Markers Of Myocardial Necrosis Research Articles

Defining a reference population to determine the 99th percentile of a contemporary sensitive cardiac troponin I assay

BackgroundDiagnosis of acute myocardial infarction (AMI) according to the universal definition is based on ischemic symptoms, imaging findings and elevated myocardial necrosis markers, preferably cardiac troponin I/T with diagnostic threshold representing the 99th percentile of a reference population. It is not clearly defined if this should be an unselected population-based or a healthy cohort with respect to cardiac diseases. Aim of the current study was to describe the distribution of troponin I using a sensitive assay and to evaluate the impact of cardiac diseases and cardiovascular risk factors in apparently healthy individuals. MethodsTroponin I was determined using a contemporary sensitive assay (TnI Ultra, Siemens) with 10% coefficient of variation (0.03ng/mL) below the published 99th percentile (0.04ng/mL) in 5000 participants (49.2% female) of the Gutenberg Health Study, a community-based, prospective, observational single-center cohort study. The calculated 99th percentile cut-offs were tested in 1818 patients with suspected AMI. ResultsTroponin I concentration representing the 99th percentile of the overall study population was 0.04ng/mL. Excluding individuals with prevalent cardiovascular disease lowers the 99th percentile to 0.034ng/mL. Exclusion of individuals with traditional risk factors or elevated natriuretic peptide leads to further reduction with 0.029/0.028ng/mL. These lower cut-offs detect more patients at risk in individuals with suspected AMI. Correlations of troponin I with age, gender and traditional risk factors were observed. ConclusionsTroponin I concentrations in apparently healthy individuals are dependent on prevalent cardiovascular diseases, traditional risk factors, gender and age. Application of corresponding cut-offs in diagnosis of AMI alters the group of patients potentially at risk.

Early cardiac changes following anthracycline chemotherapy in breast cancer: a prospective multi-centre study using advanced cardiac imaging and biochemical markers

Summary This prospective study is designed to identify novel ima- ging (utilizing cardiovascular magnetic resonance and advance echocardiography) and biochemical markers to detect early, sub-clinical cardiotoxicity following chemotherapy. Background Cardiac toxicity is an important long term side effect of anthracyline chemotherapy. We hypothesized that novel cardiovascular magnetic resonance (CMR) and echocar- diographic markers of myocardial function, oedema, and necrosis can detect early, subclinical cardiac toxicity in patients receiving anthracycline therapy for breast cancer. recovery fast-spin echo sequence (short-TI inversion recovery) was used in 3 short-axis views of the left ven- tricle. For assessment of myocardial oedema, the ratio of mean signal intensity (SI) of the myocardium was com- pared to that of skeletal muscle. Results In the study patients, the mean CMR LV end-systolic volume index (LVESVI) increased from baseline of 17.8 ± 6.2 to 20.3 ± 5.9 mL/m2 (p 1.9 as specified by Lake Louis criteria) in one or more short axis slices post chemotherapy. There was no new late gadolinium hyperenhancement to suggest focal myocar- dial necrosis/fibrosis in any patient following therapy.

Is remote ischaemic preconditioning of benefit to patients undergoing cardiac surgery?

