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Background and aims The use of high sensitivity troponin (hs-Tn) may enable early rule out of acute myocardial infarction (AMI) for patients presenting to the emergency department (ED) with chest pain. This study evaluated two approaches to the early rule out of AMI; a combination of a presentation hs-Tn < 4 ng/L and normal glucose at presentation (dual testing) and a presentation hs-Tn troponin below the limit of detection (LoD). Methods We utilised prospectively collected data on adult patients presenting with suspected ACS in two EDs in Australia and New Zealand. Blood samples were taken on presentation and tested for glucose and high sensitivity troponin I. The primary endpoint was index AMI and the secondary endpoint was 30-day acute coronary syndrome (ACS). Sensitivity, specificity, positive and negative predictive values were used to assess the diagnostic accuracy of the dual testing and LoD approaches. Results Of the 1412 participants, 182 (12.9%) had index AMI. The LoD and the dual testing approach were 100% sensitive for index AMI. The specificity of the dual testing approach (25.2%) was slightly higher than that of the LoD (20.4%). Sensitivity for ACS was similar for the two approaches (96.5% for dual testing and 98.1% for the LoD). Conclusions The dual testing and LoD approach identified all patients with index AMI and could be used to reduce the proportion of patients requiring lengthy assessment and inpatient admission. Further investigation is still required to rule out unstable angina pectoris in patients identified as low risk. [ABSTRACT FROM AUTHOR]

We achieved possibility of isolation, characterization human umbilical cord blood endothelial progenitor cells (EPCs), examination potency of EPCs to form new blood vessels and differentiation into cardiomyoctes in canines with acute myocardial infarction (AMI). EPCs were separated and cultured from umbilical cord blood. Their phenotypes were confirmed by uptake of double stains dioctadecyl tetramethylindocarbocyanine-labeled acetylated LDL and FITC-labeled Ulex europaeus agglutinin 1 (DILDL-UEA-1). EPCs of cord blood were counted. Human VEGFR-2 and eNOS from the cultured EPCs were assessed by qPCR. Human EPCs was transplanted intramyocardially in canines with AMI. ECG and cardiac enzymes (CK-MB and Troponin I) were measured to assess severity of cellular damage. Histopathology was done to assess neovascularisation. Immunostaining was done to detect EPCs transdifferentiation into cardiomyocytes in peri-infarct cardiac tissue. qPCR for human genes (hVEGFR-2, and eNOS) was done to assess homing and angiogenic function of transplanted EPCs. Cultured human cord blood exhibited an increased number of EPCs and significant high expression of hVEGFR-2 and eNOS genes in the culture cells. Histopathology showed increased neovascularization and immunostaining showed presence of EPCs newly differentiated into cardiomyocyte-like cells. Our findings suggested that hEPCs can mediate angiogenesis and differentiate into cardiomyoctes in canines with AMI. [ABSTRACT FROM AUTHOR]

Several pieces of evidence indicate that the microglial P2X 7 receptor (P2X 7 R) regulate cardiovascular activities. We explored the possible roles of microglial P2X 7 R in the PVN mediated sympathoexcitatory responses in acute myocardial infarction (AMI) rat. Sprague–Dawley rats underwent coronary artery ligation to induce AMI. The rats received intraperitoneal administration of the P2X 7 R antagonist Brilliant Blue-G (BBG, 25 or 50 mg kg −1 , once a day for 5 days) prior to myocardial ischemia. Other rats received bilateral microinjection of P2X 7 R-siRNA (0.015 or 0.03 nmol 0.1 μl per side, once a day for 2 days) targeting P2X 7 R mRNA into the PVN prior to myocardial ischemia. First, we examined the ATP levels and protein expression P2X 7 R in the PVN in different ischemia time groups, and we found that the change of P2X 7 R was positive correlated with the ATP levels in a time-dependent manner. The double-immunofluorescence evidence showed that P2X 7 R was mainly co-localizated with the microglial marker Iba-1 in the PVN. Second, gene knockdown of P2X 7 R with P2X 7 -siRNA or inhibition of P2X 7 R with BBG reduce the mRNA and protein expression of IL-1β and TNF-α in the PVN of AMI rat. Third, microinjected P2X 7 -siRNA also suppressed the up-regulation of P2X 7 R, oxytocin and vasopressin in the PVN of AMI rats. Fourth, P2X 7 -siRNA and BBG also attenuated the renal sympathetic nerve activity (RSNA) in the AMI rats. Our results indicate that microglial P2X 7 R activation in PVN mediating the production of proinflammatory cytokines that activate oxytocinergic and vasopressinergic neuron, which augmented the RSNA in the AMI rat. [ABSTRACT FROM AUTHOR]

Background: Concerns regarding the use of selected bone marrow stem cells (BMSCs) in the field of cardiac repair after acute ischemic events have been raised. The current meta-analysis aimed to assess the efficacy and safety of selected BMSC transplantation in patients with acute myocardial infarction (AMI) based on published randomized controlled trials (RCTs). Methods: A systematic literature search of PubMed, Ovid LWW, BIOSIS Previews, and the Cochrane library from 1990 to 2014 was conducted. Results from RCTs involving subjects with AMI receiving selected BMSC therapy and followed up for at least 6 months were pooled. Results: Eight trials with a total of 262 participants were included. Data were analyzed using a random effects model. Overall, selected BMSC therapy improved left ventricular ejection fraction (LVEF) by 3.17% (95% confidence interval [CI] 0.57–5.76, P = 0.02), compared with the controls. There were trends toward reduced left ventricular end-systolic volume (LVESV) and fewer major adverse cardiac events (MACEs). Subgroup analysis revealed a significant difference in LVEF in favor of selected BMSC therapy with bone marrow mesenchymal stem cells (BMMSCs) as the cell type. Conclusions: Transplantation of selected BMSCs for patients with AMI is safe and induces a significant increase in LVEF with a limited impact on left ventricular remodeling. [ABSTRACT FROM AUTHOR]

Introduction Cardiac magnetic resonance (CMR) is a unique method to determine regional and local aortic stiffness parameters. Although various methods have been validated, there are no data in patients after acute ST-segment elevation myocardial infarction (STEMI). In the present study we assessed the feasibility of different CMR derived measures of aortic stiffness in patients after first acute STEMI for the first time. Methods CMR derived aortic pulse wave velocity (PWV) determined by the regional transit-time (PWV TT ) and local flow-area (PWV QA ) method as well as local distensibility coefficients (DCs) was analyzed in 22 healthy young volunteers and 28 patients with recent acute STEMI. Results PWV TT and DC of the ascending aorta differed significantly between healthy subjects and STEMI patients (all p < 0.001). PWV QA at thoracic levels of aorta was not different between groups (p > 0.520) and did not correlate with age (p > 0.149) and PWV TT (p > 0.310). Intra- and interobserver variability was high for PWV TT (r = 0.970, p < 0.001 and r = 0.920, p < 0.001), acceptable for DC (all r > 0. 809, p < 0.001 and all r > 0.510, p < 0.001) but low for thoracic PWV QA (all r < 0.330 and all r < 0.372). Conclusion PWV TT and local DC are robust methods for the assessment of aortic stiffness in patients after acute STEMI. [ABSTRACT FROM AUTHOR]

Background Short-term mortality has been studied thoroughly in patients undergoing primary percutaneous coronary intervention (PCI), whereas long-term cause of death in patients with ST-segment elevation myocardial infarction (STEMI) remains unknown. Objectives The goal of this study was to describe the association between time and cause of death in patients with STEMI undergoing primary PCI. Methods A centralized civil registration system, patient files, and public disease and death cause registries with an accurate record linkage were used to trace time and cause of death in 2,804 consecutive patients with STEMI (age 63 ± 13 years, 72% males) treated with primary PCI. Results Patients were followed up for a median of 4.7 years. During a total of 13,447 patient-years, 717 patients died. Main causes of death within the first 30 days were cardiogenic shock and anoxic brain injury after cardiac arrest. Age, culprit vessel size and flow, and the presence of heart failure and diabetes were independent predictors of mortality. After 30 days, the annual cardiac mortality rate was <1.5%. Causes of death beyond 30 days were noncardiac in 65% of cases (mainly malignancies and pulmonary diseases). The 30-day, 1-year, and 5-year all-cause (and cardiac) mortality rates were 7.9% (7.3%), 11.4% (8.4%), and 23.3% (13.8%), respectively. Conclusions Patients who survive the first month after an STEMI treated with primary PCI have an excellent prognosis, with a <1.5% annual risk of successive cardiac death. Noncardiac causes are responsible for the majority of later deaths in these patients. [ABSTRACT FROM AUTHOR]

