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The aim of this study is to assess the prognostic value of mechanical dyssynchrony defined as the standard deviation of the time to peak longitudinal strain (SD T2P LS) in predicting the development of heart failure (HF) after an ST-segment elevation myocardial infarction (STEMI). Three hundred and seventy-three patients were admitted with STEMI and treated with primary percutaneous coronary intervention. Left ventricular (LV) mechanical dyssynchrony was examined through speckle tracking echocardiography and defined as SD T2P LS. The association with the outcome of HF hospitalization was assessed using Cox proportional hazard models. During a median follow-up of 5.12 years, 144 patients (38.6%) were admitted due to HF. Worse dyssynchrony was associated with the outcome in unadjusted and multivariable analysis (multivariable hazard ratio 1.05, 95% confidence interval 1.00-1.10, p-value 0.039, per 10 ms increase), but not after further adjustment for LV ejection fraction (LVEF), E/e' and global longitudinal strain (GLS) (hazard ratio 1.01, 95% confidence interval 1.00-1.07, p-value 0.71, per 10 ms increase), nor in a model only adjusting for GLS (hazard ratio 1.01, 95% confidence interval 1.00-1.06, p-value 0.61, per 10 ms increase). These findings were reproduced in a competing risk analysis treating all-cause mortality as a competing risk. LV mechanical dyssynchrony, as assessed by SD T2P LS is not an independent predictor of post-STEMI HF development and mechanical dyssynchrony does not provide independent prognostic information regarding HF when GLS is known. [ABSTRACT FROM AUTHOR]

Aims: Two‐dimensional speckle tracking echocardiography (2DSTE) detects early signs of left ventricular dysfunction; however, it is unknown whether layer‐specific global longitudinal strain (GLS) has incremental value in diagnosis of patients with reversible ischemia assessed by single photon emission computed tomography (SPECT). Methods and Results: Eighty patients with stable angina pectoris (SAP), normal left ventricular ejection fraction (LVEF), and no history of ischemic heart disease were retrospectively identified to have been examined by 2DSTE, SPECT, and coronary angiography (CAG). Patients with a normal SPECT constituted the control group, and patients with a positive SPECT were divided into patients with or without (true‐ or false‐ positive SPECT) significant stenosis assessed by CAG. GLS was measured for two myocardial layers (endocardial and epicardial) and as well as mid‐myocardial GLS. Patients with reversible ischemia had significantly lower GLS compared to the control group (GLSEndocardial: −19.0 ± 4.4% vs −21.4 ± 3.7%, P = .011; GLSEpicardial: −14.3 ± 2.9% vs −16.3 ± 2.9%, P = .004); GLSMid‐myocardial: −16.5 ± 3.6% vs −18.6 ± 3.2%, P = .006. This difference was even more evident in patients with a true‐positive SPECT (GLSEndocardial: −18.0 ± 4.4% vs −21.4 ± 3.7%, P < .001; GLSEpicardial: −13.6 ± 3.0% vs −16.3 ± 2.9%, P < .001); GLSMid‐myocardial: −15.6 ± 3.6% vs −18.6 ± 3.2%, P < .001. Notably, no significant differences existed in patients with a false‐positive SPECT. GLSEpicardial was the only independent predictor of coronary artery disease. In conclusion: In patients with SAP and preserved LVEF, layer‐specific GLS at rest identifies patients with reversible ischemia. This seems to be evident only in patients with a true‐positive SPECT, thus, 2DSTE at rest might improve the diagnostic accuracy of a positive SPECT. [ABSTRACT FROM AUTHOR]