A best evidence topic in cardiac surgery was written according to a structured protocol. The question addressed was whether remote ischaemic preconditioning (RIPC) is of benefit to patients undergoing cardiac surgery. Altogether, more than 264 papers were found using the reported search, 16 of which represented the best evidence to answer the clinical question. The authors, journal, date and country of publication, patient group studied, study type, relevant outcomes and results of these papers are tabulated. We conclude that RIPC is a safe protocol which could potentially be used in cardiac surgery to provide additional cardiac protection against ischaemia reperfusion injury, although it may not be appropriate for patients on K(+) ATPase channel blockers (sulphonylureas) as they seem to eliminate the effect of RIPC. In our study, we found two meta-analyses of cardiac surgery with or without RIPC. Both unequivocally showed 0.81 and 0.74 standardized mean reduction in myocardial necrosis markers in patients receiving RIPC and cardiac or vascular surgery. No difference in perioperative myocardial infarction incidence or 30-day mortality were found. In adult cardiac surgery, we found 11 randomized control trials (RCTs) ranging in size from 45 to 162 patients. Two representative studies reported no difference in postoperative cardiac troponin I concentration in RIPC vs. controls. In one of the studies (CABG ± RIPC) no additional benefit could have been observed for RIPC regarding intra-aortic balloon pump usage (controls 8.5 vs. RIPC 7.5%), inotropic support (39 vs. 50%) or vasoconstrictor usage (66 vs. 64%). On the other hand, in the other study [CABG ± AVR (aortic valve replacement) ± RIPC] significant reduction of troponin I at 8 h postoperatively (controls, 2.90 µg/l vs. RIPC, 2.54 µg/l, P = 0.043) was shown. Marked reduction in cardiac necrosis markers was also found in several smaller RCTs concerning coronary artery bypass grafting (CABG) patients receiving RIPC preoperatively: with cold crystalloid cardioplegia (44.5% reduction), with cross-clamping and fibrillation (43% reduction) and with cold blood cardioplegia (42.4% reduction). The proof of concept trials summarized here give some early evidence that RIPC may potentially provide some reduction in myocardial injury. If confirmed, in future clinical studies this technique may one day lead to a method to reduce reperfusion injury in clinical practice.

Biomarkers in Acute Myocardial Infarction

Acute coronary syndrome (ACS) is a significant cause of morbidity and mortality worldwide. Patients can be stratified by symptoms, risk factors and electrocardiogram results but cardiac biomarkers also have a prime role both diagnostically and prognostically. The proper diagnosis of ACS requires reliable and accurate biomarker assays to detect evidence of myocardial necrosis. Currently, troponin is the gold standard biomarker for myocardial injury and is used commonly in conjunction with creatine kinase-MB (CK-MB) and myoglobin to enable a more rapid diagnosis of ACS. Other markers of myocardial necrosis, inflammation and neurohormonal activity have also been shown to have either diagnostic or prognostic utility, but none have been shown to be superior to troponin. The measurement of multiple biomarkers and the use of point of care markers may accelerate current diagnostic protocols for the assessment of such patients

MASP-2 activation is involved in ischemia-related necrotic myocardial injury in humans

Background/objectivesInsufficient blood supply to the heart results in ischemic injury manifested clinically as myocardial infarction (MI). Following ischemia, inflammation is provoked and related to the clinical outcomes. A recent basic science study indicates that complement factor MASP-2 plays an important role in animal models of ischemia/reperfusion injury. We investigated the role of MASP-2 in human acute myocardial ischemia in two clinical settings: (1) Acute MI, and (2) Open heart surgery. MethodsA total of 187 human subjects were enrolled in this study, including 50 healthy individuals, 27 patients who were diagnosed of coronary artery disease (CAD) but without acute MI, 29 patients with acute MI referred for coronary angiography, and 81 cardiac surgery patients with surgically-induced global heart ischemia. Circulating MASP-2 levels were measured by ELISA. ResultsMASP-2 levels in the peripheral circulation were significantly reduced in MI patients compared with those of healthy individuals or of CAD patients without acute MI. The hypothesis that MASP-2 was activated during acute myocardial ischemia was evaluated in cardiac patients undergoing surgically-induced global heart ischemia. MASP-2 was found to be significantly reduced in the coronary circulation of such patients, and the reduction of MASP-2 levels correlated independently with the increase of the myocardial necrosis marker, cardiac troponin I. ConclusionsThese results indicate an involvement of MASP-2 in ischemia-related necrotic myocardial injury in humans.