Coronary artery thrombosis in ST-elevation myocardial infarction (STEMI) is a dynamic process often preceded by episodes of silent plaque rupture and subocclusive thrombosis. Thrombus organization is achieved by ingrowth of endothelial and smooth muscle cells. Clinical significance and impact of thrombus neovascularization on primary percutaneous coronary intervention (pPCI) outcome remain unclear. Therefore we investigated composition and neovascularization of thrombi aspirated during pPCI and their association with clinical and angiographic parameters of STEMI patients. Methods Aspirated thrombi retrieved from 84 STEMI patients were classified as fresh (1day), lytic (1-5days) or organized (5days). Thrombus neovascularization was evaluated immunohistochemically using CD34, CD31 and VEGF antibodies. CD34 and CD31 immunopositive (CD34/CD31+) cells were organized as single, clusters and microvessels. VEGF positivity was graded as low or high, based on thrombus surface immunopositive area. Results CD34/CD31+ cells were present in 67% of all aspirated thrombi. Thrombus CD34/CD31 positivity was associated with previous history of angina pectoris (χ2=6.142, p=0.013) and lower myocardial blush grade (MBG<3, χ2=12.602, p<0.001). Organization of CD34/CD31+ cells showed inverse association with the extent of VEGF positivity (χ2=10.607, p=0.005). Fresh thrombi were associated with shorter ischemic time (U=237.5, p=0.002) and MBG 3 (χ2=6.379, p=0.012). Conclusions Older thrombus age and neovascularization are associated with suboptimal myocardial perfusion in STEMI patients. Thrombus VEGF expression is inversely associated with degree of CD34+ cell organization. Therefore, neovascularization of aspirated thrombi may indicate the duration of thrombosis, coronary microcirculation status and outcome in STEMI patients. [ABSTRACT FROM AUTHOR]

[Display omitted] • A fluorescent immunosensor for rapid detection of cardiac troponin I was created. • The detection can be finished within 5 min. • The limit of detection was below 10 pM and detection range was 10 pM–1000 nM. • The immunosensor is expected to contribute to the rapid diagnosis and precise treatment of myocardial infarction. A rapid detection approach based on quench-release for cardiac troponin I (cTnI), a biomarker of myocardial infarction, was developed. To ensure detection accuracy, a rabbit monoclonal antibody, RabMG4C80A (G4), that binds specifically to cTnI was used. The antigen-binding fragment of G4 was prepared and labeled with fluorescent dyes to produce a fluorescent immunosensor G4 Q-body that can be used for cTnI detection. Using this method, an assay could be completed in as little as 5 min, enabling rapid diagnosis following myocardial infarction and providing a timely basis for patient treatment. A dose–response curve of the G4 Q-body for cTnI detection was obtained from the fluorescence spectra, from which the concentration of cTnI in the sample was determined. The limits of detection and concentration for 50% of maximal effect of the assay were found to be below 10 pM and 3.8 nM, respectively, of cTnI. The optimal detection range was 10 pM–1000 nM. After the occurrence of acute myocardial infarction, the cTnI concentration rose to 2 nM in 1 h and persisted for 6–8 days at around 20 nM; the detection range of the assay therefore covered the clinically relevant range of cTnI during myocardial infarction. This is the first Q-body based on rabbit monoclonal antibodies, and it is expected to contribute to the rapid diagnosis and precise treatment of myocardial infarction. [ABSTRACT FROM AUTHOR]

• Aortic dissection need to be considered as a cause of acute coronary syndrome before rushing into invasive treatments. • Screening for other diseases that may affect body vasculature should be assessed; IgG4-RD can cause aortitis and aortic dissection. • Histopathology findings are never diagnostic alone for IgG4-RD and must be interpreted in the context of clinical, serologic and radiologic data. Occlusion of the right coronary artery is a relatively rare complication of type A aortic dissection and an example of type 2 myocardial infarction (MI) as well but when it occurs, it may have a fatal result for the patient. Aortic pseudoaneurysms are local type A dissections with a restricted extent in which the majority of the aortic wall has been breached and luminal blood is held in only by a thin rim of the remaining wall, mainly purely the adventitia. They typically occur from iatrogenic trauma by interventional procedures or previous cardiac surgery. We present a case of a 56 years old patient who suffered an acute functional MI due to such pseudoaneurysm formed in the context of an undiagnosed aortitis. The etiology remained unclear until the surgical aortic prosthesis was deemed necessary, finding chronic IgG4 infiltrates in the aortic tissue. To our knowledge, this is the first case of IgG4-related aortitis causing functional MI and cardiogenic shock. [ABSTRACT FROM AUTHOR]

Swift and effective diagnosis of acute myocardial infarction (AMI) is critical to patient survival due to its serious life-threatening effects and increasing incidence. Creatine kinase MB (CK-MB) is one of the markers of AMI. In this work, we enabled a portable visual quantitative assay of CK-MB by incorporating target-responsive DNA hydrogel with a microfluidic chip. The CK-MB aptamer and the complementary short DNA strand were grafted onto the polyacrylamide strand separately and formed the hydrogel by base-paired linkage. Upon introduction of CK-MB, the aptamer bound to CK-MB. This led to hydrogel dissociation and subsequent release of pre-trapped gold nanoparticles (AuNPs), which is proportional to the concentration of CK-MB. To achieve portable on-site detection, we further combined the hydrogel with a microfluidic chip and utilized the color change caused by the released AuNPs to take picture and analyze the average gray value. Then, as low as 0.027 nM CK-MB could be detected by cell phone. With good portability, visualization, and simple sample handling, this method has great potential for quantitative point-of-care testing (POCT) of targets in resource-constrained settings. [Display omitted] • A POCT platform that combined a microfluidic chip with DNA hydrogel to enable accurate quantitative detection of CK-MB. • The device possessed wide source of reading instruments, reliable results and intelligent readout. • This proposed method had been successfully certified to be convenient and rapid for the detection of serum samples. [ABSTRACT FROM AUTHOR]

Background Acute myocardial infarction (AMI), is related to a diffuse active inflammation of the coronary tree associated with rupture of one of the multiple vulnerable plaques. The presence of soluble mediators of inflammation with their synergic or antagonistic actions coordinates the physiological response determining the plaque fate and the fatal event. The present study focus on the cytokines network operating in human coronary plaques of patients died from AMI and controls, pointing out that coronaries of AMI patients produce PTX3 protein twice as that of controls and express high level of PTX3 mRNA. Results The presence of CX3CR1 polymorphisms is significantly correlated with the incidence and the outcome of acute myocardial infarction inducing in the whole coronary tree a strong recruitment of Th1 polarized inflammation that is directly correlated to PTX3 expression. Conclusions Moreover we found a positive correlation between the expression of PTX3 in the plaque and the content of macrophage cells showing a M2 polarization indicating the possible role of this chemokine as mediator of immune response that would orchestrate plaque evolution and inflammatory cell type activation. [ABSTRACT FROM AUTHOR]

Acute myocardial infarction with ST-segment elevation (STEMI) initiates with intraluminal thrombosis and results in total occlusion of the coronary artery. To date, characterization of the coronary thrombus proteome in STEMI patients has not been yet accomplished. Therefore, we aimed to perform an in-depth proteomic characterization of the human coronary thrombus by means of three different approaches: 2-DE followed by mass spectrometry (MALDI MS/MS), 1-DE combined either with liquid chromatography coupled to mass spectrometry in a MALDI TOF/TOF (LC–MALDI-MS/MS), or in a LTQ-Orbitrap (LC–ESI-MS/MS). This approach allowed us to identify a total of 708 proteins in the thrombus. Expression in coronary thrombi (n = 20) of 14 proteins was verified, and the expression of fibrin and 6 cell markers (platelets, monocytes, neutrophils, eosinophils, T-cells and B-cells) quantified by selected reaction monitoring (SRM). A positive correlation of 5 proteins (fermitin homolog 3, thrombospondin-1, myosin-9, beta parvin and ras-related protein Rap-1b) with CD41 was found, pointing out the potential activation of a focal adhesion pathway within thrombus platelets. DIDO1 protein was found to correlate negatively with thrombus fibrin, and was found up-regulated in the plasma of these STEMI patients, which may constitute a starting point for further analyses in the search for biomarkers of thrombosis. Biological significance The proteomic characterization of the human coronary thrombus may contribute to a better understanding of the mechanisms involved in acute coronary syndrome, and thus pave the road for the identification of new therapeutic targets that may help addressing this and other thrombotic diseases. A novel methodology to characterize thrombus composition and expression of a sub-group of proteins is hereby described, which allowed linking protein expression with cellular and ECM matrix composition of the thrombus. Five proteins (fermitin homolog 3, thrombospondin-1, myosin-9, beta parvin and ras-related protein Rap-1b) co-express within the human coronary thrombus with CD41, pointing out the potential activation of a focal adhesion pathway within thrombus platelets during thrombus formation. Besides, the protein death-inducer obliterator 1, found to be expressed within the human coronary thrombus, has been proved to increase in the plasma of STEMI patients, which constitutes an important starting point for further analyses in the search for biomarkers of thrombosis. [ABSTRACT FROM AUTHOR]

