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Background: Psoriasis is associated with a heightened risk of cardiovascular disease and higher prevalence of metabolic syndrome.Objective: Investigate the effect of metabolic syndrome and its factors on early coronary artery disease assessed as noncalcified coronary burden by coronary computed tomography angiography in psoriasis.Methods: This cross-sectional study consisted of 260 participants with psoriasis and coronary computed tomography angiography characterization. Metabolic syndrome was defined according to the harmonized International Diabetes Federation criteria.Results: Of the 260 participants, 80 had metabolic syndrome (31%). The metabolic syndrome group had a higher burden of cardiometabolic disease, systemic inflammation, noncalcified coronary burden, and high-risk coronary plaque. After adjusting for Framingham risk score, lipid-lowering therapy, and biologic use, metabolic syndrome (β = .31; P < .001) and its individual factors of waist circumference (β = .33; P < .001), triglyceride levels (β = .17; P = .005), blood pressure (β = .18; P = .005), and fasting glucose (β = .17; P = .009) were significantly associated with noncalcified coronary burden. After adjusting for all other metabolic syndrome factors, blood pressure and waist circumference remained significantly associated with noncalcified coronary burden.Limitations: Observational nature with limited ability to control for confounders.Conclusions: In psoriasis, individuals with metabolic syndrome had more cardiovascular disease risk factors, systemic inflammation, and noncalcified coronary burden. Efforts to increase metabolic syndrome awareness in psoriasis should be undertaken to reduce the heightened cardiovascular disease risk. [ABSTRACT FROM AUTHOR]

Background: Psoriasis is associated with elevated risk of heart attack and increased accumulation of subclinical noncalcified coronary burden by coronary computed tomography angiography (CCTA). Machine learning algorithms have been shown to effectively analyze well-characterized data sets.Objective: In this study, we used machine learning algorithms to determine the top predictors of noncalcified coronary burden by CCTA in psoriasis.Methods: The analysis included 263 consecutive patients with 63 available variables from the Psoriasis Atherosclerosis Cardiometabolic Initiative. The random forest algorithm was used to determine the top predictors of noncalcified coronary burden by CCTA. We evaluated our results using linear regression models.Results: Using the random forest algorithm, we found that the top 10 predictors of noncalcified coronary burden were body mass index, visceral adiposity, total adiposity, apolipoprotein A1, high-density lipoprotein, erythrocyte sedimentation rate, subcutaneous adiposity, small low-density lipoprotein particle, cholesterol efflux capacity and the absolute granulocyte count. Linear regression of noncalcified coronary burden yielded results consistent with our machine learning output.Limitation: We were unable to provide external validation and did not study cardiovascular events.Conclusion: Machine learning methods identified the top predictors of noncalcified coronary burden in psoriasis. These factors were related to obesity, dyslipidemia, and inflammation, showing that these are important targets when treating comorbidities in psoriasis. [ABSTRACT FROM AUTHOR]

Background: The contribution of inflammation to the incidence of cardiovascular disease (CVD) has been increasingly recognized in recent years. We investigated the relationship of aortic vascular uptake of 18F-FDG by PET/CT and aortic wall thickness (AWT) by MRI in psoriasis, a chronic inflammatory disease with increased incidence of CVD. One hundred sixty-five patients with plaque psoriasis participated in an ongoing longitudinal cohort study. Subclinical atherosclerosis was assessed as aortic uptake of 18F-FDG by PET/CT reported as target-to-background ratio (TBR) and AWT by MRI reported as maximal thickness. Results: Patients with psoriasis were middle aged, predominantly male, and had mild CV risk by traditional risk factors. Psoriasis severity as measured by PASI score was a notable determinant of AWT (ρ = 0.20, p = 0.01). Moreover, aortic vascular uptake of 18F-FDG associated with AWT by MRI at baseline in unadjusted analysis (β = 0.27 p = 0.001) and following adjustment for traditional cardiovascular risk factors, waist-to-hip ratio, and statin use (β = 0.21 p = 0.01). Finally, following 1 year of psoriasis treatment, a decrease in aortic vascular uptake of 18F-FDG was associated with a reduction in AWT in fully adjusted models (β = 0.33, p = 0.02). Conclusion: In conclusion, we demonstrate that psoriasis severity and aortic vascular uptake of 18F-FDG in the aorta were associated with AWT. Following treatment of psoriasis, a decrease in aortic vascular uptake of 18F-FDG was associated with a reduction in AWT at 1 year. These findings suggest that aortic vascular uptake of 18F-FDG is associated with early evidence of vascular disease assessed by aortic wall thickness. Prospective studies in larger populations including other inflammatory diseases are warranted. [ABSTRACT FROM AUTHOR]