Nível de NT-proBNP em pacientes com síndrome coronariana aguda sem supradesnivelamento do segmento ST

Non-ST-segment elevation acute coronary syndrome is associated with elevation of brain natriuretic peptide and markers of myocardial necrosis, although its relationship with the TIMI score and left ventricular function are largely unknown. To evaluate the correlation between plasma N-terminal pro-brain natriuretic peptide (NT-proBNP) and markers of myocardial necrosis [creatine phosphokinase muscle-brain fraction (CK-MB) and troponin I], TIMI risk score and left ventricular ejection fraction in patients with non-ST-segment elevation acute coronary syndrome. Eighty-seven patients with non-ST-segment elevation acute coronary syndrome were divided into two groups: 37 (42.5%) with unstable angina and 50 (57.5%) with non-ST-segment elevation myocardial infarction. Left ventricular ejection fraction more than 40% was found in 86.2% of the total sample. Serum levels of NT-proBNP was higher in patients with non-ST elevation myocardial infarction than in those with unstable angina (p<0.001). Increased levels of NT-proBNP were associated with increases in troponin I (rs=0.425, p<0.001), peak CK-MB (rs=0.458, p<0.001) and low left ventricular ejection fraction (rs=-0.345, p=0.002); no correlation was found with the TIMI risk score (rs=0.082, p=0.44). Multivariate analysis revealed that left ventricular ejection fraction and troponin I levels were independently correlated with NT-proBNP levels (p=0.017 and p=0.002, respectively). Increased levels of NT-proBNP in patients with non-ST-segment elevation acute coronary syndrome are not related exclusively to low left ventricular ejection fraction, but can also be caused by the presence of myocardial ischemia and necrosis.

Overtures to Takotsubo's Cardiomyopathy

A cohort of 12 cases of reported TCM andCR was identified and compared to a group without rup-ture selected by random sampling. Rupture was confirmedon autopsy in 5 patients, suspected by catheterization in2 patients,andsuggestedbyechocardiographyin5patients.MorepatientswithCRhadSTelevationinleadIIandwereallolder females (76±9 years). Also, systolic blood pressure,double product, and peak creatine kinase were significantlyhigher in the CR group compared to controls. However,the difference in troponin I was not statistically significant.Furthermore, the use of β-blockers was less frequent in theCR group. These features of rupture in TCM are similarto those known to occur with rupture following myocardialinfarction (MI).TCM tends to have a clinical presentation similar toan acute MI, with substernal chest pain and dyspnea andmild elevation of markers of myocardial necrosis. The diag-nosis will ultimately depend on demonstrating the lackof occlusive coronary lesions with matching wall motionabnormalities.

Heart type fatty acid binding protein in relation to pharmacologic scintigraphy in coronary artery disease

Heart-type fatty acid-binding protein (H-FABP) is a marker of myocardial necrosis, but whether it increases during myocardial ischemia is not known. This study investigated whether serum levels of H-FABP change during adenosine stress testing and nuclear imaging in patients with stable coronary artery disease. Thirty stable patients with established coronary artery disease on their medications were studied. Sampling was performed before the stress test, at the end of adenosine infusion, as well as 1, 2 and 3 h after the completion of the infusion. No difference in H-FABP serum levels were found at the five pre-specified time points in the overall group (p=0.99); furthermore, there was no significant difference regardless of the test result--positive (p=1) or negative (p=0.98). It is concluded that H-FABP does not change significantly during pharmacologic stress testing in patients with known coronary artery disease and there is no difference whether there is inducible ischemia or not.

