BACKGROUND In patients with non-ST-segment elevation acute coronary syndrome (NSTEACS), coronary pathology may range from structurally normal vessels to severe coronary artery disease. OBJECTIVES The purpose of this study was to test if coronary computed tomography angiography (CTA) may be used to exclude coronary artery stenosis $50% in patients with NSTEACS. METHODS The VERDICT (Very Early Versus Deferred Invasive Evaluation Using Computerized Tomography in Patients With Acute Coronary Syndromes) trial (NCT02061891) evaluated the outcome of patients with confirmed NSTEACS randomized 1:1 to very early (within 12 h) or standard (48 to 72 h) invasive coronary angiography (ICA). As an observational component of the trial, a clinically blinded coronary CTA was conducted prior to ICA in both groups. The primary endpoint was the ability of coronary CTA to rule out coronary artery stenosis ($50% stenosis) in the entire population, expressed as the negative predictive value (NPV), using ICA as the reference standard. RESULTS Coronary CTA was conducted in 1,023 patients-very early, 2.5 h (interquartile range [IQR]: 1.8 to 4.2 h), n = 583; and standard, 59.9 h (IQR: 38.9 to 86.7 h); n = 440 after the diagnosis of NSTEACS was made. A coronary stenosis $50% was found by coronary CTA in 68.9% and by ICA in 67.4% of the patients. Per-patient NPV of coronary CTA was 90.9% (95% confidence interval [CI]: 86.8% to 94.1%) and the positive predictive value, sensitivity, and specificity were 87.9% (95% CI: 85.3% to 90.1%), 96.5% (95% CI: 94.9% to 97.8%) and 72.4% (95% CI: 67.2% to 77.1%), respectively. NPV was not influenced by patient characteristics or clinical risk profile and was similar in the very early and the standard strategy group. CONCLUSIONS Coronary CTA has a high diagnostic accuracy to rule out clinically significant coronary artery disease in patients with NSTEACS. (C) 2020 by the American College of Cardiology Foundation.
Background: The inflammatory biomarker soluble urokinase plasminogen activator receptor (suPAR) is associated with presence and severity of coronary artery disease (CAD) and incident death and myocardial infarction (MI). We sought to validate this finding in a further cohort of patients with suspected CAD. Methods: Plasma suPAR was available in 1635 patients (73% with CAD) undergoing coronary angiography at a single regional Danish hospital between 2003 and 2005. Patients were followed for adverse cardiovascular outcomes of death, cardiac death and MI over a median follow-up of 4.2 years. Results: In multivariate Cox models, adjusted for established cardiovascular risk factors, the biomarkers C-reactive protein, troponin-T and N-terminal-pro brain natriuretic peptide and the number of stenotic vessels, suPAR was independently associated with the combined endpoint of death/MI, hazard ratio (HR) 1.88; cardiovascular death, HR 2.01; and non-fatal MI, HR 1.53; (all p <= .037) per doubling of suPAR concentration. A plasma cutoff for suPAR >= 3.5 ng/mL was also significantly associated with death/MI, HR 1.51; p = .005. The C-statistic for the multivariate model predicting death/MI improved from 0.712 to 0.730 (p for difference .008) after inclusion of suPAR. However, suPAR was not associated with presence or extent of CAD (p > .05). Conclusion: These results validate previous findings that demonstrate suPAR to be an independent predictor of death/MI in patients with suspected or known CAD, however suPAR was not associated with presence or extent of CAD in our cohort. Probably because suPAR reflects end organ damage rather than the degree of atherosclerosis. BRIEF SUMMARY: We demonstrate that the inflammatory biomarker soluble urokinase plasminogen activator receptor is an independent predictor of death/myocardial infarction in patients with suspected or known coronary artery disease, but is not associated with the presence or severity of coronary artery disease.