Background aims. Endothelial progenitor cells (EPCs) are known to play a beneficial role by promoting postnatal vasculogenesis in pathological events, such as ischemic heart disease and peripheral artery disease. However, little is known about the potential of EPCs to restore heart damage tissue. We compared the cardiac differentiation capacity of EPCs isolated from peripheral blood of patients with acute myocardial infarction (AMI) with EPCs obtained from umbilical cord blood (UCB). Methods. EPCs from both origins were isolated by density gradient centrifugation and characterized through the use of endothelial markers (UEA-1 lectin, CD 133 and KDR) and endothelial cell colony-forming unit assay. Cardiac differentiation capacity of EPCs was assessed by immunofluorescence and reverse transcriptase-polymerase chain reaction after 5- azacytidine (5-aza) induction. Results. No significant differences were observed between the number of endothelial cell colony-forming units in peripheral blood of patients with AMI and samples from UCB. Moreover, 5-aza induced the appearance of myotube-like structures and the positive expression of sarcomeric a-actinin, cardiac troponin I and T and desmin in a similar pattern for both cell sources, which indicates a comparable acquisition of a cardiac-like phenotype. Conclusions. For the first time, we have compared, in vitro, the cardiomyogenic potential of EPCs derived from patients with AMI with UCB-derived EPCs. Our data indicate that EPCs obtained from both origins have similar plasticity and functions and suggest a potential therapeutic efficacy in cardiac cell therapy. [ABSTRACT FROM AUTHOR]

Background While sleep apnea (SA) might be a modifiable cardiovascular risk factor, recent data suggest that SA is severely underdiagnosed in patients after acute myocardial infarction (MI). There is limited evidence about day-night variation of onset of MI on dependence of having SA. We therefore investigated the prevalence of SA and examined the day-night variation of onset of MI in acute MI patients. Methods We prospectively studied 782 consecutive patients admitted to the hospital with the diagnosis of acute MI. All subjects underwent sleep evaluations using a portable device after at least 48 h post-admission. Using the apnea-hypopnea index (AHI), groups were defined as patients without SA (< 5 events/h), mild SA (5-15 events/h), moderate SA (15-30 events/h), and severe SA (≥ 30 events/h). Results Almost all patients (98%) underwent urgent coronary angiography and 91% of patients underwent primary PCI. Using a threshold of AHI ≥5 events/h, SA was present in 65.7% of patients after acute MI. Mild SA was present in 32.6%, moderate in 20.4% and severe in 12.7%. The day-night variation in the onset of MI in all groups of SA patients was similar to that observed in non-SA patients. From 6 AM to 12 PM, the frequency of MI was higher in both SA and non-SA patients, as compared to the interval from 12 AM to 6 AM (all p < 0.05). Conclusion There is a high prevalence of SA in patients presenting with acute MI. Peak time of MI onset in SA patients was between 6 AM and noon, similar to that in the general population. Whether diagnosis and treatment of SA after MI will significantly improve outcomes in these patients remains to be determined. [ABSTRACT FROM AUTHOR]

Objectives This study sought to identify clinical and procedural predictors of elevated radiation dose received by patients with acute myocardial infarction (AMI) undergoing percutaneous coronary intervention (PCI) and to determine if elevated radiation dose was predictive of mortality in this population. Background Little data exist regarding the impact of excessive radiation burden on clinical outcomes in patients undergoing PCI. Methods The study population included 1,039 patients who underwent PCI for an AMI between January 1, 2007 and December 31, 2008 at an academic tertiary care teaching hospital. Cumulative skin dose (measured in milligray [mGy]) was selected as a measurement of patient radiation burden. Clinical and procedural variables were analyzed in multiple logistic and linear regression models to determine predictors of higher skin dose, and its impact was evaluated on all-cause intermediate-term mortality at two years. Results Median skin dose was 2120 mGy (IQR 1379–3190 mGy) in the overall population, of which 153 (20.8%) patients received an elevated skin dose (defined as a skin dose > 4,000 mGy). Independent predictors of elevated skin dose included male gender, obesity, multivessel intervention, and presentation with a non-ST-elevation MI (NSTEMI) versus an ST-elevation MI (STEMI). Increased skin dose was not predictive of intermediate-term mortality by multivariate analysis in the overall population or in either subgroup of STEMI and NSTEMI. Conclusions In this contemporary observational study examining patients with AMI undergoing PCI, male gender, obesity, multivessel intervention, and presentation with a NSTEMI were associated with increased radiation exposure. [ABSTRACT FROM AUTHOR]

Background Although a higher heart rate is known to be a risk factor for cardiovascular disease (CVD) events, there have been no reports concerning bradycardia. Whether lower and higher resting pulse rates (RPRs) are associated with cardiovascular risk was investigated in subjects from a community-based, prospective cohort study. Methods After subjects with atrial fibrillation, subjects with a history of CVD, and subjects receiving antihypertensive treatment were excluded, 17,766 subjects (5958 men), aged 40-79 (mean 61.5) years, were analyzed. The RPR at baseline was categorized into four groups (RPR<60, 60-69.5, 70-79.5, ≥80 beats per minute (bpm)) using the average value of two consecutive measurements. The endpoint was set as the composite outcome of myocardial infarction, stroke, or sudden death. Results During a mean follow-up of 5.6 years, there were 213 events in men and 186 events in women. In Cox regression models, increased risks of CVD were found in the men group with RPR<60 bpm, as well as the group with RPR≥80 bpm, compared with the reference group with RPR 60-69.5 bpm (hazard ratio [HR] = 1.73, p = 0.005 and HR = 2.01, p < 0.001). These increased risks were found even when adjusted for age and other CVD risk factors (HR = 1.55, p = 0.026 with RPR<60 bpm and HR = 1.72, p = 0.009 with RPR≥80 bpm). In women, there were no significant associations between RPR and CVD risk. Conclusion Bradycardia, as well as a higher pulse rate, may be an independent risk factor for future cardiovascular events in apparently healthy men. [ABSTRACT FROM AUTHOR]

Background Blood transfusion is controversial for anemic patients with acute myocardial infarction (AMI), with some previous studies reporting increased risk of transfusion-associated mortality. Objectives The goal of this study was to examine variability in blood transfusions across hospitals and the relationship between blood transfusion and in-hospital mortality in a large, contemporary cohort of consecutive AMI patients. Methods Among 34,937 AMI hospitalizations from 57 centers, patients receiving at least 1 packed red blood cell transfusion were compared with those who were not transfused. Using 45 disease severity, comorbidity, laboratory, and in-hospital treatment variables, we propensity matched patients who did and did not receive a packed red blood cell transfusion. A conditional logistic regression model was used to identify the association between transfusion and in-hospital mortality. Results A total of 1,778 patients (5.1%) had at least 1 transfusion. In unadjusted analyses, transfusion was associated with higher in-hospital mortality (odds ratio: 2.05 [95% confidence interval: 1.76 to 2.40]). The vast majority of patients (91.1%) with and without transfusion had nonoverlapping propensity scores, reflecting incomparable clinical profiles. Thus, they were excluded from the propensity-matched analyses. After propensity matching those with overlapping scores, blood transfusion was associated with a reduced risk of in-hospital death (odds ratio: 0.73 [95% confidence interval: 0.58 to 0.92]). Conclusions The majority of patients undergoing blood transfusion in clinical practice cannot be matched with nontransfused patients due to their markedly different clinical profiles. Among comparable patients, blood transfusion was associated with a lower risk of in-hospital mortality. These findings suggest that previous observational reports of increased mortality with transfusion may have been influenced by selection bias, and they highlight the need for randomized trials to establish the role of transfusion during AMI. [ABSTRACT FROM AUTHOR]

Intermedin functions systemically as a potent vasodilator and its plasma levels have been shown to be elevated in patients with acute myocardial infarction. This study aimed to evaluate the prognostic value of plasma intermedin level in the patients with ST-segment elevation acute myocardial infarction. Plasma intermedin concentrations of 128 patients and 128 healthy controls were determined using a radioimmunoassay. Patients were followed up for 6 months for major adverse cardiovascular events (MACE) consisting of cardiovascular mortality, reinfarction, hospitalization for decompensated heart failure, and lift-threatening arrhythmia. The association of plasma intermedin levels with MACE was investigated by univariate and multivariate analyses. Plasma intermedin levels were significantly higher in patients than in healthy subjects. Elevated plasma level of intermedin was identified as an independent predictor of MACE. Receiver operating characteristic curve analysis showed that plasma intermedin levels had high predictive value for MACE. Moreover, its predictive value was similar to Global Registry of Acute Coronary Events scores' based on area under curve. Meantime, it obviously improved Global Registry of Acute Coronary Events scores' predictive value in a combined logistic-regression model. In multivariate Cox's proportional hazard analysis, plasma intermedin level emerged as an independent predictor of MACE-free survival. Thus, our results suggest that high plasma intermedin level is associated with poor outcomes of patients and may be a useful prognostic biomarker in ST-segment elevation acute myocardial infarction. [ABSTRACT FROM AUTHOR]

