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ABSTRACT: BACKGROUND: Osteopontin (OPN), a multifunctional glycoprotein, has recently been found to be an important player in cardiovascular diseases and to be implicated in a variety of acute as well as chronic inflammatory processes, including atherosclerosis. This study investigates the association between plasma OPN at admission and the long-term outcome in patients with ST segment elevation myocardial infarction (STEMI) treated with primary percutaneous coronary intervention (pPCI). METHODS: We included a total of 730 consecutive STEMI patients admitted to a single high-volume invasive heart centre between September 2006 and December 2008. Plasma OPN and high sensitivity C-reactive protein (hsCRP) were measured. RESULTS: The median follow-up time was 27 months (interquartile range: 22-33) and endpoints were all-cause mortality, re-infarction and heart failure. Even when adjusted for all baseline variables, increasing OPN was independently associated with increased all-cause mortality, and the combined endpoint, a linear increase in OPN of 10 µg/l, was associated with a hazard ratio (HR) of 1.05 (95% confidence interval (CI): 1.02-1.08; p = 0.002) for all-cause mortality and HR 1.03 (95%CI: 1.01-1.05; p = 0.047) for the combined endpoint. Importantly, OPN interacted with the predictive power of hsCRP, and the combination of high OPN levels and high hsCRP levels (>3 mg/l) were significantly associated with increased risk of all-cause mortality (HR: 2.32; CI: 1.51-3.58; p < 0.001), re-infarction (HR: 2.19; CI: 1.22-3.93; p = 0.006), heart failure (HR: 1.84; CI: 1.08-3.13; p = 0.025) and the combined endpoint (HR: 2.08; CI: 1.53-2.84; p < 0.001). CONCLUSIONS: In conclusion, a high OPN level, especially in combination with a high hsCRP level, was associated with poor long-term outcome in STEMI patients treated with pPCI.
European journal of preventive cardiology. 04/2013;
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ABSTRACT: BACKGROUND: -Color Tissue Doppler Imaging (TDI) M-mode through the mitral leaflet is an easy and precise method to estimate all cardiac time intervals from one cardiac cycle and thereby obtaining the Myocardial Performance Index (MPI). However, the prognostic value of the cardiac time intervals and the MPI assessed by color TDI M-mode through the mitral leaflet in patients with ST-segment Elevation Myocardial Infarction (STEMI) is unknown. METHODS AND RESULTS: -In total 391 patients were admitted with a STEMI, treated with primary Percutaneous Coronary Intervention (pPCI) and were examined by echocardiography median 2 days after the STEMI. Outcome was assessed according to death (n=33), hospitalization with heart failure (CHF, n=53) or new myocardial infarction (re-MI, n=25). Follow-up time was median 25 months. The population was stratified according to tertiles of the MPI. The risk of a re-MI, being admitted with CHF or death, increased with increasing tertile of MPI, being approximately three times as high for the third tertile compared to the first tertile (HR 2.8, 95% CI 1.7 to 4.7, p<0.001). MPI provided independent prognostic information in a multivariable Cox regression model adjusted for age, gender, previous MI, peak troponin, systolic and diastolic echocardiographic parameters, with a HR of 1.24 (p=0.005) for the combined endpoint per each 0.1 increase in MPI. CONCLUSIONS: -MPI assessed by TDI M-mode is a simple and reproducible measure, which provides independent prognostic information, regardless of rhythm, incremental to conventional and novel echocardiographic parameters of systolic and diastolic function in patients with STEMI treated with pPCI.
