Background Recent studies suggest that psoriasis, particularly if severe, may be a risk factor for major adverse cardiac events such as myocardial infarction, stroke, and mortality from cardiovascular disease. We compared the risk of major adverse cardiac events between patients with psoriasis and the general population and estimated the attributable risk of severe psoriasis. Methods We performed a cohort study in the General Practice Research Database. Severe psoriasis was defined as receiving a psoriasis diagnosis and systemic therapy (N=3,603). Up to 4 patients without psoriasis were selected from the same practices and start dates for each patient with psoriasis (N=14,330). Results Severe psoriasis was a risk factor for major adverse cardiac events (hazard ratio 1.53; 95% confidence interval 1.26, 1.85) after adjusting for age, gender, diabetes, hypertension, tobacco use and hyperlipidemia. After fully adjusted analysis, severe psoriasis conferred an additional 6.2% absolute risk of 10-year major adverse cardiac events. Conclusions Severe psoriasis confers an additional 6.2% absolute risk of 10-year rate of major adverse cardiac events compared to the general population. This potentially has important therapeutic implications for cardiovascular risk stratification and prevention in patients with severe psoriasis. Future prospective studies are needed to validate these findings.
To evaluate the feasibility of using [18F]fluorodeoxyglucose positron emission tomographycomputed tomography (FDG-PET/CT) to detect and quantify systemic inflammation in patients with psoriasis.Design: Case series with a nested case-control study.Setting: Referral dermatology and preventive cardiology practices.Participants: Six patients with psoriasis affecting more than 10% of their body surface area and 4 controls age and sex matched to 4 of the patients with psoriasis for a nested case-control study. Main Outcome Measures:The FDG uptake in the liver, musculoskeletal structures, and aorta measured by mean standardized uptake value, a measure of FDG tracer uptake by macrophages and other inflammatory cells.Results: FDG-PET/CT identified numerous foci of inflammation in 6 patients with psoriasis within the skin, liver, joints, tendons, and aorta. Inflammation in the joints
Objective To understand whether directly-measured psoriasis severity is associated with vascular inflammation assessed by 18F-fluorodeoxyglucose positron emission tomography computed tomography (FDG PET/CT). Approach In depth cardiovascular and metabolic phenotyping was performed in adult psoriasis patients (n=60) and controls (n=20). Psoriasis severity was measured using psoriasis area severity index (PASI). Vascular inflammation was measured using average aortic target-to-background ratio using FDG PET/CT. Results Both the psoriasis patients (28 men, 32 women, mean age 47 years) and controls (13 men, 7 women, mean age 41 years) were young with low cardiovascular risk. PASI scores (Median 5.4; IQR 2.8-8.3) were consistent with mild to moderate skin disease severity. Increasing PASI score was associated with an increase in aortic TBR (β=0.41, p=0.001), an association that changed little after adjustment for age, sex and Framingham risk score. We observed evidence of increased neutrophil frequency (mean psoriasis: 3.7±1.2; vs 2.9±1.2; p=0.02) and activation by lower neutrophil surface CD16 and CD62L in blood. Serum levels of S100A8/A9 (745.1±53.3 vs 195.4±157.8 ng/mL; p<0.01) and neutrophil elastase-1 (43.0±2.4 vs 30.8±6.7 ng/mL; p<0.001) were elevated in psoriasis. Finally, S100A8/A9 protein related to both psoriasis skin disease severity (β=0.53; p=0.02) and vascular inflammation (β=0.48; p=0.02). Conclusions Psoriasis severity is associated with vascular inflammation beyond cardiovascular risk factors. Psoriasis increased neutrophil activation and neutrophil markers, and S100A8/A9 related to both skin disease severity and vascular inflammation.
