ABSTRACT
Objectives:
To evaluate the association between Inflammatory bowel disease (IBD) and Ischemic heart disease (IHD).
Methods:
A retrospective cohort analysis included patients with and without IBD seen at the outpatient gastroenterology clinic of a large tertiary care hospital between January 2015 and October 2022. The primary outcome was the association between IBD and IHD, and the secondary outcome was predictors of IHD in patients with IBD.
Results:
The study included 400 patients; 291 were IBD patients, and 109 had other non-inflammatory GI disorders. The IBD group displayed significantly lower rates of hyperlipidemia (8.6% vs. 30.3%, p<0.001), diabetes mellitus (DM) (10% vs. 24.8%, p<0.001), and hypertension (11.7% vs. 32.1%, p<0.001) compared to the non-IBD group. Only 2.7% (n=8) of IBD patients developed IHD. Logistic regression analysis did not demonstrate a significant association between IBD and IHD (p=0.932). Among classical risk factors, only hypertension (OR: 26.2, 95% CI: 2.14–661, p=0.016) and hyperlipidemia (OR: 10.5, 95% CI: 1.32–132, p=0.0405) significantly increased the risk of developing IHD among patients with IBD.
Conclusion:
In this cohort, there is no increased risk of developing IHD in patients with IBD compared to non-IBD patients.
Keywords: Inflammatory bowel disease, ischemic heart disease, coronary artery disease, ulcerative colitis, Crohn’s disease
Crohn’s disease (CD) and ulcerative colitis (UC) are the main illnesses that are designated as “inflammatory bowel disease” (IBD). Both are prolonged inflammatory disorders that follow an episodic and remitting process of disorder activity and manifestations.1 During the past decade, more evidence has emerged about the relationship between IBD and unfavorable cardiovascular events.2 Inflammation heavily influences the pathogenesis of both IBD and coronary artery disease (CAD).3
The IBD has long been believed to be a disease of the developed world,4 and before 1982, it was uncommon in Saudi Arabia. However, between 1976 and 1994, 101 Arab patients with IBD were managed.5 Furthermore, epidemiological data have connected IBD to elevated odds of experiencing acute coronary syndrome (ACS) and heart failure.6 The evidence regarding the relationship between IBD and ischemic heart disease (IHD) is unclear, and previous analyses have identified conflicting findings and heterogeneity. One study examined the relationship between IHD and IBD with a mean follow-up period of 16 years and found a significantly higher likelihood of IHD among patients with IBD, females, and patients over 60 years of age. years of age showed the most apparent increases.7 Conversely, in 2015, Ruisi et al. found that only one patient developed IHD during the 2 years of follow-up in a retrospective analysis of 300 patients with IBD who did not have traditional IHD risk factors (diabetes, hypertension, hyperlipidemia, congestive heart failure, age 65 years or older, family history, end-stage renal disease, or a smoking history of 5 pack–years).1
In addition, a cross-sectional study examined a national sample of inpatient hospitalizations over 11 years, and after adjusting for IHD risk variables, patients with IBD had a considerably lower incidence of myocardial infarction (MI) and CAD in comparison to the average for the general population.8 However, the latest systematic research of 5 studies included a total population of 605,382 patients and reported a higher probability of MI in patients with IBD, and this probability was significantly observed only for UC, but not for CD.9 Due to contradictory findings of previous research and a scarcity of data on the connection between IHD and IBD in Saudi Arabia, our analysis aimed to determine the association between IBD and IHD and to examine predictors of IHD in established patients with IBD.
Methods
This single-center retrospective cohort study included a random selection of patients with IBD who were seen in the outpatient gastroenterology clinic at King Abdulaziz University Hospital (KAUH) in Jeddah, Saudi Arabia, between January 2015 and October 2022. A random selection of patients who were followed up at the clinic with gastrointestinal disorders other than IBD was included for comparison as the “non-IBD” group. The KAUH IBD registry (IBDIS) was used for this study to identify patients who fulfilled the inclusion criteria, which included an established diagnosis of IBD (UC or CD) based on typical clinical, endoscopic, and histological criteria and age between 18 and 60 years regardless of gender or nationality. Patients in both groups were excluded from the study if they had a history of chronic infection, other autoimmune disease, or solid organ tumor. Ethics approval was granted by the Research Ethics Committee at King Abdulaziz University (reference number 323-22).
