Table 1.
Endothelial dysfunction in psoriasis and evidence of oxidative stress and inflammation.
| First Author, Year, [Ref.] |
Country | Study Design | Study Groups | Psoriasis Severity/PASI Inclusion Criteria | PASI Mean ± SD/[SEM] or Median (IQR) | Disease Duration (Years, Mean ± SD or [SEM]) | Systemic Antipsoriatic Therapy |
Assessment Method/ Occlusion Site |
Vessel, Measurement Site | Measurements | Effect on Measured Inflammation and Oxidative Stress Parameters | |
|---|---|---|---|---|---|---|---|---|---|---|---|---|
| Psoriasis | Controls | |||||||||||
| Jensen, 2011, [208] | Denmark | Case-control Study | 30 | 30 | Mild to moderate psoriasis/PASI < 10 | 7.3 ± 3.8 | 21.3 ± 17.0 | None | PAT (reactive hyperemia index, RHI; augmentation index, %)/Brachial artery (occlusion) | both index fingers | ↔ RHI; ↔ AI% | ↑ hsCRP (p = 0.011) |
| Mallbris, 2008, [223] | Sweden | Case-control Study | 20 | 20 | Severe psoriasis/PASI > 12 | 14.3 ± 4.8 | 0.4 ± 0.3 | None | FMD, NMD (absolute value vessel dilatation (B2-B1); vessel dilatation as the % of baseline value, %)/Forearm cuff (occlusion) | BA, above the elbow | ↔ B2-B1 ↔ %FMD ↔ %NMD |
↑ hsCRP (p < 0.05) |
| Martyn-Simmons, 2011, [205] | United Kingdom | Prospective Cohort Study | 60 | 117 | Moderate to severe psoriasis/PASI > 10 | 9.15 ± [0.91] | 31 ± [1.6] | Standard systemic therapy: MTX (n = 16, 26.7%); Acitretin (n = 5, 8.3%); ciclosporin (n = 3, 5%), fumaric acid esters (n = 5, 8.3%); Biologics: anti TNF-therapy (n = 13, 21.7%) |
FMD, NMD (vessel dilatation as the % of baseline value, %)/Forearm cuff (occlusion) | BA, above the elbow | ↔ %FMD ↔ %NMD FMD associated with ciclosporin (β = 0.29, p < 0.04) |
↑ hsCRP (p < 0.05) |
| Gisondi, 2009, [224] | Italy | Case-control Study | 39 | 38 | Moderate to severe psoriasis/PASI > 10 | 12.4 ± 4.7 | 14.8 ± 12.7 | None (at least 2 months before inclusion) | cfPWV; no occlusion site crPWV(m/s); no occlusion site |
cfPWV—sensor on CA and FA; crPWV—sensors on CA and RA |
↑ cfPWV (p = 0.001); positive correlation with disease duration (p = 0.0001), not with PASI. ↔ PWVcr |
↔ CRP |
| Balci, 2008, [207] | Turkey | Case-control Study | 43 | 43 | All PASI included | 6.5 ± 4.4 | 13.26 ± 10.55 | None (n = 32, 74%) Standard systemic treatment: acitretin (n = 10, 23%) Biologics: etanercept (n = 1, 2.3%) |
cIMT (mm), no occlusion site FMD, NMD (vessel dilatation as the % of baseline value, %)/Forearm cuff (occlusion) |
cIMT—left and right CCA FMD-BA, above the elbow |
↑ cIMT (p = 0.003) ↓ FMD% (p = 0.002), correlating with disease duration (β = −0.259, p < 0.05) ↓ NMD% (p = 0.013) No association with systemic therapies found. |
/ |
| Ulusoy, 2010, [202] | Turkey | Case-control Study | 28 | 28 | Mild to moderate/PASI 0.1–49.9 | 13 ± 8 | 4 ± 3 | None | FMD, NMD (vessel dilatation as the % of baseline value, %)/3–4 cm proximal to the section of the brachial artery (occlusion) | BA, above the elbow | ↓ FMD% (p < 0.001) ↔ NMD% |
