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Aims: To improve risk prediction of cardiovascular morbidity and mortality, we need sensitive markers of cardiac dysfunction; Echocardiographic Tissue Doppler Imaging (TDI) is feasible and harmless and may be ideal for this purpose., Methods and Results: Within the community-based Copenhagen City Heart Study, 2064 participants were examined by echocardiography including TDI and followed (median 10.9 years) with regard to cardiovascular death, heart failure, or acute myocardial infarction (n = 277). Impaired systolic (s') and diastolic (e' and a') function according to age and sex as assessed by TDI was associated with increased risk of the combined end point, even in the subgroup of persons with a normal conventional echocardiographic examination [per 1 cm/s decrease: s': HR 1.32 (1.12-1.57), P < 0.001; e': HR 1.17(1.04-1.31), P < 0.01; a': HR 1.17 (1.06-1.30), P < 0.005]. Interestingly, reduced early diastolic myocardial velocity (e') was associated with risk of acute myocardial infarction, whereas reduced systolic (s') or late diastolic function (a') was associated with heart failure and cardiovascular death independently of traditional risk factors, plasma proBNP, and conventional echocardiographic measures. Combining information on early and late diastolic function by TDI provided incremental prognostic information and improved risk classification (net reclassification improvement: 27%; P < 0.001) and remained a significant predictor of the combined end point even in the subgroup with a normal conventional echocardiographic examination [per cm/s decrease: HR 1.18 (1.08-1.28), P < 0.001]., Conclusion: In the general population, TDI identifies individuals with cardiac dysfunction and high risk of cardiovascular morbidity and mortality independently of traditional risk factors, even in persons with a normal conventional echocardiographic examination., (Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2015. For permissions please email: journals.permissions@oup.com.)

Natriuretic peptides (NPs) may regulate adipocyte metabolism including adiponectin. Infusion of atrial natriuretic peptide (ANP) increases plasma adiponectin in patients with heart failure. However, this relation has not been examined in a clinical setting or in myocardial infarction (MI). Accordingly, we investigated the interplay between proANP and adiponectin and the prognostic implications in patients with MI. We prospectively included 680 patients with ST-segment elevation myocardial infarction (STEMI) treated with primary percutaneous coronary intervention from September 2006 to December 2008. Blood samples were drawn immediately before percutaneous coronary intervention. Additionally, we included 40 patients with 4 obtained blood samples during STEMI. Adiponectin and proANP were measured in all plasma samples. All patients were followed for 5 years. End points were all-cause mortality (n = 137) and the combined end point (n = 170) of major adverse cardiovascular events (MACEs). Plasma adiponectin and proANP were strongly associated at admission (r = 0.34, p <0.001). In patients with increasing proANP during STEMI, adiponectin also increased (0.5 ± 0.3 vs -0.1 ± 0.1 mg/L, p = 0.026). During follow-up, patients with higher adiponectin at admission had increased risk of all-cause mortality and MACE (both, p <0.001). After adjustment for confounding risk factors by Cox regression analysis, adiponectin remained an independent predictor of all-cause mortality and MACE: hazard ratio 1.31 (95% confidence interval 1.07 to 1.60; p = 0.009) and 1.31 (95% confidence interval 1.09 to 1.57; p = 0.004), respectively, for each SD increase. However, the association vanished when proANP was included in the analysis. In conclusion, adiponectin is associated with an increased risk of all-cause mortality and MACE. However, concomitantly elevated proANP levels appear to confound the association between adiponectin and worsened outcome., (Copyright © 2015 Elsevier Inc. All rights reserved.)