Background: The optimal timing of invasive coronary angiography (ICA) and revascularization in patients with non-ST-segment elevation acute coronary syndrome (NSTE-ACS) is not well defined. We tested the hypothesis, that a strategy of very early invasive coronary angiography (ICA) and possible revascularization within 12 hours of diagnosis, is superior to an invasive strategy performed within 48-72 hours in terms of clinical outcomes. Methods: Patients admitted with clinical suspicion of NSTE-ACS in the Capital Region of Copenhagen, Denmark were screened for inclusion in the VERDICT trial (ClinicalTrials.gov NCT02061891). Patients with ECG changes indicating new ischemia and/or elevated troponin, in whom ICA was clinically indicated and deemed logistically feasible within 12 hours, were randomized 1:1 to ICA within 12 hours or standard invasive care within 48-72 hours. The primary endpoint was a combination of all-cause death, non-fatal recurrent myocardial infarction, hospital admission for refractory my...
Background: The optimal timing of invasive coronary angiography (ICA) and revascularization in patients with non-ST-segment elevation acute coronary syndrome is not well defined. We tested the hypothesis that a strategy of very early ICA and possible revascularization within 12 hours of diagnosis is superior to an invasive strategy performed within 48 to 72 hours in terms of clinical outcomes. Methods: Patients admitted with clinical suspicion of non-ST-segment elevation acute coronary syndrome in the Capital Region of Copenhagen, Denmark, were screened for inclusion in the VERDICT trial (Very Early Versus Deferred Invasive Evaluation Using Computerized Tomography) ( ClinicalTrials.gov NCT02061891). Patients with ECG changes indicating new ischemia or elevated troponin, in whom ICA was clinically indicated and deemed logistically feasible within 12 hours, were randomized 1:1 to ICA within 12 hours or standard invasive care within 48 to 72 hours. The primary end point was a combination of all-cause death, nonfatal recurrent myocardial infarction, hospital admission for refractory myocardial ischemia, or hospital admission for heart failure. Results: A total of 2147 patients were randomized; 1075 patients allocated to very early invasive evaluation had ICA performed at a median of 4.7 hours after randomization, whereas 1072 patients assigned to standard invasive care had ICA performed 61.6 hours after randomization. Among patients with significant coronary artery disease identified by ICA, coronary revascularization was performed in 88.4% (very early ICA) and 83.1% (standard invasive care). Within a median follow-up time of 4.3 (interquartile range, 4.1–4.4) years, the primary end point occurred in 296 (27.5%) of participants in the very early ICA group and 316 (29.5%) in the standard care group (hazard ratio, 0.92; 95% CI, 0.78–1.08). Among patients with a GRACE risk score (Global Registry of Acute Coronary Events) >140, a very early invasive treatment strategy improved the primary outcome compared with the standard invasive treatment (hazard ratio, 0.81; 95% CI, 0.67–1.01; P value for interaction=0.023). Conclusions: A strategy of very early invasive coronary evaluation does not improve overall long-term clinical outcome compared with an invasive strategy conducted within 2 to 3 days in patients with non-ST-segment elevation acute coronary syndrome. However, in patients with the highest risk, very early invasive therapy improves long-term outcomes. Clinical Trial Registration: URL: https://www.clinicaltrials.gov . Unique identifier: NCT02061891.
BACKGROUND:Common lipoprotein lipase (LPL) variants are important determinants of triglycerides (TG) and high-density lipoprotein (HDL) cholesterol (C) concentrations. High TG/low HDL-C tend to cluster with hypertension, glucose intolerance, and abdominal obesity and comprise the metabolic syndrome (MetS). The role of LPL variants as a cause of MetS is unclear. This study investigated the relationship between two common LPL variants and the presence of MetS and its individual components. METHODS:Cross-sectional study, including 2348 Danish women (50.7%) and men, age 41-72 years, without known cardiovascular disease. Carrier status for the two common LPL variants: 447Ter (low TG/high HDL-C) and 291Ser (high TG/low HDL-C) was determined. The prevalence of MetS according to the National Cholesterol Education Program criteria was 16.6%. RESULTS:Of the 2348 participants, 19.8% had the 447Ter variant and 4.9% had the 291Ser variant. Compared with the reference variant, the prevalence of MetS was lower in carriers of the 447Ter variant (11.2% vs. 17.9%, P < 0.001) but with no difference in carriers of the 291Ser variant (18.4% vs. 16.5%, P = 0.59). Adjusted for age, sex, smoking, physical activity, alcohol consumption, and highest sex-specific insulin quartile, the relative risk of MetS was 0.63 (95% confidence interval [CI] 0.45-0.89, P < 0.01) for carriers of the 447Ter variant and 1.20 (95% CI 0.70-2.03, P > 0.05) for carriers of the 291Ser variant. Both LPL variants were associated with high TG/low HDL-C (P < 0.01), but not with the MetS components waist circumference, hypertension, and glucose intolerance (P > 0.05). CONCLUSION:The two common LPL variants were associated with MetS through their effect on high TG/low HDL-C.
