Arterial structure and function in inflammatory bowel disease

Abstract

Inflammatory bowel disease (IBD) is the result of a combination of environmental, genetic and immunologic factors that trigger an uncontrolled immune response within the intestine, which results in inflammation among genetically predisposed individuals. Several studies have reported that the prevalence of classic cardiovascular risk factors is lower among subjects with IBD than in the general population, including obesity, dyslipidaemia, diabetes and hypertension. Therefore, given the risk profile of IBD subjects, the expected cardiovascular morbidity and mortality should be lower in these patients than in the general population. However, this is not the case because the standardized mortality ratio is not reduced and the risk of coronary heart disease is increased in patients with IBD. It is reasonable to hypothesize that other factors not considered in the classical stratification of cardiovascular risk may be involved in these subjects. Therefore, IBD may be a useful model with which to evaluate the effects of chronic low-grade inflammation in the development of cardiovascular diseases. Arterial stiffness is both a marker of subclinical target organ damage and a cardiovascular risk factor. In diseases characterized by chronic systemic inflammation, there is evidence that the inflammation affects arterial properties and induces both endothelial dysfunction and arterial stiffening. It has been reported that decreasing inflammation via anti tumor necrosis factor alpha therapy decreases arterial stiffness and restores endothelial function in patients with chronic inflammatory disorders. Consistent with these results, several recent studies have been conducted to determine whether arterial properties are altered among patients with IBD. In this review, we discuss the evidence pertaining to arterial structure and function and present the available data regarding arterial stiffness and endothelial function in patients with IBD.

Keywords: Arterial stiffness; Crohn’s disease; Inflammation; Pulse wave velocity; Tumour necrosis factor alpha; Ulcerative colitis.

Figure 1

Role of arterial compliance in the damping of blood flow and the pressure oscillations generated by the heart. A: During systole, a portion of the stroke volume is forwarded directly to the peripheral tissues; approximately 50% of the stroke volume is momentarily stored within the aorta and stretches the arterial walls; B: During diastole, the energy imbricated within the arterial wall is discharged, and the stored blood is forwarded into the peripheral tissues, ensuring continuous flow and contributing to the maintenance of sufficient diastolic blood pressure.

Figure 2

Arterial stiffness and reflection waves. A: Pulse wave in subjects with normal arterial stiffness; B: Pulse waves in subjects with increased arterial stiffness. DBP: Diastolic blood pressure; SBP: Systolic blood pressure.

Figure 3

Reference technique utilized to measure carotid-femoral pulse wave velocity. PWV: Pulse wave velocity; L: The distance between the two measurement sites; Δt: The time lag between the pulse waves acquired at the proximal (carotid) and distal (femoral) sites.

Figure 4

Potential mechanisms by which inflammation can induce functional (A) and structural (B) arterial stiffening. eNOS: Endothelial nitric oxide synthase; H₂O₂: Hydrogen peroxide; IL-1: Interleukin-1; MMPs: Matrix metalloproteinases; NO: Nitric oxide; O^2-: Superoxide; ROS: Reactive oxygen species; TIMP: Tissue inhibitor of matrix metalloproteinases; TNF-α: Tumor necrosis factor alpha.