Cardiovascular involvement in ankylosing spondylitis and axial spondyloarthritis: epidemiology, mechanisms, and clinical management.

Ankylosing spondylitis (AS) and axial spondyloarthritis (axSpA) are chronic inflammatory diseases primarily affecting the axial skeleton. Increasing evidence indicates that their impact extends beyond the musculoskeletal system and includes clinically relevant cardiovascular involvement. Cardiovascular disease has become an important determinant of long-term outcomes in these patients, with growing evidence showing increased risks of myocardial infarction, stroke, atrial fibrillation, and other major adverse cardiovascular events. In addition to overt clinical events, subclinical vascular abnormalities, endothelial dysfunction, arterial stiffness, and structural cardiac changes are frequently observed. Cardiovascular injury in this setting arises from a complex interplay between traditional risk factors and persistent systemic inflammation. Inflammatory pathways involving tumor necrosis factor, interleukin-17, and interleukin-6 appear to promote endothelial activation, oxidative stress, lipid dysfunction, vascular remodeling, and atherosclerosis. Current evidence suggests that tumor necrosis factor inhibitors may provide cardiovascular benefit through improved control of inflammation, whereas the long-term cardiovascular effects of interleukin-17 inhibitors, non-steroidal anti-inflammatory drugs, and Janus kinase inhibitors remain incompletely defined. These findings support a more integrated clinical approach in AS/axSpA, combining disease control with cardiovascular risk assessment, modification of conventional risk factors, and ongoing cardiovascular surveillance.