Introduction: In individuals without chronic inflammatory conditions, chronic stress independently associates with cardiovascular disease (CVD) in part via a mechanism that involves heightened activity of the amygdala. Psoriasis (PSO), a chronic inflammatory condition, with increased prevalence of stress and subclinical CVD, provides a useful human model to study the effects of perceived psychological stress on CVD. We aimed to study whether there was a relationship between resting amygdala activity (AmygA) and high risk coronary plaque in PSO. Methods: Consecutive PSO patients (N=105) underwent FDG PET/CT scans (60 minutes post-FDG injection) to quantify perceived stress as measured by AmygA target-to-background ratio. Presence of high risk plaque was determined by plaque characterization via CCTA. HRP identification was defined as either positive remodeling (index ≥ 1.1) and/or low attenuation (< 30 HU). The cohort was stratified by mean AmygA values and subsequently statistically analyzed via multivariable logistic regression (STATA 12). Results: The cohort was middle-aged, predominantly male, low CV risk by Framingham risk score and mild-moderate psoriasis severity (Table 1). Unadjusted logistic regression illustrated significant increase in odds of HRP prevalence for patients with higher AmygA (Odds ratio [Confidence Interval]: 3.33 [1.41-7.84]) which remained significant independent of cardiovascular risk factors, statin use, and PSO therapy (2.65 [1.01-6.91]). Conclusion: Perceived stress assessed by AmygA was associated with increased prevalence of HRP in PSO beyond adjustment for cardiovascular risk factors. As such, neurobiological mechanisms related to chronic psychosocial stress, may play a role in inflammatory atherogenesis. [ABSTRACT FROM AUTHOR]

Introduction: Retrospective analysis shows that individuals with history of major adverse cardiovascular events (MACE) have increased aortic wall thickness (AWT) compared to those without MACE but of similar CV risk. AWT at the infrarenal level predicted incidence of MACE in the Dallas Heart Study (HR 1.28 per 1 SD increase, equivalent to 0.33 mm). Since wall thickness varies throughout the vasculature, data on the prospective relation of max and mean thoracic AWT to MACE is needed. Hypothesis: AWT in the thoracic aorta will prospectively predict incident CV events in the MESA study. Methods: 779 participants in the MESA study who underwent MRI at baseline were followed for incident hard CHD events (MI, CHD death, resuscitated and cardiac arrest), hard CVD (also includes stroke), all CVD (including angina), CV mortality, and atrial fibrillation (AF) (detected by analysis of discharge codes for new hospitalizations). The relationship between thoracic AWT and MACE was assessed using Cox proportional hazard regression. Axial images of the descending thoracic aorta were obtained at the level of the right pulmonary artery at mid-diastole. Thoracic aortic wall thickness was obtained using MASS vessel wall (Medis, The Netherlands). Results: Median follow-up time was 14.0 years; 779 study participants were included. In these participants, 101 new CV events occurred in addition to 92 new AF events. In univariate analysis, max AWT was a predictor of hard CV disease, MI, and new AF (HR 1.33 per 1 mm increase in AWT, p=0.02; HR 1.53, p=0.01; HR 1.25, p=0.04, respectively). Unadjusted, mean AWT was a predictor of all CVD and new AF (HR 1.49, p=0.02; HR 1.93, p=0.001). After adjustment for traditional CV risk, mean AWT remained a predictor of new AF (HR 1.67, p=0.01) (Table 1). Conclusions: Mean thoracic AWT was not associated with MACE after adjustment for CV risk factors. However, mean thoracic AWT was independently associated with incident atrial fibrillation, indicating a potential role in the pathophysiology of this condition. [ABSTRACT FROM AUTHOR]