Background: Atrial natriuretic peptide (ANP) is released from the atria (on cleavage of proANP) in response to elevated intra-atrial pressure and wall stretch. Clinical data on proANP are still limited, mainly due to limitations in assaying the protein, which recently have been solved. ProANP is elevated in cardiovascular disease and predicts outcome in heart failure. However, knowledge of the prognostic value in acute myocardial infarction remains limited., Methods: We prospectively included 680 patients with STEMI treated with primary-PCI, from September 2006 to December 2008. Blood samples were drawn immediately before PCI. Plasma MR-proANP was measured using an automated processing assay. Endpoints were all-cause mortality (n = 137) and the combined endpoint (n = 170) of major adverse cardiovascular events (MACE) defined as cardiovascular mortality and admission due to recurrent MI, ischaemic stroke or heart failure., Results: During 5-year follow-up, MR-proANP was associated with increased risk of all-cause mortality and MACE (both p < 0.001). After adjustment for confounding risk factors (age, gender, hypertension, diabetes, hypercholesterolaemia, smoking, previous MI, BMI, eGFR, CRP, peak-TnI, symptom-to-balloon time, multivessel disease, complex lesion, LAD-lesion and use of glycoprotein inhibitor), MR-proANP remained an independent predictor of all-cause mortality and MACE - hazard ratio: 1.68 (95% CI 1.35-2.10; p < 0.001) and 1.68 (95% CI 1.39-2.03; p < 0.001) per standard deviation increase in MR-proANP. MR-proANP significantly increased C-statistics and reclassified 26% of the patients for all-cause mortality and 34% for MACE into higher or lower risk categories, matching actual event rates more accurately., Conclusions: Plasma MR-proANP independently predicts all-cause mortality and MACE in patients with STEMI., (© The European Society of Cardiology 2014 Reprints and permissions: sagepub.co.uk/journalsPermissions.nav.)

Background: High levels of circulating osteoprotegerin (OPG) predicts long-term outcome in patients with ST-elevation myocardial infarction (STEMI), possibly because of increased vascular inflammation resulting in myocardial damage. In the present study we aimed at elucidating the dynamic progress of OPG levels during STEMI treated with percutaneous coronary intervention (PCI) and additionally, the effect of OPG levels on cardiac function., Methods: We prospectively included 42 patients with STEMI treated with primary PCI. Four consecutive blood samples were obtained before and after PCI treatment. Plasma OPG levels were determined using an in-house immunoassay. Cardiac function was increased according to echocardiography, estimating left ventricular ejection fraction (LVEF) 1-3 days after STEMI., Results: During STEMI, OPG levels peaked after PCI and then decreased; mean concentrations (95% confidence interval) before PCI, after PCI, and on day 1 and day 2 of 2650 ng/L (2315-3036 ng/L), 2778 ng/L (2442-3363 ng/L), 2024 ng/L (1775-230 6 ng/L), and 1808 ng/L (1551-2106 ng/L), respectively (P < 0.001). Interestingly, the OPG response was observed before the response in troponin I and C-reactive protein. Patients with reduced LVEF (< 40%) exhibited an increased OPG response before, during, and after PCI (mean increase, 38%; 9%-75%; repeated measures analysis of variance, P = 0.009). Adjustment for age, sex, body mass index, and cardiovascular risk factors did not significantly affect the association between reduced LVEF and increased OPG response (mean increase 33% (4%-70%; F = 5.784; P = 0.023)., Conclusions: Circulating OPG levels are altered during STEMI treated with primary PCI. A high OPG level is independently associated with impaired LVEF., (Copyright © 2014 Canadian Cardiovascular Society. Published by Elsevier Inc. All rights reserved.)