Aims: Early identification of patients who could benefit from early re-intervention after catheter ablation is highly warranted. Our aim was to investigate the association between post-procedural burden of supraventricular ectopic complexes (SVEC) and the risk of long-term atrial fibrillation (AF) recurrence.Methods and results: A total of 125 patients undergoing catheter ablation for AF were included. Patients underwent 7-day Holter recordings immediately post-procedural. The number of SVEC in post-procedural Holter recordings was categorized into quartiles: 0-72, 73-212, 213-782 and ≥ 783 SVEC/day. Long-term AF recurrence was defined as a combined endpoint of AF ≥ 1 min during follow-up Holter recordings, cardioversion or hospitalization for AF after a 3-month blanking period and within 24 months of follow-up. High post-procedural supraventricular ectopy burden was associated with an increased risk of long-term AF recurrence in a dose-dependent manner (≥ 783 SVEC: HR 4.6 [1.9-11.5], P < 0.001) irrespective of AF recurrence during the blanking period or other risk factors. In patients with early AF recurrence < 90 days after catheter ablation ectopy burden was also highly predictive of long-term AF recurrence (SVEC ≥ 213: HR 3.0 [1.3-6.7], P = 0.007). Correspondingly, patients with early AF recurrence but low ectopy burden remained at low risk of long-term AF recurrence after the blanking period.Conclusion: Our results indicate that post-procedural ectopy burden is highly associated with long-term AF recurrence and could be a potent risk marker for selection of patients for early re-ablation. Development of future ablation risk stratification and strategies should include focus on post-procedural ectopy burden. [ABSTRACT FROM AUTHOR]

Aims: Diabetes is associated with higher arterial stiffness—an early marker of cardiovascular disease. The coupling between arterial stiffness and myocardial function is still unresolved. We investigate associations between arterial stiffness and early myocardial impairment assessed with advanced echocardiography.Methods: In 305 type 1 diabetes (T1D) patients without known heart disease and with normal left ventricular ejection fraction (LVEF) (biplane LVEF > 45%), we measured arterial stiffness as pulse wave velocity (PWV) and performed conventional and speckle-tracking echocardiography assessing global longitudinal strain (GLS) as a measure of systolic myocardial function. Associations between PWV and myocardial function were reported as standardized beta values from adjusted regression models including age, sex, mean arterial pressure, body mass index, HbA1c, diabetes duration, estimated glomerular filtration rate, degree of albuminuria, total cholesterol, heart rate and smoking.Results: Patients were 54 (12) years [mean (SD)], 152 (50%) females, diabetes duration 31 (16) years, HbA1c 65 (12) mmol/mol, LVEF 58 (5) %, GLS −18.2 (2.6) % and PWV 10.2 (3.4) m/s. There was no association between PWV and LVEF (p = 0.93). Conversely, there was a highly significant association between PWV and GLS in crude and multivariable models (standardized β-coefficient 0.25, p < 0.001 and 0.16, p = 0.036, respectively). Also, diastolic function measured as E/e′ was highly associated with PWV in crude and multivariable models (standardized β-coefficient 0.43, p < 0.001 and 0.17, p = 0.016, respectively).Conclusions: In T1D patients with normal LVEF and without known heart disease, higher arterial stiffness is independently associated with early systolic and diastolic myocardial impairment detectable by advanced echocardiography. Although unable to demonstrate causality, we display a relationship between diabetic angiopathy and diabetic cardiomyopathy (H-3-2009-139 and PROFIL-H-B-2009-056). [ABSTRACT FROM AUTHOR]

In patients with type 2 diabetes, both supervised exercise and treatment with the glucagon-like peptide-1 ( GLP-1) receptor agonist ( GLP-1RA) liraglutide may improve cardiac function. We evaluated cardiac function before and after 16 weeks of treatment with the GLP-1RA liraglutide or placebo, combined with supervised exercise, in 33 dysregulated patients with type 2 diabetes on diet and/or metformin. Early diastolic myocardial tissue velocity was improved by exercise in the placebo group (mean ± standard deviation [s.d.] −7.1 ± 1.6 to −7.7 ± 1.8 cm/s, P = .01), but not in the liraglutide group (−7.1 ± 1.4 to −7.0 ± 1.4 cm/s, P = .60; between groups, P = .02). Similarly, the mean ± s.d. ratio of early and atrial mitral annular tissue velocities improved in the placebo group (1.0 ± 0.4 to 1.2 ± 0.4, P = .003), but not in the liraglutide group (1.0 ± 0.3 to 1.0 ± 0.3, P = .87; between groups, P = .03). We found no significant differences in heart rate, left ventricular ( LV) structure or function within or between the groups. In conclusion, the addition of liraglutide to exercise in sedentary patients with dysregulated type 2 diabetes may blunt the suggested beneficial effect of exercise on LV diastolic function. [ABSTRACT FROM AUTHOR]