Background Although cerebrovascular accident (CVA) is a relatively infrequent complication of acute myocardial infarction (AMI), the occurrence of CVA in patients with AMI is associated with increased morbidity and mortality. We wanted to assess post-AMI CVA rate in the United States and identify the associated patient characteristics, comorbidities, type of AMI, and utilization of invasive procedures. Methods This is an observational study from the Nationwide Inpatient Sample, 2006-2008. Using multivariate regression models, we assessed predictive risk factors for post-AMI CVA among patients admitted for AMI. Results Among the 1,924,413 patients admitted for AMI, the overall rate of CVA was 2% (ischemic stroke: 1.47%, transient ischemic attack [TIA]: 0.35% and hemorrhagic stroke: 0.21%). In this sample of AMI patient, higher incidence of CVA was associated with: CHF (adjusted odds ratio [AOR] 1.71; 95% confidence interval [CI], 1.58-1.84,), age over 65 AOR, 1.65; 95% CI, 1.60-1.70, alcohol abuse AOR, 1.60; 95% CI, 1.49-1.73, cocaine use AOR, 1.48; 95% CI, 1.29-1.70, atrial fibrillation AOR, 1.43; 95% CI, 1.39-1.46, Black race AOR, 1.35; 95% CI, 1.30-1.40, female gender AOR, 1.32; 95% CI, 1.29-1.35, peripheral vascular disease [PVD] AOR, 1.26; 95% CI, 1.22-1.30, coronary artery bypass graft (CABG) AOR, 1.22; 95% CI, 1.17-1.27, P <0.0001, STEMI AOR, 1.17; 95% CI, 1.14-1.20 and teaching hospitals AOR, 1.09; 95% CI, 1.06-1.12. Conclusion Female gender, older age (age≥65), black ethnicity, comorbidities including CHF, PVD, atrial fibrillation as well as STEMI and undergoing CABG were associated with the highest risk of CVA post-AMI. [ABSTRACT FROM AUTHOR]

Objectives To compare management of patients with acute non-ST segment elevation myocardial infarction (NSTEMI) in three developed countries with national ongoing registries. Background Results from clinical trials suggest significant variation in care across the world. However, international comparisons in "real world" registries are limited. Methods We compared the use of in-hospital procedures and discharge medications for patients admitted with NSTEMI from 2007 to 2010 using the unselective MINAP/NICOR [England and Wales (UK); n=137,009], the unselective SWEDEHEART/RIKS-HIA (Sweden; n=45,069), and the selective ACTION Registry-GWTG/NCDR [United States (US); n=147,438] clinical registries. Results Patients enrolled among the three registries were generally similar except those in the US who were younger but had higher rates of smoking, diabetes, hypertension, prior heart failure, and prior MI than in Sweden or in UK. Angiography and percutaneous coronary intervention (PCI) were performed more often in the US (76% and 44%) and Sweden (65% and 42%) relative to the UK (32% and 22%). Discharge betablockers were also prescribed more often in the US (89%) and Sweden (89%) than in the UK (76%). In contrast, discharge statins, angiotensin converting enzyme inhibitors/angiotensin receptor blockers (ACEI/ARB), and dual antiplatelet agents (among those not receiving PCI) were higher in the UK (92%, 79%, and 71%) than in the US (85%, 65%, 41%) and Sweden (81%, 69%, and 49%). Conclusions The care for patients with NSTEMI differed substantially among the three countries. These differences in care among countries provide an opportunity for future comparative effectiveness research as well as identify opportunities for global quality improvement. [ABSTRACT FROM AUTHOR]

Background: Various national campaigns launched in recent years have focused on young women with acute myocardial infarctions (AMIs). Contemporary longitudinal data about sex differences in clinical characteristics, hospitalization rates, length of stay (LOS), and mortality have not been examined. Objectives: This study sought to determine sex differences in clinical characteristics, hospitalization rates, LOS, and in-hospital mortality by age group and race among young patients with AMIs using a large national dataset of  U.S. hospital discharges. Methods: Using the National Inpatient Sample, clinical characteristics, AMI hospitalization rates, LOS, and in-hospital mortality were compared for patients with AMI across ages 30 to 54 years, dividing them into 5-year subgroups from 2001 to 2010, using survey data analysis techniques. Results: A total of 230,684 hospitalizations were identified with principal discharge diagnoses of AMI in 30- to 54-year-old patients from Nationwide Inpatient Sample data, representing an estimated 1,129,949 hospitalizations in the United States from 2001 to 2010. No statistically significant declines in AMI hospitalization rates were observed in the age groups >55 years or stratified by sex. Prevalence of comorbidities was higher in women and increased among both sexes through the study period. Women had longer LOS and higher in-hospital mortality than men across all age groups. However, observed in-hospital mortality declined significantly for women from 2001 to 2010 (from 3.3% to 2.3%, relative change 30.5%; p for trend < 0.0001) but not for men (from 2% to 1.8%, relative change 8.6%; p for trend = 0.60). Conclusions: AMI hospitalization rates for young people have not declined over the past decade. Young women with AMIs have more comorbidity, longer LOS, and higher in-hospital mortality than young men, although their mortality rates are decreasing. [ABSTRACT FROM AUTHOR]

Abstract: We investigated disparities in rates of acute myocardial infarction (AMI) between Aboriginal and non-Aboriginal people in the 199 Statistical Local Areas (SLAs) in New South Wales, Australia. Using routinely collected and linked hospital and mortality data from 2002 to 2007, we developed multilevel Poisson regression models to estimate the relative rates of first AMI events in the study period accounting for area of residence. Rates of AMI in Aboriginal people were more than two times that in non-Aboriginal people, with the disparity greatest in more disadvantaged and remote areas. AMI rates in Aboriginal people varied significantly by SLA, as did the Aboriginal to non-Aboriginal rate ratio. We identified almost 30 priority areas for universal and targeted preventive interventions that had both high rates of AMI for Aboriginal people and large disparities in rates. [Copyright &y& Elsevier]

Abstract: Background: Silent atrial fibrillation (AF) has been suggested to be frequent after acute myocardial infarction (MI). Continuous ECG monitoring (CEM) has been shown to improve AF screening in patients at risk of stroke. Objectives: We aimed to assess the incidence and prognosis of silent AF in patients with acute MI. Methods: All the consecutive patients with acute MI were prospectively analyzed by CEM≥48h after admission. Silent AF was defined as asymptomatic episodes lasting at least 30s. The population was divided into three groups: no-AF, silent AF and symptomatic AF. Results: Among the 849 patients, 135 (16%) developed silent AF and 45 (5%) symptomatic AF. Compared with the no-AF group, patients with silent AF were markedly older (80 vs. 62y, p<0.001), more frequently women (43% vs. 30%, p=0.006) and less likely to be smokers (20% vs. 36%, p<0.001). They had impaired left ventricular ejection fraction (LVEF) and left atrial (LA) enlargement. By multivariate analysis, age, history of AF, indexed LA area and LVEF were identified as independent predictors of silent AF. In-hospital heart failure and death rates were markedly higher in silent AF group when compared with no-AF patients (41.8% vs 21.0% and 10.4% vs. 1.3%, respectively). Conclusion: Our large prospective study showed for the first time that silent AF is more frequent than symptomatic AF after MI. Our work suggests that indexed LA area could help to predict the risk of developing silent AF. Moreover, the onset of silent AF is associated with worse hospital prognosis. [Copyright &y& Elsevier]

Abstract: This study is to investigate the key genes and their possible function in acute myocardial infarction (AMI). The data of GSE4648 downloaded from the Gene Expression Omnibus (GEO) database include 6 time points (15min, 60min, 4h, 12h, 24h and 48h) of 12 left ventricle (LV) samples, 12 surviving LV free wall (FW) samples, 12 inter-ventricular septum (IVS) samples after AMI operation and corresponding sham-operated samples. The data of each sample were analyzed with Affy and Bioconductor packages, and differentially expressed genes (DEGs) were screened out using BETR package with false discovery rate (FDR)<0.01. Then, functional enrichment analysis for DEGs was conducted with Database for Annotation, Visualization and Integrated Discovery (DAVID). Totally 194 DEGs were identified in LV, and only the gene tubulin beta 2a (Tubb2a) and natriuretic peptide B (Nppb) were respectively up-regulated in surviving FW tissue and IVS tissue. The biological process response to wounding and inflammatory response were significantly enriched, as well as leukocyte transendothelial migration pathway. Besides, the expression pattern analysis showed the DEGs mostly up-regulated at 4h after AMI, and these genes were mainly associated with immunity. Additionally, in transcriptional regulatory network, early growth response 1 (Egr1), activating transcription factor 3 (Atf3), Atf4, Myc and Fos were considered as the key transcription factors related to immune response. The key transcription factors and potential target genes might provide new information for the development of AMI, and leukocyte transendothelial migration pathway might play a vital role in AMI. [Copyright &y& Elsevier]