Objective: Patients with acute myocardial infarction (MI) have increased risk of developing type 2 diabetes mellitus (T2DM). Adiponectin is an insulin-sensitizing hormone produced in adipose tissue, directly suppressing hepatic gluconeogenesis, stimulating fatty acid oxidation and glucose uptake in skeletal muscle and insulin secretion. In healthy humans, low plasma adiponectin levels associate with increased risk of T2DM; however, the relationship between adiponectin and T2DM in patients with MI has never been investigated., Research Design and Methods: We prospectively included 666 patients with ST-segment elevation MI, without diabetes, treated with percutaneous coronary intervention, from September 2006 to December 2008 at a tertiary cardiac center. Blood samples were drawn before intervention, and total plasma adiponectin was measured in all samples. During follow-up (median 5.7 years [interquartile range 5.3-6.1]) 6% (n = 38) developed T2DM. Risk of T2DM was analyzed using a competing risk analysis., Results: Low adiponectin levels were associated with increased risk of T2DM (P < 0.001). Even after adjustment for confounding risk factors (age, sex, hypertension, hypercholesterolemia, current smoking, previous MI, BMI, blood glucose, total cholesterol, HDL, LDL, triglyceride, estimated glomerular filtration rate, C-reactive protein, peak troponin I, and proatrial natriuretic peptide), low adiponectin levels remained an independent predictor of T2DM (hazard ratio [HR] 5.8 [2.3-15.0]; P < 0.001). Importantly, plasma adiponectin added to the predictive value of blood glucose, with the combination of high blood glucose and low plasma adiponectin, vastly increasing the risk of developing T2DM (HR 9.6 [3.7-25.3]; P < 0.001)., Conclusions: Low plasma adiponectin levels are independently associated with increased risk of T2DM in patients with MI and added significantly to the predictive value of blood glucose., (© 2014 by the American Diabetes Association. Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered.)

Background: Doppler tissue imaging (DTI) detects early signs of left ventricular (LV) dysfunction; however, the prognostic significance of DTI after ST-segment elevation myocardial infarction (STEMI) is unknown. The aim of this study was to evaluate the prognostic value of DTI after STEMI in patients treated with primary percutaneous coronary intervention., Method: In total, 391 patients who were admitted with STEMIs and treated with primary percutaneous coronary intervention were prospectively included. All participants were examined by echocardiography 2 days (interquartile range, 1-3 days) after STEMI. Longitudinal systolic (s'), early diastolic (e'), and late diastolic (a') myocardial velocities were measured using color DTI at six mitral annular sites and averaged to provide global estimates., Results: The median follow-up period was 25 months (interquartile range, 19-32 months). The primary end point was a composite of death, heart failure, or a new myocardial infarction. Patients with low global systolic function (s') or low global diastolic function (e') had >2 times greater risk for the combined end point compared with patients with high global s' (hazard ratio, 2.60; 95% confidence interval, 1.64-4.13; P < .001) or e' (hazard ratio, 2.26; 95% confidence interval, 1.44-3.55; P < .001), respectively. After adjustment for age, gender, peak troponin I, previous myocardial infarction, LV ejection fraction, LV mass index, and LV dimension in a multivariate Cox model, patients with low values of both global s' and e' remained at significantly higher risk than patients with high s' and/or e' (hazard ratio, 1.69; 95% confidence interval, 1.02-2.81; P = .043)., Conclusions: A pattern of low systolic and diastolic performance as assessed by DTI is a paramount marker of adverse prognosis for patients with STEMIs independent of conventional echocardiographic parameters. DTI velocities should be evaluated together as they interact with the prognosis., (Copyright © 2014 American Society of Echocardiography. Published by Mosby, Inc. All rights reserved.)

Background: Color tissue Doppler imaging M-mode through the mitral leaflet is an easy and precise method to estimate all cardiac time intervals from 1 cardiac cycle and thereby obtain the myocardial performance index (MPI). However, the prognostic value of the cardiac time intervals and the MPI assessed by color tissue Doppler imaging M-mode through the mitral leaflet in patients with ST-segment-elevation myocardial infarction (MI) is unknown., Methods and Results: In total, 391 patients were admitted with an ST-segment-elevation MI, treated with primary percutaneous coronary intervention, and examined by echocardiography a median of 2 days after the ST-segment-elevation MI. Outcome was assessed according to death (n=33), hospitalization with heart failure (n=53), or new MI (n=25). Follow-up time was a median of 25 months. The population was stratified according to tertiles of the MPI. The risk of new MI, being admitted with congestive heart failure or death, increased with increasing tertile of MPI, being ≈3 times as high for the third tertile compared with the first tertile (hazard ratio, 2.8; 95% confidence interval, 1.7-4.7; P<0.001). MPI provided independent prognostic information in a multivariable Cox regression model adjusted for age, sex, previous MI, peak troponin, and systolic and diastolic echocardiographic parameters, with a hazard ratio of 1.24 (P=0.005) for the combined end point per each 0.1 increase in MPI., Conclusions: MPI assessed by tissue Doppler imaging M-mode is a simple and reproducible measure that provides independent prognostic information, regardless of rhythm, incremental to conventional and novel echocardiographic parameters of systolic and diastolic function in patients with ST-segment-elevation MI treated with primary percutaneous coronary intervention.