Objectives: We aimed to determine the prevalence of echocardiographic abnormalities and their relation to clinical characteristics and cardiac symptoms in a large, contemporary cohort of patients with type 2 diabetes. Results: A total of 1030 patients with type 2 diabetes participated. Echocardiographic abnormalities were present in 513 (49.8%) patients, mainly driven by a high prevalence of diastolic dysfunction 178 (19.4%), left ventricular hypertrophy 213 (21.0%) and left atrial enlargement, 200 (19.6%). The prevalence increased markedly with age from 31.1% in the youngest group (<55 years) to 73.9% in the oldest group (>75 years) (p < 0.001) and was equally distributed among the sexes (p = 0.76). In univariate analyses, electrocardiographic abnormalities, age, body mass index, known coronary heart disease, hypertension, albuminuria, diabetes duration and creatinine were associated with abnormal echocardiography along with dyspnoea and characteristic chest pain (p < 0.05 for all). Neither of the cardiac symptoms nor clinical characteristics had sufficient sensitivity and specificity to accurately identify patients with abnormal echocardiography. Conclusion: Echocardiographic abnormalities are very common in outpatients with type 2 diabetes, but neither cardiac symptoms nor clinical characteristics are effective to identify patients with echocardiographic abnormalities. [ABSTRACT FROM AUTHOR]

Several clinical prediction score models have been investigated for predicting mortality in patients with cerebral infarction. However, none of these include echocardiographic measures. Our objective was to evaluate the prognostic value of tissue Doppler imaging (TDI) of the myocardium in patients with cerebral infarction. Two hundred forty-four patients with cerebral infarction and subsequent echocardiographic examination in sinus rhythm were identified. Using TDI in three apical projections, longitudinal mitral annular velocities were obtained in six segments. Cox regression models, C-statistics and reclassification analysis were performed for global and segmental e'. During a median follow-up of 3 years 42 patients died. Patients who died had significantly impaired systolic and diastolic function (determined by LVEF and E/e'). The risk of dying increased with decreasing global e', being approximately 13 times higher for patients in the lowest tertile compared to patients in the highest tertile (HR 13.4 [3.2;56.3], p < 0.001). Patients with significantly impaired global e' showed increased mortality after multivariable adjustment for: LVEF, E/e', age, gender, heart failure, chronic obstructive pulmonary disease, prior cerebral infarction, ischemic heart disease, cancer, hypertension, hypercholesterolemia, carotid stenosis, mitral regurgitation, liver disease and thromboembolisms (HR 1.9 [1.1;3.2]), per 1 cm/s decrease, p < 0.05). Similar pattern was seen in segmental analyses of the e'. In contrast to e', no conventional echocardiographic parameters remained independent predictors of mortality after multivariable adjustment. Diastolic myocardial dysfunction determined as e' by TDI is a significant predictor of mortality in patients with cerebral infarction. Applying this parameter can aid the prognostic assessment after cerebral infarction. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