BACKGROUND Our aims were to determine the incidence of symptomatic deep venous thrombosis (DVT) and pulmonary embolism (PE) that required inpatient or outpatient treatment, and to identify specific risk factors associated with DVT/PE in patients who had undergone surgery for a fracture distal to the knee. METHODS Using individual linkage of nationwide registries, we included all Danish patients who had undergone surgery for a fracture distal to the knee between 1999 and 2011. Patients were followed for 180 days from discharge. Event rates of DVT/PE were calculated, and significant risk factors were identified with use of multivariable Cox regression analyses. Routine postdischarge antithrombotic chemoprophylaxis was not given to these patients. RESULTS The study included 57,619 patients, 594 of whom had a venous thromboembolic event during the follow-up period. Thirty-nine (6.6%) of the 594 events were death due to PE. The overall event rate during the 180-day study period was 1.0%. The incidence rate was 7.28 events per 100 person-years before discharge, decreasing to a stable level below one event per 100 person-years in week 13 to 14 after discharge. Use of oral contraception by patients eighteen to fifty years of age (hazard ratio [HR] = 5.23, 95% confidence level [CI] = 3.35 to 8.18), previous DVT (HR = 6.27, 95% CI = 4.18 to 9.40), previous PE (HR = 5.45, 95% CI = 3.05 to 9.74), coagulopathy (HR = 2.47, 95% CI = 1.07 to 5.72), and peripheral artery disease (HR = 2.34, 95% CI = 1.20 to 4.56) were the factors associated with the highest risk of postoperative DVT/PE. Also, increasing age, increasing body mass index, cancer, and treatment with nonsteroidal anti-inflammatory drugs were associated with a significantly increased risk of DVT/PE. CONCLUSIONS The incidence of DVT/PE was low following surgery for fractures distal to the knee; however, the risk was increased in the presence of a number of risk factors. This study suggests that specific groups of patients undergoing surgery for a fracture distal to the knee might benefit from postdischarge antithrombotic treatment.
Background: Soluble urokinase plasminogen activator receptor (suPAR) is released in response to inflammatory stimuli, and plasma levels are associated with long-term outcomes. The ischemia/reperfusion injury caused by cardiac arrest (CA) and resuscitation triggers an inflammatory response. This pilot study aimed at investigating suPAR levels in relation to outcome after CA and mild induced hypothermia.Methods: suPAR levels were measured at 6, 36, and 72 hours in patients treated with hypothermia after CA. suPAR levels were analyzed in relation to survival after 6 months. Receiver operating characteristic curve (ROC)-analyses were performed, and area under the curve (AUC) was calculated. Time to return of spontaneous circulation (ROSC) was correlated to suPAR levels.Results: Fifty-five patients (40 male, median 65 years) were included, and 33 (60%) were alive after 6 months. The suPAR levels were significantly higher in nonsurviving patients compared with survivors at 6 and 36 hours (p=0.006 and 0.034 respectively), but not at 72 hours. The suPAR levels increased from 6 to 72 hours (p<0.0001). Time to ROSC correlated positively with suPAR levels at 6 hours (p=0.003) but not at 36 and 72 hours. ROC analysis shoved an AUC of 0.76 at 6 hours. In the subgroup of CA of cardiac cause, the AUC was 0.84.Conclusion: suPAR levels at 6 and 36 hours after CA were significantly higher in nonsurviving patients compared with survivors; however, the overlap in suPAR levels between the outcome groups was substantial, reducing the prognostic value. There was a significant increase in suPAR levels during the first 72 hours after CA.