Data were collected from patients’ electronic medical records using a predesigned data extraction sheet. The data collected included patient demographics such as age, gender, ethnicity, and residence; risk factors for IHD, including hypertension, diabetes, hyperlipidemia, obesity (defined as body mass index (BMI) > 30 kg/m2); and history of tobacco smoking. Patient status included diagnoses of UC, CD, or IBD unclassified (IBDU). The data collected concerning the disease included the age at diagnosis, duration of the diagnosis in years, and the dates of the first and last encounters for the exposed group. We used the Montreal classification to classify IBD phenotypes and behavior and differentiated IBD subtypes based on age, location, and behavior over time.10
Differences between CD and UC include disease behavior and perianal involvement for CD and disease severity and extent for UC. Age upon diagnosis was subcategorized as less than 16 years (A1), 17–40 years (A2), and >40 years (A3). The categories of CD sites were L1 (terminal ileal), L2 (colonic), L3 (ileocolonic), and L4 (upper gastrointestinal). The extent of UC was classified as E1 (ulcerative proctitis), E2 (left-sided UC), or E3 (pancolitis UC). The behavior of CD was described as non-stricturing and nonpenetrating (B1), stricturing (B2), penetrating (B3), and with or without perianal involvement (p). The levels of disease severity in UC were S0 (clinical remission), S1 (mild UC), S2 (moderate UC), and S3 (severe UC).
The clinical data included the symptoms at diagnosis and during the last visit or active flare period (whichever was most recent). We also analyzed intestinal manifestations (such as abdominal pain, diarrhea, tenesmus, etc.) and extraintestinal manifestations (joint pain, mouth ulcers, weight loss, etc.) of IBD and signs at diagnosis and the last visit or active flare period (such as pyoderma gangrenosum, uveitis, aphthous ulcer, etc.). The patient records were used to identify information regarding medical treatments for IBD, including azathioprine, 5-ASA/sulfasalazine, oral corticosteroids, and TNF-α antagonists (such as infliximab and adalimumab). The hospital database was also used to extract information about the laboratory investigations (CRP, p-ANCA, c-ANCA, ASCA, and fecal calprotectin), as well as endoscopic and radiological investigations (MRE, barium studies, CT of the abdomen and pelvis with or without contrast, and abdominal ultrasound).
Control group selection
Patients in the non-IBD control group consisted of a random selection of patients with the following conditions: irritable bowel syndrome (IBS), solitary rectal ulcer syndrome (SRUS), anal fissure, hemorrhoids, or colonic diverticulosis.
Sample size and data analysis
The required sample size was calculated using the tool Raosoft with a confidence level of 95% and a margin of error of 5%. The overall sample result was 992 participants, and the response distribution was 50%. Accordingly, the recommended estimated sample size was 278 participants.
IBM SPSS Statistics for Windows, Version 21.0 (Armonk, NY: IBM Corp) was employed to import and analyze data. Frequencies were used for descriptive statistics to characterize categorical variables, including the main variables. The mean and standard deviation were used to characterize continuous variables. Categorical variables were compared using the chi-squared test. Binary associations were evaluated using logistic regression. The p-value, odds ratios (ORs), and 95% CIs were determined, and p-values less than 0.05 were deemed significant.
Study outcomes
The primary aim of the study was to examine the association between IBD and the development of IHD. The secondary goal was to identify predictors of IHD in patients with IBD.
Results
Baseline characteristics
The study included 400 participants comprising 291 (72.8%) individuals diagnosed with IBD and 109 (27.2%) individuals without IBD. The gender distributions differed significantly between the 2 patient populations (p=0.002), with a greater percentage of females occurring in the non-IBD group (65.1%) than the IBD group (47.1%). The mean age was significantly higher in the non-IBD group than the IBD group (47.7 years vs. 35.9 years, p<0.001). The participants’ residence type was not significantly different between groups (p=0.880), with most participants residing in urban areas.
The BMI distribution varied significantly between groups (p=0.001), with more individuals in the IBD group falling into the ranges of <18.5 and 18.5–25 compared to the non-IBD group. The prevalence of hypertension, diabetes mellitus (DM), and hyperlipidemia differed significantly between the IBD and non-IBD groups (p<0.001 for all), with higher rates observed in the non-IBD group for all three conditions. The mean total serum cholesterol level was significantly higher in the non-IBD group (4.1 mmol/L, p=0.023). Smoking status did not significantly differ between groups (p=0.952). The mean levels of HbA1c, LDL, and triglycerides also did not differ significantly between groups (p=0.466, p=0.197, p=0.516, respectively). Table 1 shows a comparison of the patient characteristics in both groups.