Background: Despite 5-7 months of physical inactivity during hibernation, brown bears (Ursus arctos) are able to cope with physiological conditions that would be detrimental to humans. During hibernation, the tissue metabolic demands fall to 25% of the active state. Our objective was to assess cardiac function associated with metabolic depression in the hibernating vs. active states in free-ranging Scandinavian brown bears. Methods: We performed echocardiography on seven free-ranging brown bears in Dalarna, Sweden, anesthetized with medetomidine-zolazepam-tiletamine-ketamine during winter hibernation in February 2013 and with medetomidine-zolazepam-tiletamine during active state in June 2013. We measured cardiac output noninvasively using estimates of hemodynamics obtained by pulsed wave Doppler echocardiography and 2D imaging. Comparisons were made using paired T-tests. Results: During hibernation, all hemodynamic indices were significantly decreased (hibernating vs. active state): mean heart rate was 26.0 (standard deviation (SD): 5.6) beats per min vs. 75.0 (SD: 17.1) per min (P = 0.002), mean stroke volume 32.3 (SD: 5.2) ml vs. 47.1 (SD: 7.9) ml (P = 0.008), mean cardiac output 0.86 (SD: 0.31) l/min vs. 3.54 (SD: 1.04) l/min (P = 0.003), and mean cardiac index 0.63 (SD: 0.21) l/min/kg vs. 2.45 (SD: 0.52) l/min/m2 (P < 0.001). Spontaneous echo contrast was present in all cardiac chambers in all seven bears during hibernation, despite the absence of atrial arrhythmias and valvular disease. Conclusion: Free-ranging brown bears demonstrate hemodynamics comparable to humans during active state, whereas during hibernation, we documented extremely low-flow hemodynamics. Understanding these physiological changes in bears may help to gain insight into the mechanisms of cardiogenic shock and heart failure in humans. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

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 STEMl 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; Cl: 1.03-1.59; p = 0.03), repeat myocardial infarction (HR: 1.30; Cl: 1.00-1.68; p = 0.05) and admission with heart failure (HR: 1.50; Cl: 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. [ABSTRACT FROM AUTHOR]

Aims Exenatide, a glucagon-like-peptide-1 analogue, increases myocardial salvage in experimental settings with coronary occlusion and subsequent reperfusion. We evaluated the cardioprotective effect of exenatide at the time of reperfusion in patients with ST-segment elevation myocardial infarction (STEMI) treated with primary percutaneous coronary intervention (pPCI). Methods and results A total of 172 patients with STEMI and Thrombolysis in Myocardial Infarction flow 0/1 were randomly assigned to exenatide or placebo (saline) intravenously. Study treatment was commenced 15 min before intervention and maintained for 6 h after the procedure. The primary endpoint was salvage index calculated from myocardial area at risk (AAR), measured in the acute phase, and final infarct size measured 90 ± 21 days after pPCI by cardiac magnetic resonance (CMR). In 105 patients evaluated with CMR, a significantly larger salvage index was found in the exenatide group than in the placebo group (0.71 ± 0.13 vs. 0.62 ± 0.16; P= 0.003). Infarct size in relation to AAR was also smaller in the exenatide group (0.30 ± 0.15 vs. 0.39 ± 0.15; P= 0.003). In a regression analysis, there was a significant correlation between the infarct size and the AAR for both treatment groups and an analysis of covariance showed that datapoints in the exenatide group lay significantly lower than for the placebo group (P= 0.011). There was a trend towards smaller absolute infarct size in the exenatide group (13 ± 9 vs. 17 ± 14 g; P= 0.11). No difference was observed in left ventricular function or 30-day clinical events. No adverse effects of exenatide were observed. Conclusion In patients with STEMI undergoing pPCI, administration of exenatide at the time of reperfusion increases myocardial salvage. [ABSTRACT FROM PUBLISHER]

