COMMENTARY

Could Treating Psoriasis Slow Coronary Artery Disease Progression?

Graeme M. Lipper, MD

Disclosures

November 17, 2016

Association Between Changes in Coronary Artery Disease Progression and Treatment With Biologic Agents for Severe Psoriasis

Hjuler KF, Bøttcher M, Vestergaard C, Bøtker HE, Iversen L, Kragballe K
JAMA Dermatol. 2016;152:1114-1121

Study Summary

Moderate to severe psoriasis vulgaris has been linked to multiple potentially life-shortening comorbidities, including diabetes mellitus, metabolic syndrome, coronary artery disease, and myocardial infarction.[1,2] This has led to the concept of psoriasis as a chronic inflammatory state predisposing psoriatic individuals to cardiovascular disease.[2] In fact, psoriatic patients treated with tumor necrosis factor alpha (TNF alpha) inhibitors have shown a reduction in the proinflammatory marker C-reactive protein and a reduction in arterial intima-media thickness.[3,4] These tantalizing findings raise the possibility that biologic drugs targeting proinflammatory cytokines (TNF alpha, IL-12/23, IL-17) may delay the progression of coronary artery disease (CAD) in patients with moderate to severe psoriasis vulgaris.

To further explore this idea, Hjuler and colleagues conducted a prospective, controlled, observer-blinded clinical study in which they enrolled 56 adult patients (71% male) with severe psoriasis vulgaris (PASI scores of at least 10). Patients with symptomatic CAD were excluded from the study. All patients had baseline and follow-up coronary artery CT imaging. Half of the study participants (n = 28) started biologic therapy, primarily with adalimumab (n = 21). The 56 control patients had comparable characteristics, including PASI scores, but declined systemic therapy.

Patients receiving biologic therapy responded well to treatment, with a mean PASI score reduction of 87.6%. To assess the effect of biologic therapy on atherosclerotic plaque progression, investigators used both noncontrast coronary artery calcium CT and contrast-enhanced coronary CT angiography at baseline and after 13 months.

Blinded investigator analysis of these images showed:

  • Coronary artery calcium scores remained stable in the intervention group and progressed in the control group (P = .02).

  • The number of coronary artery segments with luminal narrowing did not change in either group.

  • In contrast, the severity of luminal narrowing did not change in the treatment group but worsened in the control group, consistent with atherosclerotic disease progression in the latter (P = .02).

  • Mean serum levels of C-reactive protein dropped in the treatment group but did not change in the control group. In contrast, mean serum lipid levels were stable in both the treatment and control groups.

Viewpoint

The link between psoriasis and cardiovascular disease is well established, with prior studies showing that blockade of proinflammatory cytokines such as TNF alpha reduces serum markers of inflammation and may even slow the progression of cardiovascular disease.[5]

Hjuler and colleagues now add to this growing body of encouraging data by showing how biologic therapy seems to slow progression of coronary atherosclerotic plaque progression—that is, at least over a 13-month period in patients with severe psoriasis lacking any symptoms of CAD. Of note, the investigators excluded all patients with symptomatic CAD or "major uncontrolled cardiovascular risk factors, prior cardiovascular events or coronary artery vascularization." Hence, these results cannot be extrapolated to the general psoriasis population, which would include individuals with symptomatic cardiovascular disease.

While results such as these are encouraging, studies have yet to show any reduction in CAD-related mortality in patients with psoriasis or other inflammatory conditions taking biologics. Future controlled studies should aim to distinguish between the potential cardioprotective effects of different classes of biologics because there is no reason to assume that drugs targeting TNF alpha, IL-12/23, and IL-17 will all have comparable cardio-protective effects.

Abstract

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