A CASE OF TAKOTSUBO SYNDROME

Takotsubo syndrome, first reported by Satoh et al in 1990, is a reversible cardiomyopathy frequently precipitated by a stressful event with a clinical presentation that mimics an acute coronary syndrome (1). The syndrome was initially reported in the Japanese literature but in recent years it has also been reported in North American and European populations (2).The clinical presentation is similar to that of acute myocar-dial infarction in the absence of any obstructive epicardial coronary artery lesion. This type of left ventricular dysfunction is characterized by preserved basal function, moderate-to-severe dysfunction in the mid-ventricle, and apical akinesis (3).We report a case of that syndrome presented to our emer -gency department in July 2007 with a history of central chest pain after a stressful event.The patient was a 66-year-old-woman with a family his-tory of cardiovascular disease. Remote pathological anamne-sis highlighted a history of depression-anxiety syndrome, gastro-oesophageal reflux disease and dyspeptic disorders.She was referred to our emergency department on July 2007, 2 hours and 30 minutes after the onset of chest pain. The patient underwent two stressful events (2 family mem-bers of the patient had passed away recently).At admission blood pressure was 110/60 mmHg, ECG revealed sinus rhythm, ST elevation of approximately 2 mm from V4 to V6 and the second ECG showed T wave inversion and QTc at the upper limits of reference, myocardial necrosis markers were elevated (peak serum mass CK-MB was 4,35 ng/mL, and the peak level of troponin T was 4,35 ng/mL). Transthoracic echocardiography revealed akinesis of theapex and distal segment of the left anterior wall, pre -served systolic function with ejection fraction of 65%, normal diameters and parietal thickness. Emergency cardiac catheterization was performed and showed normal coronary arteries; left ventriculography revealed apical dyskinesia (Figure 1).4 days later a cardio-MRI was performed. It revealed apex dyskinesia and hypokinesis of the distal segments of the anterior, inferior and lateral wall and ipokinesis of the inter-ventricular septum in the distal segment. After gadolinium-DTPA injection, no late hyperenhancement was observed (Figure 2). On discharge she remained asymptomatic. She was dismissed on medical therapy with ramipril, ASA, spironolac-tone, omeprazol.Serial ECGs and echocardiograms performed after dis-charge showed that the ECG and left ventricular contraction gradually returned to normal over a 12-week period.Follow-up MRI was performed after 3 months. It revealed no ventricular wall motion abnormalities, no myocardial per-fusion defects or late hyperenhancement.Takotsubo cardiomyopathy is an increasingly recognized diagnosis. Its clinical presentation mimics the presentation of acute ST elevation myocardial infarction without con-comitant epicardial coronary artery disease. Despite the ini-tial dramatic presentation of this disease the prognosis is quite favourable. Takotsubo cardiomyopathy could be more common than previously thought and although under-reported it is an important diagnosis to make, with an excellent prognosis.

Volatile Agents for Cardiac Protection in Noncardiac Surgery: A Randomized Controlled Study

Volatile anesthetics reduce the risk of myocardial infarction and mortality in coronary artery surgery. Recently, the American College of Cardiology/American Heart Association Guidelines suggested the use of volatile anesthetic agents for the maintenance of general anesthesia during noncardiac surgery in patients at risk for perioperative myocardial ischemia, but no randomized experience to document the cardioprotective effects of these agents exists in this setting. Therefore, the authors performed a prospective, randomized, controlled trial to compare the effects of sevoflurane versus total intravenous anesthesia, in terms of postoperative cardiac troponin I release in patients undergoing noncardiac surgery. A randomized, controlled trial. A teaching hospital. Eighty-eight consecutive patients undergoing noncardiac surgery. Patients were allocated randomly to receive either volatile anesthetic (44 patients) as the main anesthetic agent or total intravenous anesthesia (TIVA) (44 patients). Postoperative cardiac troponin I release was measured as a marker of myocardial necrosis. Patients with detectable postoperative troponin I in the sevoflurane group (12/44, 27.3%) were similar to those in the propofol group (9/44, 20.5%; p = 0.6). There was no significant reduction of postoperative median peak cTnI release (0.16 ± 0.71 ng/mL in the sevoflurane group compared with the TIVA group, 0.03 ± 0.08 ng/mL; p = 0.4). Three patients died at the 1-year follow-up for noncardiac causes (2 in the TIVA group). In the authors' experience, patients undergoing noncardiac surgery did not benefit from anesthesia based on halogenated anesthetics. Further studies are necessary to evaluate the cardioprotective effects of volatile agents in noncardiac surgery.