Objective. The mechanisms by which overweight and physical inactivity lead to hypertension are complex. Leptin, an adipocyte-derived hormone, has been linked with hypertension. We wanted to investigate the relationship between leptin, physical activity and new-onset hypertension. Methods. The study was a prospective cohort study of 744 women and 367 men, who were normotensive in the third Copenhagen City Heart Study (CCHS) examination, performed 1991-94. Based on questionnaire items, the participants were divided into two groups with low ( n == 674) and high ( n == 437) levels of leisure-time physical activity, respectively. Results. Between the third and the fourth CCHS examination, performed 2001-03, 304 had developed hypertension, defined as systolic blood pressure (SBP) ≥ 140 mmHg or diastolic blood pressure (DBP) ≥ 90 mmHg or use of antihypertensive medication. In a logistic regression model, including age, sex, body mass index, SBP, DBP, level of physical activity and leptin, we found a significant interaction between leptin and level of physical activity with new-onset hypertension as outcome variable ( p == 0.012). When we entered the interaction variables, effect of leptin with low level of physical activity and with high level of physical activity, respectively, in the original model, leptin predicted new-onset hypertension in participants with low level of physical activity [odds ratio (95% confidence interval): 1.16 (1.01-1.33) for one unit increase in log-transformed leptin levels, p == 0.038], but not in participants with high level of physical activity [0.88 (0.74-1.05), p == 0.15]. Conclusion. We found that leptin predicted new-onset hypertension but only in participants with low level of physical activity. [ABSTRACT FROM AUTHOR]

Background: An increasing proportion of patients with acute coronary syndrome (ACS) requiring percutaneous coronary intervention (PCI) are classified as elderly (aged ≥ 70 years). The glycoprotein IIb/IIIa inhibitor abciximab is known to reduce adverse outcomes in patients aged <70 years with high-risk ACS undergoing PCI, but conflicting findings relating to its effects in the elderly have been reported. Objective: The aim of this study was to evaluate the effect of abciximab in elderly high-risk ACS patients undergoing PCI. Methods: From our dedicated PCI registry we identified 2068 ACS patients with high-risk lesions that were treated with PCI. Baseline data were collected prospectively. All-cause mortality, target vessel revascularization (TVR), myocardial infarction (MI), and the combination of these were primary study endpoints. All endpoints within 1 year after PCI were registered and validated. The population was subsequently stratified according to age and use of abciximab. Results: Elderly patients constituted 42% of the total population. They presented with more co-morbidities, were less frequently treated with abciximab and had a higher risk of reaching the combined endpoint and higher all-cause mortality than younger patients. The age/abciximab stratified analysis revealed no effect of abciximab on any of the endpoints in elderly patients (combined endpoint: no abciximab 22.6% vs abciximab 23.4%, p = 0.85; all-cause mortality: no abciximab 15.4% vs abciximab 15.9%, p = 0.91; TVR: no abciximab 3.4% vs abciximab 5.5%, p = 0.21; MI: no abciximab 7.0% vs abciximab 8.5%, p = 0.54), whereas all-cause mortality and the risk of reaching the combined endpoint were significantly reduced in younger patients (combined endpoint: no abciximab 14.0% vs abciximab 9.4%, p = 0.03; all-cause mortality: no abciximab 4.5% vs abciximab 1.7%, p = 0.02; TVR: no abciximab 5.5% vs abciximab 4.3%, p = 0.39; MI: no abciximab 7.2% vs abciximab 6.6%, p = 0.80). These findings were confirmed in our adjusted analyses. Conclusions: In this large observational study we found no benefit of abciximab treatment in elderly high-risk ACS patients who underwent PCI. These findings should be taken into consideration when deciding on the treatment strategy for elderly ACS patients undergoing PCI. [ABSTRACT FROM AUTHOR]