/ |
| Von Stebut, 2019, [220] | Germany | Randomized Controlled Trial | 151 (35 + PsA) |
44 | Moderate to severe/PASI > 10 | A. 19.3 ± 7.9 B. 21.7 ± 10.5 C. 17.5 ± 4.2 D. 19.5 ± 6.1 |
A. 20.6 ± 12.7 B. 20.8 ± 13.3 C. 18.9 ± 11.7 D. 20.3 ± 11.7 |
A. secukinumab 300 mg from baseline to week 52 (n = 48) B. secukinumab 150 mg from baseline to week 52 (n = 54) C. placebo until week 12, then secukinumab 300 mg until week 52 (n = 26) D. placebo until week 12, then secukinumab 150 mg until week 52 (n = 23) |
FMD (vessel dilatation as the % of baseline value, %)/5 cm distal to the measurement site (occlusion) PWVcf (distance/Δtime [m/s]), AI [%], no occlusion site |
FMD—BA, 5–10 cm proximal to the antecubital fossa PWVcf—on CA and FA |
Psoriasis patients compared to healthy controls: ↓ FMD% (at baseline), (p < 0.01) Group A and B compared to 3 and 4 at 12 weeks: ↔ FMD% Group A compared to baseline: ↑ FMD% (p < 0.002) Group B compared to baseline: ↑ FMD% (p = 0.0034) Group D compared to baseline: ↔ FMD%, ↔ PWVcf |
A compared with C + D at week 12: ↓ S100B (mean −0.02, 95%CI −0.03 to 0.01) |
| de Simone, 2011, [201] | Italy | Case-control Study | 32 | 31 | Not specified/all PASI included | 17.9 ± 10.9 | 12.6 ± 10.2 | None (at least 3 months prior) | FMD, NMD (vessel dilatation as the % of baseline value, %)/forearm (occlusion) | Right BA, 2 to 15 cm proximal to the antecubital fossa | ↓ FMD% (p = 0.012), no correlation found with PASI or disease duration ↔NMD% |
↔ CRP ↔ ESR |
| Erfan, 2005, [225] | Turkey | Case-control Study | 60 | 30 | Moderate to severe/PASI ≥ 5 | Pso-ED 10.9 (5–24.6) Pso + ED 10.3 (5–26.9) |
Pso-ED 7.8 (1–30) Pso + ED 15.5 (1–50) |
none | FMD, NMD (vessel dilatation as the % of baseline value, %)/not specified (occlusion) | BA | ↓ FMD (p < 0.05) | ↑ YKL-40 (p < 0.05) ↑ CRP (p < 0.05) Pso + ED vs. controls + ED: ↑ YKL-40 (p < 0.05) |
| Haberka, 2018, [226] | Poland | Case-control Study | 80 | 39 | Mild to moderate | 18.6 ± 10.5 | 15.3 ± 11.2 | none | cfPWV (m/s), no occlusion site, FMD (vessel dilatation as the % of baseline value, %)/proximal portion of the arm (occlusion) cIMT (mm), no occlusion site |
cfPWV—sensors (CCA and CFA) FMD- BA, above the antecubital fossa cIMT—CCA |
↑ cIMT(mm) (p < 0.05) ↓ FMD% (p < 0.001) ↔ PWV m/s |
↑ AOPPs (p < 0.001), sign. assoc. with IMT (r = 0.3), FMD (r = -0.25) ↑ visfatin (p < 0.001) ↔ osteoprogerin, ↔ nesfatin |
| Holzer, 2021, [227] | Austria | Randomized Controlled Trial | 65 | Moderate to severe/PASI ≥ 10 | Adalimumab group: 16.3 ± 5.8 FAE group:16.4 ± 5.9 |
Adalimumab group: 11.9 ± 11.3 FAE group:10.1 ± 8.8 |
Intervention with: Adalimumab (n = 33, 50.8%) FAE (n = 32, 49.2%) + NB-UVB (for non-responders) |
FMD, NMD (vessel dilatation as the % of baseline value, %)/not specified (occlusion) cIMT (mm), no occlusion site |
FMD—BA, above the antecubital fossa cIMT—1st cm of the CCA |
Adalimumab group: ↑ FMD% after intervention (p = 0.048) FAE group: ↔FMD% Both groups: ↔ NMD%, ↔cIMT (mm) |
