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C-reactive protein to albumin ratio provides important long-term prognostic information in patients undergoing endovascular abdominal aortic repair
Abstract
Background
The prognostic value of C-reactive protein/albumin ratio (CAR) is of import in cardiovascular diseases. Our aim was to evaluate the impact of the CAR in patients with asymptomatic abdominal aortic aneurysm (AAA) undergoing endovascular aneurysm repair (EVAR).
Material and Method
We retrospectively evaluated 127 consecutive patients who underwent technically successful elective EVAR procedure between December 2014 and September 2020. The optimal CAR cut-off value was determined by using receiver operating characteristic (ROC) curve analysis. Based on the cut-off value, we investigated the association of CAR with long-term all-cause mortality.
Results
32 (25.1%) of the patients experienced all-cause mortality during a mean 32.7 ± 21.7 months’ follow-up. In the group with mortality, CAR was significantly higher than in the survivor group (4.63 (2.60–11.88) versus 1.63 (0.72–3.24), p < 0.001). Kaplan–Meier curves showed a higher incidence of all-cause mortality in patients with high CAR compared to patients with low CAR (log-rank test, p < 0.001). Multivariable Cox regression analysis revealed that glucose ≥ 110 mg/dL (HR: 2.740; 95% CI: 1.354–5.542; p = 0.005), creatinine ≥ 0.99 mg/dL (HR: 2.957, 95% CI: 1.282–6.819, p = 0.011) and CAR > 2.05 (HR: 8.190, 95% CI: 1.899–35.320, p = 0.005) were the independent predictors of mortality.
Conclusion
CAR was associated with a significant increase in postoperative long-term mortality in patients who underwent EVAR. Preoperatively calculated CAR can be used as an important prognostic factor.
This review assesses how publications interpret factors that influence the serum or plasma albumin (PA) level in prognostic indices, focusing on inflammation and nutrition. On PubMed, a search for “albumin AND prognosis” yielded 23,919 results. From these records, prognostic indices were retrieved, and their names were used as search strings on PubMed. Indices found in 10 or more original research articles were included. The same search strings, restricted to “Review” or “Systematic review”, retrieved yielded on the indices. The data comprised the 10 latest original research articles and up to 10 of the latest reviews. Thirty indices had 294 original research articles (6 covering two indices) and 131 reviews, most of which were from recent years. A total of 106 articles related the PA level to inflammation, and 136 related the PA level to nutrition. For the reviews, the equivalent numbers were 54 and 65. In conclusion, more publications mention the PA level as a marker of nutrition rather than inflammation. This is in contrast to several general reviews on albumin and nutritional guidelines, which state that the PA level is a marker of inflammation but not nutrition. Hypoalbuminemia should prompt clinicians to focus on the inflammatory aspects in their patients.
Objective:
To evaluate the prognostic value of C-reactive protein to albumin ratio (CAR) in patients with severe aortic valve stenosis undergoing surgical aortic valve replacement (AVR).
Methods:
Four hundred seventy-six patients with severe degenerative aortic stenosis who underwent successful isolated surgical AVR were enrolled. Hospitalization due to heart failure, surgical aortic reoperation, paravalvular leakage rates, and long-term mortality were evaluated in the whole study group. The participants were divided into two groups, as 443 patients without mortality (group 1) and 33 patients with mortality (group 2) during the follow-up time.
Results:
CAR was lower in patients without mortality than in those with mortality during the follow-up time (0.84 [0.03-23.43] vs. 2.50 [0.22-26.55], respectively, P<0.001). Age (odds ratio [OR]: 1.062, confidence interval [CI]: 1.012-1.114, P=0.014), CAR (OR: 1.221, CI: 1.125-1.325, P<0.001), ejection fraction (OR: 0.956, CI: 0.916-0.998, P=0.042), and valve type (OR: 2.634, CI: 1.045-6.638, P=0.040) were also found to be independent predictors of long-term mortality. Additionally, rehospitalization (0.86 [0.03-26.55] vs. 1.6 [0.17-24.05], P=0.006), aortic reoperation (0.87 [0.03-26.55] vs. 1.6 [0.20-23.43], P=0.016), and moderate to severe aortic paravalvular leakage (0.86 [0.03-26.55] vs. 1.86 [0.21-19.50], P=0.023) ratios were associated with higher CAR.
Conclusion:
It was firstly described that CAR was strongly related with increased mortality rates in patients with isolated severe aortic stenosis after surgical AVR. Additionally, rehospitalization, risk of paravalvular leakage, and aortic reoperation rates were higher in patients with increased CAR than in those without it.
Introduction:
Stent restenosis remains a clinical challenge for patients with ischemic heart disease, since it is associated with repeated coronary interventions as well as higher hospitalization rates and medical costs. Inflammation plays a significant role. Although an association between stent restenosis, increased C-reactive protein (CRP) and decreased albumin levels has been previously reported, no studies have investigated the ability of the CRP/albumin ratio to predict stent restenosis.
Methods:
This retrospective study included 448 patients who had previously undergone primary percutaneous coronary intervention and who were referred for subsequent reintervention due to recurrence of anginal symptoms. The study population was divided into two groups based on whether the patient had developed stent restenosis. They were then stratified into three groups according to their CRP/albumin ratio.
Results:
Out of 448 patients, stent restenosis was observed in 24.5% (n=110), as determined by coronary angiography. Patients with stent restenosis had a higher CRP/albumin ratio, greater platelet distribution width (PDW), higher CRP levels, and lower levels of both high-density lipoprotein (HDL) cholesterol and serum albumin. The CRP/albumin ratio (OR: 2.289, 95% CI: 1.056-4.959; p=0.036), stent diameter, PDW and HDL cholesterol levels were found to be independent predictors of stent restenosis. A ROC curve comparison demonstrated that the CRP/albumin ratio was a better predictor of restenosis than either albumin and CRP individually, but it was not better than PDW and HDL cholesterol.
Conclusion:
As a novel inflammation-based risk score, the CRP/albumin ratio may be an easily accessible marker for assessment of stent restenosis risk.
Purpose:
This study was performed to compare the treatment outcomes between endovascular aneurysm repair (EVAR) and open surgical repair (OSR) of abdominal aortic aneurysms (AAAs) in a South Korean population.
Materials and methods:
We performed a retrospective review of the medical records of 99 patients with AAAs who were managed at Gyeongsang National University Hospital between January 2005 and December 2014. We reviewed the demographic characteristics and perioperative treatment outcomes of patients with AAA undergoing EVAR or OSR. In-hospital mortality and reintervention rates were assessed and compared between the EVAR and OSR groups.