Estudio de los niveles de ligando CD40 en pacientes con síndrome coronario agudo

Introduction The CD40 ligand (CD40L) is a member of the tumor necrosis factor superfamily and plays an important role in the regulation of thymus-dependent humoral immunity and cell-mediated immune responses. This ligand is a 39 kDa, 261 amino acid (aa) glycoprotein that can form either homotrimers or undergo proteolytic cleavage to produce soluble forms of CD40 (i.e. 15-18 KDa). Elevated levels of soluble CD40L (sCD40L) have been observed in the sera of patients with systemic lupus erythematosus, chronic lymphocytic leukemia and unstable angina. Enhanced levels of both soluble and membrane-bound CD40L in angina patients suggest that CD40L plays a pathogenic role in the atherosclerotic process and in promoting acute coronary syndromes (ACS). Material and methods We analyzed serum sCD40L levels in 56 patients with ACS (aged 54.4 ± 13.4 years) from the internal medicine department of our hospital compared with levels in 22 healthy controls (aged 43 ± 8 years). To measure sCD40 we used the Quantikine CD40 ligand immunoassay, a solid-phase ELISA designed to measure human CD40 in serum using E. coli-expressed recombinant human CD40. For comparison purposes, troponin T data was measured in patients with ACS. These data were obtained by a chemiluminescent method using the Elecsys 2100 Roche Diagnostics analyzer. Results Mean values of CD40L were significantly higher in healthy controls (546.7 ± 64.7 pg/mL) than in ACS patients: 1,048 ± 157 pg/mL (p < 0.05). The comparison study between troponin T and CD40L generated the following regression equation: Troponin T = 1.48 * CD40L - 0.004. Discussion The proinflammatory and procoagulant protein CD40L represents a novel target in the treatment of atherosclerosis and ACS. Currently, risk evaluation in patients with ACS can be carried out by troponin analysis. Although troponins are only markers of myocardial necrosis, sCD40L is a marker of platelet activation and unstable plaques and can thus be used to identify disease activity before the development of cardiac cell necrosis.

Circulation : Clinical Summaries

<i>Circulation</i> : Clinical Summaries

Heart-type fatty acid binding protein in elective cardioversion of atrial fibrillation

Objectives We sought to investigate whether heart-type fatty acid binding protein (H-FABP), a new marker of myocardial necrosis, increases in relation to elective cardioversion of atrial fibrillation (AF). Methods We studied 25 consecutive patients (61 ± 16 years old, 21 men) admitted to our hospital for elective cardioversion of AF. Peripheral venous samples were drawn immediately before cardioversion, one hour and 24 h after the procedure and assayed for H-FABP. Results A mean of 309 ± 183 J was used for cardioversion. Successful cardioversion in sinus rhythm was achieved in 18 patients (72%). Serum levels of H-FABP did not change significantly either in relation to the procedure [1385 (256–17,127) pg/mL at baseline, 1125 (290–15,238) pg/mL 1 h post and 1045.5 (66–2981) pg/mL 24 h post cardioversion, p = 0.37] or to the success of the procedure. Conclusion H-FABP does not significantly change following elective cardioversion for AF and we, therefore, speculate that myocardial necrosis does not occur during cardioversion.

Impact of perfusion restoration at epicardial and tissue levels on markers of myocardial necrosis and clinical outcome of patients with acute myocardial infarction