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 to 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 to 34) months. Follow-up was 99.7% complete. Outcomes were all-cause and cardiovascular mortality, re-myocardial infarction and admission due to heart failure., 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 patients with shock (n = 51) catecholamines correlated strongly with thrombomodulin and syndecan-1 (rho = 0.31 to 0.42, all P <0.05). During follow-up, 78 (14%) patients died (37 cardiovascular deaths) and 65 (11%) were admitted with heart failure. 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 heart failure (30-day all-cause mortality hazard ratio (95% CI) 1.39 (1.01 to 1.92), P = 0.046; 30-day heart failure 1.65 (1.17 to 2.34), P = 0.005; and long-term cardiovascular mortality 1.49 (1.08 to 2.04), P = 0.014). Furthermore, one quartile higher syndecan-1 was also weakly but independently associated with long-term all cause mortality (1.26 (1.02 to 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 patients with shock. Furthermore, adrenaline and syndecan-1 were weakly but independently associated with mortality and heart failure. Acute myocardial infarction appears to cause significant endothelial cell and glycocalyx injury and a parallel increase in circulating catecholamines.

Background: 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)., Methods: 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., Results: 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])., Conclusions: High plasma sMAC independently predicts all-cause mortality and MACE in STEMI-patients treated with PCI., (Copyright © 2012 Mosby, Inc. All rights reserved.)

Objectives: 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., Background: 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., Methods: 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)., Results: 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)., Conclusions: High plasma NGAL independently predicts all-cause mortality and MACE in ST-segment elevation myocardial infarction patients treated with primary percutaneous coronary intervention., (Copyright © 2012 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.)

Aims: In individuals without known heart disease, electrocardiographic Q-waves predict a poor prognosis. We aimed to examine whether prognostic information can be derived from the size and location of Q-waves in persons from the general population without known ischaemic heart disease (IHD) or heart failure (HF)., Methods and Results: Electrocardiograms (ECGs) of 5381 persons without known IHD or HF from the 4th Copenhagen City Heart Study were reviewed and Q-waves were classified according to their size and location. Multivariate Cox proportional hazards regression models were used to examine the associations of Q-waves adjusted for age, hypertension, diabetes, and estimated glomerular filtration rate with the risk of the combined endpoint of death and hospitalization for IHD. During a median of 7.8 years of follow-up, 1003 persons reached the combined endpoint. One hundred and fourteen (2.1%) had pathological Q-waves, of whom 44% suffered from an event compared with 18% from the control group, P< 0.001. Persons with hypertension, diabetes, and impaired renal function were more likely to have Q-waves. Even small Q-waves (i.e. Minnesota code 1.2.x-1.3.x) were associated with a poor prognosis, hazard ratio (HR) 1.4 [95% confidence interval (CI): 1.0-2.0; P< 0.05], though not as grave as large Q-waves (i.e. Minnesota code 1.1.x) HR 2.8 (95%CI: 1.6-5.0; P< 0.001). Conversely, there was no difference in the outcome of patients with anteriorly HR 1.6 (95%CI: 1.1-2.4) vs. posteriorly HR 1.5 (95%CI: 0.9-2.4) located Q-waves (P= 0.85)., Conclusion: In the general population without known IHD or HF, even small Q-waves in the ECG are associated with a poor prognosis.