Objectives Psoriasis is a Th-1/17 mediated inflammatory disease associated with increased risk of cardiovascular disease (CVD). Inflammation may modulate lipoprotein particle number and directly impair HDL functions, in particular reverse cholesterol transport (RCT). We sought to study how chronic in vivo inflammation modulates lipoprotein particle composition using nuclear magnetic resonance spectroscopy (NMR) and HDL efflux in psoriasis. Methods and Results We prospectively enrolled a consecutive sample of patients with psoriasis (n=122) and compared lipoprotein and metabolic risk factors to patients without psoriasis (n=134). Fasting lipids, insulin, glucose were measured by standard assays, and lipoprotein concentration and size were measured by NMR. In a random subset (n=100 each group), HDL efflux capacity was quantified using a validated ex vivo system involving the incubation of macrophages with apolipoprotein B-depleted serum from patients. Traditional lipid concentrations were similar in both groups except for HDL concentration which was lower in psoriasis (43 mg/dL (36–58) vs 50 (42–62), p<0.01). However, NMR showed an atherogenic profile in psoriasis similar to that observed in diabetes, with significant increase in LDL particle concentration [1210.5 (1002–1498) vs 1115 (935–1291), p=0.03] with decrease in LDL size [20.6 (20.3–21.1) vs 21.3 (20.6–21.1), p<0.001] beyond CV risk factors and HOMA-IR (p=0.001). Finally, HDL efflux capacity was lower in psoriasis compared to controls in fully adjusted models (beta −0.14, p=0.001). Conclusions These data support a more atherogenic lipoprotein profile by NMR and decreased HDL efflux capacity in psoriasis patients compared to controls beyond CVD risk factors. The abnormal lipoprotein particle composition and HDL efflux capacity in psoriasis may provide a link between psoriasis and CVD.
Rationale GlycA, an emerging inflammatory biomarker, predicted cardiovascular events in population-based studies. Psoriasis, an inflammatory disease associated with increased cardiovascular risk, provides a model to study inflammatory biomarkers in cardiovascular disease (CVD). Whether GlycA associates with psoriasis and how it predicts subclinical CVD beyond hsCRP in psoriasis is unknown. Objective To investigate the relationships between GlycA and psoriasis, and between GlycA and subclinical CVD. Methods and Results Psoriasis patients and controls (n=412) participated in a two-stage study. We measured GlycA by NMR spectroscopy. NIH participants underwent 18-FDG PET/CT scans to assess vascular inflammation (VI) and coronary CT angiography to quantify coronary artery disease (CAD) burden. Psoriasis cohorts were young (mean age=47.9), with low cardiovascular risk and moderate skin disease. HsCRP and GlycA were increased in psoriasis compared to controls [GlycA: (PENN: 408.8±75.4 vs. 289.4±60.2, p<0.0001, NIH: 415.8±63.2 vs. 346.2±46, p<0.0001)] and demonstrated a dose-response with psoriasis severity. In stage 2, VI (β=0.36, p<0.001) and CAD (β=0.29, p=0.004) associated with GlycA beyond CV risk factors in psoriasis. In ROC analysis, GlycA added value in predicting VI (p=0.01) and CAD (p<0.01). Finally, initiating anti-TNF therapy (n=16) reduced psoriasis severity (p<0.001), GlycA (463.7±92.5 vs. 370.1±78.5; p<0.001) and VI (1.93±0.36 vs. 1.76±0.19; p<0.001), while GlycA remained associated with VI (β=0.56, p<0.001) post-treatment. Conclusions GlycA associated with psoriasis severity and subclinical CVD beyond traditional CV risk and hsCRP. Moreover, psoriasis treatment reduced GlycA and VI. These findings support the potential utility of GlycA in subclinical CVD risk assessment in psoriasis and potentially other inflammatory diseases.
COVID-19 infection can affect the cardiovascular system. We sought to determine if left ventricular global longitudinal strain (LVGLS) is affected by COVID-19 and if this has prognostic implications. Materials & methods: Retrospective study, with LVGLS was measured in 58 COVID-19 patients. Patients discharged were compared with those who died. Results: The mean LV ejection fraction (LVEF) and LVGLS for the cohort was 52.1 and -12.9 ± 4.0%, respectively. Among 30 patients with preserved LVEF(>50%), LVGLS was -15.7 ± 2.8%, which is lower than the reference mean LVGLS for a normal, healthy population. There was no significant difference in LVGLS or LVEF when comparing patients who survived to discharge or died. Conclusion: LVGLS was reduced in COVID-19 patients, although not significantly lower in those who died compared with survivors.
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