Adalimumab a.i.:↓hsCRP (p = 0.022); FAE a.i.: ↔ hsCRP; ↓ p-selectin (p = 0.034) Both groups a.i.: ↓E-selectin (FAE: p = 0.041; adalimumab: p = 0.001) |
|
| Erturan, 2014, [228] | Turkey | Case-control Study | 56 | 53 | Mild to moderate/PASI 0.1–49.9 | 3 (range 0.6–27) | 5.5 (range 0.5–50) | None (at least 3 months prior) | FMD (vessel dilatation as the % of baseline value, %)/forearm, bottom of the cuff on the wrist (occlusion) IMT(mm), no occlusion site |
FMD—BA, 2–5 cm proximal to the antecubital fossa cIMT—previous segment of the bifurcation of the CA |
↓ FMD % (p = 0.0001) ↔ cIMT |
↑ sCD40L (p = 0.012) ↔ homocysteine ↔ ESR ↔ hsCRP |
| Karadag, 2010, [204] | Turkey | Case-control Study | 75 (24 + PsA) | 50 | All PASI included | 4.4 (1.8–34) | No data provided | No data obtained | FMD (vessel dilatation as the % of baseline value, %)/proximal forearm (occlusion) | BA | Pso vs. controls: ↓ FMD% (p < 0.001), no correlation with PASI PsA vs. Pso: ↓ FMD (p = 0.096) |
↑ ESR (p = 0.006) |
| Białecka, 2021, [229] | Poland | Case-control Study | 62 (6 + PsA) | 42 | All PASI included | 14.92 ± 6.99 | Assessed, data not provided | Data obtained on past use of systemic therapy (systemic treatment was used in n = 39; 62.9%) | cIMT (mm), no occlusion site cardiac CT: calcium score according to the Agatston scale (CS); mass of calcifications (CM, mg); the volume of calcifications in coronary arteries (CV, mm3) |
cIMT—Both CCA, 2 cm from their bifurcation | ↑ cIMT (p < 0.0001); no correlation with PASI or CRP ↑ amount of calcification |
↑ CRP (p < 0.0001) |
| Bańska-Kisiel, 2016, [230] | Poland | Cross-sectional Study | 74 | none | Mild to moderate/PASI ≤ 50 | 18.7 ± 10.6 | 17.1 ± 11.2 | Biologics (n = 5; 7%) | cIMT (mm), no occlusion site | Both CCA, distal segments | Association between cIMT and PASI (r = 0.33; p = 0.007) | / |
| Troitzsch, 2012, [231] | Germany | Cross-sectional Study | 72 | 1955 | No data | No data | No data | No data provided | cIMT (mm), no occlusion site | Both CCA (10 consecutive measurement points, in 1 mm steps, from the bulb of both sides) | ↑ cIMT (p = 0.001) ↔ carotid plaque prevalence |
↑ hsCRP (p = 0.003) |
| de Oliveira, 2019, [232] | Brazil | Case-control Study | 11 | 33 | Severe/PASI > 10 | No data | No data | MTX (n = 2, 18%) | PWV (m/s), AIx, arm (occlusion) cIMT(mm), no occlusion site |
PWV—not specified cIMT—1 cm from the posterior wall of the CCA |
↑ PWV (p = 0.033) ↑ IMT (left CCA) above the 75th centile (p = 0.045) |
↑ CRP (p < 0.001) |
| Fabi, 2022, [233] | Italy | Case-control Study | 20 * age < 18 |
20 | Not specified | 2.64 ± 2.6 | 1.84 ± 1.18 | Cyclosporine (n = 3, 15%), 2 switched to guselkumab | cIMT(mm), no occlusion site | Both CCA, at least 5 mm below its end | ↑ cIMT (right, p = 0.001; left, p = 0.00), positively correlating with disease duration | / |
