230 Understanding UK cardiologists’ perception of systemic inflammation and hsCRP in atherosclerotic cardiovascular disease and chronic kidney disease: insights from UK respondents to the multinational flame-ASCVD survey
Suraj PathakAlberico L. CatapanoIssei KomuroNikolaus MarxPreethy PrasadJuying QianJosé Francisco K SaraivaAbhijit Shete
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Abstract:
Introduction
Despite advancements in managing atherosclerotic cardiovascular disease (ASCVD), mortality and morbidity rates remain high. This is partially attributed to systemic inflammation (SI) which leads to increased cardiovascular risk in people with both ASCVD and CKD. An early understanding of the clinical perception towards SI and usage of high sensitivity C-reactive protein (hsCRP) could help improve identification and management in people with ASCVD and CKD. The FLAME-ASCVD (systemic inFLAMmation and rolE of hsCRP as a biomarker in AtheroSclerotic CardioVascular Disease) study aimed to assess cardiologists' awareness of SI and hsCRP in this population across ten countries.Methods
The FLAME-ASCVD study employed a real-world, cross-sectional, survey involving cardiologists from ten countries, including the United Kingdom. Participants included cardiologists with at least three years of clinical practice experience, seeing a minimum of 15 people with both ASCVD and CKD per month. Responses from 602 cardiologists were evaluated, with this analysis focussing on the subset of 60 UK cardiologists.Results
While SI was acknowledged as a CV risk factor by 65% of UK cardiologists, with 77% of UK cardiologists acknowledging the role of SI in recurrent CV events, 54% of UK cardiologists reported not considering SI in decision-making, due to the lack of available treatments. Despite acknowledging CRP (87%) and hsCRP (32%) as valid biomarkers, UK cardiologists reported lower utilization of SI in patient management, with only 23% intending to test for SI in this patient population (compared to 64% globally), highlighting a discrepancy in clinical practice. Similarly, discussions with patients about SI were less common among UK cardiologists (30%) compared to the global average (43%). However, UK cardiologists were more likely to identify the lack of effective SI treatments as the most common unmet need for people with both ASCVD and CKD (58%), compared to cardiologists globally (41%).Conclusions
The UK subgroup analysis of the FLAME-ASCVD study provides valuable insights into UK cardiologists' perceptions of SI and hsCRP in people with ASCVD and CKD. Addressing the identified gaps requires increased efforts towards education, guideline development, and further research targeting the residual inflammatory risk in patients with ASCVD and CKD. This study was fully funded by Novo Nordisk. Novo Nordisk employees were involved in all aspects of study conduct and are coauthors of this abstract.Conflict of Interest
This study was fully funded by Novo Nordisk. Novo Nordisk employees were involved in all aspects of study conduct and are coauthors of this abstract.Keywords:
Atherosclerotic cardiovascular disease
Introduction: C-reactive protein is a stable and excellent biomarker of systemic inflammation which is easy to measure. COPD is an inflammatory disorder of lung with widespread Systemic manifestations and associated Systemic inflammatory response. C-reactive protein levels are increased in COPD patients. Present study investigated C-reactive protein level in stable COPD patients and its relation with clinically important outcome variable, exercise capacity. Method: Study included 56 stable COPD patients with mild to moderate severity in age group 40-70 years and 56 nonsmoking controls in the same age group. Clinical and physiological characteristics were determined and C-reactive protein levels were measured. Result: This study confirms the finding of higher C-reactive protein levels in smoker COPD patients (4.9 vs 4.0 mg-L-1) as compared to nonsmoker COPD patients. It also confirms that level of C-reactive protein in ex-smoker COPD population remains significantly higher than nonsmoker control group (4.9±0.5 vs 3.1mg/l). Conclusion: C-reactive protein level was strongly associated and correlated with 6 minute walk distance, FEV1 and GOLD stages, so C-reactive protein level can indirectly reflect prognosis of COPD patient and his exercise capacity. We recommend that measurement of C-reactive protein levels may be a useful tool to predict the prognosis and patient outcome in COPD patients. It also provides strong argument to develop therapies aimed at decreasing inflammation independent of smoking cessation.
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Imaging biomarker
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Aim was to study the correlation between dyslipoproteinemia and systemic inflammation marker C-reactive protein in COPD patients. Materials and methods. Retrospective data analysis of 66 cases of COPD patients aged 40-60 years was conducted. C-reactive protein (CRP) was assessed as a marker of systemic inflammation. We also measured the dyslipoproteinemia markers, such as total cholesterol (TC) and low-density lipoprotein cholesterol (LDLC). Using paired linear regression method there was studied an effect of CRP level on some dyslipoproteinemia indices in COPD patients. Results. The average level of CRP was 11.60 ± 5.54 mg/l, demonstrating the presence of a systemic inflammation in study patients. We revealed a linear correlation between CRP and TC (r = 0,7 ± 4,7). There was even stronger correlation between CRP and LDLC ( r = 0,8 ± 3,5). Conclusion. In patients from this retrospective study, a correlation between the levels of CRP and TC/LDLC as the indicators of high risk of atherosclerosis was found. Therefore, it is possible to assume in COPD patients, it is feasible to screen the level of TC and LDLC for prevention/ early diagnosing of atherosclerosis, which in turn is the leading cause of death worlwide. Key words: chronic inflammation, atherosclerosis, COPD, C-reactive protein, dyslipoproteinemia.