Circulation Cardiovascular Imaging 03/2013; · 5.94 Impact Factor
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ABSTRACT: INTRODUCTION: Excessive sympathoadrenal activation in critical illness contributes directly to organ damage and high concentrations of catecholamines damage the vascular endothelium. This study investigated associations between potential drivers of sympathoadrenal activation, circulating catecholamines and biomarkers of endothelial damage and outcome in ST segment elevation myocardial infarction (STEMI)-patients, hypothesizing that the catecholamine surge would reflect shock degree and correlate with biomarkers of endothelial damage. METHODS: This was a prospective study of 678 consecutive STEMI-patients admitted to a single high-volume invasive heart centre for primary percutaneous coronary intervention (pPCI) from September 2006-July 2008. Blood samples were drawn immediately before pPCI. Plasma adrenaline, noradrenaline, syndecan-1 and thrombomodulin were measured retrospectively with complete data in 571 patients (84%). Median follow-up time was 28 (IQR 23-34) months. Follow-up was 99.7% complete. Outcomes were all-cause and cardiovascular mortality, re-myocardial infarction and admission due to heart failure (HF). RESULTS: Circulating noradrenaline and adrenaline correlated weakly but independently with syndecan-1 (rho=0.15 and rho=0.13, both p<0.01) and thrombomodulin (rho=0.11 and rho=0.17, both p<0.01), biomarkers of glycocalyx and endothelial cell damage, respectively. Considering biomarkers, patients with shock pre-pPCI had higher adrenaline and syndecan-1 and patients admitted to ICU post-pPCI had higher syndecan-1 (all p<0.05), and in the shocked patients (n=51) catecholamines correlated strongly with thrombomodulin and syndecan-1 (rho=0.31-0.42, all p<0.05). During follow-up, 78 (14%) patients died (37 cardiovascular deaths) and 65 (11%) were admitted with HF. By multivariate Cox proportional hazards analyses, one quartile higher plasma adrenaline was weakly but independently associated with both 30-day and long term mortality and HF (30-day all-cause mortality Hazard Ratio (95% CI) 1.39 (1.01-1.92), p=0.046; 30-day HF 1.65 (1.17-2.34), p=0.005; long-term cardiovascular mortality 1.49 (1.08-2.04), p=0.014). Furthermore, one quartile higher syndecan-1 was also weakly independently associated with long-term all cause mortality (1.26 (1.02-1.57), p=0.034). CONCLUSIONS: In STEMI-patients treated with pPCI, catecholamines correlated weakly with biomarkers of endothelial damage, with the strongest correlations and highest adrenaline and syndecan-1 levels in shocked patients. Furthermore, adrenaline and syndecan-1 were weakly independently associated with mortality and HF. Acute MI appears to cause significant endothelial cell and glycocalyx injury and a parallel increase in circulating catecholamines.
Critical care (London, England) 02/2013; 17(1):R32. · 4.61 Impact Factor
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ABSTRACT: Adiponectin exerts anti-inflammatory and antiatherogenic effects and appears to protect against arteriosclerosis. Accordingly, an association between low concentrations of plasma adiponectin and cardiovascular (CV) disease has been demonstrated in several studies. In contrast, elevated plasma adiponectin has been associated with increased mortality and an increasing number of major adverse CV events (MACE). Because of these conflicting results, the true role of adiponectin remains to be elucidated. In the Copenhagen City Heart Study, we prospectively followed up 5,624 randomly selected men and women from the community without CV disease. Plasma adiponectin was measured at the beginning of the study. The median follow-up time was 7.8 years (interquartile range 7.3 to 8.3). The end point was all-cause mortality (n = 801), and the combined end point was MACE, consisting of CV mortality or nonfatal myocardial infarction or ischemic stroke (n = 502). High adiponectin was inversely associated with an increasing number of traditional CV risk factors (p <0.0001). The geometric mean adiponectin concentrations were 10.0 mg/L (95% confidence interval [CI] 9.7 to 10.4) for persons with no CV risk factors present versus 8.1 mg/L (95% CI 7.8 to 8.4) for persons with 4 CV risk factors. After adjustment for confounding risk factors by Cox regression analysis, adiponectin remained an independent predictor of death and MACE. The hazard ratio for each increase in adiponectin of 5 mg/L for death and MACE was 1.20 (95% CI 1.14 to 1.27; p <0.0001) and 1.14 (95% CI 1.05-1.23; p <0.0001), respectively. In conclusion, an increasing number of risk factors for CV disease is associated with decreased plasma adiponectin. High plasma adiponectin independently predicted death and MACE in a large community-based population. These results have confirmed the dual expression indicated by previous studies.
The American journal of cardiology 01/2013; · 3.58 Impact Factor
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ABSTRACT: The complement system is an important mediator of inflammation, which plays a pivotal role in atherosclerosis and acute myocardial infarction (AMI). Animal studies suggest that activation of the complement cascade resulting in the formation of soluble membrane attack complex (sMAC), contributes to both atherosclerosis and plaque rupture and may be the direct cause of tissue damage related to ischemia/reperfusion injury. However clinical data of sMAC during an AMI is sparse. Accordingly the aim was to investigate the prognostic role of sMAC in patients with ST-segment elevation myocardial infarction (STEMI).
We included 725 STEMI-patients admitted to a single, high-volume invasive heart centre, treated with primary percutaneous coronary intervention (PCI), from September 2006 to December 2008. Blood samples were drawn immediately before PCI. Plasma sMAC was measured using an in-house immunoassay. Endpoints were all-cause mortality (n = 62) and the combined endpoint (n = 122) of major cardiovascular events (MACE) defined as cardiovascular mortality and admission due recurrent AMI or heart failure. Follow-up time was 12 months.
During 12 months of follow-up 62 patients died from all causes and 122 patients reached the combined end-point of MACE. Patients with high sMAC (>75th percentile) had increased risk of both all-cause mortality and MACE. Even after adjustment for confounding risk factors by Cox-regression analyses, high levels of sMAC remained an independent predictor of all-cause mortality (hazard ratio 1.81 [95% CI 1.06-3.06; P = .029]) and MACE (hazard ratio 1.70 [95% CI 1.16-2.48; P = .006]).