Table 1.
- Baseline characteristics of the study cohort including patients with Inflammatory bowel disease (IBD group) and without IBD (non-IBD group). Values shown are n (%) except for those marked as “Mean (SD).”
| Baseline characteristic | Non-IBD | IBD | Total | p-value |
|---|---|---|---|---|
| Total n (%) | 109 (27.2) | 291 (72.8) | 400 | |
| Gender | ||||
| Female | 71 (65.1) | 137 (47.1) | 208 (52.0) | 0.002 |
| Male | 38 (34.9) | 154 (52.9) | 192 (48.0) | |
| Age in years | ||||
| Mean (SD) | 47.7 (15.3) | 35.9 (13.1) | 39.1 (14.7) | <0.001 |
| Area of residence | ||||
| Rural | 4 (3.7) | 8 (2.7) | 12 (3.0) | 0.880 |
| Urban | 105 (96.3) | 283 (97.3) | 388 (97.0) | |
| Body mass index (BMI) | ||||
| <18.5 | 7 (6.4) | 45 (15.5) | 52 (13.0) | 0.001 |
| 18.5–25 | 39 (35.8) | 137 (47.1) | 176 (44.0) | |
| 25–30 | 29 (26.6) | 61 (21.0) | 90 (22.5) | |
| >30.0 | 34 (31.2) | 48 (16.5) | 82 (20.5) | |
| Hypertension | ||||
| No | 74 (67.9) | 257 (88.3) | 331 (82.8) | <0.001 |
| Yes | 35 (32.1) | 34 (11.7) | 69 (17.2) | |
| Diabetes mellitus | ||||
| No | 82 (75.2) | 262 (90.0) | 344 (86.0) | <0.001 |
| Yes | 27 (24.8) | 29 (10.0) | 56 (14.0) | |
| Hyperlipidemia | ||||
| No | 76 (69.7) | 266 (91.4) | 342 (85.5) | <0.001 |
| Yes | 33 (30.3) | 25 (8.6) | 58 (14.5) | |
| Smoking status | ||||
| Smoker | 8 (15.1) | 37 (15.8) | 45 (15.7) | 0.952 |
| Ex-smoker | 2 (3.8) | 7 (3.0) | 9 (3.1) | |
| Non-smoker | 43 (81.1) | 190 (81.2) | 233 (81.2) | |
| Last HbA1c reading | ||||
| Mean±SD | 6.2±1.9 | 6.0±1.3 | 6.1±1.6 | 0.466 |
| Serum total cholesterol (mmol/L) | ||||
| Mean±SD | 4.1±1.7 | 3.4±1.9 | 3.7±1.8 | 0.023 |
| Serum LDL (mmol/L) | ||||
| Mean±SD | 2.9 (1.2) | 2.4±1.9 | 2.6±1.6 | 0.197 |
| Serum triglyceride (mmol/L) | ||||
| Mean±SD | 1.3±1.5 | 1.2±0.8 | 1.2±1.1 | 0.516 |
Out of the 400 participants included in the analysis, 16 (4.0%) had established IHD. Patient status (IBD vs. non-IBD) demonstrated a significant association with the presence of IHD (p=0.046), with an equal number of cases of individuals diagnosed with IBD (50.0%) exhibiting IHD compared to the non-IBD group (50.0%). The mean age was significantly higher among participants diagnosed with IHD compared to those without it (58.9 years vs. 38.3 years, p<0.001). BMI categories did not demonstrate a significant association with IHD (p=0.148).
Higher proportions of individuals diagnosed with hypertension (81%, p<0.001) and hyperlipidemia (69%, p<0.001) developed IHD. Those not diagnosed with DM were significantly more likely to develop IHD (56%, p=0.003). No significant association was found between smoking status (19%, p=0.107), duration of IBD diagnosis (9.7 years vs. 7.3 years, p=0.231), or IBD follow-up duration (3.8 years vs. 4.5, p=0.658) and IHD. The mean age at IBD diagnosis (48.7 years vs. 28 years, p<0.001) was significantly higher among patients who developed IHD compared to those who did not (Table 2).
Table 2.