Abciximab is beneficial in patients with ST-segment elevation myocardial infarction (STEMI) undergoing primary percutaneous coronary intervention (pPCI) . However, the optimal administration route of the initial bolus of abciximab, that is, intravenous (IV) versus intracoronary (IC), has been questioned. Preliminary studies suggest that IC-bolus is superior, probably due to high local concentration. In this study, we assess the short-term efficacy and safety of IC compared to IV bolus of abciximab in patients with STEMI during pPCI. In 2006-2008, we randomized 355 STEMI patients who underwent pPCI and had indication for abciximab to either IV or IC bolus followed by a 12-hour IV infusion. Primary end-points at 30 days were target vessel revascularization (TVR), recurrent myocardial infarction (MI) or death, and the composite of the three. Secondary end-points were bleeding complications. The two groups (IV n = 170;IC n = 185) were similar with respect to baseline characteristics. Mortality at 30 days was 5.3% in the IV group compared to only 1.1% in the IC group (P = 0.02). TVR was performed in 9.4% in the IV group compared to 3.8% in the IC group (P = 0.03). No significant difference in MI rates was seen (IV 4.7% vs. IC 2.7%; P = 0.32). We found a significant reduction in the composite end-point (IV 19.4% vs. IC 7.6%; P = 0.001) in favor of IC use. Major bleeding complications were similar (IV 2.4% vs. IC 1.6%; P = 0.62). Neither difference was observed in minor bleedings (IV 14.1% vs. IC 9.7%; P = 0.20). IC administration of bolus abciximab in STEMI patients undergoing pPCI reduces 30-day mortality and TVR and tends to reduce MI, compared to IV-bolus. (J Interven Cardiol 2011;24:105-111) [ABSTRACT FROM AUTHOR]

BackgroundLeptin and adiponectin are hormones secreted by adipose tissue, and both hormones are candidate intermediaries between adipose tissue and overweight-related diseases. So far, no prospective study has been published where the independent effects of these two hormones on the development of hypertension have been directly compared. The objective of this study was to investigate the relationships between plasma levels of leptin and adiponectin and new-onset hypertension in the Copenhagen City Heart Study (CCHS).MethodsIn a prospective study design, we examined new-onset hypertension in 620 women and 300 men who were normotensive in the third CCHS examination, which was performed in 1991–1994.ResultsBetween the third and the fourth CCHS examination, which was performed in 2001–2003, 254 had developed hypertension, defined as systolic blood pressure (SBP) ≥140 mm Hg, or diastolic blood pressure (DBP) ≥90 mm Hg, or use of antihypertensive medication. Using logistic regression analysis, adjusting for age, sex, estimated glomerular filtration rate, triglycerides, high-density lipoprotein cholesterol (HDL-C), fibrinogen, and glucose, and with leptin and adiponectin included in the same model, leptin was significantly associated with new-onset hypertension with an odds ratio (95% confidence interval) of 1.28 (1.08–1.53; P < 0.005) for 1 s.d. higher level of log-transformed leptin, whereas adiponectin was not significantly associated with new-onset hypertension having an odds ratio of 1.02 (0.84–1.24; P = 0.83) for 1 s.d. higher level of log-transformed adiponectin.ConclusionsIn the CCHS, leptin, but not adiponectin, was a significant independent predictor of new-onset hypertension.American Journal of Hypertension 2010; doi:10.1038/ajh.2009.244 [ABSTRACT FROM AUTHOR]

Alkaline-fermented food condiments play an important role in the diets of many people in developing and a few developed countries. The rise in pH during production of these foods is due to the ability of the dominant microorganisms, Bacillus spp., to hydrolyze proteins into amino acids and ammonia. Studies have been undertaken which have investigated a number of these products like dawadawa, ugba, bikalga, kinema, natto, and thua- nao. In this review, current knowledge about the principal microbiological activities and biochemical modifications which occur during the processing of the alkaline condiments including nutritional, antimicrobial, and probiotic aspects are discussed. The current use of molecular biology methods in microbiological research has allowed unambiguous and more reliable identification of microorganisms involved in these fermentations generating sufficient knowledge for the selection of potential starter cultures for controlled and better production procedures for alkaline-fermented seeds condiments. [ABSTRACT FROM AUTHOR]