High plasma sMAC independently predicts all-cause mortality and MACE in STEMI-patients treated with PCI.
American heart journal 11/2012; 164(5):786-92. · 4.65 Impact Factor
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ABSTRACT: The aim of this study was to investigate the prognostic role of neutrophil gelatinase-associated lipocalin (NGAL) in a large population of patients with ST-segment elevation myocardial infarction.
NGAL is a glycoprotein released by damaged renal tubular cells and is a sensitive maker of both clinical and subclinical acute kidney injury. New data have demonstrated that NGAL is also stored in granules of mature neutrophils, and recent data suggest that NGAL may also be involved in the development of atherosclerosis. NGAL is significantly increased in patients with myocardial infarction compared with patients with stable coronary artery disease and healthy subjects. However, the prognostic value of NGAL has never been studied in patients with myocardial infarction.
We included 584 consecutive ST-segment elevation myocardial infarction patients admitted to the heart center of Gentofte University Hospital, Denmark, and treated with primary percutaneous coronary intervention, from September 2006 to December 2008. Blood samples were drawn immediately before primary percutaneous coronary intervention. Plasma NGAL levels were measured using a time-resolved immunofluorometric assay. The endpoints were all-cause mortality (n = 69) and the combined endpoints (n = 116) of major adverse cardiac events (MACE) defined as cardiovascular mortality and admission due to recurrent myocardial infarction or heart failure. The median follow-up time was 23 months (interquartile range, 20 to 24 months).
Patients with high NGAL (>75th percentile) had increased risk of all-cause mortality and MACE compared with patients with low NGAL (log-rank test, p < 0.001). After adjustment for confounding risk factors chosen by backward elimination by Cox regression analysis, high NGAL remained an independent predictor of all-cause mortality and MACE (hazard ratio: 2.00; 95% confidence interval: 1.16 to 3.44; p = 0.01 and hazard ratio: 1.51; 95% confidence interval: 1.00 to 2.30; p = 0.05, respectively).
High plasma NGAL independently predicts all-cause mortality and MACE in ST-segment elevation myocardial infarction patients treated with primary percutaneous coronary intervention.
Journal of the American College of Cardiology 07/2012; 60(4):339-45. · 14.16 Impact Factor
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ABSTRACT: Substantial evidence points to a protective role of adiponectin against atherosclerosis and cardiovascular (CV) disease. However, in the setting of an acute myocardial infarction (AMI), the role of adiponectin has not previously been studied. Consequently, the aim of this study was to investigate the prognostic role of adiponectin after AMI in a large population of patients with ST-segment elevation myocardial infarction treated with primary percutaneous coronary intervention. A total of 735 consecutive patients with ST-segment elevation myocardial infarction admitted to a single high-volume invasive heart center and treated with primary percutaneous coronary intervention from September 2006 to December 2008 were included. Blood samples were drawn immediately before the invasive procedure. Plasma adiponectin was measured using a validated immunoassay. End points were all-cause mortality, CV mortality, and admission for new AMI or heart failure. The median follow-up time was 27 months (interquartile range 22 to 33). Patients with high adiponectin (quartile 4) had increased mortality compared to patients with low adiponectin (quartiles 1 to 3) (log-rank p <0.001). After adjustment for conventional risk factors (age, gender, smoking, hypertension, hypercholesterolemia, diabetes, body mass index, C-reactive protein, peak troponin I, creatinine, estimated glomerular filtration rate, previous AMI, multivessel disease, complex lesions, left anterior descending coronary artery lesion, and symptom-to-balloon time) by Cox regression analysis, high adiponectin remained an independent predictor of all-cause mortality (hazard ratio 2.1, 95% confidence interval 1.3 to 3.2, p = 0.001) and CV mortality (hazard ratio 2.6, 95% confidence interval 1.5 to 4.5, p = 0.001). In conclusion, increased plasma adiponectin independently predicts all-cause and CV mortality in patients with ST-segment elevation myocardial infarction treated with primary percutaneous coronary intervention.