Results:
In-hospital mortality was not significantly higher in the OSR group versus the EVAR group (3.8% vs. 8.7%, respectively, P=0.41). Intervention time (209.6 mins vs. 350.9 mins, P<0.001) and length of hospital stay (7.79 days vs. 17.46 days, P<0.001) were significantly longer in the OSR group vs. the EVAR group. Median follow-up time was 24.1±20 months for the EVAR group and 43.9±28 months for the OSR group. The cumulative rate of freedom from reintervention at 60 months was 62.0% for the EVAR group and 100% for the OSR group (P<0.001).
Conclusion:
EVAR was favorable in terms of intervention time and length of hospital stay, but the long-term durability of EVAR remains open for further debate.
Background:
Short-term survival benefits of endovascular aneurysm repair (EVAR) versus open repair of intact abdominal aortic aneurysms have been shown in randomised trials, but this early survival benefit is lost after a few years. We investigated whether EVAR had a long-term survival benefit compared with open repair.
Methods:
We used data from the EVAR randomised controlled trial (EVAR trial 1), which enrolled 1252 patients from 37 centres in the UK between Sept 1, 1999, and Aug 31, 2004. Patients had to be aged 60 years or older, have aneurysms of at least 5·5 cm in diameter, and deemed suitable and fit for either EVAR or open repair. Eligible patients were randomly assigned (1:1) using computer-generated sequences of randomly permuted blocks stratified by centre to receive either EVAR (n=626) or open repair (n=626). Patients and treating clinicians were aware of group assignments, no masking was used. The primary analysis compared total and aneurysm-related deaths in groups until mid-2015 in the intention-to-treat population. This trial is registered at ISRCTN (ISRCTN55703451).
Findings:
We recruited 1252 patients between Sept 1, 1999, and Aug 31, 2004. 25 patients (four for mortality outcome) were lost to follow-up by June 30, 2015. Over a mean of 12·7 years (SD 1·5; maximum 15·8 years) of follow-up, we recorded 9·3 deaths per 100 person-years in the EVAR group and 8·9 deaths per 100 person-years in the open-repair group (adjusted hazard ratio [HR] 1·11, 95% CI 0·97-1·27, p=0·14). At 0-6 months after randomisation, patients in the EVAR group had a lower mortality (adjusted HR 0·61, 95% CI 0·37-1·02 for total mortality; and 0·47, 0·23-0·93 for aneurysm-related mortality, p=0·031), but beyond 8 years of follow-up open-repair had a significantly lower mortality (adjusted HR 1·25, 95% CI 1·00-1·56, p=0·048 for total mortality; and 5·82, 1·64-20·65, p=0·0064 for aneurysm-related mortality). The increased aneurysm-related mortality in the EVAR group after 8 years was mainly attributable to secondary aneurysm sac rupture (13 deaths [7%] in EVAR vs two [1%] in open repair), with increased cancer mortality also observed in the EVAR group.
Interpretation:
EVAR has an early survival benefit but an inferior late survival compared with open repair, which needs to be addressed by lifelong surveillance of EVAR and re-intervention if necessary.
Funding:
UK National Institute for Health Research, Camelia Botnar Arterial Research Foundation.
Serum albumin concentration (CP) is a remarkably strong prognostic indicator of morbidity and mortality in both sick and seemingly healthy subjects. Surprisingly, the specifics of the pathophysiology underlying the relationship between CP and ill-health are poorly understood. This review provides a summary that is not previously available in the literature, concerning how synthesis, catabolism, and renal and gastrointestinal clearance of albumin interact to bring about albumin homeostasis, with a focus on the clinical factors that influence this homeostasis. In normal humans, the albumin turnover time of about 25 days reflects a liver albumin synthesis rate of about 10.5 g/day balanced by renal (≈6%), gastrointestinal (≈10%), and catabolic (≈84%) clearances. The acute development of hypoalbuminemia with sepsis or trauma results from increased albumin capillary permeability leading to redistribution of albumin from the vascular to interstitial space. The best understood mechanism of chronic hypoalbuminemia is the decreased albumin synthesis observed in liver disease. Decreased albumin production also accounts for hypoalbuminemia observed with a low-protein and normal caloric diet. However, a calorie- and protein-deficient diet does not reduce albumin synthesis and is not associated with hypoalbuminemia, and CP is not a useful marker of malnutrition. In most disease states other than liver disease, albumin synthesis is normal or increased, and hypoalbuminemia reflects an enhanced rate of albumin turnover resulting either from an increased rate of catabolism (a poorly understood phenomenon) or enhanced loss of albumin into the urine (nephrosis) or intestine (protein-losing enteropathy). The latter may occur with subtle intestinal pathology and hence may be more prevalent than commonly appreciated. Clinically, reduced CP appears to be a result rather than a cause of ill-health, and therapy designed to increase CP has limited benefit. The ubiquitous occurrence of hypoalbuminemia in disease states limits the diagnostic utility of the CP measurement.
Background
Inflammation of the aortic wall is recognised as a key pathogenesis of abdominal aortic aneurysm (AAA). This study was undertaken to determine whether inflammatory cytokines could be used as biomarkers for the presence of AAA.
Methods and Results
Tissue profiles of 27 inflammatory cytokine were examined in AAA (n=14) and nonaneurysmal (n=14) aortic tissues. Three cytokines, regulated upon activation normally T‐cell expressed and secreted (RANTES), eotaxin, and macrophage inflammatory protein 1 beta (MIP‐1b), had increased expression in AAA, particularly within the adventitial layer of the aortic wall. Basic fibroblast growth factor (bFGF) had reduced expression in all layers of the AAA wall. Examination of the circulating plasma profiles of AAA (n=442) and AAA‐free controls (n=970) suggested a (risk factor adjusted) AAA‐association with eotaxin, RANTES, and high sensitivity C‐reactive protein (hsCRP). A plasma inflammatory cytokine score, calculated using these three markers, suggested a strong risk association with AAA (odds ratio, 4.8; 95% CI, 3.5–6.7; P<0.0001), independent of age, sex, history of ischemic heart disease, and smoking.
Conclusions
Contrary to reports suggesting a distinct T helper 2–associated inflammatory profile in AAA, this current study suggests a more‐generalized pattern of inflammation, albeit with some potentially distinct features, including elevated plasma eotaxin and decreased plasma RANTES. In combination with hsCRP, these markers may have potential utility as AAA biomarkers.
Objective:
This study aimed to clarify long-term mortality and its predictors in patients with abdominal aortic aneurysm (AAA) who underwent endovascular aneurysm repair (EVAR).
Materials and methods:
Patients with AAA who underwent elective EVAR at Tokyo Medical and Dental University hospital between 2008 and 2011 were reviewed. The patients' data were retrospectively collected from medical records.
Results:
Sixty-four patients were identified for this study. In long-term follow-up, the survival rate was significantly lower in patients with high preoperative C-reactive protein (CRP) levels. Patients with obstructive lung disease (FEV1/FVC <70%) or anemia tended to have a poorer prognosis but the association was not statistically significant. Age, concurrent hyperlipidemia, and blood pressure levels were not predictors of mortality rates.