Introduction: Psoriasis (PSO) is a chronic inflammatory disorder associated with increased cardiovascular (CV) risk and lipoprotein dysfunction. Small dense LDL particle number (s-LDLp) is now recognized as an important predictor of CV events. Furthermore, non-calcified coronary plaque burden (NCB) is associated with future CV events and is increased in PSO. Hypothesis: A reduction in psoriasis severity at one year would be associated with a reduction in s-LDLp levels and change in NCB. Methods: Consecutive PSO patients (N = 138) underwent CCTA (Toshiba, 320-dector row) for coronary NCB characterization using QAngio (Medis) at baseline and 1-year. Lipoprotein profiling was done using NMR spectroscopy. Psoriasis severity was assessed using the Psoriasis Area Severity Index (PASI). Results: The cohort was middle aged, predominantly male, low CV risk by FRS, and had moderate-to-severe PSO severity at baseline (Table 1). PSO patients with decreased psoriasis at one-year had a decrease in s-LDLp (537.5 ± 37.5 vs 338.8 ± 34.9, p<0.001) with comparable LDL concentration (LDLc 105.9 ± 4.1 vs 109.4 ± 6.9, p=0.27) at 1-year. NCB (1.22 ± 0.004 vs 1.14 ± 0.004, p <0.001) decreased concurrent with improvement in PASI. In contrast, PSO patients with worsening psoriasis severity at one-year had increased LDLc (103.1 ± 7.1 vs 126.2 ± 13.0, p = 0.01), comparable s-LDLp (487.5 ± 37.5 vs 447.1 ± 40.8, p = 0.11) levels, and a non-significant increase in NCB (1.05 ± 0.05 vs 1.11 ± 0.06, p =0.15). Finally, change in NCB associated with change in s-LDLp in all PSO patients beyond adjustment for CV risk factors (Beta= 0.13, p=0.03). Conclusions: Psoriasis improvement was associated with improvement in s-LDLp and NCB beyond traditional CV risk factors. These findings underscore the need to understand the spectrum of LDL characterization in context of sub-clinical atherosclerosis and demonstrate the potential incremental value NMR profiling may provide to better capture CV risk in chronic inflammatory diseases. [ABSTRACT FROM AUTHOR]

Introduction: Evidence suggests that inflammatory mediators are important in the pathogenesis of atherosclerosis and their inhibition not only reduces cardiovascular (CV) events, but also may favorably modify plaque morphology. Psoriasis (PSO) is a chronic inflammatory disease associated with early myocardial infarction and it was recently shown that it is associated with non-calcified plaque. We hypothesized that anti-inflammatory biologic therapy for psoriasis will favorably modify coronary plaque morphology compared to non-biologic treated patients. Methods: Consecutive patients (n=107) stratified by biologic therapy underwent coronary computed tomography angiography (320 detector row, Toshiba) at baseline and one-year. Coronary plaque indices and attenuation-based plaque sub-components were quantified using dedicated software (QAngio, Medis). Reader was blinded to both time of scan and treatment. Results: PSO patients were middle aged and at low CV risk by traditional risk scores with no significant differences in demographics, laboratory values, or coronary indices between the two groups. At one-year (Table 1) , there was a reduction in non-calcified plaque burden in the biologic treated group only (1.12 ± 0.46 mm2 vs. 1.04 ± 0.40 mm2; p<0.001). While there was a significant reduction in necrotic core (NC) in the biologic group, there was progression of NC in the non-biologic group (ΔNC, Biologic: -0.11 mm2 vs. Non-biologic: 0.005 mm2; p=0.02). Additionally, there was an increase in fibrous burden in both groups; however, the difference between change in fibrous burden (FB) in the biologic group was greater (ΔFB, Biologic: 0.02 mm2 vs. Non-biologic: 0.008 mm2; p=0.02). After adjustment for traditional CV risk factors including age, gender, body mass index, and statin use, biologic therapy was associated with reduction in NC (β=0.13, p=0.02). Conclusions: Biologic therapy had significant effects on coronary plaque morphology, with a reduction in overall non-calcified plaque burden driven by increases in fibrous burden and decrease in necrotic core. These findings suggest that biologic therapies may reduce both coronary plaque burden and high-risk features. Larger, randomized studies are needed to confirm these results. [ABSTRACT FROM AUTHOR]