| Awad, 2017, [234] | Egypt | Case-control Study | 45 | 45 | Not specified/all PASI included | 10.18 ± 4.6 | cIMT < 1 mm: 10.27 ± 14.07 cIMT > 1 mm: 11.33 ± 6.98 |
none | cIMT(mm), no occlusion site | Both CCA, distal portion of the CCA (10–20 mm proximal to the carotid bulb) | ↑ cIMT (p < 0.001), positively correlating with PASI (r = 0.78, p < 0.001), serum psoriasin (r = 0.48, p > 0.01) and serum koebnerisin (r = 0.48, p < 0.01), but not with disease duration | ↑ psoriasin (p < 0.001) ↑ koebnerisin (p = 0.001), higher levels in patients with subclinical atherosclerosis (p = 0.04) |
| Liu, 2015, [235] | China | Case-control Study | 35 | 20 | BSA > 10% | 15.5 ± 12.7 | 14.0 ± 7.2 | MTX (n = 13, 37.1%) Retinoids (n = 2, 5.7%) |
haPWV (m/s), no occlusion site, cIMT(mm), no occlusion site AI |
haPWV—precordium and both posterior PA cIMT—max. thickness point along a 1-cm section of the CCA proximal to the carotid bulb, both sides |
CD34 + EPC was independently predictive of increased haPWV | ↓ CD34 + EPC (p = 0.02); neg. correlating with haPWV (r = -0.43, p = 0.01) ↔ CD34/KDR + EPC, ↔ CD133/KDR + EPC and ↔ CD133 + EPC |
| El-Mongy, 2009, [236] | Egypt | Case-control Study | 80 (25 + PsA) |
50 | Not specified/all PASI included | 29.1 ± 16 | 12.6 ± 9.5 | No data provided (patients treated with cyclosporine or retinoid were excluded) | cIMT(mm), no occlusion site | right CCA, 1 cm distal to the carotid bifurcation in the posterior wall | ↑ cIMT (p < 0.001), positively correlating with age (r = 0.6, p ≤ 0.001), duration of the disease (r = 0.4, p = 0.001) and PASI (r= 0.5, p ≤ 0.001) | ↑ CRP (p ≤ 0.001) ↑ ESR (p = 0.004) |
| Martinez-Lopez, 2018, [237] | Spain | Prospective Cohort Study | 53 (21 + PsA) |
Self-controlled, 8 m | PASI ≥ 5 | 9.46 ± 3.62 | 17.33 ± 10.78 | Systemic therapy (n = 30, 56.6%) Cyclosporine (n = 10, 18.8%), MTX (n = 10, 18.8%), acitretin (n = 10, 18.8%); Biologics (n = 23, 43.4%); TNF-α inhibitor (etanercept, infliximab, adalimumab), (n = 13, 24.5%); anti-IL12/23 (ustekinumab), (n = 10, 18.8%) Wash out period of 3 months before baseline |
cIMT (mm), no occlusion site | cIMT—left CCA, 1 cm from the carotid bifurcation (6 measurements) | All patients: Decreasing tendency IMT (p = 0.086) MTX a.i.: ↓ IMT (p = 0.045) ustekinumab a.i.: ↓ IMT (p = 0.010) |
/ |
| Piros, 2021, [238] | Hungary | Prospective Cohort Study | 31 (17 + PsA) | Self-controlled, 6 m | Severe psoriasis/PASI > 10 | 18 (14–24) | 24 (16–28) | anti-IL-17 therapy- intervention: secukinumab (n = 20, 64.5%), ixekizumab (n = 11, 35.5%) |
cIMT (mm) bIMT (mm) fIMT (mm); no occlusion site |
cIMT—CCA; bIMT—middle third of the BA fIMT—middle third of the CFA * on both sides |
6 months after baseline, a.i. ↓ cIMT, ↓ bIMT, ↓ fIMT (p < 0.001 for all)—the improvement was more significant in non-calcified arteries than in calcified arteries |
/ |
| Jokai, 2013, [239] | Hungary | Prospective Cohort Study | 16 | Self-controlled, 6 m | Severe psoriasis/PASI > 15 | Baseline: 25.64 (21.2–32.4); ↓ of PASI after 6 months for 1.04 (0–8.8) |