- Comparison between patients with and without ischemic heart disease (IHD). Values shown are n (%) except for those marked as “Mean (SD).”
| Baseline characteristic | Yes | No | Total | p-value |
|---|---|---|---|---|
| Ischemic heart disease | ||||
| Total n (%) | 16 (4.0) | 384 (96.0) | 400 | |
| Patient status | ||||
| Non-IBD | 8 (50.0) | 101 (26.3) | 109 (27.2) | 0.046 |
| IBD | 8 (50.0) | 283 (73.7) | 291 (72.8) | |
| Gender | ||||
| Female | 6 (37.5) | 202 (52.6) | 208 (52.0) | 0.309 |
| Male | 10 (62.5) | 182 (47.4) | 192 (48.0) | |
| Age in years | ||||
| Mean (SD) | 58.9 (14.6) | 38.3 (14.1) | 39.1 (14.7) | <0.001 |
| Body mass index (BMI) n (%) | ||||
| < 18.5 | 0 (0.0) | 52 (13.5) | 52 (13.0) | 0.148 |
| 18.5–25 | 6 (37.5) | 170 (44.3) | 176 (44.0) | |
| 25–30 | 7 (43.8) | 83 (21.6) | 90 (22.5) | |
| > 30.0 | 3 (18.8) | 79 (20.6) | 82 (20.5) | |
| Hypertension | ||||
| No | 3 (18.8) | 328 (85.4) | 331 (82.8) | <0.001 |
| Yes | 13 (81.2) | 56 (14.6) | 69 (17.2) | |
| Diabetes mellitus | ||||
| No | 9 (56.2) | 335 (87.2) | 344 (86.0) | 0.003 |
| Yes | 7 (43.8) | 49 (12.8) | 56 (14.0) | |
| Hyperlipidemia | ||||
| No | 5 (31.2) | 337 (87.8) | 342 (85.5) | <0.001 |
| Yes | 11 (68.8) | 47 (12.2) | 58 (14.5) | |
| Smoking status | ||||
| Smoker | 2 (25.0) | 43 (15.4) | 45 (15.7) | 0.107 |
| Ex-smoker | 1 (12.5) | 8 (2.9) | 9 (3.1) | |
| Non-smoker | 5 (62.5) | 228 (81.7) | 233 (81.2) | |
| Age at IBD diagnosis in years | ||||
| Mean±SD | 48.7±18.5 | 28.0±12.1 | 28.6±12.7 | <0.001 |
| Duration since IBD diagnosis (years) | ||||
| Mean±SD | 9.7±10.2 | 7.3±5.1 | 7.4±5.3 | 0.231 |
| IBD Follow-up duration | ||||
| Mean±SD | 3.8±3.5 | 4.5±4.1 | 4.5±4.0 | 0.658 |
Study outcomes
According to the logistic regression analysis, individuals with hypertension (OR=17.421, p≤0.001) and hyperlipidemia (OR=6.338, p=0.013) were more likely to develop IHD. However, the risk of IHD did not differ between the IBD and non-IBD groups (OR=1.05, p=0.932) (Table 3). No significant associations were observed between medication and the development of IHD (Figure 1).
Table 3.
- Results of binomial logistic regression analysis of predictors of ischemic heart disease (IHD).
| Predictor | Estimate | SE | Z | p-value | Odds ratio | Lower | Upper |
|---|---|---|---|---|---|---|---|
| 95% Confidence Interval | |||||||
| Intercept | -5.3439 | 0.873 | -6.1245 | <.001 | 0.00478 | 8.64e-4 | 0.0264 |
| Gender | |||||||
| Male –Female | 0.7352 | 0.583 | 1.2609 | 0.207 | 2.08594 | 0.6652 | 6.5407 |
| Patient status | |||||||
| IBD – Non-IBD | 0.0517 | 0.608 | 0.0850 | 0.932 | 1.05307 | 0.3199 | 3.4669 |
| Hypertension | |||||||
| Yes – No | 2.8577 | 0.792 | 3.6098 | < .001 | 17.42069 | 3.6917 | 82.2056 |
| Diabetes mellitus | |||||||
| Yes – No | -1.0535 | 0.707 | -1.4897 | 0.136 | 0.34870 | 0.0872 | 1.3946 |
| Hyperlipidemia | |||||||
| Yes – No | 1.8466 | 0.742 | 2.4875 | 0.013 | 6.33808 | 1.4794 | 27.1541 |
Estimates represent the log odds of “Ischemic heart disease = Yes” vs. “Ischemic heart disease = No”
Figure 1.
- Odds-ratio plot for IBD medications and the development of ischemic heart disease (IHD).
