythmia.

Inflammatory bowel disease (IBD), which affects over 2.3 million people in the USA, involves chronic gut inflammation and can lead to cardiovascular complications, including pericarditis. Whether pericarditis in IBD patients is caused by medication, or by the disease itself, remains unclear. Our study aimed to determine the prevalence of pericarditis in IBD and its impact on cardiac complications, outcomes and resource utilization.

NIS data were obtained for IBD patients from 2016-2020. Outcomes were assessed using multivariate logistic regression, adjusting for demographics, hospital characteristics, comorbidities, and IBD etiology.

In our study of 1.52 million IBD patients, 0.6% had pericarditis, of whom a majority were women (54.1%) and white (76.3%), over 65 years old (43.1%), enrolled in Medicare (51.7%), and living in urban areas (96.3%). Adjusting for confounding factors, IBD patients with pericarditis had higher odds of cardiac arrest (adjusted odds ratio [aOR] 2.73, 95% confidence interval [CI] 1.90-3.91), cardiogenic shock (aOR 6.42, 95%CI 4.77-8.64), and ventricular arrhythmia (aOR 2.13, 95%CI 1.63-2.78 (P<0.001 for all).

Our study found that pericarditis, though rare at 0.6%, significantly impacts cardiovascular health and healthcare utilization in IBD patients, with higher prevalence of pericarditis in older individuals, females, and those with comorbidities such as diabetes, hypertension or chronic kidney disease highlighting the need for further research to enhance therapeutic approaches and patient care.

Inflammatory bowel disease (IBD) presents a complex interplay of chronic inflammation in the gastrointestinal tract and is associated with various extraintestinal manifestations, including cardiovascular complications (CVCs). IBD patients face an elevated risk of CVCs, including coronary artery disease, heart failure, arrhythmias, stroke, peripheral artery disease, venous thromboembolism, and mesenteric ischemia, necessitating comprehensive cardiovascular risk assessment and management. The intricate interplay between chronic inflammation, genetic predisposition, environmental factors, and immune dysregulation likely contributes to the development of CVCs in IBD patients. While the exact mechanisms linking IBD and CVCs remain speculative, potential pathways may involve shared inflammatory pathways, endothelial dysfunction, dysbiosis of the gut microbiome, and traditional cardiovascular risk factors exacerbated by the chronic inflammatory state. Moreover, IBD medications, particularly corticosteroids, may impact cardiovascular health by inducing hypertension, insulin resistance, and dyslipidemia, further amplifying the overall CVC risk. Lifestyle factors such as smoking, obesity, and dietary habits may also exacerbate cardiovascular risks in individuals with IBD. Lifestyle modifications, including smoking cessation, adoption of a heart-healthy diet, regular exercise, and optimization of traditional cardiovascular risk factors, play a fundamental role in mitigating CVC risk. Emerging preventive strategies targeting inflammation modulation and gut microbiome interventions hold promise for future interventions, although further research is warranted to elucidate their efficacy and safety profiles in the context of IBD. Continued interdisciplinary collaboration, advanced research methodologies, and innovative interventions are essential to address the growing burden of CVCs in individuals living with IBD and to improve their long-term cardiovascular outcomes.

Emerging data highlights the heightened risk of atherosclerotic cardiovascular diseases (ASCVD) in patients with chronic inflammatory disorders, particularly those afflicted with inflammatory bowel disease (IBD). This review delves into the epidemiological connections between IBD and ASCVD, elucidating potential underlying mechanisms. Furthermore, it discusses the impact of current IBD treatments on cardiovascular risk. Additionally, the cardiovascular adverse effects of novel small molecule drugs used in moderate-to-severe IBD are investigated, drawing parallels with observations in patients with rheumatoid arthritis. This article aims to comprehensively evaluate the existing evidence supporting these associations. To achieve this, we conducted a meticulous search of PubMed, spanning from inception to August 2023, using a carefully selected set of keywords. The search encompassed topics related to IBD, such as Crohn's disease and ulcerative colitis, as well as ASCVD, including coronary artery disease, cardiovascular disease, atrial fibrillation, heart failure, conduction abnormalities, heart blocks, and premature coronary artery disease. This review encompasses various types of literature, including retrospective and prospective cohort studies, clinical trials, meta-analyses, and relevant guidelines, with the objective of providing a comprehensive overview of this critical intersection of inflammatory bowel disease and cardiovascular health.

Although previous evidence has suggested an increased risk of cardiovascular disease (CVD) in patients with inflammatory bowel disease (IBD), its association with arrhythmias is inconclusive. In this study, we aimed to explore the long-term risk of arrhythmias in patients with IBD.