Discussion:
High CRP level, COPD, and anemia reflect inflammation, which is associated with the pathogenesis of AAA. These inflammatory markers are predictors of long-term mortality after EVAR for AAA as well as for other diseases.
Conclusions:
A high preoperative CRP level was a predictor of increased long-term mortality in patients with AAA who underwent EVAR. No specific leading causes of death were identified for this increase in the mortality rate.
Residual inflammation at ICU discharge may have impact upon long-term mortality. However, the significance of ongoing inflammation on mortality after ICU discharge is poorly described. C-reactive protein (CRP) and albumin are measured frequently in the ICU and exhibit opposing patterns during inflammation. Since infection is a potent trigger of inflammation, we hypothesized that CRP levels at discharge would correlate with long-term mortality in septic patients and that the CRP/albumin ratio would be a better marker of prognosis than CRP alone.
We evaluated 334 patients admitted to the ICU as a result of severe sepsis or septic shock who were discharged alive after a minimum of 72 hours in the ICU. We evaluated the performance of both CRP and CRP/albumin to predict mortality at 90 days after ICU discharge. Two multivariate logistic models were generated based on measurements at discharge: one model included CRP (Model-CRP), and the other included the CRP/albumin ratio (Model-CRP/albumin).
There were 229 (67%) and 111 (33%) patients with severe sepsis and septic shock, respectively. During the 90 days of follow-up, 73 (22%) patients died. CRP/albumin ratios at admission and at discharge were associated with a poor outcome and showed greater accuracy than CRP alone at these time points (p = 0.0455 and p = 0.0438, respectively). CRP levels and the CRP/albumin ratio were independent predictors of mortality at 90 days (Model-CRP: adjusted OR 2.34, 95% CI 1.14-4.83, p = 0.021; Model-CRP/albumin: adjusted OR 2.18, 95% CI 1.10-4.67, p = 0.035). Both models showed similar accuracy (p = 0.2483). However, Model-CRP was not calibrated.
Residual inflammation at ICU discharge assessed using the CRP/albumin ratio is an independent risk factor for mortality at 90 days in septic patients. The use of the CRP/albumin ratio as a long-term marker of prognosis provides more consistent results than standard CRP values alone.
Background
Inflammation, hypoalbuminaemia and peritoneal protein clearance are important predictors of survival in patients treated with peritoneal dialysis (PD). We hypothesized that the common link is abnormal endothelial barrier function. To test this, we explored associations between hypoalbuminaemia, systemic albumin leak and soluble markers of systemic inflammation and endothelial injury.Methods
This was a cross-sectional study of 41 prevalent PD patients. Endothelial barrier function was measured as transcapillary escape rate of 125I albumin [transcapillary escape rate of albumin (TERalb)]. Seventeen plasma biomarkers including pro-inflammatory cytokines, endothelial biomarkers and metalloproteinases were measured. Hierarchical clustering analysis (HCA) and principal component analysis (PCA) were used to explore the hypothesis.ResultsThe mean TER alb was 13.7 ± 8.9 (%/h), higher than in non-uraemic subjects 8.22 ± 5.8 (%/h). Three patient clusters were defined from HCA according to their biomarker patterns. Cluster 1 was characterized by inflammation, hypoalbuminaemia, overhydration and intermediate TERalb. Cluster 2 was non-inflamed, preserved muscle mass and more normal TERalb. Cluster 3 had highest TERalb, platelet activation, preserved plasma albumin and intermediate high-sensitivity C-reactive protein levels. Two principal components (PCs) were identified from the biomarker matrix, PC1, indicating platelet activation and PC2, pro-inflammatory. TERalb was positively related to PC1 but not PC2. Diabetes and ischaemic heart disease were associated with PC1 and PC2, respectively.Conclusions
This exploratory analysis indicates that endothelial barrier function is decreased in PD patients and is associated with diabetic status and markers of platelet activation more than inflammation. In contrast, hypoalbuminaemia is associated more with inflammation and atherosclerotic disease indicating a more complex relationship between systemic endothelial barrier function, inflammation and hypoalbuminaemia which requires further validation.
The modified early warning score (MEWS) was developed as a track and trigger tool for the prompt identification of seriously ill patients on an acute medical ward. This paper examines its value in the setting of an acute medical admissions unit (MAU) and compares it to biochemical markers of acute and chronic disease. Three hundred unselected acute admissions to the MAU of the Queen Elizabeth Hospital, Gateshead, were assessed. Correlations between MEWS score and C-reactive protein (CRP) and albumin separately were assessed, and then the relationship between MEWS and the CRP/albumin ratio across the age spectrum was examined. The findings demonstrated a strong correlation between the MEWS score and CRP/albumin ratio (r=0.88, p<0.001) across the whole age spectrum. Length of stay correlated poorly with MEWS (r=0.08) and CRP/albumin ratio (r=0.15). Overall mortality was 5% and was predicted by both tools, with a MEWS score of >4 (relative risk (RR)=7.8) outperforming a CRP/albumin of >2 (RR=2.6). MEWS remains the gold standard for assessing outcome in acute medical admissions, but does have limitations in the elderly (those aged over 70 years). A raised CRP/albumin ratio was less sensitive for overall mortality than MEWS. It did, however, appear to be of greater value in the elderly, especially in those with acute exacerbations of chronic disease. Neither test accurately predicted length of stay.
In a population-based study of 6,386 men and women aged 25--84 years in Tromsø, Norway, in 1994--1995, the authors assessed the age- and sex-specific distribution of the abdominal aortic diameter and the prevalence of and risk factors for abdominal aortic aneurysm. Renal and infrarenal aortic diameters were measured with ultrasound. The mean infrarenal aortic diameter increased with age. The increase was more pronounced in men than in women. The age-related increase in the median diameter was less than that in the mean diameter. An aneurysm was present in 263 (8.9%) men and 74 (2.2%) women (p < 0.001). The prevalence of abdominal aortic aneurysm increased with age. No person aged less than 48 years was found with an abdominal aortic aneurysm. Persons who had smoked for more than 40 years had an odds ratio of 8.0 for abdominal aortic aneurysm (95% confidence interval: 5.0, 12.6) compared with never smokers. Low serum high density lipoprotein cholesterol was associated with an increased risk for abdominal aortic aneurysm. Other factors associated with abdominal aortic aneurysm were a high level of plasma fibrinogen and a low blood platelet count. Antihypertensive medication (ever use) was significantly associated with abdominal aortic aneurysm, but high systolic blood pressure was a risk factor in women only. This study indicates that risk factors for atherosclerosis are also associated with increased risk for abdominal aortic aneurysm.