To assess the impact of reperfusion after primary percutaneous coronary intervention (PCI) on myocardial salvage and outcome of patients with acute ST-segment elevation myocardial infarction (STEMI). This study included 1,406 patients with STEMI undergoing primary PCI. Blood flow restoration at epicardial and tissue levels was assessed by Thrombolysis in Myocardial Infarction (TIMI) and myocardial perfusion grade (MPG). Patients had paired scintigraphic examinations before, and 7-14 days after intervention. Based on TIMI and MPG grades, patients were divided into three groups: patients with optimal epicardial/optimal tissue perfusion (TIMI=3/MPG=3; n=801), patients with optimal epicardial/suboptimal tissue reperfusion (TIMI=3/MPG ≤ 2; n=412) and patients with suboptimal epicardial/suboptimal tissue reperfusion (TIMI ≤ 2/MPG ≤ 2; n=193). In these groups, the median infarct size (25th-75th quartiles) in the 7-14 days scintigraphy was: 7.0% (1.0%-19.0%), 12.6% (5.0%-27.6%) and 18.7% (10.4%-33.7%) of the left ventricle (p<0.001); frequency of aborted myocardial infarction was: 15.5%, 10.0% and 4.7%, (p<0.001); estimates of 5-year mortality were: 7.8%, 16.0% and 20.1% (adjusted hazard ratio=0.43, 95% confidence interval 0.21-0.89; p=0.02 for optimal epicardial/optimal tissue vs suboptimal epicardial/suboptimal tissue reperfusion). In patients with STEMI undergoing primary PCI, restoration of blood flow at epicardial and tissue levels was associated with increased myocardial salvage and improved long-term survival.

Pre-Therapy With Statins in Percutaneous Coronary Interventions

Statins present a number of beneficial effects on endothelial function and atherosclerotic plaque, modulating oxidative stress and inflammation. The benefits of long-term statin treatment in the entire spectrum of atherosclerotic vascular disease can largely be explained by its cholesterol-lowering effects and the associated reduction of the progression of atherosclerosis. The short-term benefits of statins use are most likely due to their non-lipid, pleiotropic effects. Myocardial injury during percutaneous coronary intervention (PCI) occurs in 10-40% of cases and is often characterized by a slight increase in the markers of myocardial necrosis, sometimes without symptoms, electrocardiographic changes or impairment of cardiac function. Periprocedural myocardial infarction is associated with a worse outcome on long term follow-up. Several randomized trials have suggested a beneficial effect of pre-treatment with statins in the outcome of the procedure. Myocardial protection by statin pre-therapy in PCI has been studied in several trials published over the last decade. The mechanisms underlying the beneficial pleiotropic effects of statins may be an anti-inflammatory action reducing myocardial injury necrosis due to microembolization, an improvement in endothelial function on microcirculation, and direct myocardial protection. This article reviews the major randomized trials which have studied the use of statins as pre-treatment in PCI and explores future perspectives. Key words: statins, percutaneous coronary intervention, acute coronary syndromes

Scintigraphic Techniques for Early Detection of Cancer Treatment–Induced Cardiotoxicity

New antitumor agents have resulted in significant survival benefits for cancer patients. However, several agents may have serious cardiovascular side effects. Left ventricular ejection fraction measurement by (99m)Tc multigated radionuclide angiography is regarded as the gold standard to measure cardiotoxicity in adult patients. It identifies left ventricular dysfunction with high reproducibility and low interobserver variability. A decrease in left ventricular ejection fraction, however, is a relatively late manifestation of myocardial damage. Nuclear cardiologic techniques that visualize pathophysiologic processes at the tissue level could detect myocardial injury at an earlier stage. These techniques may give the opportunity for timely intervention to prevent further damage and could provide insights into the mechanisms and pathophysiology of cardiotoxicity caused by anticancer agents. This review provides an overview of past, current, and promising newly developed radiopharmaceuticals and describes the role and recent advances of scintigraphic techniques to measure cardiotoxicity. Both first-order functional imaging techniques (visualizing mechanical [pump] function), such as (99m)Tc multigated radionuclide angiography and (99m)Tc gated blood-pool SPECT, and third-order functional imaging techniques (visualizing pathophysiologic and neurophysiologic processes at the tissue level) are discussed. Third-order functional imaging techniques comprise (123)I-metaiodobenzylguanidine scintigraphy, which images the efferent sympathetic nervous innervations; sympathetic neuronal PET, with its wide range of tracers; (111)In-antimyosin, which is a specific marker for myocardial cell injury and necrosis; (99m)Tc-annexin V scintigraphy, which visualizes apoptosis and cell death; fatty-acid-use scintigraphy, which visualizes the storage of free fatty acids in the lipid pool of the cytosol (which can be impaired by cardiotoxic agents); and (111)In-trastuzumab imaging, to study trastuzumab targeting to the myocardium. To define the prognostic importance and clinical value of each of these functional imaging techniques, prospective clinical trials are warranted.

