Patients with long-standing psoriasis are high-risk cardiac patients and should be managed accordingly. Especially in young patients with first cardiological symptoms an intensive work-up is indicated.
Cardiovascular comorbidities in psoriasis may lead to a reciprocal influence – with implications for disease progression. About 70% of all psoriasis patients have at least one concomitant disease [1]. There is a significantly increased prevalence of cardiovascular diseases, obesity, diabetes, metabolic syndrome, depression, inflammatory autoimmune diseases and addiction. Severe psoriasis not only increases the risk of myocardial infarction and stroke, but also cardiovascular mortality [3]. According to data from a secondary analysis, the prevalence of moderate to severe coronary calcification is fivefold higher in patients with psoriasis than in a healthy control group [4]. In addition, psoriasis sufferers have been shown to have a similar risk of coronary heart disease as patients 10 years older with hyperlipidemia [2,5]. Cytokine-mediated inflammatory processes, which play a role in the etiology of psoriasis, are thought to be an independent risk factor for cardiovascular comorbidities. These in turn influence the inflammatory mechanisms underlying psoriasis [2] (Fig. 1) . For example, the cytokine IL-6 is associated with an increased risk of cardiovascular events. However, interleukin-17A, which is central in chronic skin disease, also plays an important role in the genesis of vascular dysfunction and inflammation. In addition, inflammation of the aorta in psoriatic patients correlates positively with the presence of CHD. An ultrasound study published in 2019 showed that psoriasis patients have an increased number of arteriosclerotic plaques in the femoral artery compared to a control group and insulin resistance is the most important determinant of atherosclerosis [6]. Obesity is a risk factor for both psoriasis and cardiovascular disease and is associated at the cellular level (proinflammatory cytokines, inflammatory adipokines, anti-inflammatory adipokines) with a state of chronic inflammation [2].
Comprehensive therapy management indicated
Efficient anti-inflammatory treatment with a general reduction in inflammatory burden may therefore also reduce cardiovascular risk. However, attention should also be paid to the fact that some medications used to treat cardiovascular comorbidities may affect psoriasis therapy [2]: Antihypertensives including beta-blockers and ACE inhibitors may worsen psoriasis symptoms in some patients, and interactions between ciclosporins and statins may induce rabdomiolysis. A cohort study demonstrated that improvement in psoriasis severity was associated with a reduction in aortic vascular inflammation at one-year follow-up [8]. A cohort study published in 2019 in patients with moderate to severe psoriasis demonstrated that in biologic-naïve patients, biologics therapy resulted in a significant reduction in coronary inflammation compared with the conventionally treated control group [6].
Literature:
- Augustin M, et al: Use of system therapeutics and biologics in guideline-based therapy of moderate to severe psoriasis vulgaris. PsoNet Magazine 2017/1.
- Torres T: Treating psoriasis in patients with metabolic comorbidities. Psoriasis treatment, slide presentation, Tiago Torres, MD, PhD, EADV Congress, Madrid, Oct. 12, 2019.
- Armstrong EJ, Harskamp CT, Armstrong AW: Psoriasis and Major Adverse Cardiovascular Events: A Systematic Review and Meta-Analysis of Observational Studies. J Am Heart Assoc 2013; 2(2): e000062.
- Mansouri B, et al: Comparison of Coronary Artery Calcium Scores Between Patients With Psoriasis and Type 2 Diabetes. JAMA Dermatol 2016; 152(11): 1244-1253.
- Lerman JB, et al: Coronary Plaque Characterization in Psoriasis Reveals High-Risk Features That Improve After Treatment in a Prospective Observational Study Circulation 2017; 136(3): 263-276.
- Elnabawi YA, et al: Association of Biologic Therapy With Coronary Inflammation in Patients With Psoriasis as Assessed by Perivascular Fat Attenuation Index. JAMA Cardiol 2019; 4(9): 885-891.
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