ObjectivesSoluble urokinase plasminogen activator receptor (suPAR) is a marker of inflammation and endothelial dysfunction. We investigated the associations between suPAR and diabetes, including diabetes duration and complications, in patients with type 1 diabetes.Design, setting and subjectsFrom 2009 to 2011, 667 patients with type 1 diabetes and 51 nondiabetic control subjects were included in a cross-sectional study at Steno Diabetes Center, Gentofte, Denmark. suPAR levels were measured with an enzyme-linked immunosorbent assay.Main outcome measuresThe investigated diabetic complications were cardiovascular disease (CVD: previous myocardial infarction, revascularisation, peripheral arterial disease and stroke), autonomic dysfunction (heart rate variability during deep breathing <11 beatsmin(-1)), albuminuria [urinary albumin excretion rate (UAER) 30mg/24h] or a high degree of arterial stiffness (pulse wave velocity 10ms(-1)). Analyses were adjusted for gender, age, systolic blood pressure, estimated glomerular filtration rate, UAER, glycated haemoglobin (HbA(1c)), total cholesterol, body mass index, C-reactive protein, antihypertensive treatment and smoking.ResultsSoluble urokinase plasminogen activator receptor levels were lower in control subjects versus all patients, in control subjects versus normoalbuminuric patients (UAER <30mg/24h), in normoalbuminuric patients with short (<10 years) versus long diabetes duration and were increased with degree of albuminuria (adjusted P<0.001 for all). Furthermore, suPAR levels were higher in patients with versus without CVD (n=144; 21.3%), autonomic dysfunction (n= 369; 59.2%), albuminuria (n=357; 53.1%) and a high degree of arterial stiffness (n=298; 47.2%) (adjusted P0.024). The adjusted odds ratio (95% confidence interval) values per 1 ln unit increase in suPAR were as follows: 2.5 (1.1-5.7) for CVD: 2.7 (1.2-6.2) for autonomic dysfunction; 3.8 (1.3-10.9) for albuminuria and 2.5 (1.1-6.1) for a high degree of arterial stiffness (P0.039).ConclusionThe suPAR level is higher in patients with type 1 diabetes and is associated with diabetes duration and complications independent of other risk factors. suPAR is a potential novel risk marker for the management of diabetes.
Aims Low prevalence of detectable cardiac troponin in healthy people and low-risk patients previously curtailed its use. With a new high-sensitive cardiac troponin assay (hs-cTnT), concentrations below conventional detection may have prognostic value, notably in combination with N-terminal pro-B-type natriuretic peptide (NT-pro-BNP).Methods and results Biomarker concentrations were determined from serum obtained at enrolment in the CLARICOR trial involving 4197 patients with stable coronary artery disease (CAD) followed for 2.6 years. Serum hs-cTnT was detectable (above 3ng/l) in 78% and above the conventional 99th percentile (13.5ng/l) in 23%. Across all levels of hs-cTnT there was a graded increase in the risk of cardiovascular death after adjustment for known prognostic indicators: hazard ratio (HR) per unit increase in the natural logarithm of the hs-cTnT level, 1.49; 95% confidence interval (CI), 1.23-1.81; similarly for all-cause mortality (HR 1.48, 95% CI 1.29-1.70) and myocardial infarction (HR 1.37, 95% CI 1.13-1.67). Increasing values of hs-cTnT were associated with increased mortality across all values of NT-pro-BNP, but this was particularly prominent when NT-pro-BNP >400ng/l.Conclusions In patients with stable CAD, any detectable hs-cTnT level is significantly associated with all-cause mortality, cardiovascular death, and myocardial infarction after adjustment for traditional risk factors and NT-pro-BNP. Excess mortality is particularly pronounced in patients with NT-pro-BNP >400ng/l.