BackgroundLow-grade chronic inflammation has been proposed to play a major role in the pathogenesis of hypertension. Low-grade chronic inflammation is also closely associated with obesity, an established causative factor in the development of hypertension. The purpose of this study was to investigate the relationship between two markers of inflammation, C-reactive protein (CRP) and fibrinogen, and blood pressure (BP) and other hemodynamic variables in obese subjects.MethodsFrom a large cardiovascular study based in the general population, we selected subjects with a body mass index (BMI) ≥30 kg/m2, free of major cardiovascular diseases, not taking BP-lowering or lipid-lowering drugs (n = 487; women = 51.1%; median (5th to 95th percentile) age = 62 years (36–80)). The cardiovascular study included measurements of traditional and new risk factors, including ankle brachial BP index, a measure of subclinical atherosclerosis. CRP was determined by a high-sensitive assay.ResultsIn partial Spearman rank correlation analysis, adjusted for age and sex, we found no significant relationships between either CRP or fibrinogen and systolic BP, diastolic BP, pulse pressure, or ankle brachial index (ρ: −0.057 to 0.068; P > 0.13). However, fibrinogen and CRP were found to be significantly related to heart rate (ρ: 0.127–0.169; P < 0.01).ConclusionsIn this study of generally healthy obese subjects from the general population, we found no significant relationships between markers of inflammation and systolic BP or diastolic BP, showing that obese subjects with higher levels of inflammatory markers do not have higher BP levels than their obese counterparts with lower levels of inflammatory markers.American Journal of Hypertension 2009; doi:10.1038/ajh.2009.1American Journal of Hypertension (2009); 22, 4, 451–456. doi:10.1038/ajh.2009.1 [ABSTRACT FROM AUTHOR]

This article presents the results of a clinical trial that compared two drug-eluting stents used in heart patients. Stent implantation has reduced the mortality rate of patients with coronary artery obstructions and the goal of drug-eluting stents is to reduce neointima formation by using antiprofilerative drugs built into the stent. This study chose to compare stents that are sirolimus-eluting to those that are paclitaxel-eluting. The study did not find a significant difference in adverse cardiac events between the two stents nor did they differ much in thrombosis rates.

An elevated urinary albumin excretion (UAE) in non-diabetic subjects without renal or cardiovascular disease has been shown to be predictive of ischaemic heart disease. An insertion (I)/deletion (D) polymorphism in the angiotensin I-converting enzyme (ACE) gene has been identified and the D allele may be associated with cardiovascular disease. The aim of this study was to find a potential linkage between this polymorphism and elevated UAE. For studies of UAE and cardiovascular pathophysiology, a highly selected population sample has been identified comprising all clinically healthy subjects aged 40-65 years with elevated UAE in a dipstick negative urinary sample (n = 27) from The Copenhagen City Heart Study. Neither the ACE genotype distribution (p = 0.12) nor the D and I allele frequencies (p = 0.69) differed significantly between subjects with elevated UAE and a matched normoalbuminuric control group (n = 46). Elevated UAE in clinically healthy subjects is not linked to the ACE gene polymorphism. [ABSTRACT FROM AUTHOR]

Objectives. To assess prevalence of positive urinary dipstick analysis for leucocyte esterase, nitrite, haemoglobin, or glucose in the general population and measure the urinary albumin excretion rate (UAER) in subjects with or without a positive dipstick analysis. Design. A cross-sectional study of 3645 subjects. Setting. An unselected urban population study. Main outcome measures. Prevalence data of positive dipstick analyses and UAER values. Results. Prevalence data of a positive dipstick analysis were 12%, 4%, 3% and 6%, respectively, for leucocyte esterase, nitrite, haemoglobin, and glucose. Subjects with any positive dipstick analysis had significantly higher UAER than subjects with a negative analysis: 4.9 (4.4-5.3) (geometric mean (95% confidence interval)) vs 3.0 (2.9-3.1) mg 24 h[sup -1] (p < 0.001). Conclusions. Prevalence data of positive urinary dipstick analyses in a large population based study are provided. Subjects with any positive finding had higher UAER than controls. Exclusion of subjects with a positive finding is recommended in studies of UAER as a cardiovascular risk factor in non-diabetic subjects. [ABSTRACT FROM AUTHOR]

