Discussing coronary risk with patients to improve blood pressure treatment: secondary results from the CHECK-UP study.

OBJECTIVES: Hypertension is common among patients with dyslipidemia but is often poorly treated. The objective of this analysis was to evaluate how a decision aid, used by primary care physicians to improve lipid therapy, impacted on the treatment of hypertension. STUDY DESIGN: Data were analyzed from patients enrolled in a randomized trial focusing primarily on the treatment of dyslipidemia. Patients received usual care or a coronary risk profile every three months to monitor the risk reduction following lifestyle changes and/or pharmacotherapy to treat dyslipidemia. Hypertension management was assessed based on a post hoc analysis of individuals whose blood pressure exceeded current national hypertension guidelines. RESULTS: There were 2,631 subjects who completed the study. Among 1,352 patients without diagnosed hypertension, 30% were above target on at least three consecutive visits. Among 1,279 individuals with known hypertension, 69% were above target on at least two consecutive visits. Overall, patients receiving risk profiles were more likely to receive appropriate antihypertensive therapy (OR = 1.40, 95% CI 1.11-1.78) compared to those receiving usual care. After adjustment for inter-physician variability and potential confounders, the use of the risk profile was associated with an increased likelihood of starting therapy (OR = 1.78, 95% CI 1.06-3.00) or modifying therapy (OR = 1.40, 95% CI 1.03-1.91). CONCLUSIONS: In this clinical trial of dyslipidemia management, inadequately controlled hypertension was common, occurring in nearly 50% of individuals. Ongoing coronary risk assessment was associated with more appropriate blood pressure management. Cardiovascular risk assessment decision aids should be further evaluated in a randomized trial of hypertension therapy.

Patient knowledge of coronary risk profile improves the effectiveness of dyslipidemia therapy: the CHECK-UP study: a randomized controlled trial.

BACKGROUND: Despite increasing evidence that treating dyslipidemia reduces cardiovascular events, many patients do not achieve recommended lipid targets. METHODS: To determine whether showing physicians and patients the patient's calculated coronary risk can improve the effectiveness of treating dyslipidemia in a primary care setting, patients were randomized to receive usual care or ongoing feedback regarding their calculated coronary risk and the change in this risk after lifestyle changes, pharmacotherapy, or both to treat dyslipidemia. Outcomes, based on intention-to-treat analysis, included changes in blood lipid levels, coronary risk, and the frequency of reaching lipid targets. RESULTS: Two hundred thirty primary care physicians enrolled 3,053 patients. After 12 months of follow-up, 2,687 patients (88.0%) remained in the study. After adjustment for baseline lipid values, significantly greater mean reductions in low-density lipoprotein cholesterol levels and the total cholesterol to high-density lipoprotein cholesterol ratio were observed in patients receiving risk profiles (51.2 mg/dL [to convert to millimoles per liter, multiply by 0.0259] and 1.5, respectively) vs usual care (48.0 mg/dL and 1.3, respectively), but the differences were small (-3.3 mg/dL; 95% confidence interval [CI], -5.4 to -1.1 mg/dL; and -0.1; 95% CI, -0.2 to -0.1, respectively). Patients in the risk profile group were also more likely to reach lipid targets (odds ratio, 1.26; 95% CI, 1.07 to 1.48). A significant dose-response effect was also noted when the impact of the risk profile was stronger in those with worse profiles. CONCLUSIONS: Discussing coronary risk with the patient is associated with a small but measurable improvement in the efficacy of lipid therapy. The value of incorporating risk assessment in preventive care should be further evaluated.

Vimentin exposed on activated platelets and platelet microparticles localizes vitronectin and plasminogen activator inhibitor complexes on their surface.

Type 1 plasminogen activator inhibitor (PAI-1), the primary inhibitor of tissue-type plasminogen activator (t-PA), is found in plasma and platelets. PAI-1 circulates in complex with vitronectin (Vn), an interaction that stabilizes PAI-1 in its active conform. In this study, we examined the binding of platelet-derived Vn and PAI-1 to the surface of isolated platelets. Flow cytometry indicate that, like P-selectin, PAI-1, and Vn are found on the surface of thrombin- or calcium ionophore-activated platelets and platelet microparticles. The binding of PAI-1 to the activated platelet surface is Vn-dependent. Vn mediates the binding of PAI-1 to platelet surfaces through a high affinity (K(d) of 80 nm) binding interaction with the NH(2) terminus of vimentin, and this Vn-binding domain is expressed on the surface of activated platelets and platelet microparticles. Immunological and functional assays indicate that only -5% of the total PAI-1 in platelet releasates is functionally active, and it co-precipitates with Vn, and the vimentin-enriched cytoskeleton fraction of activated platelet debris. The remaining platelet PAI-1 is inactive, and does not associate with the cytoskeletal debris of activated platelets. Confocal microscopic analysis of platelet-rich plasma clots confirm the co-localization of PAI-1 with Vn and vimentin on the surface of activated platelets, and platelet microparticles. These findings suggest that platelet vimentin may regulate fibrinolysis in plasma and thrombi by binding platelet-derived Vn.PAI-1 complexes.