16.8 (4–40) | No biologic therapy at baseline; intervention with TNF-α inhibitors: etanercept (n = 3, 18.8%), infliximab (n = 7, 43.8%), adalimumab (n = 6, 37.5%) during 6 months | cIMT (mm), bIMT (mm), no occlusion site | cIMT—carotid bifurcation bIMT—middle third of the BA |
Group 1— no apparent atherosclerosis (n = 13) ↓ after intervention cIMT(mm) (p = 0.011) ↓ after intervention bIMT(mm) (p = 0.006) Group 2—atherosclerosis present (n = 3) ↔ cIMT, ↔ bIMT (but increasing tendency) |
/ |
| Ikonomidis, 2015, [240] | Greece | Case-control Study | 59 | 59 CAD patients; 40 healthy controls | All PASI included | 11.5 ± 8 | 5.1 ± 1.25 | Ciclosporine (n = 59, 100%) | cfPWV (m/s), augmentation index (CAI, %), no occlusion site, FMD (vessel dilatation as the % of baseline value, %)/occlusion site not specified cIMT(mm), no occlusion site CFR (ratio of peak diastolic velocity after adenosine infusion to peak diastolic velocity at rest), no occlusion site |
cfPWV—sensors (CCA and CFA FMD—BA cIMT—CCA, bulb, ICA; on both sides CFR—color Doppler on LAD |
Compared to healthy controls: ↑ cfPWV; ↑ CAI, ↑ IMT (p < 0.05 for all); IMT values correlating with PASI (r = 0.67, p < 0.01) ↓ FMD, ↓ CFR Compared to CAD patients: ↔ cfPWV; ↔ CAI, ↔ IMT ↔ FMD, ↔ CFR |
Compared to healthy controls: ↑ MDA, ↑ IL-6 (p < 0.05 for both), correlating with cIMT (r = 0.35, p = 0.01 and r = 0.58, p < 0.001) Compared to CAD patients: ↔ MDA, ↔ IL-6 |
| Robati, 2014, [241] | Iran | Case-control Study | 60 | 60 | All PASI included | 23.45 (14.92–33.18) | 10 (4–16.5) | None (exclusion criteria was systemic therapy within the last 6 months) | cIMT (mm), no occlusion site | Right CCA, 1 cm proximal to the bifurcation (at least 3 measurements) | ↑ cIMT (p < 0.0001) | ↑ leptin, ↑ resistin (p < 0.0001) |
| Antonucci, 2014, [242] | Italy | Case-control Study | 40 | 40 | Moderate to severe/PASI > 10 | 16.1 ± ? | Not assessed | Exclusion criteria were: cyclosporine, oral retinoids, systemic steroids; no other data on therapy available | cIMT (mm), no occlusion site | cIMT—CCA, 1 cm proximal to the bifurcation | ↑ IMT (p < 0.001), positively correlating with PASI (r = 0.515, p < 0.01), not with BMI | / |
| Marovt, 2020, [243] | Slovenia | Prospective Cohort Study | 15 (4 + PsA) |
Self-controlled | Moderate to severe/PASI > 10 | PASI 16.78 (11.0–19.8) BSA 12.62 (8–20) |
20.9 (range 3–52) | Intervention with anti-IL-23/IL-17: ustekinumab (n = 4, 26.67%); secukinumab (n = 10, 66.67%); ixekizumab (n = 1, 6.67%) | cfPWV (m/s), no occlusion site, aortic AIx, cIMT (mm), no occlusion site |
CfPWV—CA, FA cIMT—CA, bifurcation level, both sides |
↔ cfPWV ↔ cIMT ↑ central aortic diastolic pressure (mmHg) (p = 0.03) |
/ |
| Elsheikh, 2013, [244] | Egypt | Case-control Study | 60 | 20 | Mild, moderate, severe/all PASI included | 18.49 ± 11.29 | 11.25 ± 6.95 | None (at least 6 weeks prior to cIMT) | cIMT (mm; internal diameter—ID; arterial wall mass index—AWMI), no occlusion site | Both sides at three points: - CCA (10 mm before the bulb) - Bulb (5–10 mm cranially to the start of the bulb - Internal carotid artery column after the flow divider |
