Cardiovascular Manifestations of Inflammatory Bowel Disease: Pathogenesis, Diagnosis, and Preventive Strategies

Table 1

Cardiovascular manifestations in IBD.

Cardiovascular manifestations	Possible pathogenic mechanisms	References
Pericarditis and myocarditis	(i) Immune-mediated myocarditis in IBD as a result of exposure to autoantigens	[40–43]
	(ii) Cardiotoxicity as an adverse effect of the treatment with 5-ASA and its derivatives
Venous thromboembolism	(i) Hypercoagulability induced by the systemic inflammation	[22, 53–61]
	(ii) Platelet abnormalities
	(iii) Endothelial dysfunction induced by mechanical and systemic factors
	(iv) Venous stasis
	(v) Acquired risk factors (prolonged hospitalization, surgical interventions, central venous catheters, prolonged immobilization and bed rest, glucocorticoids, smoking, oral contraceptives, vitamin deficiencies, dehydration, hormone replacement therapy, and hyperhomocysteinemia)
	(vi) Genetic risk factors (dysfibrinogenemias, prothrombin gene mutation, factor V Leiden thrombophilia, and deficiency of proteins C, S, and antithrombin)
Arterial thromboembolism	(i) Structural and functional vascular alterations induced by chronic systemic inflammation	[57, 68–78]
	(ii) Accelerated development of atherosclerosis and highly unstable atherosclerotic plaques
	(iii) Endothelial dysfunction induced by microbial lipopolysaccharides
	(iv) Altered gut microbiota
	(v) Adipokines
	(vi) Calprotectin
	(vii) NOD2/CARD15 gene polymorphism
	(viii) Dyslipidemia
Heart failure	(i) Myocardial fibrosis secondary to altered collagen metabolism, impaired nitric oxide-mediated vasodilation, and deficiencies of vitamins and essential trace elements	[83–87]
	(ii) Heart muscle atrophy due to prolonged use of corticosteroids, total parenteral nutrition, and chronic inflammatory status
	(iii) Myocarditis, endocarditis, and valvulopathy
Arrhythmias and conduction disorders	(i) Interstitial fibrosis and structural and functional cardiac remodeling	[91–95, 99–101]
	(ii) Impaired autonomic nervous system: increased sympathetic and decreased parasympathetic activity
Endocarditis	(i) Bacteremia due to increased transmucosal permeability	[16, 103–106]
	(ii) Predisposing risk factors: immunosuppression, preexistent valvular heart disease, and central venous catheters
Valvulopathies	(i) Myxomatous degeneration	[110, 111]
	(ii) Ascending aorta changes due to chronic systemic inflammation
Takayasu arteritis	(i) Genetic risk factors: HLA-A24:02, HLA-B52:01, and HLA-DRB-115:02	[114, 115]