Abstract: Background: Patients undergoing primary percutaneous coronary intervention (PCI) are at high risk for contrast-induced nephropathy (CIN), a complication that has been demonstrated to negatively affect outcomes. It has been suggested that, when compared to males, female patients present higher incidence of CIN and higher mortality after primary PCI. However, the specific role of gender in this setting remains ill-defined given its complex interplay with several co-morbidities and clinical characteristics. We investigated the relationship of patients' variables, including gender, with CIN and mortality after primary PCI. Methods: In a single center study in 323 consecutive patients undergoing primary PCI, the development of CIN and mortality during an 18-month median follow-up period was assessed. CIN was defined as an increase in serum creatinine (≥25% or ≥0.5mg/dl) from baseline occurring at any time during the first 3 post-procedural days. Results: CIN occurred in 23 female and 26 male patients (25.0% vs 11.2%, p =0.003), while cumulative mortality was 10.6%. Women presented unfavorable basal characteristics and underwent myocardial reperfusion less quickly. At multivariable analysis, reduced left ventricular ejection fraction (LVEF) (odds ratio [OR] 7.32 95% confidence interval [CI]: 2.60–21, p <0.001) and female gender (OR 2.49 95%CI 1.22–5.07, p =0.01) predicted CIN, whereas the occurrence of CIN (hazard ratio [HR] 3.65 95%CI 1.55–8.59, p =0.003) and a Mehran risk score (MRS) ≥6 (HR 1.76 95%CI 1.13–2.74, p =0.01) independently predicted long-term mortality. Conclusions: After primary PCI, female gender and LVEF are associated with an increased risk of CIN, whereas MRS and development of CIN predict long-term mortality. [Copyright &y& Elsevier]

Abstract: Background: Cell-based pro-angiogenic therapy by bone marrow mesenchymal stem cells (MSCs) has been touted as a means to reducing the adverse effects of cardiac remodeling after myocardial infarction (MI). Milieu-dependent regulation of pro-angiogenic potential of MSCs after infarction remains to be elucidated. In this study, the effects of marrow-derived MSCs on the kinetics of angiogenesis signaling factors were investigated in a rabbit model of MI. Methods: MI was induced in rabbits, and the animals were randomized into two groups (cell transplantation and control, each group with 21 animals). 1×106 autologous marrow-derived MSCs were injected into the myocardium of the border zone after transfection with a green fluorescent protein (GFP) lentiviral reporter vector. Control animals received PBS vehicle only. Effect of the transplanted cells on the hearts was evaluated over time by pathological, immunofluorescence, western blotting, immuno-electron microscopy, and echocardiographic analyses. Results: Transplanted GFP-positive MSCs were enriched with time in the peri-infarct border zone with differentiation potential into three major cell types of the heart, including cardiomyocytes, endothelial cells, and smooth muscle cells, and there was significant augmentation of microvascular density. The transplanted cells could change the milieu of the injured myocardium to increase the expression levels of VEGF as well as the ratio of Ang-2 to Ang-1, and to reduce the ratio of phosphorylated Tie2 to Tie2. Conclusion: An angiogenesis-promoting milieu was induced after the transplantation of marrow MSCs in the injured myocardium. Compared with the resident cells, the transplanted cells had a greater rate of cellular kinetics in the infarcted myocardium. [Copyright &y& Elsevier]

Abstract: Background: This study tested whether adipose-derived mesenchymal stem cells (ADMSC) embedded in platelet-rich fibrin (PRF) scaffold is superior to direct ADMSC implantation in improving left ventricular (LV) performance and reducing LV remodeling in a rat acute myocardial infarction (AMI) model of left anterior descending coronary artery (LAD) ligation. Methods: Twenty-eight male adult Sprague Dawley rats equally divided into group 1 [sham control], group 2 (AMI only), group 3 (AMI+direct ADMSC implantation), and group 4 (AMI+PRF-embedded autologous ADMSC) were sacrificed on day 42 after AMI. Results: LV systolic and diastolic dimensions and volumes, and infarct/fibrotic areas were highest in group 2, lowest in group 1 and significantly higher in group 3 than in group 4, whereas LV performance and LV fractional shortening exhibited a reversed pattern (p<0.005). Protein expressions of inflammation (oxidative stress, IL-1β, MMP-9), apoptosis (mitochondrial Bax, cleaved PARP), fibrosis (Smad3, TGF-β), and pressure-overload biomarkers (BNP, MHC-β) displayed a pattern similar to that of LV dimensions, whereas anti-inflammatory (IL-10), anti-apoptotic (Bcl-2), and anti-fibrotic (Smad1/5, BMP-2) indices showed a pattern similar to that of LV performance among the four groups (all p<0.05). Angiogenesis biomarkers at protein (CXCR4, SDF-1α, VEGF), cellular (CD31+, CXCR4+, SDF-1α+), and immunohistochemical (small vessels) levels, and cardiac stem cell markers (C-kit+, Sca-1+) in infarct myocardium were highest in group 4, lowest in group 1, and significantly higher in group 3 than in group 2 (all p<0.005). Conclusion: PRF-embedded ADMSC is superior to direct ADMSC implantation in preserving LV function and attenuating LV remodeling. [Copyright &y& Elsevier]

Abstract: Objective: Adropin is a recently identified bioactive protein that is important for energy homeostasis and maintaining insulin sensitivity. We sought to detect serum adropin levels in acute myocardial infarction (AMI) patients. Methods: We enrolled 138 AMI patients, 114 stable angina pectoris (SAP) patients and 75 controls. Adropin levels were measured by enzyme-linked immunosorbent assay (ELISA). Results: Serum adropin levels were significantly lower in patients with AMI compared with SAP patients or controls (P <0.01). Multivariate logistic regression demonstrated that lower adropin was the independent predictor for the presence of AMI in coronary artery disease (CAD) patients (P <0.01). Serum adropin levels were negatively associated with body mass index (BMI) (P <0.01) and triglyceride levels (P <0.05) in AMI patients. Conclusion: Decreased serum adropin levels are associated with the presence of AMI in CAD patients. These results revealed that adropin might represent as a novel biomarker for predicting AMI onset in CAD patients. [Copyright &y& Elsevier]

Objective: Coronary artery embolism resulting in acute myocardial infarction (AMI) is an infrequent but potentially life-threatening occurrence. To date, there is still no consensus in the literature regarding the optimal therapeutic algorithm for embolic myocardial infarction. Patients: We present our experience with three patients who had mechanical valve prosthesis and suffered from AMI due to coronary artery embolism in the setting of sub-therapeutic or interrupted anti-coagulation therapy. Those patients were treated with intracoronary thrombolysis, thrombus aspiration followed by balloon angioplasty and thrombus aspiration alone, respectively. Results: In our case 1, the coronary angiogram demonstrated extensive thrombus within the left circumflex coronary artery and extending into the left anterior descending (LAD). We performed intracoronary thrombolytic therapy, which results in completed thrombus resolution and favourable clinical outcome. In our case 3, coronary angiography revealed massive thrombus within the middle-LAD with a TIMI grade 3 distal flow. The patient underwent a successful thrombus aspiration procedure without stent implantation. In our case 2, the coronary angiography revealed total occlusion of the middle LAD, and thrombus aspiration was initially performed because of the large thrombus burden. However, this approach was unsuccessful and so the patient was then treated with balloon angioplasty, resulting in TIMI 2 flow. Conclusion: Embolic myocardial infarction, although uncommon, can occur in predisposed groups such as those with prosthetic mechanical valves with sub-therapeutic anticoagulation. The treatment for this specific group of patients needs to be tailored individually. [ABSTRACT FROM AUTHOR]

Highlights: [•] The patients were grouped according to the quartile of CST concentration. [•] A correlation between CST and malignant arrhythmia in AMI patients is found. [•] Age, CST and NT-proBNP are independent predictors for MACE. [•] Increased blood glucose (≥6.1mmol/L) predicts malignant arrhythmia in AMI patients. [•] CST is a new predictor for prediction of malignant arrhythmia in patients with AMI. [Copyright &y& Elsevier]

Acute myocardial infarction (AMI) leads to molecular, structural, geometric, and functional changes in the heart in a process known as ventricular remodeling. An intense organized inflammatory response is triggered after myocardial ischemia and necrosis and involves all components of the innate immunity, affecting both cardiomyocytes and noncardiomyocyte cells. Inflammation is triggered by tissue injury; it mediates wound healing and scar formation and affects ventricular remodeling. Many therapeutic attempts aimed at reducing inflammation in AMI during the past 3 decades presented issues of impaired healing or increased risk of cardiac rupture or failed to show any additional benefit in addition to standard therapies. More recent strategies aimed at selectively blocking one of the key factors upstream rather than globally suppressing the response downstream have shown some promising results in pilot trials. We herein review the pathophysiological mechanisms of inflammation and ventricular remodeling after AMI and the results of clinical trials with anti-inflammatory strategies. [Copyright &y& Elsevier]