↑ cIMT (p = 0.001); ↑ AWMI (p = 0.010) ↓ ID (p = 0.001) - independent predictor of cIMT: duration of disease (r = 0.425, p = 0.008); age (r = 0.362, p = 0.021), PASI score (r = 0.326, p = 0.014); BMI (r = 0.243, p = 0.019) |
/ |
| Yiu, 2010, [206] | China | Case-control Study | 52 | 50 | BSA > 10 | 14.7 ± 12.1 | 15.4 ± 7.1 | Methotrexate (n = 26, 50%) | baPWV (m/s), no occlusion, PAT (index), proximal forearm of the studied hand (occlusion) |
baPWV—ATP and BA; PAT—tip of both middle fingers |
Psoriasis vs. controls: ↑ baPWV (p < 0.01) ↔ PAT index Psoriasis patients on MTX vs. without MTX: ↔ baPWV ↔ PAT index no correlation between baPWV and PAT index (r = 0.09, p = 0.40) |
↑ hsCRP (p < 0.01)—correlating with baPWV (r = 0.51, p < 0.01) and with PASI (r = 0.48, p < 0.01) |
| Kim, 2015, [245] | South Korea | Case-control Study | 54 | 60 | Mild and moderate to severe/all PASI included | 10.7 + 7.0 | 10.4 + 9.7 | Data on previous systemic treatment obtained: n = 49, 90.7% had received systemic treatment at some point | BSI (β) cIMT (mm), no occlusion site |
BSI—region 2 cm from the carotid bifurcation toward the center of the body cIMT—1 cm distal to the far wall of each CCA |
↑ BSI (p < 0.001), correlating with PASI ↔ cIMT (intended to be ↑, no significance) |
/ |
| Patschan, 2018, [246] | Germany | Case-control Study | 30 | 26 | Not specified | 10.2 ± 2.0 | 18.3 ± 2.7 | Past/present treatment with biological drug (n = 10, 33%) | cfPWV (m/s), augmentation index, AI; no occlusion site | Sensors on CA and FA | ↔ PWV (m/s) | ↑CRP ↔ CD133+/KDR+ (EPC) cells |
| Pina, 2016, [219] | Spain | Prospective Cohort Study | 29 | Self-controlled | Moderate to severe psoriasis | 18.9 ± 7.8 | 18.2 ± 12.1 | Anti-TNF-α (intervention): adalimumab Washout period from other systemic therapies of 4 weeks |
FMD (vessel dilatation as the % of baseline value, %), forearm (occlusion); PWV |
FMD—BA, 2–12 cm proximal to the antecubital fossa PWV—right CCA |
A.i. vs. baseline: ↑ FMD%(p = 0.008) ↓ PWV (p = 0.03) |
hsCRP? |
| Balta, 2014, [247] | Turkey | Case-control Study | 32 | 35 | All PASI included | Assessed, but values not presented in paper | Assessed, but values not presented in paper | No data provided | PWV (m/s), augmentation index (AIx), BA (occlusion) | Distance between jugular notch and symphysis pubis | ↑ PWV (m/s), (p = 0.01), no correlation with disease duration or PASI | ↑ hsCRP (p = 0.01) |
| Dregan, 2018, [248] | United Kingdom | Cross-sectional Study | 2091 | 165 149 | Presence of psoriasis diagnosis/all included | Not assessed | Not assessed | Corticosteroids (n = 166, 8% DMARDs (n = 168, 8%) |
photoplethysmography (arterial stiffness index, SI, m/s), no occlusion | Index finger of the dominant hand | ↑ SI (p = 0.016) | / |