The American journal of cardiology 11/2011; 109(4):492-6. · 3.58 Impact Factor
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ABSTRACT: Atherosclerosis is the main cause of cardiovascular disease, but the extent of atherosclerosis in individual patients is difficult to estimate. A biomarker of the atherosclerotic burden would be very valuable. The aim of the present study was to evaluate the association of plasma osteoprotegerin (OPG) to clinical and subclinical atherosclerotic disease in a large community-based, cross-sectional population study. In the Copenhagen City Heart Study, OPG concentrations were measured in 5,863 men and women. A total of 494 participants had been hospitalized for ischemic heart disease or ischemic stroke, and compared to controls, this group with clinical atherosclerosis had higher mean OPG (1,773 vs 1,337 ng/L, p <0.001) and high-sensitivity C-reactive protein (2.3 vs 1.6 mg/L, p <0.001). In a multivariate model with age, gender, body mass index, hypertension, diabetes, hypercholesterolemia, smoking status, estimated glomerular filtration rate, high-sensitivity C-reactive protein, and OPG, OPG remained significantly associated with clinical atherosclerosis (p <0.01); high-sensitivity C-reactive protein, in contrast, did not (p = 0.74). In the control group without clinical atherosclerosis, OPG was independently associated with hypertension, diabetes, hypercholesterolemia, smoking, and subclinical peripheral atherosclerosis as measured by ankle brachial index. For each doubling of the plasma OPG concentration, the risk for subclinical peripheral atherosclerosis increased by 50% (p <0.001) after multivariate adjustment. In conclusion, OPG appears to be a promising biomarker of atherosclerosis that is independently associated with traditional risk factors of atherosclerosis, subclinical peripheral atherosclerosis, and clinical atherosclerotic disease such as ischemic heart disease and ischemic stroke.
The American journal of cardiology 11/2011; 109(4):515-20. · 3.58 Impact Factor
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ABSTRACT: The prevalence of diabetes mellitus (DM) and ischemic heart disease is increasing. Moreover, patients with DM experiencing an acute coronary syndrome (ACS) have an increased risk of adverse outcomes after revascularization compared to non-diabetics. Data have suggested that the glycoprotein IIb/IIIa inhibitor abciximab might be more efficient in diabetics than in those without DM.
We evaluated the effect of abciximab in patients with DM and ACS from our percutaneous coronary intervention (PCI) registry. Among 5,003 patients with ACS who underwent PCI, 629 had DM. Patients were followed for up to 3 years with regard to mortality, myocardial infarction (MI) and target vessel revascularization (TVR). Despite a more severe risk profile, adjusted analyses revealed a marked reduction in TVR (hazard ratio [HR], 0.30; confidence interval [CI], 0.14-0.63; p = 0.002), mortality (HR, 0.53; CI, 0.28-0.97; p = 0.04) and the combined endpoint, also including MI (HR, 0.53; CI, 0.35-0.79; p = 0.002) in the DM patients who received abciximab compared to those who did not, resulting in a risk of reaching the endpoints at levels similar to the risk in patients without DM. The reduction in MI was not significant.
Our findings suggest that abciximab administered to ACS patients with DM during PCI reduces mortality and the need for TVR to rates similar to those seen in patients without DM and far below the risk in DM patients who do not receive abciximab.
The Journal of invasive cardiology 01/2011; 23(1):21-6. · 1.84 Impact Factor
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Sune H Pedersen,
Soren Galatius,
Peter R Hansen,
Rasmus Mogelvang,
Steen Z Abildstrom,
Rikke Sørensen,
Ulla Davidsen,
Anders Galloe,
Ulrik Abildgaard,
Allan Iversen,
Jan Bech,
Jan K Madsen,
Jan S Jensen
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ABSTRACT: We evaluated the independent impact of field triage on treatment delay and long-term clinical outcome in a large contemporary, consecutive population of ST-segment elevation myocardial infarction (STEMI) patients undergoing primary percutaneous coronary intervention (pPCI).
Reduction of treatment delay is crucial for patients with STEMI.
From January 2005 to July 2008, 1,437 STEMI patients were treated with pPCI at a single high-volume invasive center. We present the 1-year outcome in this observational registry study.
A total of 616 patients were admitted by field triage and 821 by emergency departments. Baseline and angiographic variables were similar in the 2 populations. Patients admitted by field triage had a significantly shorter median door-to-balloon time compared with patients admitted by emergency department triage (83 min, interquartile range 67 to 100 min vs. 103 min, interquartile range 80 to 135 min; p<0.001). Door-to-balloon times of less than the recommended 90 min were achieved in 61% of field triage patients, but only in 36% of nonfield-triage patients (p<0.001). After adjustment for relevant baseline variables, patients admitted by field triage had a reduced risk of reaching the combined end point of all-cause mortality or nonfatal myocardial infarction (hazard ratio: 0.67; 95% confidence interval: 0.46 to 0.97; p=0.035).
This study shows that field triage of STEMI patients to pPCI significantly reduces treatment delay and improves outcome. These results emphasize the value of field triage as an important tool in the quest to improve clinical outcomes in STEMI patients undergoing pPCI.
Journal of the American College of Cardiology 12/2009; 54(24):2296-302. · 14.16 Impact Factor