Predictors of IHD among patients with IBD
Among classical risk factors for IHD, only hypertension (OR: 26.2, 95% CI: 2.14, 661; p=0.016) and hyperlipidemia (OR: 10.5, 95% CI: 1.32, 132; p=0.0405) significantly elevated the risk of developing IHD among patients with IBD. The age at IBD diagnosis (OR: 0.79, 95% CI: 0.54, 1.28; p=0.237) and the duration since the diagnosis (OR: 0.77, 95% CI: 0.51, 1.26; p=0.222) were not associated with IHD (Table 4).
Table 4.
- Predictors of ischemic heart disease among patients with Inflammatory Bowel Disease (IBD).
| Predictor | Estimate | SE | Z | p-value | Odds ratio | Lower | Upper |
|---|---|---|---|---|---|---|---|
| 95% Confidence Interval | |||||||
| Intercept | -6.28 | 1.721 | -3.650 | <.001 | 0.002 | 0.000004 | 0.038 |
| Gender | |||||||
| Male – Female | 0.901 | 0.878 | 1.027 | 0.304 | 2.46 | 0.46 | 15.9 |
| Age in years | -0.002 | 0.036 | -0.070 | 0.944 | 1.00 | 0.92 | 1.07 |
| Hypertension | |||||||
| Yes – No | 3.268 | 1.352 | 2.417 | 0.016 | 26.2 | 2.14 | 661 |
| Diabetes mellitus | |||||||
| Yes – No | -0.131 | 1.125 | -0.117 | 0.907 | 0.88 | 0.09 | 8.64 |
| Hyperlipidemia | |||||||
| Yes – No | 2.354 | 1.149 | 2.048 | 0.0405 | 10.5 | 1.32 | 132 |
| Age at diagnosis | -0.240 | 0.203 | -1.183 | 0.237 | 0.79 | 0.54 | 1.28 |
| Duration since diagnosis | -0.264 | 0.216 | -1.222 | 0.222 | 0.77 | 0.51 | 1.26 |
CI: Confidence interval, Adjusted R squared: 0.462
Discussion
Chronic inflammatory pathways are common in both IHD and IBD, but the underlying pathophysiology of each disease and unidentified confounding factors may be reasons why their relationship has been unclear. This study examined the association between these 2 distinct diseases and revealed that patients with IBD had no increased probability of IHD occurrence. The OR for IHD development among patients with IBD was 1.05 (95% CI: 0.32–3.5), indicating a lack of elevated risk of IHD incidence among such patients. Considering that most of our cohort (97.8%) was Middle Eastern, this might be explained by the ethnic background of the participants. The clinical features of Arab and Jewish patients with IBD were recently examined, and it was shown that while there were no variations in IHD risk between CD patients of the 2 ethnic groups, Arab patients with UC had a significantly lower risk of IHD than the Jewish patients.11
Furthermore, a local retrospective study assessing various characteristics of IBD in North-Central Saudi Arabia showed that the risk of thromboembolism in patients with IBD was 1.5%, which is less than the rates documented in other countries.12 According to a large prospective study with a follow-up period of 9–13 years, there was no evidence of a causal relationship between genetically determined CD or UC and cardiometabolic diseases (MI, ischemic stroke, heart failure, and type 2 DM).13 Moreover, no causal link between IBD and CAD or IHD was found according to a 2-sample Mendelian randomization (MR) analysis after controlling for BMI and smoking.14 The present findings are consistent with those of prior research,1,8,15–19 which had similar sample sizes and were retrospective in nature. The findings could support future studies to examine the potential effects that ethnicity and genetics have on the probability of IHD in patients with IBD.
Our findings demonstrated that classic cardiovascular risk variables such as hyperlipidemia and high blood pressure might predict the development of IHD. However, it was unexpected that IHD was substantially more common in those without DM. This might be explained by the fact that only a minority of patients in our cohort (n=16) had IHD. A recent randomized Mendelian study reported that type 2 DM and IBD were not causally related.20 Interestingly, the mean age at IBD diagnosis was significantly higher (48.7 years vs. 28.0, p<0.001) among individuals diagnosed with IHD. This indicates that the interaction between known risk factors and age may have an effect on the development of IHD among patients with IBD. Remarkably, hypothesis testing in comparisons suggested evidence of IBD subtype and duration of disease being predictors of IHD development. However, this was not confirmed in logistic regression analysis.