Background: Osteoprotegerin (OPG) is a glycoprotein with a regulatory role in immune, skeletal and vascular systems. Data suggest that high circulating OPG levels are associated with an increased risk of cardiovascular disease. We analyzed the association between OPG and long-term outcome in patients with ST-segment elevation myocardial infarction (STEMI) treated with primary percutaneous coronary intervention (pPCI)., Methods: We included 716 consecutive STEMI patients admitted to a single high-volume invasive heart center from September 2006 to December 2008. Endpoints were all-cause mortality, repeat myocardial infarction, admission due to heart failure and combinations thereof. Median follow-up lasted 27 months (interquartile range: 22-33)., Results: OPG levels exhibited a non-Gaussian distribution and were therefore divided into quartiles. High levels of OPG were significantly associated with a worse outcome. After adjustment for conventional risk factors (e.g. C-reactive protein, estimated glomerular filtration rate, symptom-to-balloon time and troponin I) using Cox regression, OPG remained a significantly independent predictor of death (HR per increase in OPG quartile: 1.28; CI: 1.03-1.59; p = 0.03), repeat myocardial infarction (HR: 1.30; CI: 1.00-1.68; p = 0.05) and admission with heart failure (HR: 1.50; CI: 1.18-1.90; p = 0.001)., Conclusion: This study shows that OPG independently predicts long-term outcome in STEMI patients treated with pPCI. Eventually, this knowledge could improve risk stratification and overall outcome., (Copyright © 2012 S. Karger AG, Basel.)

Objective: Use of drug-eluting stents (DES) in patients with ST-elevation myocardial infarction (STEMI) during routine primary percutaneous coronary intervention (pPCI) is controversial., Methods: From January 2004 to July 2008, a total of 2,155 STEMI patients were treated with pPCI [DES or bare-metal stent (BMS)] at a single high-volume invasive center. We present 4-year outcomes in this observational registry study., Results: A total of 1,725 were treated with DES and 430 with BMS. Patients treated with DES were younger and had more complex angiographic characteristics compared to BMS patients. Patients treated with DES had lower adjusted risk of target lesion revascularization (TLR) [hazard ratio (HR) = 0.68; 95% confidence interval (CI): 0.40-0.98; p = 0.04], but had a trend toward increased risk of definite stent thrombosis (HR = 1.96; 95% CI: 0.83-4.61; p = 0.12). No difference was found when evaluating all-cause mortality and non-fatal myocardial infarction., Conclusions: In this study, we set out to evaluate the independent impact of DES or BMS treatment on long-term clinical outcomes in STEMI patients treated with pPCI in a real-life setting. DES use was associated with a reduced risk of TLR, but a trend toward increased risk of stent thrombosis was found. However, this safety issue did not translate into an increased risk of death or overall non-fatal myocardial infarction for DES patients.

Objectives: 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)., Background: Reduction of treatment delay is crucial for patients with STEMI., Methods: 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., Results: 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)., Conclusions: 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.

Background: We sought to describe the long-term prognosis after routine primary percutaneous coronary intervention (pPCI) in a contemporary consecutive population of patients with presumed ST-segment elevation myocardial infarction, compare it with similar results from the landmark DANAMI-2 trial, and to identify a possible impact of time of presentation and referral pattern., Methods and Results: Long-term prognosis in 1019 presumed ST-segment elevation myocardial infarction patients, treated according to modern routine pPCI during the year 2004, was analyzed and compared with similar data from the DANAMI-2 trial. Furthermore, we analyzed the impact of patient presentation to the angioplasty center during "off hours" (4 pm to 8 am plus weekends and holidays) and the impact of being referred from noninvasive hospitals. At 3 years, 20.4% in the routinely treated population versus 19.6% in the DANAMI-2 trial reached the combined end point of death, reinfarction, or stroke (P=0.68), whereas the all-cause mortality was 13.0% and 13.7%, respectively (P=0.65). Patients admitted during off hours had the same risk of reaching the combined end point of death, reinfarction, or stroke compared with patients admitted during office hours (hazards ratio, 1.04; 95% CI, 0.8 to 1.5; P=0.81). Door-to-balloon times of less than 90 minutes were achieved in 60% among patients admitted directly to an invasive center but only in 40% among transferred patients (P<0.001). Despite this difference, no difference in unadjusted or adjusted long-term prognosis was found between the 2 groups., Conclusions: This study shows that ST-segment elevation myocardial infarction patients treated with contemporary routine pPCI achieve a similar long-term prognosis as patients in the landmark randomized pPCI trial (DANAMI-2). Furthermore, the long-term prognosis was the same regardless of whether the pPCI was performed during off hours or office hours. Thus, pPCI including transportation of patients from noninvasive centers can be applied successfully in a real-life population.