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A pathophysiologic model of Alzheimer's disease (AD) has been recently proposed in which beta amyloid accumulation occurs earlier (indexed by abnormal CSF Abeta42), followed by tau-mediated neuronal injury and dysfunction (abnormal CSF tau or FDG-PET) and lastly atrophic changes (abnormal hippocampal volume, HV). The aim of this study is to validate this model by comparing clinical features and conversion to AD and other dementias among groups of patients with mild cognitive impairment (MCI) with different abnormal biomarker profiles. The patients of this study were 58 with MCI in whom AD biomarkers (CSF Abeta42 and tau, temporoparietal hypometabolism on 18F-FDG PET, and hippocampal volume) were collected. Patients were divided into 3 groups of no abnormal biomarker, AD biomarker pattern (including 3 subgroups of early = only abnormal Abeta42, intermediate = abnormal Abeta42 and FDG-PET or tau, and late = abnormal Abeta42, FDG-PET or tau, and HV), and any other biomarker combination. MCI patients with AD biomarker pattern had lower behavioral disturbances than patients with any other biomarker combination (P <.0005) and lower performance on verbal and nonverbal memory than the other two groups (P = .07 and P = .004, respectively). Within the 3 subgroups with AD biomarker pattern there was a significant trend to higher rate of conversion to dementia (p for trend = .006). Moreover, AD was the type of incident dementia in 100% of patients with an AD biomarker pattern, but 0% and 27% in converters with no abnormal biomarker and any other biomarker combination, respectively (P = .002). Clinical cases representative of the three groups were also described. The results of this study provide evidence in favor of the dynamic biomarker model and support the use of biomarkers for the diagnosis of MCI due to AD according to the new recently published research criteria.
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C-Reactive protein serum levels were measured in 57 pediatric patients with 3% to 92% total body surface area burns to determine whether a defined rise in C-reactive protein serum levels could indicate sepsis earlier in burn patients. A rise in C-reactive protein serum levels was defined as an increase of at least 3 mg/dL for 2 days or 10 mg for 1 day. Increases the first 2 days after the burn or the day after surgery were excluded, since these injuries increase C-reactive protein serum levels. Patients were defined as septic when they were on systemic antibiotics and exhibited at least two of 16 specific clinical parameters. C-Reactive protein serum levels correctly predicted sepsis 82% of the time (efficiency=82%). Nonseptic patients generally did not show increased C-reactive protein serum levels (specificity=69%). When sepsis did occur, it always was preceded by increased C-reactive protein (sensitivity=100%), and the increased C-reactive protein occurred 2.3+/-0.5 days before the patient was deemed septic clinically. Hence, a defined rise in C-reactive protein serum levels can predict sepsis sooner in burned children.
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Atherosclerosis is the main cause of myocardial infarction (MI) and inflammation is considered as a main cause of atherosclerosis. Inflammatory indicators such as C-reactive protein (CRP) are considered as a diagnostic marker for MI in recent years. We studied the relationship between seropositivity to CRP and high-sensitivity- reactive protein (hsCRP) with MI and compared their relationship and diagnostic values. All sera of patients and control cases were examined by a commercial quantitative ELISA kit for measuring hsCRP and by a non-quantitative latex agglutination kit for detecting CRP, simultaneously. Results were analyzed by chi -square statistic test in SPSS software version 16. About 62.0% of patients were positive for CRP and 100% positive for hsCRP but in control group, seropositivity rate was 6.6% for CRP and 52.6% for hsCRP. Mean titer of hsCRP in patients was 23.2 but 6.3 mg/l in control group. We found significant relationship between CRP and MI (P=0.004) and with hsCRP with MI (P=0.002). hsCRP and CRP have significant relationship to MI as diagnostic indicators and hsCRP is more sensitive than CRP but regarding to their false positive and negative values, and for decreasing their accuracy, it is recommended to perform both simultaneously. Key words: C-reactive protein (CRP), high-sensitivity- reactive protein (hsCRP), myocardial infarction.
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It is now recognized that inflammatory processes regulate all stages of atherosclerosis, from disease initiation to thrombotic complications. C-reactive protein (CRP) is a plasmatic protein used as a general marker of inflammation. The high sensitivity C-reactive protein (hsCRP) refers to the measurement of CRP in blood samples using assays with sufficient sensitivity to quantify low (baseline) levels of this biomarker. Low-grade chronic inflammatory processes are linked to atherosclerosis and may be screened with the use of hsCRP, thus providing additional information in cardiovascular risk prediction. This review elaborates the role of CRP in atherogenesis and the value of hsCRP as a biomarker in cardiovascular risk prediction in both primary and secondary prevention setting. Keywords: Atherogenesis, biomarker, cardiovascular disease, C-reactive protein, high sensitivity C-reactive protein, inflammation, prevention.