Free radicals are a normal component of cellular oxygen metabolism in mammals. However, free radical-associated damage is an important factor in many pathological processes. Glycation and oxidative damage cause protein modifications, frequently observed in numerous diseases. Albumin represents a very abundant and important circulating antioxidant. This review brings together recent insights on albumin antioxidant properties. First, it focuses on the different activities of albumin concerning protein antioxidation. In particular, we describe the role of albumin in ligand binding and free radical-trapping activities. In addition, physiological and pathological situations that modify the antioxidant properties of albumin are reported.
Objectives:
Malnutrition has been shown to be associated with survival in a variety of diseases. Our aim is to evaluate the prognostic value of objective nutritional indexes indicating malnutrition, in patients underwent endovascular aortic replacement.
Methods:
We retrospectively evaluated 149 consecutive patients who underwent technically successful endovascular aortic replacement operation between October 2010 and August 2019. Objective nutritional indexes, prognostic nutritional index, geriatric nutritional risk index and controlling nutritional status, scores were calculated using the preoperative data. Optimal cut-off values were obtained by receiver operating characteristic analysis. According to the cut-off values, we investigated the relationship between indexes and the long-term all-cause mortality.
Results:
During mean 48.0 ± 30.3 months follow-up duration, in 47 of patients (31.5%), all-cause mortality were documented. In mortality group, prognostic nutritional index (42.8 ± 7.1 vs 51.3 ± 5.2, p < 0.001) and geriatric nutritional risk index (100.7 ± 10.1 vs 107.6 ± 9.2, p < 0.001) were significantly lower, controlling nutritional status score (2.0 (1.0-4.0) vs 1.0 (0.0-2.0), p < 0.001) was higher when compared to survivor group. Kaplan-Meier curves presented higher mortality incidence in malnutrition patients evaluated with objective nutritional indexes (Log-rang test, for all three indexes p < 0.001). Besides Cox-proportional hazard analysis showed all three nutritional indexes may be a predictive marker for all-cause mortality, prognostic nutritional index introduced more valuable data than other two indexes.
Conclusions:
Malnutrition is associated with significant increase in postoperative long-term mortality in endovascular aortic replacement patients. Preoperatively calculated objective nutritional indexes especially prognostic nutritional index can be used as an important prognostic tool.
Aim: The present study aimed to examine the correlation between high-sensitivity C-reactive protein to albumin ratio (CAR) and in-hospital and short-term major adverse cardiac events (MACEs) in patients with acute coronary syndrome (ACS). Materials & methods: We analyzed 652 consecutive patients who had been hospitalized for ACS. The MACEs were defined as cardiogenic shock, reinfarction, acute heart failure and all-cause death. Results: The incidence rate of MACEs was significantly higher in the high CAR (≥0.114) group than in the low CAR (<0.114) group. Multivariate analysis revealed that CAR, high-sensitivity C-reactive protein and albumin were independent predictors for increased risk for MACEs. Conclusion: The CAR was independently correlated with in-hospital and short-term MACEs and can be used for risk stratification in patients with ACS.
Purpose:
To investigate the effect of abdominal aortic aneurysm (AAA) size on mid- and long-term survival after endovascular aneurysm repair (EVAR).
Materials and methods:
Retrospective data were collected from 325 consecutive patients (mean age 69.7 ± 8.5 years; 323 men) who underwent EVAR for intact AAA at a single institution between January 2003 and December 2013. The primary endpoint was death at 3, 5, and 10 years after EVAR. Optimal cutoff points for AAA size and age were determined using receiver operating characteristics (ROC) curves. Time to event analyses (Kaplan-Meier curves and Cox proportional hazard models) were employed to determine any differences in all-cause mortality outcomes between AAA size groups. Cox models were adjusted for age and other comorbidities (hypertension, hyperlipidemia, coronary artery disease, smoking status, symptomatic status, and creatinine); the outcomes are reported as the hazard ratio (HR) with 95% confidence interval (CI).
Results:
The cohort was dichotomized according to the ROC analysis, which defined an optimal cutoff point of 5.6 cm for AAA size and >70 years for age. The mean follow-up period post EVAR was 45.5±29.2 months. In total, 134 (41.2%) patients died during the 10-year follow-up. Thirty-day mortality was 1.1% (2/184) in the patients with AAA <5.6 cm and 2.1% (3/141) in patients with AAA ≥5.6 cm (p=0.45). All-cause mortality was not significantly affected by comorbidities. However, AAA size ≥5.6 cm was associated with increased 3-year mortality risk (HR 1.59, 95% CI 1.001 to 2.52, p<0.049) but not 5-year (HR 1.44, 95% CI 0.98 to 2.10, p=0.062) or 10-year mortality (HR 1.28, 95% CI 0.91 to 1.80, p=0.149). After adjusting for comorbidities, AAA size ≥5.6 cm was no longer significantly associated with morality at any time point. Using a larger size cutoff (AAA size ≥6.0 cm) resulted in improved statistical significance in the unadjusted model. In the adjusted Cox model, AAA size ≥6.0 cm was significantly associated with increased risk of mortality at 3 years (HR 1.67, 95% CI 1.01 to 2.77, p<0.047), but not at longer time points.
Conclusion:
Our study demonstrates that midterm survival after EVAR is significantly and independently associated with AAA size even after correcting for comorbidities. However, in the long term, preoperative AAA size is not an independent predictor of mortality.
The relationship between C-reactive protein (CRP) level on admission and mortality after transcatheter aortic valve implantation (TAVI) remains unclear. To evaluate the impact of serum CRP level on mortality after TAVI, we assessed 1016 TAVI patients with CRP and 538 TAVI patients with high-sensitive CRP (hs-CRP) level on admission in the OCEAN (Optimized transCathEter vAlvular interveNtion)-TAVI registry. Study population was stratified into two groups (high/low), according to the median of CRP and hs-CRP on admission. We assessed the impact of high CRP and hs-CRP level on all-cause death after TAVI. During 2-year follow-up, all-cause death after TAVI was 9.4% in patients with CRP and 11.9% in patients with hs-CRP. Median value of serum CRP was 0.10mg/dL in both CRP and hs-CRP. Patients with high CRP (> 0.10mg/dL) had significantly higher incidence of all-cause death compared to those with low CRP (11.5% vs. 7.6%, log-rank P = 0.015). Multivariate Cox regression analysis with a time-varying covariate demonstrated that high CRP was an independent predictor of all-cause death within the first 3-month (HR, 2.78; 95%CI, 1.30–5.95) compared to from 3-month onward to 2-year (HR, 0.80; 95%CI, 0.47–1.36) (P for interaction = 0.008). Inversely, these results were not observed in the stratification using hs-CRP on admission. In conclusions, high CRP on admission was significantly associated with an increased risk of all-cause death after TAVI, particularly within the first 3-month after TAVI. Risk stratification using CRP may be a simple and useful strategy to identify high-risk patients who undergo TAVI.
Background
Here, we report the mid-term results of endovascular treatment of isolated dissection of the abdominal aorta, which is a very rare pathology.