Abstract: Background: Epidemiologic studies of heme iron and non-heme iron intake in relation to risk of acute myocardial infarction (AMI) are lacking. Therefore, we examine the associations between heme iron and non-heme iron intake and fatal and nonfatal AMI in men. Moreover, we investigated whether the associations were modified by intake of minerals (calcium, magnesium, and zinc) that decreases iron absorption. Methods: The population-based prospective cohort of Swedish Men (COSM) included 36882 men, aged 45–79years, who completed a self-administered questionnaire on diet and had no history of coronary heart disease, stroke, diabetes, or cancer at baseline. Results: During an 11.7year follow-up, 678 fatal and 2593 nonfatal AMI events were registered. The hazard ratio (HR) of fatal AMI among men in the highest compared with the lowest quintile of heme iron intake was 1.51 (95%CI: 1.07–2.13, P-trend=0.02). The association was confined to men with a low intake of minerals that can decrease iron absorption. Among men with combined intakes of calcium, magnesium, and zinc below the medians, the HR of fatal AMI was 2.89 (95%CI: 1.43–5.82) for the highest vs. the lowest quintile of heme iron intake. There was no association between heme iron intake and nonfatal AMI, or between non-heme iron intake and fatal or nonfatal AMI. Conclusions: Findings from this prospective study indicate that a high heme iron intake, particularly with simultaneous low intake of minerals that can decrease iron absorption, may increase the risk of fatal AMI. [Copyright &y& Elsevier]

Abstract: Background: This nationwide population-based study investigated the relationship between individual and neighborhood socioeconomic status (SES) and mortality rates for acute myocardial infarction (AMI) in Taiwan. Methods: A population-based follow-up study included 23,568 patients diagnosed with AMI from 2004 to 2008. Each patient was monitored for 2years, or until their death, whichever came first. The individual income-related insurance payment amount was used as a proxy measure of patient's individual SES. Neighborhood SES was defined by household income, and neighborhoods were grouped as advantaged or disadvantaged. The Cox proportional hazards model was used to compare the mortality rates between the different SES groups after adjusting for possible confounding risk factors. Results: After adjusting for potential confounding factors, AMI patients with low individual SES had an increased risk of death than those with high individual SES who resided in advantaged neighborhoods. In contrast, the cumulative readmission rate from major adverse cardiovascular events did not differ significantly between the different individual and neighborhood SES groups. AMI patients with low individual SES had a lower rate of diagnostic angiography and subsequent percutaneous coronary intervention (P<0.001). The presence of congestive heart failure, chronic kidney disease, chronic obstructive pulmonary disease, pneumonia, septicemia, and shock revealed an incremental increase with worse SES (P<0.001). Conclusions: The findings indicate that AMI patients with low individual SES have the greatest risk of short-term mortality despite being under a universal health-care system. Public health strategies and welfare policies must continue to focus on this vulnerable group. [Copyright &y& Elsevier]

Background The objective of this study was to analyze the effects of cardiac rehabilitation (CR) on the atrial function of patients with acute myocardial infarction (AMI) who had been successfully revascularized through percutaneous coronary intervention (PCI). Methods Forty-two AMI patients having undergone CR were enrolled in this observational study. Assessments were performed before and after 6 weeks of CR. Left atrial strain analysis was carried out by two-dimensional speckle tracking echocardiography. Left ventricular ejection fraction (LVEF) was measured by the biplane Simpson's method. Pulsed-wave Doppler at the tip of mitral valve leaflets enabled us to measure early (E) and late (A) diastolic filling velocities, deceleration time (DT) of early filling velocity and isovolumic relaxation time (IVRT). Left ventricle tissue velocity was measured by tissue Doppler imaging of the lateral mitral annulus (e’) and E/e’ was subsequently calculated. Ratio of E/e’ to left atrium (LA) peak strain was used to estimate LA stiffness. Results Following CR, LVEF ( P = 0.010), LA strain ( P < 0.001) and LA stiffness ( P = 0.013) all showed improvement, while other parameters remained unchanged. Conclusion Post-AMI cardiac rehabilitation and revascularization by PCI might have favourable effects on LA function. [ABSTRACT FROM AUTHOR]

Abstract: Objective: This study aimed to explore the correlates for mortality in patients treated with both primary percutaneous coronary intervention (PCI) and intra-aortic balloon pump counter-pulsation (IABP). Background: Acute myocardial infarction (AMI) complicated by cardiogenic shock (CS) is associated with high mortality rates. Methods: From a cohort of patients with AMI, treated with both primary PCI and IABP and who met strict definitions for CS to identify correlates associated with mortality, the study compared patients who died in-hospital to those who survived to discharge. Results: A cohort of 93 patients met the inclusion/exclusion criteria. Of them, 66.7% were male, and the average age was 64.96±13.06years. The overall in-hospital mortality rate for this cohort was 33%. The baseline characteristics were balanced save for older average age and left ventricular ejection fraction in those who died (p=0.049 and p=0.014, respectively). Insertion of IABP pre-PCI and cardiac arrest at the catheterization lab were more frequent in those who died (p=0.027 and p=0.008, respectively). The insertion of IABP pre-PCI, cardiac arrest at the cath lab, and lower ejection fraction were correlated with in-hospital mortality (ORs 2.68, 5.93, and 0.02, respectively). Conclusions: In the era of primary PCI and IABP as standard of care in AMI complicated by CS, patients with low EF, those who necessitate IABP insertion pre-PCI, and those who necessitate cardiopulmonary resuscitation during PCI are at higher risk for in-hospital mortality and should be considered for more robust hemodynamic support devices with an attempt to improve their prognosis. [Copyright &y& Elsevier]

Abstract: Background: Hospital acute myocardial infarction (AMI) care is increasingly evaluated using composite quality scores. We investigated the influence of three aggregation methods for an AMI indicator on mortality and hospital rank. Methods and results: We studied 136,392 patients discharged alive from 199 hospitals with AMI recorded in the Myocardial Ischaemia National Audit Project, between 01/01/2008 and 31/12/2009. A composite of prescription of aspirin, thienopyridine inhibitor, β-blocker, angiotensin converting enzyme inhibitor, HMG CoA reductase enzyme inhibitor and enrolment in cardiac rehabilitation at discharge was aggregated as opportunity based (OBCS), weighted opportunity-based (WOBCS) and all-or-nothing (ANCS) scores. We quantified adjusted 30-day, 6-month and 1-year mortality rates and hospital performance rank. Median (IQR) scores were OBCS: 95.0% (3.5), WOBCS: 94.7% (0.8) and ANCS: 80.9% (11.8). The three methods affected the proportion of hospitals outside 99.8% credible limits of the national median (OBCS: 52.2%, WOBCS: 64.3% and ANCS: 37.7%) and hospital rank. Each 1% increase in composite score was significantly associated with a 1 to 3% and a 4% reduction in 6-month and 1-year mortality, respectively. However, the ANCS had fewer cases and no significant association with 30-day mortality. Conclusions: A hospital composite score, incorporating 6 aspects of AMI care, was significantly inversely associated with mortality. However, composite aggregation method influenced hospital rank, number of cases available for analysis and size of the association with all-cause mortality, with the ANCS performing least well. The use and choice of composite scores in hospital AMI quality improvement requires careful evaluation. [Copyright &y& Elsevier]

Abstract: Background: ST-segment elevation myocardial infarction (STEMI) due to coronary artery occlusion in the setting of acute carbon monoxide (CO) poisoning is a very rare presentation. Objective: Our aim was to report on the use of primary angioplasty in a patient with STEMI in the setting of CO poisoning. Case Report: A 36-year-old man with retrosternal chest pain was admitted after exposure to CO. The initial electrocardiogram (ECG) showed ST depression in I, aVL, and V3−V4 with slight ST elevation in II, III, aVF leads. Toxic carboxyhemoglobin level of 22% and troponin I of 2.19 μg/L were confirmed. After oxygen therapy the chest pain diminished, but after about 15 h it returned. The repeat ECG revealed normalization of previous ST depression with persistent ST elevation in II, III, aVF leads. The troponin I concentration was 5.94 μg/L. An echocardiogram demonstrated an apex hypokinesia involving the adjacent segments of the anterior and lateral wall. On the coronary angiogram, an acute occlusion of the distal left anterior descending coronary artery was confirmed. Primary percutaneous coronary intervention (PCI) of the infarct-related artery was performed. After PCI, the patient was symptom free and had partial ST-segment elevation resolution. The patient was discharged home after 7 days, with persistent ST-T changes and mild hypokinesia of the apex suggesting myocardial injury. Conclusions: Patients with toxic CO exposure who have symptoms of STEMI should be carefully evaluated with serial ECG, cardiac necrosis marker measurements, and an echocardiogram. When there is evidence of myocardial injury, a wider use of coronary angiography can identify patients who could benefit from PCI. [Copyright &y& Elsevier]

