RESUMEN
Objectives: This study assessed cardiovascular disease (CVD) risk classification according to QRISK2, JBS3 'heart age' and the prevalence of elevated high-sensitivity C reactive protein (hsCRP) in UK primary prevention patients. Method: The European Study on Cardiovascular Prevention and Management in Usual Daily Practice (EURIKA) (NCT00882336) was a cross-sectional study conducted in 12 European countries. 673 UK outpatients aged ≥50 years, without clinical CVD but with at least one conventional CVD risk factor, were recruited. 10-year CVD risk was calculated using QRISK2. JBS3 'heart age' and hsCRP level were assessed according to risk category. Results: QRISK2 and JBS3 heart age was calculated for 285 of the 305 patients free from diabetes mellitus and not receiving a statin. QRISK2 classified 28%, 39% and 33% of patients as low (<10%), intermediate (10% to <20%) and high (≥20%) risk, respectively. Two-thirds of low-risk patients and half of intermediate-risk patients had a heart age ≥5 years and ≥10 years higher than their chronological age, respectively. Half of low-risk patients had hsCRP levels ≥2 mg/L and approximately 40% had levels ≥3 mg/L. Approximately 80% of low-risk patients had both elevated hsCRP and heart age relative to their chronological age. Conclusions: Almost 40% more patients in this 'at risk' group would be eligible for statin therapy following the lowering of the National Institute for Health and Care Excellence treatment threshold to ≥10% 10-year risk. Of patients falling below this treatment threshold, almost all were at increased lifetime risk as measured by JBS3, and of these, the majority had elevated hsCRP levels. These patients with high absolute risk may benefit from early primary CVD prevention.
RESUMEN
BACKGROUND: High on treatment platelet reactivity (HTPR) is common in patients receiving clopidogrel following an acute coronary syndrome (ACS); it's also associated with increased morbidity and mortality. More potent and predictable antiplatelet drugs have addressed this issue at the expense of increased bleeding. Identification of HTPR and the targeted use of more potent antiplatelet drugs has, so far, broadly failed. We investigate this approach in terms of the timing of platelet function testing and how this can impact on the ability of these bedside tests to predict HTPR around the time of coronary intervention. METHODS: High risk ACS patients treated with 5 days of clopidogrel had platelet function assessed using the multiple electrode aggregometry system (MEA) pre, post and 24 h following percutaneous coronary intervention (PCI). Simultaneous detailed analysis of platelet status was undertaken with quantification of platelet bound and soluble p-selectin and mass spectrometry quantification of the eicosanoid 12-HETE. RESULTS: As assessed by MEA 40.5% of patients had HTPR pre-PCI; mean aggregation units (AU) in response to ADP were 499.1 ± 46.3 pre-PCI, 407.6 ± 37.7 post-PCI and 269.1 ± 24.6 AU 24 h post-PCI (pre to post PCI p > 0.05, pre to 24 h post-PCI p = 0.0002). This highly significant drop in platelet reactivity was contrasted with on-going expression of platelet bound p-selectin, increased soluble p-selectin and rising 12-HETE concentrations. CONCLUSIONS: This study outlines significant changes in ex-vivo platelet aggregation that occur within 24 h of PCI in high risk NSTEMI patients using bedside PFT. Whilst there were no changes in antiplatelet therapy during the study period its clear that timing is crucial when assessing high on treatment residual platelet activity.