BACKGROUND Plasma concentrations of soluble urokinase plasminogen activator receptor (suPAR) predict mortality in several clinical settings, but the long-term prognostic importance of suPAR in chest pain patients admitted on suspicion of non-ST-segment elevation acute coronary syndrome (NSTEACS) is uncertain. METHODS suPAR concentrations were measured on admission in 449 consecutive chest pain patients in a single center between January 3, 2005, and February 14, 2006. Patients were followed for all-cause mortality from discharge until July 28, 2011. RESULTS The diagnoses at discharge comprised high-risk NSTEACS [non-ST elevation myocardial infarction or unstable angina with electrocardiogram (ECG) abnormalities] in 77 patients (17.2%) and low-risk NSTEACS without evidence of myocardial ischemia in 257 (57.2%) of patients. Another 115 (25.6%) of patients received other diagnoses. During a median follow-up of 5.7 years (range, 0.01-6.6 years) there were 162 (36.1%) deaths. suPAR was predictive of mortality independent of age, sex, smoking, final diagnosis for the hospitalization, comorbidities (diabetes, hypertension, previous myocardial infarction, and heart failure), and variables measured on the day of admission (renal function, inflammatory markers, and markers of myocardial ischemia) with a hazard ratio (95% CI) of 1.93 (1.48-2.51) per SD increase in log-transformed suPAR, P < 0.0001. The use of suPAR improved the predictive accuracy of abnormal ECG findings and increased troponin concentrations regarding all-cause mortality (c statistics, 0.751-0.805; P < 0.0001). CONCLUSIONS suPAR is a strong predictor of adverse long-term outcomes and improves risk stratification beyond traditional risk variables in chest pain patients admitted with suspected NSTEACS.
The plasma level of the inflammatory biomarker soluble urokinase plasminogen activator receptor (suPAR) is an independent predictor of cardiovascular disease and all-cause mortality in healthy subjects. The prognostic capability of suPAR, its temporal course, and its relation to plasma C-reactive protein (CRP) in patients with ST-segment elevation myocardial infarction undergoing primary percutaneous intervention (PCI) is unknown. Therefore, the plasma suPAR and CRP levels were measured in 296 consecutive patients with ST-segment elevation myocardial infarction admitted for primary PCI at baseline and every 6 to 8 hours thereafter until the cardiac biomarker levels had peaked. The end points were all-cause mortality and fatal or nonfatal recurrent myocardial infarction (MI). During a median follow-up period of 5.75 years, 69 deaths and 48 nonfatal and 14 fatal recurrent MIs occurred. All-cause mortality increased significantly from 8.1% to 41.5% across increasing quartiles of suPAR levels at the end of follow-up (log-rank p <0.0001). After adjustment for other independent prognostic factors, a highly significant increase was seen in all-cause mortality (hazard ratio 1.45, 95% confidence interval, 1.19 to 1.76; p <0.001) and recurrent MI (hazard ratio 1.53, 95% confidence interval 1.16 to 2.01; p <0.01) for each standard deviation increment of suPAR levels). In contrast to plasma CRP, the suPAR levels remained stable after primary PCI. Furthermore, CRP did not predict mortality or reinfarction after adjustment for age and gender (p = 0.34). In conclusion, suPAR is a stable plasma biomarker after ST-segment elevation myocardial infarction treated with primary PCI that predicts all-cause mortality and recurrent MI.
Background The inflammatory biomarkers soluble urokinase plasminogen activator receptor (suPAR) and C-reactive protein (CRP) independently predict cardiovascular disease (CVD). The prognostic implications of suPAR and CRP combined with Framingham Risk Score (FRS) have not been determined. Methods From 1993 to 1994, baseline levels of suPAR and CRP were obtained from 2315 generally healthy Danish individuals (mean [SD] age: 53.9 [10.6] years) who were followed for the composite outcome of ischemic heart disease, stroke and CVD mortality. Results During a median follow-up of 12.7years, 302 events were recorded. After adjusting for FRS, women with suPAR levels in the highest tertile had a 1.74-fold (95% confidence interval [CI]: 1.08–2.81, p=0.027) and men a 2.09-fold (95% CI: 1.37–3.18, p<0.001) increase in risk compared to the lowest tertile. Including suPAR and CRP together resulted in stronger risk prediction with a 3.30-fold (95% CI: 1.36–7.99, p<0.01) increase for women and a 3.53-fold (1.78–7.02, p<0.001) increase for men when both biomarkers were in the highest compared to the lowest tertile. The combined extreme tertiles of suPAR and CRP reallocated individuals predicted to an intermediate 10-year risk of CVD of 10–20% based on FRS, to low (<10%) or high (>20%) risk categories, respectively. This was reflected in a significant improvement of C statistics for men (p=0.034) and borderline significant for women (p=0.054), while the integrated discrimination improvement was highly significant (P≤0.001) for both genders. Conclusions suPAR provides prognostic information of CVD risk beyond FRS and improves risk prediction substantially when combined with CRP in this setting.