Role of ischemia-modified albumin in estimating the extent and scope of cardiac ischemia in patients with ST elevation myocardial infarction

Ischemia-modified albumin (IMA) is a laboratory biomarker of cardiac ischemia. Our study aims to determine whether IMA can estimate or represent to any degree the extent of myocardial ischemia. We expect that the higher the marker of cardiac necrosis (maximum value after serial measurements) the greater the preceding cardiac ischemia, indicated by IMA in patients diagnosed with STEMI prior to direct percutaneous coronary intervention (PCI). We studied 216 patients indicated for direct PCI with a diagnosis of ST elevation myocardial infarction. Biochemical analysis of IMA was carried out using the albumin cobalt binding (ACB®) test. We also obtained relevant values for markers of myocardial necrosis (CK, CK-MB, cTnT). In all patients, there was an increased level of IMA prior to the procedure (116 ± 16.9 kU/l); also raised were levels of CK (17.32 μkat/l), CK-MB (4.85 μkat/l) and cTnT (2.97 μg/l) taken as the maximum values obtained after serial measurements at 12, 18, and 24 h after the procedure. We observed that there was no significant association between increase in IMA and cTnT (R2 = 0.0068, p = 0.483). This was also the case for CK-MB (R2 = 0.0011, p = 0.637). IMA does not estimate the extent of ischemia in patients with ST elevation myocardial infarction. However, its absence can be used qualitatively to rule out cardiac ischemia.

An Oral Charcoal Adsorbent, AST-120, Reduces Renal Fibrosis as well as Cardiac Pro-fibrotic and Pro-inflammatory mRNA Expression Post-MI in the Rat

Background: The predictors of cardiotoxicity with current chemotherapy regimen of anthracyclines and trastuzumab in patients with breast cancer are unclear. We hypothesised that novel cardiovascular magnetic resonance (CMR) and echocardiographic markers of myocardial function, oedema, and necrosis can detect early, subclinical cardiac toxicity in such patients. Methods: Sixteen patients (four HER2 positive) recently diagnosed with breast cancer were examined with serial CMR (for LV function, myocardial oedema and necrosis), echocardiography (for global longitudinal strain (GLS)), pro brain natriuretic peptide (pro-BNP) and Troponin T measurements at baseline, one month, and three months following commencement of (anthracycline/trastuzumab or both) chemotherapy. Results: CMR left ventricular end-systolic volume 144 An Oral Charcoal Adsorbent, AST-120, Reduces Renal Fibrosis as well as Cardiac Pro-fibrotic and Proinflammatory mRNA Expression Post-MI in the Rat