Materials and methods
A total of 11 patients (4 males (36.3%) and 7 females (63.6%)) aged 42–72 (mean, 60.3 ± 10.45) years with isolated dissection of the abdominal aorta underwent endovascular stent-graft treatment at our institution between August 2010 and September 2015. Eight patients were symptomatic, and the remaining three were asymptomatic. The asymptomatic patients had aortic aneurysms coexisting with dissection. Eight patients without aneurysm had spontaneous dissections, and the most common symptom was unresponsive abdominal pain.
Results
The mean abdominal aorta diameter was 46.7 ± 20.6 (range, 31.2–100.9) mm and the mean dissection length was 71.1 ± 47.3 (range, 17–162) mm. Aorto-bi-iliac stent grafts were used in all patients, and were placed successfully under spinal anesthesia in all but one (90.9%) patient. Occlusion developed in one patient due to compression of the aorto-bi-iliac graft. Right–left femoral–femoral bypass was performed in this patient, who could not be placed on the opposite side. In addition, the graft was placed in one patient using the left renal artery chimney technique. No intraoperative mortality occurred, and open surgery was not required. In addition, no death occurred and no additional intervention was required during the mean follow-up period of 25.5 ± 17.1 (range, 6–60) months.
Conclusion
Limited data regarding endovascular treatment of isolated dissection of the abdominal aorta are available in the literature. Based on data obtained in a limited number of patients, we consider endovascular aortic repair to be a good alternative to surgery due to its low morbidity and mortality rates.
The association of coronary artery disease (CAD) severity with increased C-reactive protein (CRP) and decreased albumin levels has been reported. However, to our knowledge, no study has investigated the usefulness of the CRP to albumin ratio (CAR) in predicting intermediate–high SYNergy between Percutaneous Coronary Intervention with TAXus and cardiac surgery (SYNTAX) score (SS) and high SS II. Consecutive patients (n = 344) treated with percutaneous coronary intervention comprised the study population. The study population was divided into 2 groups according to SS >22 and mean SS II values, respectively. Patients with intermediate–high SS and high SS II had higher CAR than patients with low SS and SS II. History of diabetes mellitus, decreased albumin, lower left ventricular ejection fraction, and elevated CAR (odds ratio [OR]: 1.020; 95% confidence interval [CI], 1.009-1.031; P < .001) were independent predictors of high SS. The presence of hypertension, decreased hemoglobin and albumin levels, and increased CAR (OR: 1.014; 95% CI, 1.004-1.023; P < .001) were independent predictors of SS II. In receiver operating characteristic curve comparison, CAR was superior to CRP and albumin in prediction of intermediate–high SS, but only CRP in prediction of high SS II. The CAR calculated from the admission blood samples could be a useful parameter for predicting CAD severity using SS and SS II.
Background:
Abdominal aortic aneurysm (AAA) development involves an inflammatory process with a potential genetic background. C-reactive protein (CRP) is an acute phase protein and was elevated in patients with AAA. The aim of this study was to investigate the association among serum high-sensitive CRP (hsCRP) concentration, its CRP genetic polymorphisms and AAA.
Methods:
Serum hsCRP concentrations and abdominal aorta diameters were measured, correlation analysis between them were performed in 155 unrelated participants with AAA and 310 non-AAA controls. Tagging single nucleotide polymorphisms (SNPs) in the CRP gene (rs1417938, rs1130864, rs1205, rs1800947) were identified via HapMap. Stratification analysis was performed to evaluate the effects of SNPs on the concentration of serum hsCRP. The association between four SNPs and AAA was assessed by unconditional logistic regressions (ULR).
Results:
Elevated serum hsCRP level was found to be an independent risk factor for AAA (OR=3.91,95%CI:2.45,6.23) after adjustment for confounding factors. Concentrations of serum hsCRP were significant different (P=0.01) in four subgroups derived from participants with abdominal aorta diameter <20mm, 20 to 29mm, 30 to 54mm, and ≥55mm. Stratification analysis revealed there was significant high frequency of elevated hsCRP levels in subjects carrying rs1205-CC genotype compared with those carrying rs1205-TT or CT genotypes (P=0.004, OR=2.31, 95%CI: 1.30, 4.11), suggesting that the genotype CC of rs1205 was associated with higher serum hsCRP levels. However, the frequency of rs1205-CC in AAA patients (15.3%) was similar to control subjects (17.6%) and we could not confirm rs1205-CC was the genetic risk factor of AAA (OR=1.18, 95%CI: 0.69, 2.01). Moreover, we found another CRP polymorphism rs1417938-TT had a significantly higher likelihood of AAA than the AT genotype (OR=2.07, 95%CI: 1.06-4.03) for the first time, indicating there was perhaps a role for rs14117938-T polymorphism that correlate with AAA.
Conclusion:
Serum hsCRP may be related to the presence of AAA and abdominal aorta diameter. Genetic polymorphisms in CRP gene could influence the concentration of serum hsCRP and the likelihood of AAA, but the causal relationship between AAA and CRP should be demonstrated further.
Introduction:
Advances in endovascular aneurysm repair now allow surgeons to treat high risk patients with complex aortic aneurysms. Stringent selection criteria for repair exists from an anatomic and technical perspective, however there is a paucity of literature examining frailty in patients being evaluated for fenestrated and branched endovascular aortic repair (FEVAR). As a marker of frailty well supported in the literature, we hypothesized that preoperative hypoalbuminemia would increase risk for short-term mortality following endovascular juxtarenal and thoracoabdominal aortic aneurysm repair.
Methods:
1089 consecutive patients with juxtarenal and thoracoabdominal aortic aneurysms considered high risk for open surgery from a single institution who underwent FEVAR from 2001-2014 were included in the study. Risk factors for all-cause mortality were identified via a Cox regression model on time to death.
Results:
The patients with severe hypoalbuminemia (albumin < 2.4 g/dl) had significantly increased 30-day mortality (P=0.025, OR 4.967 (95% CI [1.385, 17.814], Normal vs. Severe) and 2-year mortality P=0.006, OR 2.4, 95% CI [1.05, 5.73], Normal vs. Severe), as well as increased 30-day complication rates P=0.026, OR 1.91, 95% CI [0.9, 4.17], Normal vs. Severe). A univariate analysis for 30-day mortality revealed no significant difference in median age: 75.1 years vs. 72.5 years (Alive at 30-days (Q1, Q3 69.8, 80.1) vs. Expired (Q1, Q3 69.3, 77.8), P=0.24.
Conclusion:
Patients with hypoalbuminemia have significantly increased mortality risk. Albumin level is regulated by nutritional intake and inflammation due to chronic disease, which make it a useful part of a preoperative frailty assessment. Further studies are needed to identify whether optimizing nutrition status will affect albumin levels or decrease mortality.
Objective:
The effect of preoperative malnutrition on outcomes in patients undergoing major vascular surgery is unclear. We investigated the effects of preoperative hypoalbuminemia, a marker for malnutrition, on outcomes after open abdominal aortic aneurysm repair (OAR) and endovascular abdominal aortic aneurysm repair (EVAR).