Background: Low-grade inflammation is a marker for cardiovascular disease (CVD). The inflammatory biomarkers C-reactive protein (CRP) and soluble urokinase plasminogen activator receptor (suPAR) independently predict CVD. We tested the hypothesis that these biomarkers reflect different aspects of the inflammation associated with CVD.Methods: We studied 2273 subjects without CVD. Log-transformed CRP and suPAR were included in general linear and logistic regression models to compare associations with measures of anthropometry and subclinical organ damage (SOD). Owing to interactions on body mass index (BMI) (P<0.0001), the population was stratified by gender and smoking concerning anthropometry.Results: In both genders, independent of smoking, log-CRP was positively associated with BMI (beta: 0.28 to 0.40, P<0.001) and waist circumference (WC) (beta: 0.27 to 0.42, P<0.001). In contrast, in smoking women and men, log-suPAR was negatively associated with BMI and WC (beta: -0.09 to -0.19, P<0.05). In nonsmoking women, log-suPAR was positively associated with BMI and WC (beta: 0.14 and 0.16, P<0.001), whereas no associations were found in non-smoking men. No interactions were found on SOD. Adjusted for age, sex, smoking, and physical activity, log-suPAR was associated with an increased urine albumin/creatinine ratio (standardized odds ratio (95% confidence interval (CI)) for highest vs. lower quartiles: 1.36 (1.21-1.52), whereas log-CRP was not (1.10 (0.99-1.22))), and extent of atherosclerosis (standardized proportional odds ratio (95% CI) for carotid plaques 0, 1 <= to <= 3, > 3: 1.31 (1.16-1.47), whereas log-CRP was not (1.00 (0.89-1.11))).Conclusions: CRP is positively associated with anthropometric measures, whereas suPAR is linked to endothelial dysfunction and atherosclerosis. (C) 2012 Elsevier Ireland Ltd. All rights reserved.
CONTEXT:Pharmacodynamic studies have shown that persistently high platelet reactivity is common in patients with diabetes in spite of clopidogrel treatment. Clinical trials have not convincingly demonstrated that clopidogrel benefits patients with diabetes as much patients without diabetes.OBJECTIVES:To estimate the clinical effectiveness associated with clopidogrel treatment after myocardial infarction (MI) in patients with diabetes.DESIGN, SETTING, AND PATIENTS:By individual-level linkage of the Danish nationwide administrative registries between 2002-2009, patients who were hospitalized with incident MI and who had survived and not undergone coronary artery bypass surgery 30 days after discharge were followed up for as long as 1 year (maximally until December 31, 2009). Adjusted for age, sex, comorbidity, calendar year, concomitant pharmacotherapy, and invasive interventions, hazard ratios that were associated with clopidogrel in patients with and without diabetes were analyzed by Cox proportional-hazard models and propensity score-matched models.MAIN OUTCOME MEASURES:All-cause mortality, cardiovascular mortality, and a composite end point of recurrent MI and all-cause mortality.RESULTS:Of the 58,851 patients included in the study, 7247 (12%) had diabetes and 35,380 (60%) received clopidogrel. In total, 1790 patients (25%) with diabetes and 7931 patients (15%) without diabetes met the composite end point. Of these, 1225 (17%) with and 5377 (10%) without diabetes died. In total, 978 patients (80%) with and 4100 patients (76%) without diabetes died of events of cardiovascular origin. For patients with diabetes who were treated with clopidogrel, the unadjusted mortality rates (events/100 person-years) were 13.4 (95% CI, 12.8-14.0) vs 29.3 (95% CI, 28.3-30.4) for those not treated. For patients without diabetes who were treated with clopidogrel, the unadjusted mortality rates were 6.4 (95% CI, 6.3-6.6) vs 21.3 (95% CI, 21.0-21.7) for those not treated. However, among patients with diabetes vs those without diabetes, clopidogrel was associated with less effectiveness for all-cause mortality (HR, 0.89 [95% CI, 0.79-1.00] vs 0.75 [95% CI, 0.70-0.80]; P for interaction, .001) and for cardiovascular mortality (HR, 0.93 [95% CI, 0.81-1.06] vs 0.77 [95% CI, 0.72-0.83]; P for interaction, .01) but not for the composite end point (HR, 1.00 [95% CI, 0.91-1.10] vs 0.91 [95% CI, 0.87-0.96]; P for interaction, .08). Propensity score-matched models gave similar results.CONCLUSION:Among patients with diabetes compared with patients without diabetes, the use of conventional clopidogrel treatment after MI was associated with lower reduction in the risk of all-cause death and cardiovascular death.