Abstract: Ethnopharmacological relevance: The decoction of American Ginseng and Corydalis Tuber has been widely used for treatment of cardiovascular diseases due to their anti-ischemic and anti-arrhythmic effects. The aim of this study is to evaluate the anti-apoptotic effect of Shenyuan, which is composed of the bioactive components extracted from the mixture of American Ginseng and Corydalis Tuber, and to explore potential mechanisms involved in the regulation of apoptosis. Materials and methods: A porcine model of acute myocardial infarction (AMI) was established by ligation of the left anterior descending coronary artery. Thirty-eight pigs were randomized into six groups: Group S, sham (n=6); Group C, AMI controls (n=8); Group L, AMI+low-dose Shenyuan (240mg/kg d, n=6); Group M, AMI+moderate-dose Shenyuan (320mg/kg d, n=6); Group H, AMI+high-dose Shenyuan (400mg/kg d, n=6); Group B, AMI+Metoprolol Tartrate (1mg/kg d, n=6). The treatment of Shenyuan or Metoprolol started one week before AMI and continued for another two weeks after AMI. Results: Treatment with all doses of Shenyuan as well as Metoprolol produced a significant decrease of apoptotic index (P<0.05), which was confirmed by TUNEL staining method. This anti-apoptotic effect was accompanied by less release of cardiac enzymes and limit of infarct size. In Group H, levels of MDA, 8-iso-prostaglandin F2α, GRP78/bip, calregulin, CHOP/GADD153, Bax, caspase-3, cleaved caspase-3 and activity of caspase-3 were reduced, while GSH, SOD, Bcl-2 and the Bcl-2/Bax ratio were significantly increased (P<0.05). In groups M and L, some results did not show statistical difference. There was no statistical difference in cardiac function between treatment groups and Group C. Conclusion: Shenyuan treatment significantly inhibited ERS and oxidative stress, balanced the Bcl-2/Bax ratio, suppressed activation of caspase-3, and finally exerted an anti-apoptotic effect in pigs with a large anterior wall AMI. This was accompanied by less release of cardiac enzymes and limit of infarct size. Shenyuan treatment inhibited apoptosis and may have a therapeutic role in improving the natural process of AMI. [Copyright &y& Elsevier]

Abstract: Backgrounds: The disparity between ST-segment elevation myocardial infarction (STEMI) and non-STEMI (NSTEMI) remains controversial. We compared clinical outcomes and prognostic factors between STEMI and NSTEMI using large-scale registry data. Methods: We recruited 28,421 patients with STEMI (n=16,607) and NSTEMI (n=11,814) between November 2005 and April 2010 from a nationwide registry in Korea. We performed landmark analysis of cardiac death, recurrent acute myocardial infarction (re-AMI), revascularization, and major adverse cardiac events (MACE) at 30days (early term) and 1year (late term) after admission. Results: Patients with NSTEMI had a greater number of co-morbidities than STEMI patients. Early term MACE (6.9% vs. 4.5%, p<0.001) and cardiac death (6.1% vs. 3.7%, p<0.001) were higher in STEMI patients. However, late-term MACE (8.0% vs. 9.1%, p=0.007), cardiac death (1.9% vs. 2.6%, p=0.001), and re-AMI (0.6% vs. 1.3%, p<0.001) were lower in the STEMI group. The independent predictors of cardiac death were old age, renal dysfunction, LV dysfunction, Killip class, post-thrombolysis in myocardial infarction (TIMI) flow, and major bleeding in both groups. Female gender, previous ischemic heart disease, diabetes, current smoking, multivessel disease, and body mass index were MI type- or time-dependent predictors. Conclusion: The STEMI group displayed poor early term clinical outcome, whereas the NSTEMI group displayed poor late-term clinical outcome. The STEMI and NSTEMI groups had different predictor profiles for cardiac death, suggesting that different strategies are required for improving the late-term outcome of STEMI and NSTEMI patients. [Copyright &y& Elsevier]

Abstract: Background: Adipose tissue-derived progenitor cells (ATDPCs) isolated from human cardiac adipose tissue are useful for cardiac regeneration in rodent models. These cells do not express cardiac troponin I (cTnI) and only express low levels of PECAM-1 when cultured under standard conditions. The purpose of the present study was to evaluate changes in cTnI and PECAM-1 gene expression in cardiac ATDPCs following their delivery through a fibrin patch to a murine model of myocardial infarction using a non-invasive bioluminescence imaging procedure. Methods and results: Cardiac and subcutaneous ATDPCs were doubly transduced with lentiviral vectors for the expression of chimerical bioluminescent–fluorescent reporters driven by constitutively active and tissue-specific promoters (cardiac and endothelial for cTnI and PECAM-1, respectively). Labeled cells mixed with fibrin were applied as a 3-D fibrin patch over the infarcted tissue. Both cell types exhibited de novo expression of cTnI, though the levels were remarkably higher in cardiac ATDPCs. Endothelial differentiation was similar in both ATDPCs, though cardiac cells induced vascularization more effectively. The imaging results were corroborated by standard techniques, validating the use of bioluminescence imaging for in vivo analysis of tissue repair strategies. Accordingly, ATDPC treatment translated into detectable functional and morphological improvements in heart function. Conclusions: Both ATDPCs differentiate to the endothelial lineage at a similar level, cardiac ATDPCs differentiated more readily to the cardiomyogenic lineage than subcutaneous ATDPCs. Non-invasive bioluminescence imaging was a useful tool for real time monitoring of gene expression changes in implanted ATDPCs that could facilitate the development of procedures for tissue repair. [Copyright &y& Elsevier]

Highlights: [•] We introduce novel optical immunosensors for cardiac biomarkers. [•] We discuss recent advances in optical immunosensing of cardiac biomarkers. [•] We discuss multiplex optical immunosensors for detection of cardiac biomarkers. [•] We discuss the most serious problems in optical immunosensing of cardiac biomarkers. [ABSTRACT FROM AUTHOR]

Aim: To assess the impact on in-hospital and long-term survival of thrombus aspiration (TA) during primary percutaneous coronary intervention (PPCI) for ST-segment elevation myocardial infarction (STEMI) complicated by cardiogenic shock (CS). Methods and Results: From September 2001 to May 2010 we collected data from 155 patients affected with STEMI complicated by CS undergoing PPCI (12.4% of all PPCI) including 70 patients (45.2%) in TA group and 85 patients (54.8%) in conventional PCI group. Patients in TA group were more likely to have right ventricular infarction (24.3% vs 5.9%, p=0.002), higher mean left ventricular ejection fraction (40%±9% vs 35%±7%, p<0.0001) and lower left main coronary artery occlusion (2.8% vs 21.2%, p=0.002). TA was associated with a lower rate of in-hospital and long-term mortality (31.4% vs 48.2%, p=0.05 and 42.8% vs 64.7%, p=0.01 respectively) at a mean follow-up time of 6.1±2.1years. At multivariate analysis the only independent predictor of in-hospital and long-term survival was the procedural success (HR 0.18 95% CI 0.025–0.31, p=0.03 and HR 0.46 95% CI 0.09–0.74, p=0.034 respectively). Conclusions: In this retrospective study TA, performed during PPCI for STEMI complicated by CS, was not an independent predictor of in-hospital and long-term survival. [ABSTRACT FROM AUTHOR]

Aims: The role of Neutrophil elastase (NE) and proteinase 3 (PR3) in the occurrence and severity of stroke and acute myocardial infarction (AMI) have not been explored in type 2 diabetes mellitus (T2DM). This study aimed to investigate the relationship and predictive ability of NE and PR3 in the development of stroke and AMI in patients with T2DM, and to explore the pattern of NE and PR3 in atherosclerotic plaques.Methods: 465 patients with T2DM (stroke or AMI, n = 234; non stroke or AMI, n = 231) were recruited. Clinical characteristics, and NE and PR3 concentration were measured in all subjects. Semi-quantitative analysis of immunohistochemistry staining for NE and PR3 was performed in detached emboli and stable plaques.Results: Patients with stroke or AMI had a higher level of NE and PR3, with a more pronounced increase in more severe cases (higher mRS score in stroke and Gensini score in AMI) and associated with clinical markers. An increase in NE and PR3 was an independent risk factor for stroke (OR = 4.318, P = 0.017; OR = 2.979, P = 0.048, respectively) and AMI (OR = 8.385, P = 0.015; OR = 5.540, P = 0.047). Finally, immunohistochemistry staining revealed that the NE and PR3 positive area increased significantly in detached emboli compared with stable plaques.Conclusion: Increased NE and PR3 was associated with occurrence and severity of stroke and AMI in patients with T2DM. Enriched NE and PR3 in detached emboli may be associated with plaque vulnerability. [ABSTRACT FROM AUTHOR]