Through a nationwide histopathology cohort, we identified patients with biopsy-confirmed IBD in Sweden during 1969 to 2017, including Crohn's disease (CD: n = 24,954; median age at diagnosis: 38.4 years; female: 52.2%), ulcerative colitis (UC: n = 46,856; 42.1 years; 46.3%), and IBD-unclassified (IBD-U: n = 12,067; 43.8 years; 49.6%), as well as their matched reference individuals and IBD-free full siblings. Outcomes included overall and specific arrhythmias (e.g., atrial fibrillation/flutter, bradyarrhythmias, other supraventricular arrhythmias, and ventricular arrhythmias/cardiac arrest). Flexible parametric survival models estimated hazard ratios (aHR) with 95% confidence intervals (95% CIs), after adjustment for birth year, sex, county of residence, calendar year, country of birth, educational attainment, number of healthcare visits, and cardiovascular-related comorbidities. Over a median of approximately 10 years of follow-up, 1,904 (7.6%) patients with CD, 4,154 (8.9%) patients with UC, and 990 (8.2%) patients with IBD-U developed arrhythmias, compared with 6.7%, 7.5%, and 6.0% in reference individuals, respectively. Compared with reference individuals, overall arrhythmias were increased in patients with CD [54.6 versus 46.1 per 10,000 person-years; aHR = 1.15 (95% CI [1.09, 1.21], P < 0.001)], patients with UC [64.7 versus 53.3 per 10,000 person-years; aHR = 1.14 (95% CI [1.10, 1.18], P < 0.001)], and patients with IBD-U [78.1 versus 53.5 per 10,000 person-years; aHR = 1.30 (95% CI [1.20, 1.41], P < 0.001)]. The increased risk persisted 25 years after diagnosis, corresponding to 1 extra arrhythmia case per 80 CD, 58 UC, and 29 IBD-U cases over the same period. Patients with IBD also had a significantly increased risk of specific arrhythmias, except for bradyarrhythmias. Sibling comparison analyses confirmed the main findings. Study limitations include lack of clinical data to define IBD activity, not considering the potential role of IBD medications and disease activity, and the potential residual confounding from unmeasured factors for arrhythmias.

In this study, we observed that patients with IBD were at an increased risk of developing arrhythmias. The excess risk persisted even 25 years after IBD diagnosis. Our findings indicate a need for awareness of this excess risk among healthcare professionals.

Atrial fibrillation is the most common arrhythmia in clinical practice and it is associated with increased morbidity and mortality. Atrial fibrillation is linked with inflammatory signaling while inflammation and oxidative stress promote atrial remodeling promoting the development and perpetuation of the arrhythmia. On the other hand, inflammatory bowel disease (IBD) is considered a chronic inflammatory condition with flares and remissions. IBD has been associated with an increased risk of atherosclerotic cardiovascular disease but its relationship with atrial fibrillation has not been studied well. Recent epidemiological evidence indicates an association between IBD and atrial fibrillation, especially during flares/hospitalizations. This brief review provides a concise overview of all available data regarding the association between IBD and atrial fibrillation including the predictive role of electrocardiographic and echocardiographic markers. Several unresolved issues including the thromboembolic risk in this setting and the potential role of antiinflammatory interventions are also discussed.

There is limited and conflicting data available regarding the cardiovascular disease outcomes associated with inflammatory bowel disease (IBD).

We aim to perform a systematic review to evaluate the cardiovascular outcomes and mortality associated with IBD patients.

A systematic literature search has been performed on PubMed, Embase, Cochrane, and Scopus from inception till May 2022 without any language restrictions.

A total of 2,029,941 patients were included in the analysis from 16 studies. The mean age of the patients was 45.6 years. More females were found compared with males (57% vs 43%). The most common risk factors for cardiovascular disease (CVD) included smoking (24.19%) and alcohol (4.60%). The most common comorbidities includes hypertension (30%), diabetes mellitus (14.41%), dyslipidemia (18.42%), previous CVD (22%), and renal disease (10%). Among outcomes, all-cause mortality among IBD patients was 1.66%; ulcerative colitis (UC): 15.92%; and Crohn disease (CD): 0.30%. Myocardial Infarction (MI) among IBD patients were 1.47%, UC: 30.96%; and CD: 34.14%. CVD events among IBD patients were 1.95%. Heart failure events among IBD patients were 5.49%, stroke events among IBD patients were 0.95%, UC: 2.63%, and CD: 2.41%, respectively.

IBD patients are at higher risk for adverse cardiovascular outcomes, especially in women. Although there remains a lack of concrete treatment algorithms and assessment parameters that better characterize IBD risk factors, nutritional modifications and physical activity should be at the forefront of CVD prevention in IBD.