Consistent with previous research, a single-center hospital-based cohort study reported that the risk of atherosclerotic cardiovascular disease (ASCVD) in patients with IBD was significantly associated with age at diagnosis >50 years, hypertension, dyslipidemia, male sex, and a prior history of ASCVD.21 Eriksson et al22 found that among patients with IBD, those with extraintestinal symptoms and elderly-onset IBD (≥60 years) had the greatest likelihood of developing ACS. Moreover, our analysis revealed that classic CAD risk factors (hypertension, DM, and hyperlipidemia) were significantly less common in patients with IBD. This outcome aligns with previous research.23 An evidence-synthesis study that encompassed eight studies revealed that patients with IBD conditions comprising CD and UC had a reduced chance of hypertension, DM, and dyslipidemia compared to the control group.24 In line with previous studies, despite the decreased prevalence of conventional risk predictors of CAD, the presence of hypertension and hyperlipidemia predicted IHD development among patients with IBD in the present study.25–28
The current study found no significant association between IBD treatments (oral corticosteroids, TNF-alpha antagonist, azathioprine, and 5-ASA) and risk of IHD. However, the results of the univariable analysis suggested an association between oral corticosteroid use and IHD (OR=6.49, 95% CI: 1.29–118.09; p=0.072), which was slightly attenuated in the multivariable analysis (OR=5.61, 95% CI: 0.94–108.74; p=0.117). On the other hand, multiple studies have reported an association between systemic corticosteroid use and venous thromboembolism.29-31 According to a nationwide cohort study, patients who received oral corticosteroids showed a considerably more significant risk of IHD (incidence rate ratio (IRR) 1.37, 95% CI 1.25–1.50) compared to those who had never used oral corticosteroids.32 Furthermore, a study examining the links between corticosteroid use and the development of ACS has indicated that exposure to corticosteroids is protective against ACS in patients with known IHD. After accounting for cardiovascular risk variables such as DM, dyslipidemia, smoking, family history of IHD, BMI, aspirin usage, and white blood count, such exposure lowered the incidence of ACS by 82%.3
Contrary to earlier research, 5-ASA did not show any protective effects in the present study. Previous analyses have shown that users of 5-ASA demonstrated a noteworthy decrease in IHD risks compared to non-users. In spite of controlling for corticosteroid use as a substitute for the extent of disease, 5-ASA users exhibited lower odds of IHD than non-users (IRR 1.16 vs. 1.36; p=0.02), and the risk was even reduced among those who had used 5-ASA for extended periods (those with at least three prescriptions).32 Compared to non-users, users of TNF-α antagonists were shown to have a threefold increased risk, which was marginally reduced in the multivariate analysis to nearly two-fold (1.91; 95% CI: 0.44–13.96, p=0.446), although the difference was not significant. The risk factors identified for ACS and ischemic stroke among a cohort of 30 patients with IBD comprised clinical disease activity, conventional CAD risk factors like hypertension, DM, and dyslipidemia, and persistent systemic inflammation. The analysis revealed that the treatment for IBD did not exhibit any discernible protective or exacerbating influence on the susceptibility to ACS in individuals with IBD.28
Despite the valuable contributions of this study, several limitations should be considered when interpreting our findings. The retrospective nature of the study’s design inherently introduces the potential for selection bias and incomplete data collection as relying on medical records may lead to missing or inaccurate information. Additionally, secondary data limited our ability to control for confounding variables adequately. Furthermore, the single-center setting may have constrained the generalizability of the findings to broader populations.
A small proportion of our sample (n=16) developed IHD, of which only 8 were patients with IBD. This small sample size limits the generalizability of the findings to broader populations as it could affect the statistical power. Those who had developed IHD were older, had traditional risk factors for ASCVD, and had a higher age at IBD diagnosis. Lastly, the study’s observational nature precluded the establishment of causal relationships between IBD and IHD, which highlights the need for further prospective studies to confirm and elucidate the observed associations. Despite these limitations, this study provides important perspectives on the possible connections between IBD and IHD and could serve as a foundation for future research.
In conclusion, this research has clarified the complex interplay between IHD, IBD, and other clinical variables. An important finding was that individuals with IBD do not have an increased risk of IHD. IHD was only significantly predicted by the conventional risk factors of both hypertension and hyperlipidemia. Similarly, among patients with IBD, hypertension and hyperlipidemia significantly increased the risk of developing IHD. Lastly, classic CAD risk variables (dyslipidemia, DM, and hypertension) were less common in patients with IBD.
Acknowledgment
The authors gratefully acknowledge Yarah A. Alsaggaf, Layan H. Baagil, Norah A. Alharbi, Shuroog S. Almishiagih, and Majda T. Al-Sharif for their efforts as data collectors. We would like to thank American Manuscript Editors (www.americanmanuscripteditors.com) for English language editing.
Footnotes
References
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