Clinical trial NCT03228017: Subclinical Cardiovascular Disease in Psoriatic Disease
Official title: Subclinical Cardiovascular Disease in Psoriatic Disease
Study type: INTERVENTIONAL
Overall status: COMPLETED
Phase: PHASE4
Conditions: Cardiovascular Diseases
Myocardial Infarction
Atherosclerotic Cardiovascular Disease
Thrombotic Vascular Disease
Keywords: cardiovascular disease
CVD
Lead sponsor: NYU Langone Health
Sponsor class: OTHER
First posted: 2017-07-24
Enrollment: 63
Sex: ALL
Minimum age (years): 18
Maximum age (years): 90
Standard ages: ADULT
OLDER_ADULT
Accepts healthy volunteers: yes
Allocation: NON_RANDOMIZED
Intervention model: PARALLEL
Primary purpose: TREATMENT

Brief summary: This study will look at how chronic inflammation seen in psoriatic disease translates into the increased atherosclerotic and thrombotic risk and how treatment reduces this CVD risk. The Aim of this study is to 1) Evaluate the association between moderate to severe psoriatic disease and measures of vascular function. 2) Evaluate the association between moderate to severe psoriatic disease and measures of thrombotic risk. 3) Understand how traditional medications used in cardiovascular disease (CVD) prevention such as aspirin and statins affect vascular function and thrombotic risk in those with moderate to severe psoriatic disease.

Detailed description: Cardiovascular disease (CVD) remains the leading cause of death in the US. Five modifiable risk factors: smoking, hyperlipidemia, diabetes, hypertension and obesity, account for 50% of CVD mortality between the ages of 45 - 79.1 These traditional cardiac risk factors dictate who to treat with primary prevention measures but do not take into account patient-specific disease states such as psoriatic disease including psoriasis and psoriatic arthritis, which predispose to chronic inflammation. Patients with psoriatic disease have an increased risk of atherosclerotic heart disease and myocardial infarctions compared to matched controls.

Eligibility criteria: Inclusion Criteria:

* Subjects with a history of moderate to severe psoriatic disease
* Group 2: Healthy subjects without known psoriatic disease or cardiovascular disease

Exclusion Criteria:

* Unable to speak Spanish or English
* Active smoking (within the past year)
* Autoimmune, rheumatologic or inflammatory disease which are not psoriasis or psoriatic arthritis
* Known active cancer receiving treatment
* Pregnancy
* Anemia (hemoglobin \< 9 mg/dl) or thrombocytopenia (Platelet count \<75), or thrombocytosis (Platelet count \>600)
* A history of severe bleeding or bleeding disorders
* Current medication use which interact with either aspirin or atorvastatin
* Chronic kidney disease (CrCl \< 30ml/min)
* Congestive heart failure
* Currently taking aspirin or a statin.
* NSAID use within the past 48 hours

Primary outcomes:
measure: Mean Fold Change in Brachial Vein Endothelial Inflammatory Transcript
timeFrame: Baseline, 5 Months
Secondary outcomes:
measure: Fold Change Change in Composite Endothelial Inflammation
timeFrame: Baseline (pre-Aspirin), 2 weeks (post-Aspirin)
measure: Fold Change in Composite Endothelial Inflammation
timeFrame: Baseline (pre-Atorvastatin), 2 weeks (post-Atorvastatin)
measure: Change in Levels of Circulating Thromboxane B2
timeFrame: Baseline (pre-Aspirin), 2 weeks (post-Aspirin)
Other outcomes:
Locations:
city: New York
country: United States
facility: New York University School of Medicine
state: New York
Study officials:
affiliation: NYU Langone Health
name: Jeffrey Berger, MD
role: PRINCIPAL_INVESTIGATOR
References:
citation: Garshick MS, Block R, Drenkova K, Tawil M, James G, Brenna JT. Statin therapy upregulates arachidonic acid status via enhanced endogenous synthesis in patients with plaque psoriasis. Prostaglandins Leukot Essent Fatty Acids. 2022 May;180:102428. doi: 10.1016/j.plefa.2022.102428. Epub 2022 Apr 16.
citation: Garshick MS, Tawil M, Barrett TJ, Salud-Gnilo CM, Eppler M, Lee A, Scher JU, Neimann AL, Jelic S, Mehta NN, Fisher EA, Krueger JG, Berger JS. Activated Platelets Induce Endothelial Cell Inflammatory Response in Psoriasis via COX-1. Arterioscler Thromb Vasc Biol. 2020 May;40(5):1340-1351. doi: 10.1161/ATVBAHA.119.314008. Epub 2020 Mar 5.
citation: Garshick MS, Barrett TJ, Wechter T, Azarchi S, Scher JU, Neimann A, Katz S, Fuentes-Duculan J, Cannizzaro MV, Jelic S, Fisher EA, Krueger JG, Berger JS. Inflammasome Signaling and Impaired Vascular Health in Psoriasis. Arterioscler Thromb Vasc Biol. 2019 Apr;39(4):787-798. doi: 10.1161/ATVBAHA.118.312246.