Stent thrombosis is a devastating complication after percutaneous coronary intervention (PCI), but the influence of obesity on risk of stent thrombosis is unclear, and it is unknown if this relation is dependent on stent type. The objective of this study was to examine the relation between body mass index (BMI) and stent thrombosis after PCI with bare-metal stent (BMS) or drug-eluting stent (DES). We followed 5,515 patients who underwent PCI with implantation of ≥1 BMS or DES at a high-volume tertiary invasive cardiology center from 2000 through 2006. Only patients with a single type of stent (BMS or DES) implanted at the index PCI were included. Median follow-up period was 26 months (interquartile range 12 to 44) and definite stent thrombosis occurred in 78 patients. Hazard ratio of definite stent thrombosis adjusted for number of stents at the index PCI was 0.92 (95% confidence interval [CI] 0.86 to 0.97) for each increase in kilograms per square meter of BMI. There was no significant interaction between stent type and BMI (p = 0.48). Hazard ratios for probable stent thrombosis and possible stent thrombosis adjusted for numbers of stents at the index PCI were 1.01 (CI 0.99 to 1.03) and 0.99 (CI 0.98 to 1.01) for each increase in kilograms per square meter of BMI, respectively. In conclusion, BMI was inversely correlated with risk of definite stent thrombosis after PCI irrespective of stent type.
OBJECTIVE:The soluble urokinase plasminogen activator receptor (suPAR) is a plasma marker of low grade inflammation and has been associated with cardiovascular risk. We wanted to investigate whether suPAR was associated with markers of subclinical organ damage. METHODS:In a population sample of 2038 individuals, aged 41, 51, 61 and 71 years, without diabetes, prior stroke or myocardial infarction, not receiving any cardiovascular, anti-diabetic or lipid-lowering medications, we measured urine albumin/creatinine ratio (UACR), carotid atherosclerotic plaques and carotid/femoral pulse wave-velocity (PWV) together with traditional cardiovascular risk factors and high sensitivity C-reactive protein (hsCRP). RESULTS:suPAR was significantly associated with the presence of plaques (P = 0.003) and UACR (P < 0.001), but not PWV (P = 0.17) when adjusting for age, gender, systolic blood pressure, cholesterol, plasma glucose, waist/hip ratio, smoking and hsCRP. However, suPAR explained only a small part of the variation in the markers of subclinical organ damage (R(2) 0.02-0.04). During a median follow-up of 12.7 years (5th-95th percentile 5.1-13.4 years) a total of 174 composite endpoints (CEP) of cardiovascular death, non-fatal myocardial infarction and stroke occurred. suPAR was associated with CEP independent of plaques, PWV, UACR, and hsCRP as well as age, gender, systolic blood pressure, cholesterol, plasma glucose, waist/hip ratio and smoking with a standardized hazard ratio of 1.16 (95% confidence interval 1.04-1.28, P = 0.006). CONCLUSION:suPAR was associated with subclinical organ damage, but predicted cardiovascular events independent of subclinical organ damage, traditional risk factors and hsCRP. Further studies must investigate whether suPAR plays an independent role in the pathogenesis of cardiovascular disease.