Background: Myocardial velocities can be measured with both pulsed-wave tissue Doppler (PWTD) and color tissue Doppler (CTD) echocardiography. We aimed to (A) to explore which of the two methods better approximates true tissue motion and (B) to examine the agreement and the reproducibility of the two methods in a routine clinical setting., Methods: For Study A, the displacements of 63 basal myocardial segments from 13 patients were examined with M-mode and compared with the velocity-time integral of PWTD and CTD velocities. For Study B, the basal lateral segments from 58 patients were examined with PWTD and CTD, and the peak myocardial velocities during systole (Sm), early diastole (Em), and late diastole (Am) were measured., Results: Study A: CTD-based measurements of displacement were 12% lower than M-mode measurements (95% CI: -18%; -6%). PWTD velocity-time integrals measured at the outer edge of the spectral band were 40% higher (33%; 46%) than M-mode measurements. Study B: PWTD measurements of myocardial velocity were systematically higher than CTD measurements: Sm 7.51 versus 5.54, difference 1.97 +/- 1.41 cm/sec; Em 8.74 versus 6.86, difference 1.88 +/- 1.70 cm/sec; Am 7.46 versus 5.17, difference 2.29 +/- 1.82 cm/sec; P < 0.001 for all. Intraobserver coefficient of variation for Sm, Em, and Am were 6%, 12%, and 12% for PWTD, 14%, 13%, and 20% for CTD., Conclusions: CTD measures numerically smaller tissue velocities than PWTD, mostly due to an overestimation of true tissue motion by PWTD. The methods have good agreement and comparable reproducibility.

Background: The positive effect of reperfusion after ST-elevation myocardial infarction (STEMI) can be reduced by ischemic/reperfusion (I/R) injury.Mannose-binding-lectin (MBL) and soluble C5b-9 (membrane-attack-complex) are involved in complement-driven cell lysis and may play a role in human myocardial I/R injury. We evaluated the potential association between MBL and sC5b-9 in plasma and subsequent cardiac dysfunction in patients with STEMI treated with primary percutaneous coronary intervention (pPCI)., Methods: The study included 74 STEMI-patients with acute occlusion of the left anterior descending coronary artery who were successfully treated with pPCI. Cardiac dysfunction was defined as left ventricular ejection fraction LVEF < 35%., Results: Patients with subsequent LVEF < 35% had significantly higher median MBL and lower sC5b-9 compared to patients with LVEF > or = 35%. After adjustment of the multivariate logistic regression analysis, the odds for reduced LVEF was 5.5 (95% CI:1.5-19.3; p = 0.01) for patients with MBL > or = 800 mcg/L, and 5.0 (95% CI 1.4-18.4; p = 0.01) for patients with sC5b-9 < or = 160 mcg/L., Conclusion: High plasma MBL and low plasma sC5b-9 are independently associated with increased risk of cardiac dysfunction in STEMI patients treated with pPCI, probably due to increased complement activity during the ischemic and reperfusion process. The predictive value of low peripheral plasma sC5b-9 may be explained by an accumulation and activation of sC5b-9 in the infarcted myocardium.