| Choi, 2016, [249] | South Korea | Case-control Study | 103 | 103 | All PASI included | 8.7 + 5.5 | 3 (0.5–10) | No data provided | CAVI, right brachial, right ankle (occlusion) PWV(m/s), cAIx |
PWV—between aortic valve and ankle cAIx—BA, RA |
↑ CAVI (p = 0.03) cAIx, correlating with disease duration (r = 0.319, p = 0.001), not with PASI |
↑ CRP (p = 0.025) |
| Hansen, 2018, [250] | Denmark | Cross-sectional Study | 254 | 4431 | Self-reported psoriasis/all included | Not assessed | Not assessed | Not assessed | photoplethysmography (arterial stiffness index, SI), no occlusion | Index finger of the non-dominant hand | ↑ SI (p = 0.04) | ↑ hsCRP |
| Jensen, 2014, [251] | Denmark | Randomized Controlled Trial | 30 Pso, low energy diet | 30 Pso, normal diet | All PASI included | 4.8 (3.8–8.2) intervention group; 5.5 (3.6–6.8) controls |
Not assessed | Not assessed | PAT (reactive hyperemia index, RHI)/Brachial artery (occlusion on the upper arm) | Both index fingers | ↔ RHI | ↔ hsCRP ↔ VCAM ↔ ICAM |
| Nakao, 2018, [222] | Japan | Cohort Study | 15 (7 + PsA) | Self-controlled | Not specified | 5.7 (3.2–12.8) | Mean 18.7 | Intervention with anti TNF-α: infliximab | RH-PAT (RHI), arm opposite to the dominant arm (occlusion) | Fingers of each hand | 6 weeks: ↔ RHI in responders ↓ trend RHI in non-responders (p = 0.09) |
↓ CRP, ↓ ESR (p = 0.016) |
| Sunbul, 2015, [252] | Turkey | Case-control Study | 50 | 50 | Not specified | 13.7 ± 8.9 | 13.5 ± 10.7 | No data (data obtained about previous medication) | PWV(m/s), AIx | ↑ PWV (p = 0.001) ↑ AIx (p = 0.001), no correlation with PASI observed |
↑ NLR (p = 0.002) | |
| Altekin, 2012, [253] | Turkey | Case-control Study | 57 | 60 | Not specified/all PASI included | 7.8 ± 7.4 | 11.3 ± 8.5 | None (no systemic immunosuppressive therapy at least 6 months prior) | cfPWV(m/s), cIMT (mm), no occlusion site |
cfPWV—CA, FA cIMT—1 cm segment of both CCA, 2–3 cm distal to the bulb |
↑ cfPWV (p < 0.001), positively correlating with PASI (r = 0.417, p = 0.001) ↑ max cIMT (p < 0.001) ↑ mean cIMT (p < 0.001) |
/ |
| Enany, 2011, [254] | Egypt | Case-control Study | 50 | 10 | All PASI included | 20.99 ± 16.67 | 6.50 ± 2.95 | None (at least 6 months prior) | cIMT(mm), no occlusion site | CCA, 1 cm proximal to the carotid bulb; bulb; ICA, 1 cm distal to the carotid bifurcation |
↑ cIMT (p < 0.05), correlating with age, disease duration, BMI, PASI score, systolic blood pressure, diastolic blood pressure, leptin levels, LDL levels and triglyceride levels | ↑ leptin (p < 0.05) |
| Divito, 2018, [255] | Italy | Case-control Study | ↓ CV R 34; ↑ CVR 23 | ↓ CVR 39; ↑ CVR15 | Severe/PASI not specified | No data provided | No data provided | No data provided | PWV (m/s) | Not specified | Low CV risk, Pso vs. controls: ↔ PWV High CV risk, Pso vs. controls: ↑ PWV (p = 0.037) |
/ |
