Evaluation of adalimumab effects on left ventricle performance by echocardiography indexes among patients with immunosuppressant refractory ulcerative colitis

Abstract

Background and aims: Inflammatory bases lead to a simultaneous flourishing of cardiovascular complications with inflammatory bowel disease (IBD). As a released cytokine, tumor necrosis factor-α (TNF-α) can either disrupt or preserve cardiovascular performance. Due to this controversy, this study aimed to appraise the short-term anti-TNF (adalimumab [ADA]) relics on cardiac function by gauging the echocardiography indexes in patients with immunosuppressant refractory ulcerative colitis (UC).

Methods: All cases with a definite diagnosis of UC were included based on providing written informed consent and owning the severe form of active disease (Mayo score ≥7), which did not dampen with immunosuppressant. Patients were excluded in the case of previous cardiac ailments/risk factors and prior related surgical or pharmaceutical intervention. Transthoracic echocardiography (TTE) was carried out before and 3 months after biological regimen allocation and changes in indexes [ejection fraction (EF), left ventricular end-diastolic volume (LVEDV)/left ventricular end-systolic volume (LVESV), and global longitudinal strain (GLS) in standard parasternal short axis from mid-ventricular level, two-, three-, and four-chamber apical long axes] were compared via statistical analyses.

Results: The study consisted of 13 (65%) men and 7 (35%) women, with a mean age of 36.54 ± 11.3 years. Participants mainly possessed Montreal class I (45%) and an average of 3.25 years of disease duration. The intervention significantly controlled inflammation [endoscopic Mayo score (P = 0.001), partial Mayo score (P = 0.001), and C-reactive protein (P = 0.001)]. Endoscopic and clinical remission was obtained in 7 (35%) and 9 (45%) patients, respectively; however, no significant discrepancy related to the LVEDV (P = 0.86), LVESV (P-value = 0.25), EF (P-value = 0.06), and GLS in standard parasternal short axis (P = 0.73), long axis [apical 2-chamber (P-value = 0.61), apical 3-chamber (P-value = 0.15), and apical 4-chamber (P-value = 0.19) views] was observed before and after the intervention. Furthermore, no statistically significant correlation between disease activity and cardiac function was found, neither before nor after ADA administration.

Conclusion: The present perusal found no deterioration in left ventricular function indexes with ADA intervention among patients with IBD without cardiac ailment. Thus, prescribing the anti-TNF to alleviate the inflammation can be carried out with less concern about cardiac consequences and considering other adverse traces in the target group.

Keywords: adalimumab; anti-TNF-α; echocardiography; heart failure; inflammatory bowel disease; longitudinal global strain; ulcerative colitis; vascular stiffness.

Figure 1

Diagram of the participants' selection process. Among 105 patients referred to the gastrointestinal outpatient clinic, 52 were eligible for the study. A total of 24 patients were excluded, and eight participants failed to complete the study. Thus, the data from 20 patients were analyzed.

Figure 2

Comparison of traditional echocardiographic indices. No significant discrepancy for EF, LVESV, and LVEDV is seen before and after the intervention.

Figure 3

GLS percentage alteration. GLS did not change significantly in the standard parasternal short axis or two-, three-, and four-chamber apical long axes before and after the ADA administration.

Figure 4

The dual role of TNF-α in cardiovascular consequences. (A) Cardiac effects: TNF-α can enhance contractility, concentric hypertrophy, cell survival, and angiogenesis by instigating type 2 TNF-α receptors on heart tissue, protective mechanisms against heart failure development; also, it can either exert its role with type 1 TNF-α receptor provocation in the contractility decrement, cell death, and fibrosis. (B) Vascular effects: production of NO decreases with the impact of TNF-α on the Arginase enzyme, resulting in vascular hypertonicity. In addition, with the influence of this cytokine on muscle fibers and extracellular matrix, vascular hypertrophy, and calcification, accompanied by less flexible ECM, are shaped. As a result of vascular stiffness (structural and functional), cardiac afterload raises, and microvascular perfusion diminishes. The other vascular sequel of TNF-α is atherosclerosis or plaque formation which is facilitated by the expression of cellular adhesion molecules such as VCAM, ICAM, and E-selectin. Both heart and vessels adverse outcomes contribute to cardiovascular event predisposition.