CardioPulse Articles

Patients with an acute coronary syndrome (ACS) and ST-segment elevation (STEMI) benefit from immediate revascularization by percutaneous coronary intervention (PCI) or, if such is not readily available, from thrombolytic therapy. Furthermore, some of those without such electrocardiographic (ECG) findings benefit from early revascularization. Therefore, patients with a possible ACS should be assessed immediately to confirm the diagnosis, to initiate medical therapy, and to verify whether ECG findings and subsequent biochemical markers of myocardial necrosis (preferable troponin T or I) warrant invasive therapy. In order to provide a rapid response, different methods of working have been developed: pre-hospital diagnosis of STEMI, chest pain clinics, and fast track at the emergency unit. When an ambulance is called by the patient, his/her relatives or a physician, a complete 12-lead ECG should be taken to decide whether an ACS with ST elevation is present. This ECG may be interpreted by a physician if present on the ambulance, or by an onsite computer system, as was introduced in Rotterdam in the 1980s. Alternatively, the ECG may be transmitted to a hospital for interpretation by a physician. Patients with ST elevation can be immediately transferred to a hospital with PCI facilities or may receive immediate, pre-hospital thrombolytic therapy. A chest pain unit, adjacent to the general emergency unit, was introduced in Amsterdam in the 1980s. This principle was subsequently adopted by other hospitals in The Netherlands and abroad. Patients with chest pain and a possible ACS are assessed in this unit and can stay in the chest pain unit for a maximum of a few hours, until a final diagnosis is made, based on ECG, repeat troponin measurements, or other markers of myocardial injury or other investigations as appropriate. Once a diagnosis is confirmed, the patient is either admitted to the appropriate hospital ward or discharged. The chest pain unit is supervised by a cardiologist and managed by a cardiology resident. In many hospitals worldwide, patients are assessed at the general emergency unit in a hospital. In the emergency unit, a patient may be seen by an emergency physician, an internist, or a cardiologist. Several studies have shown that in patients with ACS, optimal treatment according to guidelines is best provided if a cardiologist is in charge. Nevertheless, other physicians can assume responsibility provided that they comply with the same guidelines, avoiding unnecessary delay of treatment in those patients with evolving myocardial infarction (STEMI). Such delay may be avoided when the nurses are instructed to record an ECG immediately upon arrival of the patient and call for attention if ST elevation or ST depression is apparent. It should be appreciated that patients with STEMI are a minority among those presenting with chest pain or similar symptoms. Accordingly, it is a challenge to differentiate those patients requiring immediate PCI from those with other diagnoses in whom, generally, a longer observation period is warranted. The protocol of the emergency department is crucial to guarantee optimal treatment of patients with chest pain. It should include registration of the admission diagnoses of all patients seen at the unit, with the time from entry to ECG recording and diagnosis. A regular review of such registry will help to optimize patient management.

Soluble Lectin-Like Oxidized Low-Density Lipoprotein Receptor-1 as an Early Biomarker for ST Elevation Myocardial Infarction - Time-Dependent Comparison With Other Biomarkers -

The diagnostic sensitivity of myocardial necrosis markers, such as creatine kinase-MB (CK-MB), cardiac troponins, myoglobin and heart-type fatty acid-binding protein (H-FABP) for the earliest stage of ST-elevation myocardial infarction (STEMI), remains insufficient. We compared a new biomarker of plaque vulnerability (soluble lectin-like oxidized low-density lipoprotein receptor-1, sLOX-1) with other biomarkers at the earliest stage of STEMI. Plasma sLOX-1 levels were measured in 125 STEMI, 44 non-STEMI (NSTEMI) and 125 non-acute myocardial infarction (non-AMI) patients and were significantly (P < 0.0001) higher in the STEMI and NSTEMI than in the non-AMI patients (median, 25th and 75th percentiles: 241.0, 132.3 and 472.2 vs. 147.3, 92.9 and 262.4 vs. 64.3, 54.4 and 84.3 pg/ml, respectively). At the optimal cut-off value of 91.0 pg/ml, sLOX-1 discriminated STEMI from non-AMI with 89.6% sensitivity and 82.4% specificity. Time-dependent changes in sLOX-1, H-FABP, myoglobin, troponin T and CK-MB were analyzed in 27 STEMI patients. Elevated plasma sLOX-1 levels persisted for 24h after admission, whereas other markers were not elevated at the time of admission and peaked at ≥ 2h thereafter. The diagnostic sensitivity of sLOX-1, H-FABP, myoglobin, troponin T and CK-MB for STEMI upon admission (89 min after onset) was 93%, 78%, 70%, 56% and 33%, respectively. Plasma sLOX-1 diagnosed the early stages of STEMI more accurately than H-FABP, myoglobin, troponin T and CK-MB.