Non-steroidal anti-inflammatory drugs and risk of pulmonary embolism in patients with inflammatory joint disease—results from the nationwide Norwegian Cardio-rheuma registry

Aims Patients with inflammatory joint diseases (IJD), including rheumatoid arthritis (RA), psoriatic arthritis (PsA), and axial spondyloarthritis (axSpA) have increased rates of pulmonary embolism (PE). Non-steroidal anti-inflammatory drugs (NSAIDs) use is associated with PE in the general population. Our aim was to evaluate the association between NSAIDs use and PE in IJD patients. Methods and results Using individual-level registry data from the whole Norwegian population, including data from the Norwegian Patient Registry and the Norwegian Prescription Database, we: (1) evaluated PE risk in IJD compared to non-IJD individuals, (2) applied the self-controlled case series method to evaluate if PE risks were associated with use of traditional NSAIDs (tNSAIDs) and selective cox-2 inhibitors (coxibs). After a one-year wash-out period, we followed 4 660 475 adults, including 74 001 with IJD (RA: 39 050, PsA: 20 803, and axSpA: 18 591) for a median of 9.0 years. Crude PE incidence rates per 1000 patient years were 2.02 in IJD and 1.01 in non-IJD individuals. Age and sex adjusted hazard ratios for PE events were 1.57 for IJD patients compared to non-IJD. Incidence rate ratios (IRR) [95% confidence interval (CI)] for PE during tNSAIDs use were 0.78 (0.64–0.94, P = 0.010) in IJD and 1.68 (1.61–1.76, P < 0.001) in non-IJD. IRR (95% CI) for PE during coxibs use was 1.75 (1.10–2.79, P = 0.018) in IJD and 2.80 (2.47–3.18, P < 0.001) for non-IJD. Conclusion Pulmonary embolism rates appeared to be higher in IJD than among non-IJD subjects in our study. Traditional NSAIDs may protect against PE in IJD patients, while coxibs may associated with increased PE risk.Non-steroidal anti-inflammatory drugs and risk of pulmonary embolism in patients with inflammatory joint disease—results from the nationwide Norwegian Cardio-rheuma registrypublishedVersio

Treatment to lipid targets in patients with inflammatory joint diseases in a preventive cardio-rheuma clinic

Objectives: To perform cardiovascular (CV) risk stratification in patients with inflammatory joint diseases (IJD) and treat to lipid targets according to recommendations. Methods: We initiated a preventive cardio-rheuma clinic based on the unmet need of adequate CV prevention in IJD patients. A full CV risk stratification was performed at the first consultation (history of conventional risk factors and of CV disease, lipid measurement, blood pressure and ultrasound examination of both carotid arteries), and the patient was classified to either a primary or secondary CV prevention regime, or to have low risk (no intervention). Lipid lowering (LL) treatment was adjusted until at least two lipid targets were achieved. Results: Of the 426 patients referred, 36.6% had a systematic coronary risk evaluation (SCORE) <5% (no LL intervention). The remaining 270 patients [(rheumatoid arthritis (RA): n=165, ankylosing spondylitis (AS): n=70, and psoriatic arthritis (PsA): n=35] were categorized to either primary (n=63) or secondary prevention (n=207). There were significant differences between the patient groups regarding age (p<0.001), sex (p<0.001) and disease duration (p<0.001). Lipid changes in IJD patients were; total cholesterol: 1.86±1.20 mmol/L (p<0.001), low density lipoprotein cholesterol: 1.74±1.11 (p<0.001), high density lipoprotein cholesterol: -0.01±0.30 (p=0.61), triglycerides: 0.28±0.72 (p<0.001). The proportions of patients reaching at least 2 lipid targets were for RA/AS/PsA: 92.1/90.0/82.9% respectively. No serious adverse events were observed. Conclusions: There was indication for CV prevention in a high proportion of IJD patients referred for CV risk stratification. Treatment to lipid targets was successful in approximately 90% of patients with IJD

Intensiv lipidsenkende behandling som sekundærprofylakse etter kardiovaskulær hendelse i allmennpraksis

Sammendrag For pasienter som har gjennomgått en kardiovaskulær hendelse eller har fått påvist aterosklerotisk sykdom ved invasiv eller non-invasive prosedyrer er det indikasjon for sekundærprofylakse. Disse pasientene skal i følge nye retningslinjer (1) settes på intensiv lipidsenkende behandling, slik at LDL- nivået senkes. En stor metaanalyse har bekreftet at å senke LDL-kolesterol <1,8 mmol/L er forbundet med lavest risiko for å få tilbakevendende kardiovaskulær hendelser. (2) Det omtalte målivået er en sterk anbefaling (GRADE 1A). Vi vil ved å referere til studier, og ved å presentere en kartlegging av en utvalgt allmennpraksis i Norge, vise at det i varierende grad er rutinemessig oppfølging av kolesterolverdier hos disse pasientene som sikrer at de når målnivå for LDL ved statinbruk. Vi hevder at svært få av allmennlegene i Norge, av ulike grunner, kommer til behandlingsmålet her. Derfor vil vi presentere et forbedringsprosjekt for den utvalgte allmennpraksisen som har som mål å endre fastlegenes oppfølging og behandling av de overnevnte pasientene, slik at målet om LDL-verdi < 1.8 mmol/L i større grad nås. Etter å ha rådført oss med fastlegene , foreslår vi en tettere oppfølging og en mer intensiv statinbehandling av pasientene. Kvalitetsindikatoren vår måles ved å sammenligne LDL-verdi hos de aktuelle pasientene ved start av prosjektet med verdien etter 6 mnd og ett år. For å selge inn prosjektet til fastlegene presenterer vi overbevisende dokumentasjon på hvorfor praksisendring er nødvendig. Dette kommuniseres ved hjelp av foredrag, brosjyrer og sjekklister. Siden fastlegene har en flat struktur i sin organisering mener vi det blir helt avgjørende at en ekstern gruppe tar ansvar for at prosessen gjennomføres. Vår KLoK-gruppe er denne eksterne aktøren. Det blir også avgjørende for et vellykket resultat at dialogen med legene blir tett og kontinuerlig, slik at motstand mot gjennomføringen av prosjektet blir minst mulig. Gjentatte evalueringer av prosessen og eventuelle justeringer blir viktig her