Methods:
Patients undergoing OAR or EVAR were identified in the 2005 to 2012 American College of Surgeons National Surgical Quality Improvement Program database and stratified into three groups: normal albumin (serum albumin >3.5 g/dL), moderate hypoalbuminemia (2.8-3.5 g/dL), and severe hypoalbuminemia (<2.8 g/dL). Multivariable analyses were performed to assess the association of preoperative hypoalbuminemia with 30-day morbidity and mortality.
Results:
We identified 15,002 patients with a recorded preoperative serum albumin who underwent OAR (n = 4956) or EVAR (n = 10,046). Patients in both cohorts with hypoalbuminemia had a higher burden of comorbidity. In OAR patients, multivariable analyses demonstrated that moderate hypoalbuminemia was associated with an increased risk of 30-day mortality (odds ratio [OR], 1.32; 95% confidence interval [CI], 1.02-1.70) and postoperative length of stay (LOS; means ratio [MR], 1.10; 95% CI, 1.04-1.16), whereas severe hypoalbuminemia was associated with increased 30-day mortality (OR, 1.92; 95% CI, 1.37-2.70), reoperation ≤30 days (OR, 1.80; 95% CI, 1.32-2.48), pulmonary complications (OR, 1.40; 95% CI, 1.06-1.86), and postoperative LOS (MR, 1.33; 95% CI, 1.21-1.45). In EVAR patients, moderate hypoalbuminemia was associated with an increased risk of 30-day mortality (OR, 1.90; 95% CI, 1.38-2.62), pulmonary complications (OR, 1.61; 95% CI, 1.26-2.04), reoperation ≤30 days (OR, 1.39; 95% CI, 1.12-1.74), and postoperative LOS (MR, 1.23; 95% CI, 1.18-1.29), whereas severe hypoalbuminemia was associated with increased 30-day mortality (OR, 2.98; 95% CI, 1.96-4.53), pulmonary complications (OR, 1.88; 95% CI, 1.32-2.67), reoperation ≤30 days (OR, 1.54; 95% CI, 1.08-2.19), and postoperative LOS (MR, 1.52; 95% CI, 1.40-1.65).
Conclusions:
Preoperative hypoalbuminemia is associated with increased postoperative morbidity and mortality in a severity-dependent manner among patients undergoing OAR or EVAR. Evaluation and optimization of nutritional status should be performed preoperatively in this high-risk population.
Background: The Revised Cardiac Risk Index (RCRI) is widely used to predict perioperative cardiac complications. Purpose: To evaluate the ability of the RCRI to predict cardiac complications and death after noncardiac surgery. Data Sources: MEDLINE, EMBASE, and ISI Web of Science (1966 to 31 December 2008). Study Selection: Cohort studies that reported the association of the RCRI with major cardiac complications (cardiac death, myocardial infarction, and nonfatal cardiac arrest) or death in the hospital or within 30 days of surgery. Data Extraction: Two reviewers independently extracted study characteristics, documented outcome data, and evaluated study quality. Data Synthesis: Of 24 studies (792 740 patients), 18 reported cardiac complications; 6 of the 18 studies were prospective and had uniform outcome surveillance and blinded outcome adjudication. The RCRI discriminated moderately well between patients at low versus high risk for cardiac events after mixed noncardiac surgery (area under the receiver-operating characteristic curve [AUC], 0.75 [95% CI, 0.72 to 0.79]); sensitivity, 0.65 [CI, 0.46 to 0.81]; specificity, 0.76 [CI, 0.58 to 0.88]; positive likelihood ratio, 2.78 [CI, 1.74 to 4.45]; negative likelihood ratio, 0.45 [CI, 0.31 to 0.67]). Prediction of cardiac events after vascular noncardiac surgery was less accurate (AUC, 0.64 [CI, 0.61 to 0.66]; sensitivity, 0.70 [CI, 0.53 to 0.82]; specificity, 0.55 [CI, 0.45 to 0.66]; positive likelihood ratio, 1.56 [CI, 1.42 to 1.73]; negative likelihood ratio, 0.55 [CI, 0.40 to 0.76]). Six studies reported death, with a median AUC of 0.62 (range, 0.54 to 0.78). A pooled AUC for predicting death could not be calculated because of very high heterogeneity (I 2 = 95%). Limitation: Studies generally were of low methodological quality, had varied definitions of cardiac events, and were statistically and clinically heterogeneous. Conclusion: The RCRI discriminated moderately well between patients at low versus high risk for cardiac events after mixed noncardiac surgery. It did not perform well at predicting cardiac events after vascular noncardiac surgery or at predicting death. High-quality research is needed in this area of perioperative medicine. Primary Funding Source: None.
To report the contemporary life expectancy of patients undergoing abdominal (AAA) or thoracic aortic aneurysm (TAA) repair in England, relative to a healthy control population.
A retrospective observational case-control study was carried out of Hospital Episode Statistics (HES) data, an administrative dataset covering the entire English National Health Service. Patients undergoing elective repair of an abdominal or thoracic aortic aneurysm in an English NHS hospital between April 2006 and March 2011 were included. Outcome measures were 5-year all-cause mortality (in- and out-of-hospital) and adverse cardiovascular events (myocardial infarction, stroke, emergency amputation or limb revascularisation).
19,505 AAA and 730 TAA repairs were identified, with 75,260 and 2,721 control participants, respectively, and 27.5 (1.0-60.0) months' median (range) follow-up. Five-year survival was 67.4% for AAA against 81.1% for control participants, and 65.3% for TAA against 89.1% for control participants (p < .001). Freedom from adverse cardiovascular events was 86.1% for AAA against 93% for control participants and 89.1% for TAA against 94.4% for control participants (p < .001).
Long-term survival remains poor after aneurysm repair and adverse cardiovascular events are common relative to the wider population. Further research is required to characterise and optimise cardiovascular risk prevention in patients with aortic aneurysms.
C-reactive protein (CRP) is an independent risk factor for arteriosclerosis, but its role in abdominal aortic aneurysm (AAA) expansion remains not completely verified. There are no data about the prognostic significance of rates of variation of the CRP levels in asymptomatic AAAs. This study investigated the association between plasma CRP levels and AAA diameter and assessed the relationship between the gradient of CRP levels and rates of expansion in asymptomatic AAAs.
Plasma levels of high-sensitive CRP (hs-CRP) were measured using a high-sensitivity technique and AAA size was determined by computed tomography in 435 patients with asymptomatic AAAs followed up in our outpatient department.