Microalbuminuria, a subclinical rise in the urinary albumin excretion, is a risk indicator of atherosclerotic cardiovascular disease. The aim of this study was to measure the urinary albumin excretion in patients with acute myocardial infarction, and to correlate this with known atherosclerotic risk factors. One-hundred-and-twenty-six patients and 56 healthy controls matched for age and sex were studied. The albumin/creatinine concentration ratio in morning urine specimens was calculated as an index of the albumin excretion. Microalbuminuria was defined as a urinary albumin/creatinine concentration ratio above 1 mg/mmol. Urinary albumin excretion (0.88 [95% confidence interval 0.69-1.11] versus 0.51 [0.40-0.63] mg/mmol; p = 0.001) and frequency of microalbuminuria (33 [95% confidence interval 25-41] versus 16 [9-23]%; p = 0.03) were higher in patients than controls. This difference was independent of blood pressure, body weight, smoking, diabetes mellitus, renal disease, and thrombolytic treatment. There was a positive correlation between urinary albumin excretion and thickness of the left ventricle wall (R = 0.28; p = 0.001) which was independent of blood pressure. Follow-up examination of the patients will reveal whether microalbuminuria increases the risk for recurrence of acute myocardial infarction. [ABSTRACT FROM AUTHOR]

Background: Despite 5-7 months of physical inactivity during hibernation, brown bears (Ursus arctos) are able to cope with physiological conditions that would be detrimental to humans. During hibernation, the tissue metabolic demands fall to 25% of the active state. Our objective was to assess cardiac function associated with metabolic depression in the hibernating vs. active states in free-ranging Scandinavian brown bears.Methods: We performed echocardiography on seven free-ranging brown bears in Dalarna, Sweden, anesthetized with medetomidine-zolazepam-tiletamine-ketamine during winter hibernation in February 2013 and with medetomidine-zolazepam-tiletamine during active state in June 2013. We measured cardiac output noninvasively using estimates of hemodynamics obtained by pulsed wave Doppler echocardiography and 2D imaging. Comparisons were made using paired T-tests.Results: During hibernation, all hemodynamic indices were significantly decreased (hibernating vs. active state): mean heart rate was 26.0 (standard deviation (SD): 5.6) beats per min vs. 75.0 (SD: 17.1) per min (P=0.002), mean stroke volume 32.3 (SD: 5.2) ml vs. 47.1 (SD: 7.9) ml (P=0.008), mean cardiac output 0.86 (SD: 0.31) l/min vs. 3.54 (SD: 1.04) l/min (P=0.003), and mean cardiac index 0.63 (SD: 0.21) l/min/kg vs. 2.45 (SD: 0.52) l/min/ m2 (P<0.001). Spontaneous echo contrast was present in all cardiac chambers in all seven bears during hibernation, despite the absence of atrial arrhythmias and valvular disease.Conclusion: Free-ranging brown bears demonstrate hemodynamics comparable to humans during active state, whereas during hibernation, we documented extremely low-flow hemodynamics. Understanding these physiological changes in bears may help to gain insight into the mechanisms of cardiogenic shock and heart failure in humans. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

Abstracts for the 36th International Congress of the European Association of Poisons Centres and Clinical Toxicologists on May 24-27, 2016 in Madrid, Spain are presented including "Liquid Detergent Capsules: How to Make the Product and Its Use Safer" by Jan Meulenbelt et al, "Hot-cold Packs: Trifle or Threat?" by Jutta Trompelt et al and "An Analytically-Confirmed Case of Benzylglycinamide Consumption" by Antonella Valli, Pietro Papa and Carlo A. Locatelli.