Relationship between C‐reactive protein/albumin ratio and coronary artery disease severity in patients with stable angina pectoris

Background

Syntax score (SS), which is an angiographic tool used in grading the complexity of coronary artery disease (CAD), has prognostic importance in coronary artery disease (CAD) and provides important information regarding selection of revascularization strategy. C‐reactive protein (CRP) and albumin are indicators of inflammation, and high levels of them are associated with high SS. We aimed to investigate whether baseline CRP to albumin ratio C‐Reactive Protein/Albumin Ratio (CAR), an easily available and novel inflammatory marker, is associated with SS.

Method

A total 403 consecutive patients with stabile angina pectoris, who underwent coronary angiography for suspected CAD from January 2015 to June 2016, were classified into two groups, low SS (≤22) and intermediate‐high SS (>22).

Results

C‐Reactive Protein/Albumin Ratio was significantly higher in patients with intermediate‐high SS group (P < .001). In multivariate regression analysis, CAR remained an independent predictor of intermediate‐high SS group together with hypertension and LDL. The predictive performance of CAR, CRP, and albumin was compared by ROC curve analysis. CAR surpassed CRP and albumin in predicting intermediate‐high SS group. CAR >6.3 predicted an intermediate‐high SS with sensitivity and specificity of 86.8% and 43.4%, respectively.

Conclusion

C‐Reactive Protein/Albumin Ratio was more tightly associated with the complexity and severity of CAD than CRP and albumin alone and was found to be an independent predictor for intermediate‐high SS group.

     

Selective apheresis of C‐reactive protein: A new therapeutic option in myocardial infarction?

Background : There is substantial evidence that C‐reactive protein (CRP) mediates secondary damage of the myocardium after acute myocardial infarction (AMI). The aim of this animal trial in pigs was to specifically deplete CRP from porcine plasma after AMI and to study possible beneficial effects of the reduced CRP concentration on the infarcted area. Methods : Ten pigs received balloon catheter‐induced myocardial infarction. CRP was depleted from five animals utilizing a new specific CRP‐adsorber, five animals served as controls. The area of infarction was analyzed by cardiovascular magnetic resonance imaging on day 1 and day 14 after AMI. Porcine CRP levels were determined by ELISA. Results : CRP‐apheresis resulted in a mean reduction of the CRP levels up to 48.3%. The area of infarction was significantly reduced by 30 ± 6% (P = 0.003) within 14 days in the treatment group, whereas it increased by 19 ± 11% (P = 0.260) in the controls. Fourteen days after infarction, the infarcted area revealed compact, transmural scars in the controls, whereas animals receiving CRP‐apheresis showed spotted scar morphology. In the interventional group, a significantly higher left ventricular ejection fraction (LVEF) was observed after 14 days as compared to the controls (57.6 ± 2.4% vs. 46.4 ± 2.7%; P = 0.007). Conclusions : In a pig model for AMI, we observed that selective CRP‐apheresis significantly reduces CRP levels and the volume of the infarction zone after AMI. Additionally, it changes the morphology of the scars and preserves cardiac output (LVEF). J. Clin. Apheresis 30:15–21, 2015. © 2014 Wiley Periodicals, Inc.     

Elevated procalcitonin and C‐reactive protein as potential biomarkers of sepsis in a subpopulation of thrombotic microangiopathy patients

Thrombotic microangiopathy (TMA) comprises a group of microvascular thrombosis syndromes associated with multiple pathogenic factors. Deficient activity of ADAMTS13 is a pathogenic factor in a subset of TMA patients that provides a strong rationale for plasma exchange treatment. However, the subset of TMA patients with normal ADAMTS13 activity remains a heterogeneous group of patients in which the appropriate treatment is not well understood. In addition to the common forms of TMA thrombotic thrombocytopenic purpura and the hemolytic uremic syndrome, the differential diagnosis of TMA may include sepsis, autoimmune disorders, and disseminated intravascular coagulation. Optimal treatment of TMA depends on timely recognition of treatable pathogenic factors. We hypothesized that sepsis is a rapidly identifiable pathogenic factor in a subset of TMA patients. To test this hypothesis, we retrospectively measured the rapid biomarkers of sepsis C‐reactive protein (CRP) and procalcitonin (PCT), in a repository of pretreatment plasma samples from 61 TMA patients treated with plasma exchange. Levels were analyzed in 31 severely ADAMTS13‐deficient and 30 ADAMTS13‐normal patients. None of the 31 patients with severe deficiency of ADAMTS13 had elevated PCT. However, 11 of 30 (37%) non‐ADAMTS13‐deficient patient samples were strongly positive for PCT. These patient samples also had a >10‐fold higher median CRP level than patients with normal PCT. We conclude that rapid assays may help identify sepsis in a subset of TMA patients. J. Clin. Apheresis, 2009. © 2009 Wiley‐Liss, Inc.     

Effect of rosuvastatin on risk markers for venous thromboembolism in cancer

Essentials

• Statins lower venous thromboembolism risk in general but have not been studied in cancer patients.
• We completed a randomized trial of rosuvastatin vs. placebo among cancer patients on chemotherapy.
• Rosuvastatin did not significantly lower prothrombotic biomarkers including D‐dimer.
• The role of statins in venous thrombosis prevention in cancer patients remains unknown.

Summary

Background

Statin therapy is associated with lower risk of venous thromboembolism (VTE) but has not been prospectively evaluated in patients with advanced cancer.

Objectives

We determined if statin administration in this high‐risk population reduces the risk of VTE, based on established and emerging biomarkers.

Patients/Methods

This double‐blind, crossover, randomized controlled trial among patients with advanced cancer receiving systemic therapy allocated participants to rosuvastatin 20 mg daily or placebo for 3–4 weeks prior to crossover to the alternative therapy, with a 3–5‐week washout. D‐dimer, C‐reactive protein (CRP), soluble (s)P‐selectin, factor VIII (FVIII), thrombin generation and exploratory biomarkers focusing on endogenous thrombin potential, including tissue factor (TF), activated factor IX (FIXa) and activated factor XI (FXIa), were measured at the start and end of both treatment periods. The primary outcome was change in D‐dimer with rosuvastatin compared with placebo.

Results

Of 38 enrolled participants, 24 (63%) completed the study. Rosuvastatin did not cause statistically significant changes in D‐dimer levels or any other biomarker. CRP levels decreased by 40%; 4.3 mg L^?1 (95% confidence interval, ?11.0 to +2.5 mg L^?1) compared with placebo. In post‐hoc analysis, participants who received rosuvastatin initially during their first line of treatment had a 13% decrease in D‐dimer. Circulating TF, FIXa and FXIa were detected in 26%, 68% and 71% of cancer patients despite not being found in healthy individuals.

Conclusions

Rosuvastatin did not cause favorable changes in biomarkers of VTE risk in advanced cancer patients receiving chemotherapy. The role of statin therapy as thromboprophylaxis in the cancer population remains uncertain.

     

Venous thromboembolism and risk of cancer in patients with rheumatoid arthritis

Essentials

• Can venous thromboembolism (VTE) in rheumatoid arthritis (RA) patients be marker of cancer?
• RA patients with VTE and comparison cohorts from population‐based registries were compared.
• Increased risk of cancer in RA patients with VTE during the first year of VTE was observed.
• Risk of cancer in RA patients was increased also during the longer period following VTE.