| Asha, 2014, [256] | India | Case-control Study | 80 | 80 | Not specified/all PASI included | 15.60 ± 10.79 | 3.42 ± 2.56 | No data provided | cIMT(mm), no occlusion site | Both CA | ↑ mean cIMT (p < 0.001), significant cumulative association with leptin and apoB/apoA-I | ↑ leptin (p < 0.001) |
| Usta, 2011, [203] | Turkey | Case-control Study | 29 | 25 | Not specified/all PASI included | 4.6 ± 3.8 | 13 ± 10 | None (at least 1 month prior) | FMD, NMD (vessel dilatation as the % of baseline value, %), upper arm proximal to the imaged artery segment (occlusion); | BA, 2–4 cm above the antecubital fossa | ↔ FMD ↔ NMD |
↑ CRP (p = 0.011) ↑ fibrinogen (p = 0.011) ↔ ADMA |
| Arias-Santiago, 2012, [257] | Spain | Case-control Study | 72 (25 +PsA) |
61 | Severe/PASI > 10 | mean 19.25 | mean 17.64 | None (at least 2 months prior) | cIMT(mm), no occlusion site | Distal portion of the both CCA, 1 to 2 cm proximal to the carotid bulb | ↑ right cIMT (p = 0.013) ↑ left cIMT (p = 0.042) ↑ presence of carotid atheroma plaques (p < 0.001) |
↑ fibrinogen, ↑ CRP, ↑ ESR, ↑ D-dimer, ↑ homocysteine |
| Alba, 2018, [210] | USA | Case-control Study | 9 (1+ PsA) | 9 | ≥5% BSA | 16 ± 2 BSA | No data provided | None | LDF (NO-dependent vasodilatation—ΔCVClocal heating and CVCpost-l-NAME SNP-induced vasodilatation (flux/mmHg); vascular adrenergic responsiveness, logEC50) |
Cutaneous microcirculation, forearm skin | ↓ NO-dependent vasodilation (p < 0.01), correlating with BSA (r = 0.54, p = 0.04) ↔ SNP-induced vasodilatation After ascorbate infusion: ↔ NO-dependent vasodilation ↔ vascular adrenergic responsiveness ↔ max NE-induced vasoconstriction |
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Legend. PAT—digital peripheral artery tomography; FMD—flow-mediated dilatation; NMD—nitroglycerin-mediated dilatation; cfPWV—carotid-femoral pulse wave velocity; crPWV—carotid-radial pulse wave velocity; cIMT—carotid intima-media thickness; bIMT—brachial intima-media thickness; CFR—coronary flow reserve, by doppler echocardiography; baPWV—brachial-ankle pulse wave velocity; haPWV—heart to ankle pulse wave velocity; PWA—pulse wave analysis; CAVI—Cardio-Ankle Vascular Index; cAIx—central augmentation index; RH-PAT—reactive hyperemia-peripheral arterial tonometry; LDF—Laser Doppler flowmetry; CCA—common carotid artery; FA—femoral artery, BA—brachial artery; CFA—common femoral artery; RA—radial artery; ICA—internal carotid artery; LAD—left anterior descending; CFA—common femoral artery; ATP—posterior tibial artery; FAE—fumaric acid esters; a.i.—after intervention; PsA—psoriatic arthritis; CT—computed tomography; MTX—methotrexate; BSI—beta stiffness index; AI/AIx—augmentation index; ESR—erythrocyte sedimentation rate; ED—endothelial dysfunction; CVR—cardiovascular risk; NLR—neutrophil-to-lymphocyte ratio; PBR—perfused boundary region, a marker of glycocalyx barrier function; PA—popliteal artery; CVC—cutaneous vascular conductance; m- months; β—standard regression coefficient; ↔, no significant difference between groups; ↑, increased; ↓, decreased; *—special remark.