A novel potential-resolved molecularly imprinted electrochemical luminescence (ECL) immunosensor has been developed for the first time for the dual sensitive detection of markers of acute myocardial infarction (AMI): cardiac troponin I (cTnI) and myoglobin (Mb). In this work, cost-effective and robust molecularly imprinted polymer (MIP) as biomimetic antibody was used to construct the immunosensors through electropolymerization and elution to form polydopamine (PDA)-MIP modified electrode. In the presence of AMI biomarkers, two ECL probes including Ru(bpy) 3 2+@ MOCs and MoS 2 QDs functionalized by cTnI antibody and Mb aptamer could be specifically captured respectively. And two potential distinct ECL signals will be generated in one potential scan. The intensity of ECL reflects the concentrations of cTnI and Mb. The two ECL probes were characterized with field emission scanning electron microscopy, X-ray diffraction, FT-IR spectrum and UV–Vis diffuse reflectance spectroscopy. The prepared sensor exhibited a wide linear range (0.05–104 ng/mL) and a low detection limit (0.0184 ng/mL for cTnI and 0.0492 ng/mL for Mb). Additionally, the MIP-ECL sensor displayed excellent anti-interference, sensitivity and stability to detect cTnI and Mb. Therefore, it will be conducive to accelerate more precise and credible early diagnosis for AMI. • A novel potential-resolved ECL-MIP immunosensor has been developed for the first time to achieve the simultaneously sensitive detection of dual acute myocardial infarction (AMI) markers - cTnI and Mb. •Potential distinct ECL signals for double detection immunoassay are generated in one potential scan based on two ECL probes containing MoS 2 QDs/K 2 S 2 O 8 and Ru(bpy) 3 2+@MOCs/TPA system. •Molecularly imprinted polymer (MIP) as biomimetic antibody represents a cost-effective and robust alternative in immunoassays. •The as-constructed MIP-ECL immunosensor displays high sensitivity, excellent specificity, selectivity and stability. [ABSTRACT FROM AUTHOR]

Heart-type fatty acid binding protein (H-FABP) has been regarded as a promising biomarker for early diagnosis of acute myocardial infarction (AMI). Developing fast and reliable method for H-FABP detection is still highly desirable but challenging. Herein, an ascorbic acid (AA)-mediated organic photoelectrochemical transistor (OPECT) sensing strategy was reported for the detection of H-FABP in phosphate buffer saline (PBS) solution and human serum. A primary antibody/H-FABP/secondary antibody-Au NPs-alkaline phosphatase (ALP) sandwich immunorecognition structure was constructed. The modified ALP could catalytically convert ascorbic acid-2-phosphate to AA, which was then analyzed by OPECT. As a result, the AA-mediated OPECT sensing strategy realized highly sensitive detection of H-FABP with a detection limit of 3.23 × 10−14 g/mL which is two orders of magnitude lower than that of PEC method. Under optimal experimental conditions, H-FABP concentration could be obtained in ∼90 min. Importantly, the analysis of H-FABP was resistant to the interference from immunoglobulin G, bovine serum albumin, cysteine, AA and human serum. The proposed AA-mediated OPECT sensing strategy provides a simple, fast, and accurate way for H-FABP detection in AMI suspected patients. • Ascorbic acid-mediated OPECT sensing strategy was developed. • Selective and rapid detection of H-FABP was realized. • Enhanced sensitivity compared with traditional PEC technique. • Sensing mechanism of proposed strategy was demonstrated. [ABSTRACT FROM AUTHOR]

• Inspiratory muscle strength predicts post-acute myocardial infarction pneumonia. • Inspiratory muscle strength testing should be safe in current selected patients. • Inspiratory muscle training may prevent post-acute myocardial infarction pneumonia. Inspiratory muscle strength is associated with pneumonia in patients after surgery or those with subacute stroke. However, inspiratory muscle strength in patients with acute myocardial infarction (AMI) has not been studied. To evaluate the predictive value of inspiratory muscle strength for pneumonia in patients with AMI. Patients with AMI were consecutively enrolled from March 2019 to September 2019. Measurements of maximal inspiratory pressure (MIP) were used to estimate inspiratory muscle strength and mostly were taken within 24 hr after culprit-vessel revascularization. Patients were divided into 3 groups by MIP tertile (T1: < 56.1 cm H 2 O, n = 88; T2: 56.1–84.9 cm H 2 O, n = 88; T3: > 84.9 cm H 2 O, n = 89). The primary endpoint was in-hospital pneumonia. Among 265 enrolled patients, pneumonia developed in 26 (10%). The rates of pneumonia were decreased from MIP T1 to T3 (T1: 17%, T2: 10%, T3: 2%, P = 0.004). In-hospital all-cause mortality and major adverse cardiovascular events (MACEs) did not differ between groups. Multivariate logistic regression confirmed increased MIP associated with reduced risk of pneumonia (odds ratio 0.78, 95% confidence interval 0.65–0.94, P = 0.008). Receiver operating characteristic curve analysis indicated that MIP had good performance for predicting in-hospital pneumonia, with an area under the curve of 0.72 (95% confidence interval 0.64–0.81, P < 0.001). The risk of pneumonia but not in-hospital mortality and MACEs was increased in AMI patients with inspiratory muscle weakness. Future study focused on training inspiratory muscle may be helpful. [ABSTRACT FROM AUTHOR]

B cells and immunoglobulins are implicated in the pathogenesis of chronic diseases, including coronary artery disease (CAD). However, it remains elusive how the humoral immunity is incriminated in the disease progression of CAD. Using serum samples of chronic coronary syndrome (CCS) and acute myocardial infarction (AMI), we conducted a quantitative profiling of the proteomic landscape recognized by immunoglobulins, which we term immunoglobulin-associated proteome (IgAP). Intriguingly, CCS and AMI patients displayed distinctive IgAP profiles that enriched proteins in the pathways of blood coagulation regulation and lipoprotein transport, suggesting that CCS-AMI transition involves changes of these pathways that are associated with immunoglobulins. Furthermore, we identified immunoglobulin-bound coagulation factor X (F10) as a potential biomarker and validated it with an independent cohort of CCS, AMI and healthy individuals. Our study indicates that IgAP proteins may serve as novel diagnostic biomarkers for CCS and AMI. Our work it demonstrates a clear implication of immunoglobulin-associated proteome (IgAP), the proteomic landscape recognized by immunoglobulins, in the pathogenesis of CAD. In addition, it reports for the first time that immunoglobulin-bound F10 is implicated in CAD. [Display omitted] • Analysis of immunoglobulin-associated proteome (IgAP) using 20 μL of serum samples • Distinct IgAP between acute Myocardial Infarction (AMI) and Chronic Coronary Syndromes (CCS) patients • Enrichment of blood coagulation regulation and lipoprotein transport processes with differential AMI-CCS IgAP proteins • A progressive increase of immunoglobulin-bound coagulation factor X (F10) in healthy, CCS and AMI individuals [ABSTRACT FROM AUTHOR]

The objective of this study was to evaluate the association between frailty, evaluated by the Clinical Frailty Scale (CFS) and FRAIL scale, and C-terminal agrin fragment (CAF) levels with 3-month mortality following ST-segment elevation myocardial infarction (STEMI). This was a prospective observational study that included patients over the age of 18 years with STEMI admitted to the coronary intensive care unit. Within 48 h of admission, the CFS and FRAIL scale were applied and blood samples collected for serum CAF evaluation. Patients were followed for 3 months after hospital discharge, and mortality was recorded. One hundred and eleven patients were included; mean age was 62.3 ± 12.4 years, 61.3% were male and 11.7% died during the 3 months of follow-up. According to the CFS, 79.3% of the patients were classified as not frail, 12.6% as pre-frail and 8.1% as frail. According to the FRAIL scale, 31.5% of the patients were classified as not frail, 53.2% as pre-frail and 15.3% as frail. In univariate analysis, the CFS but not FRAIL scale was associated with mortality. In multiple logistic regression analysis, pre-frail/frail according to CFS (odds ratio [OR]: 6.118; CI 95%: 1.344–27.848; p = 0.019) and CAF levels (OR: 0.943; CI 95%: 0.896–0.992; p = 0.024) were associated with increased 3-month mortality. In a sub-analysis of 53 patients ≥65 years, CFS and CAF levels were associated with 3-month mortality. In conclusion, CAF levels and frailty determined by the CFS were associated with 3-month mortality after STEMI in the general and older population. • The relationship of C-terminal agrin fragment (CAF) with outcomes after myocardial infarction (STEMI) was not yet evaluated. • CAF levels were not associated with frailty evaluated by Clinical Frailty Scale (CFS) and FRAIL scale. • CAF levels and frailty were associated with 3-month mortality after STEMI in the general and older population. [ABSTRACT FROM AUTHOR]