Degree of arterial stiffness is comparable across inflammatory joint disease entities

Objectives: Inflammatory joint disease (IJD) is associated with an increased risk of developing cardiovascular disease (CVD). Arterial stiffness is both a risk factor and a surrogate marker for CVD. This study aims to compare arterial stiffness across patients with rheumatoid arthritis, ankylosing spondylitis, and psoriatic arthritis, and, by extension, to explore the relationship between arterial stiffness and the estimated CVD risk by the Systematic COronary Risk Evaluation (SCORE) algorithm. Method: During the study period, from April 2017 to June 2018, 196 patients with IJD visited the Preventive Cardio-Rheuma Clinic in Oslo, Norway. A CVD risk stratification was performed, including the assessment of traditional risk factors and the measurement of arterial stiffness. Results: Thirty-six patients (18.4%) had elevated aortic pulse wave velocity (aPWV) (≥ 10 m/s). After adjustment for age and heart rate, arterial stiffness was comparable across the IJD entities (p = 0.69). Associated factors, revealed by regression analysis, were age, blood pressure, heart rate, presence of carotid plaques, establis hed CVD, non-steroidal anti-inflammatory drugs, and statin use. Furthermore, aPWV was positively correlated with estimated CVD risk (r = 0.7, p < 0.001) and patients with a very high predicted CVD risk (SCORE ≥ 10%) had significantly higher aPWV than patients at lower CVD risk (9.2 vs 7.5 m/s, p < 0.001). Conclusion: The degree of arterial stiffness was comparable across the IJD entities and was highly associated with the estimated CVD risk. Our findings support the need for an increased focus on prevention of CVD in all patients with IJD

Effects of Long-Term Statin-Treatment on Coronary Atherosclerosis in Patients With Inflammatory Joint Diseases

Background The effect of statins over time on coronary atherosclerosis in patients with inflammatory joint diseases (IJD) is unknown. Our aim was to evaluate the change in coronary plaque morphology and volume in long-term statin-treated patients with IJD. Methods Sixty-eight patients with IJD and carotid artery plaque(s) underwent coronary computed tomography angiography before and after a mean of 4.7 (range 4.0–6.0) years of statin treatment. The treatment target for low density lipoprotein cholesterol (LDL-c) was ≤1.8 mmol/L. Changes in plaque volume (calcified, mixed/soft and total) and coronary artery calcification (CAC) from baseline to follow-up were assessed using the 17-segment American Heart Association-model. Results Median (IQR) increase in CAC after statin treatment was 38 (5–236) Agatston units (p1.8mmol/L (21 [2–143] vs. 69 [16–423], p = 0.006 and 0.65 [-1.0–13.9] vs. 13.0 [0.0–60.8] mm3, p = 0.019, respectively). Conclusions A progression of total atherosclerotic plaque volume in statin-treated patients with IJD was observed. However, soft/mixed plaque volume was reduced, suggesting an alteration in plaque composition. Patients with recommended LDL-c levels at follow-up had reduced atherosclerotic progression compared to patients with LDL-c levels above the treatment target, suggesting a beneficial effect of treatment to guideline-recommended lipid targets in IJD patients

Change in cardiovascular risk factors in patients who develop psoriatic arthritis: longitudinal data from the Nord-Trøndelag Health Study (HUNT)

Objectives The aim of this population-based study was to compare changes in cardiovascular (CV) risk factors over a decade-long period in patients who developed psoriatic arthritis (PsA) and the background population. Methods Patients diagnosed with PsA (n=151) between 1998 and 2008 and matched controls (n=755) who participated in both the Nord-Trøndelag Health Study (HUNT) 2 (1995–1997) and HUNT3 (2006–2008) were included. Mixed linear and logistic models were used to analyse the difference in mean change between HUNT2 and HUNT3 in patients and controls for body mass index (BMI), total cholesterol (TC), triglycerides, low-density lipoprotein cholesterol (LDL-c), high-density lipoprotein cholesterol (HDL-c) and blood pressure (BP). Results At baseline (HUNT2), the patients who developed PsA compared with controls had higher BMI (27.2 vs 25.9 kg/m2, p<0.001) and lower HDL-c (1.32 vs 1.40 mmol/L, p<0.03) and more were smokers (41.1 vs 28.5%, p<0.01). Seventy-eight per cent had skin psoriasis. The mean PsA disease duration at HUNT3 was 4.8 (+/–3.0) years. The patients who developed PsA gained less weight from HUNT2 to HUNT3 compared with the control group (2.1 vs 3.9 kg, difference in mean change −1.8 kg, 95% CI −3.9 to −0.5, p<0.01). TC, triglycerides, LDL-c or HDL-c values and BP declined in both groups, with no significant differences between groups