The median hs-CRP level was 4.23 mg/L. The aorta diameter increased in the four groups of patients determined according to hs-CRP quartiles (35 ± 2, 40 ± 3, 49 ± 4, and 58 ± 5 mm; P = .01). The median rate of CRP level variation per year was 1.4 mg/L. Patients with an elevation >1.4 mg/L had an expansion rate of 4.8 mm vs 3.9 mm in those <1.4 mg/L (P < .01). The multivariate age-adjusted logistic model confirmed initial diameter and variation of CRP level were the only factors associated with expansion, with odds ratios (95% confidence intervals) of 6.3 (3.1-7.5) and 3.4 (2.1-5.6).
These results confirm a statistical association between AAA diameter and hs-CRP plasma levels. This cohort study corroborates this potential causal association and contributes information about the value of the hs-CRP plasma level gradient as a marker of disease progression and rate of expansion.
Abdominal aortic aneurysm (AAA) is a complex disease with a largely unknown pathophysiological background and a strong genetic component. Various studies have tried to link specific genetic variants with AAA.
Systematic review of the literature (1947-2009).
A total of 249 studies were identified, 89 of which were eventually deemed relevant to this review. Genetic variants (polymorphisms) in a wide variety of genes, most of which encode proteolytic enzymes and inflammatory molecules, have been associated with AAA development and progression.
The genetic basis of AAA remains unknown, and most results from ''candidate-gene'' association studies are contradictory. Further analyses in appropriately powered studies in large, phenotypically well-characterized populations, including genome-wide association studies, are necessary to elucidate the exact genetic contribution to the pathophysiology of AAA.
The purpose of this review is to highlight the indications, complications, and outcomes observed with endovascular or open repair for abdominal aortic aneurysms. We selected literature published during 2005 to 2008, encompassing a research period from 1987 to 2005 which compared these 2 techniques and followed various outcomes of morbidity and mortality.
To examine and compare existing pre-operative risk prediction methods for elective abdominal aortic aneurysm (AAA) repair.
Systematic review.
Medline, EMBASE and the Cochrane library were searched for articles that related to risk prediction models used for elective AAA repair.
680 abstracts were reviewed and after exclusions 28 articles encompassing 10 risk models were identified. The most frequently studied of these were the Glasgow Aneurysm Score (GAS), the Physiological and Operative Severity Score for enUmeration of Mortality (POSSUM) predictor equation and the Vascular Biochemistry and Haematology Outcome Model (VBHOM). All models had strengths and weaknesses and some had unique features which were identified and discussed.
The GAS appeared to be the most useful and consistently validated score at present for open repair. Other systems were either not validated fully or were not consistently accurate. Some had significant drawbacks which appeared to severely limit their clinical application. Recent work has shown that no scores consistently predicted the risk associated with endovascular aneurysm repair (EVAR). Pre-operative risk stratification is a vital component of modern surgical practice, and we propose the need for a comprehensive new risk scoring method for AAA repair incorporating anatomical and physiological data.
This study was undertaken to determine the late survival of patients operated successfully for abdominal aortic aneurysm (AAA) repair, to compare survival data with that of the age- and sex-matched general population, to identify the causes of late death, and to determine the factors influencing late survival.
A total of 187 consecutive patients underwent elective surgical AAA repair between January 1987 and December 1991. There were 11 postoperative deaths (early mortality rate 5.9%). The remaining 176 patients formed the basis of this cohort-based retrospective study. Six patients (3.4%) were lost to follow-up. Mean follow-up was 71 months.
A total of 70 patients (39.8%) died during the study period. Coronary artery disease (CAD) and cancer were the two main causes. The survival rate at five years (71.6%) was lower than that of the sex- and age-matched general population (90.6%). Neither arterial hypertension nor CAD had any influence on late survival. In contrast, age and chronic renal failure were predictive variables of late survival.
The life expectancy of patients who undergo successful AAA repair is not as good as that of the age- and sex-matched general population. Late survival depends on the patients' age at the time of surgery and the existence of preoperative chronic renal failure.
The purpose of this study was to assess atherosclerotic plaque deposition and aortic wall responses in the abdominal aorta in relation to the development of aneurysmal and occlusive disease in the infrarenal aorta.
Morphologic differences at five standardized locations in the infrarenal aorta in 67 pressure perfusion-fixed male cadaver aortas (aged, 41-98 years; mean, 66 years) were studied and compared with the supraceliac segment. Quantitative computer-assisted morphometry of histologic sections included measurement of plaque area, lumen area, lumen diameter, media thickness, number of medial elastic lamellae, and the area encompassed by the internal elastic lamina that best represents the artery size of each segment. The ratio of the supraceliac segment to the midabdominal segment (normally greater than 1.3) was used to define three groups: Group I (normal): ratio greater than or equal to 1.30 (n = 31); Group II (intermediate): ratio greater than or equal to 1.20 but less than 1.30 (n = 20); and Group III: ratio less than 1.20 (n = 16), which represented dilated midabdominal aortas. There was no significant difference in age among the groups.
Group I had minimal intimal plaque and little gross evidence of atherosclerosis. Group II had increased intimal plaque compared with Group I (P <.01) and gross evidence of atherosclerosis, which was maximally localized in the distal aorta; there was no aortic enlargement or thinning of the media underneath the plaque. Group III had more intimal plaque than Group I (P <.01) and Group II (P <.01) and was associated with localized aortic enlargement and media thinning compared with Group I (P <.05) and Group II (P <.01). Increasing intimal plaque in Group III correlated with an increase in lumen diameter (r = 0.61, P <.05), but this relationship was not significant in Group I and Group II. The aortic media in Group III had a reduced number of medial elastic lamellae, was reduced in thickness, and was more exposed to increased wall stress than the aortas in Groups I and II.
These results suggest that there may be different local responses to atherosclerosis in the abdominal aorta in human beings. Plaque deposition associated with localized dilation, thinning of the media, and loss of medial elastic lamellae may predispose that segment of aorta to subsequent aneurysm formation. Plaque deposits without media thinning, without loss of elastic lamellae, and without artery wall dilation may predispose the aorta, in the event of continuing plaque accumulation, to the development of lumen stenosis.
Unlabelled:
The pathogenesis of abdominal aortic aneurysms (AAA) is a complex process in which atherosclerosis and inflammation play a leading role. Cytokines are important mediators of both processes. The aim of our study was to determine whether plasma levels of cytokines which are most involved in AAA pathogenesis can be used as endogenous markers of AAA development, and thus to facilitate the decision on surgical intervention in cases when this is clinically unclear (e.g. small AAA). In the prospective study a total of 90 patients with AAA were examined. These patients were divided into the following groups according to symptoms and AAA diameter: symptomatic AAAs, including ruptures (n=16); asymptomatic AAAs (n=74); AAAs with a diameter of up to 5 cm (n=30), AAAs of 5-8 cm (n=38), and AAAs with a diameter over 8 cm (n=22). The average age of the patients was 70.7 (56-82) years. The male to female ratio was 4:1 (71:19). A control group consisted of 30 healthy individuals of similar age and sex presentation with no manifestation of atherosclerosis. Plasma levels of cytokines were assessed in venous blood by means of radio- or enzymo-immunoassay. Statistical processing of the results was conducted with ANOVA and Wilcoxon tests with Spearman correlation, where p<0.05 was considered to be statistically significant. Plasma concentrations of cytokines were significantly higher in AAA patients than in healthy individuals. In AAA patients the tumour necrosis factor-alpha (TNF-alpha) and interleukin (IL-8) levels were low in large and in symptomatic AAAs. IL-6 levels were increased with increasing AAA diameter and symptoms. IL-8 levels (p<0.05) showed a statistically significant correlation with the diameter, and TNF-alpha (p<0.05) with the symptoms of AAA. IL-1beta, IL-2 and IL-6 did not show any significant changes with different AAA diameter or symptomatology.