Cardiovascular diseases (CVDs) remain the leading cause of morbidity and mortality despite aggressive treatment of traditional risk factors. Chronic inflammation plays an important role in the initiation and progression of CVDs. Inflammatory bowel disease (IBD) is a systemic state of inflammation exhibiting increased levels of pro-inflammatory cytokines including tumour necrosis factor-α (TNF-α), interleukin (IL)-1β, and IL-6. Importantly, IBD is associated with increased risk for CVDs especially in women and young adults, including coronary artery disease, stroke, thromboembolic diseases, and arrhythmias. Potential mechanisms underlying the increased risk for CVDs in IBD patients include increased levels of inflammatory cytokines and oxidative stress, altered platelet function, hypercoagulability, decreased numbers of circulating endothelial progenitor cells, endothelial dysfunction, and possible interruption of gut microbiota. Although IBD does not appear to exacerbate the traditional risk factors for CVDs, including hypertension, hyperlipidaemia, diabetes mellitus, and obesity, aggressive risk stratifications are important for primary and secondary prevention of CVDs for IBD patients. Compared to 5-aminosalicylates and corticosteroids, anti-TNF-α therapy in IBD patients was consistently associated with decreasing cardiovascular events. In the absence of contraindications, low-dose aspirin and statins appear to be beneficial for IBD patients. Low-molecular-weight heparin is also recommended for patients who are hospitalized with acute IBD flares without major bleeding risk. A multidisciplinary team approach should be considered for the management of IBD patients.

Systemic inflammation seen in inflammatory bowel disease (IBD) may cause electrophysiological changes in the atria leading to atrial fibrillation (AF). We analyzed data from the National Inpatient Sample for 2018 to identify all adult hospitalizations with a primary diagnosis of IBD, which were further divided based on the presence or absence of AF. The primary outcome was inpatient mortality while the secondary outcomes included inpatient complications, mean length of stay, and mean total hospital charge. We identified 92,055 IBD hospitalizations, of which 3900 (4.2%) had AF and 88,155 (95.8%) served as controls. IBD hospitalizations with AF were older (70.9 vs. 45.0 years, P < 0.001) and had a higher association with comorbidities compared to the non-AF cohort. Furthermore, the AF cohort had significantly higher adjusted odds of inpatient mortality (2.05% vs. 0.24%; adjusted odds ratio 2.07; 95% confidence interval [CI] 1.09-3.90; P = 0.025), longer length of stay (6.5 vs. 4.9 days; incidence rate ratio 1.23; 95% CI 1.14-1.33; P < 0.001), and higher total hospital charge ($14,587 vs. $11,475; incidence rate ratio 1.26; 95% CI 1.15-1.38; P < 0.001). Additionally, complications such as acute respiratory failure, pulmonary embolism, and necessity of blood product transfusion were more common for IBD hospitalizations with AF than those without.

Background: Inflammatory bowel disease (IBD), comprising ulcerative colitis (UC), and Crohn's disease (CD), has been reported to be associated with an increased risk of atrial fibrillation (AF). However, the causal role of the chronic intestinal inflammation (CII) in the development of AF remains controversial. We use Mendelian randomization (MR) analysis to explore the causal inference of CII on AF. Methods: A two-sample MR analysis was performed to estimate the potential causal effect of CII on AF. Statistical summaries for the associations between single nucleotide polymorphisms (SNPs) and phenotypes of CII were obtained from genome-wide association studies (GWAS) with cohorts of CD (n = 51,874), UC (n = 47,745), and IBD (n = 65,642) of European descent. The GWAS of 1,030,836 people of European ancestry, including 60,620 AF cases and 970,216 controls was collected to identify genetic variants underlying AF. The causal inference was estimated using the multiplicative random effects inverse-variance weighted method (IVW). The methods of MR-Egger, simple median, and weighted median were also employed to avoid the bias of pleiotropy effects. Results: Using three sets of SNPs (75 SNPs of CD, 60 SNPs of UC, and 95 SNPs of IBD), multiplicative random-effect IVW model estimated a universal null effect of CII on AF (CD: OR = 1.0059, 95% CI: 0.9900, 1.0220, p = 0.47; UC: OR = 1.0087, 95% CI: 0.9896, 1.0281, p = 0.38; IBD: OR = 1.0080, 95% CI: 0.9908, 1.0255, p = 0.37). Similar results were observed using the MR-Egger, simple median, weighted median methods. Conclusion: As opposing to the traditional observational studies, our two-sample MR analysis did not find enough evidence to support a causal role of either CD or UC in the development of AF.