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The diagnostic performance of canine serum amyloid A (SAA) was compared with that of C-reactive protein (CRP) in the detection of systemic inflammation in dogs. Sera from 500 dogs were retrospectively included in the study. C-reactive protein and SAA were measured using validated automated assays. The overlap performance, clinical decision limits, overall diagnostic performance, correlations, and agreement in the clinical classification between these 2 diagnostic markers were compared. Significantly higher concentrations of both proteins were detected in dogs with systemic inflammation (SAA range: 48.75 to > 2700 mg/L; CRP range: 0.4 to 907.4 mg/L) compared to dogs without systemic inflammation (SAA range: 1.06 to 56.4 mg/L; CRP range: 0.07 to 24.7 mg/L). Both proteins were shown to be sensitive and specific markers of systemic inflammation in dogs. Significant correlations and excellent diagnostic agreement were observed between the 2 markers. However, SAA showed a wider range of concentrations and a significantly superior overall diagnostic performance compared with CRP. Comparaison de la protéine amyloïde sérique A et de la protéine C réactive comme marqueurs diagnostiques de l’inflammation systémique chez les chiens. La performance diagnostique de l’amyloïde sérique canine A (SAA) a été comparée à celle de la protéine C réactive (PCR) dans la détection de l’inflammation systémique chez les chiens. Le sérum de 500 chiens a été inclus rétrospectivement dans l’étude. La protéine C réactive et la SAA ont été mesurées en utilisant des bioanalyses automatisées validées. La performance de chevauchement, les limites de décision cliniques, la performance diagnostique globale, les corrélations et la concordance dans la classification clinique entre ces 2 marqueurs diagnostiques ont été comparés. Des concentrations significativement supérieures des deux protéines ont été détectées chez les chiens avec une inflammation systémique (plage de la SAA : de 48,75 à > 2700 mg/L; plage de la PCR : de 0,4 à 907,4 mg/L) comparativement aux chiens sans inflammation systémique (plage de la SAA : de 1,06 à 56,4 mg/L; plage de la PCR : de 0,07 à 24,7 mg/L). Il a été démontré que les deux protéines étaient sensibles et des marqueurs spécifiques de l’inflammation systémique chez les chiens. Des corrélations significatives et une concordance diagnostique excellente ont été observées entre les deux marqueurs. Cependant, la SAA a indiqué un écart plus vaste pour les concentrations et une performance diagnostique significativement supérieure comparativement à la PCR.(Traduit par Isabelle Vallières).
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Amyloid (mycology)
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Different CSF biomarker combinations can provide conflicting diagnostic information in Alzheimer′s disease (AD). This is often attributed to differences in sensitivity and specificity, at the cohort level, between CSF markers (Aβ42, t-Tau, p-Tau181, t-Tau/Aβ42, and p-Tau181/Aβ42). When these biomarkers are analyzed against the same gold standard independently, conflicting biomarker information can also result from biomarker substructures not obvious to investigators. Previous studies have not examined conflicting biomarker information at the individual level (e.g., a profile showing normal Aβ42 levels but abnormal t-Tau/Aβ42 ratio may be interprted as AD-like even though the normal Aβ42 level argues against amyloid pathology). The prevalence of these conflicts and ways to resolve them are unknown. We measured CSF AD biomarker levels in one consecutive series (n=431) from Emory University using the multiplex AlzBio3 assay and surveyed the concordance rates between CSF biomarkers at the individual level. We also compared these results with those from clinical testing through a comparable ELISA. To resolve the issue of differential sensitivity and biomarker substructure, we then analyzed CSF AD biomarker levels through two-step clustering to identify naturally existing subgroups of biomarker profiles. Finally, to determine if the cluster membership or the combination of independent biomarker information confers greater information on prognosis, we analyzed if either predicted longitudinal cognitive changes in the Alzheimer’s Disease Neuro-Imaging Initiative (ADNI, n=409). Conflicting CSF biomarker information was very common: 59% of the Emory subjects and 37% of ADNI subjects had at least one biomarker providing diagnostic information distinct from the other biomarkers. Clustering analysis revealed three groupings: one characterized by p-Tau181/Aβ42>0.131 and longitudinal cognitive decline in MCI, and two others (including one characterized by Aβ42>258.5pg/mL) associated with cognitive stability. Within each cluster, concordant or discordant biomarker findings did not further distinguish rates of longitudinal cognitive decline. Conflicting information from different CSF AD biomarkers was common. A data-driven strategy accounting for all biomarker combinations identified naturally existing groupings each characterized by similar biochemical and prognostic profiles.
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