In conclusion:
IL-8 and TNF-alpha can be used as endogenous markers of the process of AAA development, in deciding for either surgical or endovascular treatment of patients when the clinical indication is not entirely clear.
Abdominal aortic aneurysm is a multifactorial disorder in which inflammation is an important pathophysiological feature. In explant culture, aneurysm biopsies secrete large amounts of interleukin-6 (IL-6), and among aneurysm patients, the circulating concentration of IL-6 appears to be increased.
We investigated, in 19 patients, whether aneurysm wall was an important source of circulating IL-6. We also tested the hypotheses, in 466 patients with a small aneurysm, that (1) high concentrations of circulating IL-6 signaled rapid aneurysm growth and (2) the -174 G-->C polymorphism in the IL-6 promoter predicted survival. For 19 patients with large or inflammatory aneurysms, the concentration of IL-6 was higher in the iliac arteries than the brachial arteries (median difference 26.5 pg/mL, this difference increasing with aneurysm diameter, P=0.01). In 466 patients with small aneurysms, the frequency of the -174 C allele (0.40) was similar to that in a normal healthy population. Patients of GG genotype had lower plasma concentrations of IL-6 than patients of GC and CC genotypes (medians 1.9, 4.8, and 15.6 pg/mL, respectively, Kruskal-Wallis P=0.047). Cardiovascular and all-cause mortalities were lower for patients of GG genotype than for patients of GC and CC genotype: hazard ratios 0.32 (95% CI 0.12 to 0.93), P=0.036, and 0.51 (95% CI 0.25 to 1.00), P=0.05, respectively. There was no association between plasma IL-6 or IL-6 genotype and aneurysm growth.
Aortic aneurysms appear to be an important source of circulating IL-6, the concentration being influenced by genotype. For patients with small aneurysms, the -174 G-->C IL-6 genotype predicts future cardiovascular mortality.
Abdominal aortic aneurysms (AAA) are characterized by extensive transmural inflammation and C-reactive protein (CRP) has emerged as an independent risk factor for the development of cardiovascular disease. Therefore, we evaluated a possible association between serum CRP and aneurysm dimension in patients with asymptomatic AAA. Furthermore, the possibility of CRP production by aneurysmal tissue has been examined.
Serum CRP was determined highly sensitive (hsCRP) and aneurysmal size was measured in 39 patients with AAA. The presence of CRP mRNA was assessed in the aneurysmal tissue of 16 patients. Mean (SD) hsCRP was 3.23 (2.96) mg/L. After log-transformation, hsCRP correlated significantly with aneurysmal size (r=0.477, P=0.002). When the patients were divided into 3 equally sized groups according to hsCRP level, aortic diameter increased from lowest to upper hsCRP-tertile (49 mm, 61 mm, and 67 mm, respectively; P<0.05 for 3rd versus 1st tertile). This association persisted after correction for risk factors. CRP mRNA was found in 25% of aneurysmal aortic tissues.
This is the first report showing that serum hsCRP is associated with aneurysmal size and that-in at least some patients-CRP may be produced by aneurysmal tissue. These data underscore the inflammatory nature of AAA formation, suggesting that serum hsCRP may serve as a marker of AAA disease and that CRP produced in vascular tissue might contribute to aneurysm formation.
Atherosclerosis-related mechanisms, including inflammation and possibly infection, are likely to be involved in the pathogenesis of calcific aortic valve disease. The purpose of this study was to examine whether systemic inflammatory markers and Chlamydia pneumoniae seropositivity are associated with aortic valve sclerosis (AVS) in a sample of the general population. Transesophageal echocardiography was performed in 381 subjects (median age: 67 years, range: 51-101; 52% men), a sample of the adult population in Olmsted County, Minnesota. The associations between systemic inflammatory markers (blood counts, including white blood cells differential counts, fibrinogen, and high-sensitivity C-reactive protein [hs-CRP]), C. pneumoniae immunoglobulin G (IgG) antibody titers, and AVS were examined. AVS was present in 140 subjects (37% of the population). After adjustment for age, sex, and smoking status: (1). hs-CRP was associated with AVS (odds ratio: 1.20 per two-fold increase in hs-CRP; 95% confidence interval: 1.01-1.43; P = 0.04) but this association was not significant after adjustment for additional risk factors for AVS, including body mass index (P = 0.52). (2). Blood counts and fibrinogen were not associated with AVS (P-values >0.30). (3). C. pneumoniae IgG antibody titers (low [1:16-1:32], intermediate [1:64-1:128], or high [>or=1:256] titers, compared with titers <1:16) were not associated with AVS (P = 0.21). In conclusion, hs-CRP is weakly associated with AVS, an association that is not independent of other AVS risk factors. Blood counts, fibrinogen, and C. pneumoniae seropositivity are not associated with AVS. These findings suggest that other non-inflammatory non-infectious mechanisms are likely to have a role in the pathogenesis of calcific aortic valve disease.
The aim was to determine whether early open surgical repair would benefit patients with small abdominal aortic aneurysm compared with surveillance on long-term follow-up.
The 1090 patients who were enrolled into the UK Small Aneurysm Trial between 1991 and 1995 were followed up for aneurysm repair and mortality until November 2005.
By November 2005, 714 patients (65.5 per cent) had died, 929 (85.2 per cent) had undergone aneurysm repair, 150 (13.8 per cent) had died without aneurysm repair and 11 (1.0 per cent) remained alive without aneurysm repair. After 12 years, mortality in the surgery and surveillance groups was 63.9 and 67.3 per cent respectively, unadjusted hazard ratio 0.90 (P = 0.139). Three-quarters of the surveillance group eventually had aneurysm repair, with a 30-day elective mortality of 6.3 per cent (versus 5.0 per cent in the early surgery group, P = 0.366). Estimates suggested that the cost of treatment was 17 per cent higher in the early surgery group, with a mean difference of 1326 pounds. The death rate in these patients was about twice that in the population matched for age and sex.
There was no long-term survival benefit of early elective open repair of small abdominal aortic aneurysms. Even after successful aneurysm repair, the mortality among these patients was higher than in the general population.