Markers Of Myocardial Necrosis Research Articles

Anesthetic management of a patient with Takotsubo syndrome undergoing hip fracture repair

Introduction: Takotsubo syndrome (TTS) is a type of acute reversible left ventricular dysfunction in the form of acute catecholaminergic myocardial stunning in the absence of occlusive coronary artery, with considerable patient morbidity and mortality1. The optimal anesthetic management of patients with TTS remains unclear. We would like to share our experience with a patient with TTS presenting for hip fracture repair. Methods: An 80-year old female complained of dyspnea and retrosternal chest pain after subcapital hip fracture. Her diagnostic workup revealed elevated markers of myocardial necrosis and pathologic findings from transthoracic echocardiogram. Left ventriculography imaging along with an unremarkable coronariography was suggestive of TTS. After the initial control of acute myocardial crisis, the patient was scheduled for hip fracture repair, under spinal anesthesia. Having obtained patient’s informed consent, we performed an ultrasound guided fascia iliaca compartment block (FICB) (30 mL ropivacaine 0.5%/8 mg dexamethasone). Twenty minutes after the FICB, the patient was placed in the lateral decubitus position and 3 mL levobupivacaine 0.5% were injected intrathecally. A bolus dose of dexmedetomidine 1 mcg/kg followed by a continuous intravenous infusion at a rate of 0.5 mcg/kg/hour was initiated 10 min before lumbar puncture. The infusion was reduced to 0.25 mcg/kg/hour 30 min later due to a drop in systolic blood pressure 40% below baseline, until the end of surgery. Results: No complications occurred in the postoperative period. The patient walked on the second day and one week later she was discharged from hospital. Conclusion: To our knowledge, there are no reports of intraoperative dexmetomidine administration in TTS patients. Avoidance of adrenergic agonists and initiation of antiadrenergic therapy is suggestive by the pathogenesis of the syndrome [1]. Our main goal was the control of stress response [2, 3], performing FICB to facilitate perioperative analgesia and administering dexmetomidine, an agent with sedative, anxiolytic and analgesic properties.

Left Internal Mammary Artery Skeletonization Reduces Bleeding—A Randomized Controlled Trial

The objective of this study was to compare the impact of skeletonized versus pedicled left internal mammary artery (LIMA) harvesting on bleeding after coronary artery bypass grafting (CABG). In a randomized, single-blinded trial with a parallel group design and equal allocation, we randomly assigned 62 patients undergoing primary elective CABG in a tertiary cardiac center to skeletonized or pedicled LIMA dissection. Before surgery, all aspects of coagulation were assessed. Patients were blinded to LIMA dissection technique and monitored for cumulative drainage at 12 hours (primary outcome) as well as myocardial necrosis markers. With recruitment complete, there were 31 patients in each group; all patients were analyzed. Median postoperative drainage was 395 mL at 12 hours in all patients; it was lower by 28% at 12 hours (P= .02) in patients with skeletonized LIMA (Cohen's d, 0.6; 95% confidence interval (CI), 0.09-1.11). Patients with a LIMA pedicle received more fresh-frozen plasma transfusions than did the skeletonized LIMA group (Median 3; interquartile range 3-5 versus median 3; interquartile range 3-3; P= .03). Study arms did not differ in blood coagulation. Left internal mammary artery skeletonization (odds ratio= 0.04; 95% CI, 0.003-0.44; P= .009) and higher body mass index (odds ratio= 0.63; 95% CI, 0.45-0.89; P= .008) decreased the odds of being in the top drainage quartile at 12 hours (≥550 mL). Creatine kinase was lower in skeletonized LIMA directly after surgery (median 218 U/L; interquartile range 175-310 U/L versus median 424 U/L; interquartile range 256-510 U/L; P < .001), at 6 hours (median 324 U/L; interquartile range 239-424 U/L versus median 529 U/L; interquartile range 374-707 U/L; P < .001), and 12 hours after surgery (median 351 U/L; interquartile range 277-552 U/L versus median 695 U/L; interquartile range 509-1067 U/L; P < .001). Left internal mammary artery skeletonization results in lower mediastinal drainage after CABG than pedicled LIMA harvesting.

MYOCARDIAL INFARCTION DIAGNOSIS AND CARDIAC TROPONINS

Acute myocardial infarction is a condition that develops due to the blockage of blood flow to the heart. Serial electrocardiog- raphy follow-up should be performed in patients with suspected acute myocardial infarction, serum cardiac troponin levels should be measured, and this measurement should be repeated at regular intervals. Cardiac troponins are the main markers for the diagnosis of acute myocardial infarction, as they are sensitive and specific biochemical markers of myocardial cell necrosis. Elevated levels of cardiac troponins indicate cardiac damage, but it does not explain the cause of the damage. Increases in cardiac troponin levels can be observed in many different disease states and do not necessarily indicate acute myocardial infarction. It is necessary to check cardiac troponin levels in a patient admitted to the hospital in order to exclude other diseases before establishing the diagnosis of myocardial infarction. The one-hour “rule-in” and “rule-out” algorithms are used in the tests per- formed on patients who come to the emergency department with non-ST elevation myocardial infarction. In addition, there are point-of-care cardiac troponin tests that can be used in emergency services and ambulances. However, while using point-of-care cardiac troponin tests for the diagnosis of myocardial infarction, it should be kept in mind that these tests are less sensitive and more costly than tests performed in central laboratories

Infusion therapy in treatment of patients with acute coronary syndrome

Objective. Introduction to the basic therapy of patients with acute coronary syndrome (ACS) without ST-segment elevation cardioprotective drug Tivorel (“Yuria-Pharm”) based on L-arginine and L-carnitine.&#x0D; Materials and methods. The present study was carried out in accordance with the requirements for clinical trials of drugs in the Department of Emergency Cardiology of the RSCEMPSF. Patients were admitted to the intensive care unit with a diagnosis of ACS without ST-segment elevation in the first 12 h after the onset of the disease. The study was carried out in two groups and included the following stages: screening and treatment period (10 days). The study involved 90 patients with ACS without ST segment elevation, who were allocated for treatment in the study and control groups in a 1:1 ratio. Patients of the study group, except for basic therapy (sublingual nitroglycerin, acetylsalicylic acid or clopidogrel, analgesics, β-adrenergic blockers or angiotensin-converting enzyme inhibitors), received the drug Tivorel 100 ml intravenously at a rate of 10 drops per minute for the first 10-15 min (then the rate of administration could be increased to 30 drops per minute) 1 time per day within 10 days. Control group patients were prescribed only basic therapy. Determination of markers of myocardial necrosis (troponin T), electrocardiography (ECG), echocardiography. Compulsory calculation of end-diastolic and end-systolic indices, left ventricular ejection fraction were performed.&#x0D; Results and discussion. It was found that the drug Tivorel, prescribed as part of complex therapy immediately after admission of patients to the hospital, improves the electrophysiological properties of the myocardium and prevents the appearance of temporary ECG disturbances, stabilizes the condition of patients. In patients of the main group, already in the first day after the development of acute myocardial infarction (AMI), late ventricular potentials were less often recorded, markers of the so-called arrhythmogenic substrate – 9.5 % compared to 18.7 % in patients in the control group. In the course of further observation, the prostate gland in the control group disappeared, and during treatment with Tivorel, it did not appear anymore. This suggests the presence of a pronounced anti-ischemic effect of the drug, which is also confirmed by clinical data. We have noted a reliably expressed positive dynamics of changes in the end part of the ventricular complex under the influence of therapy with Tivorel. Analysis of standard ECG and 24-hour monitoring data in a number of patients revealed rhythm disturbances. There were no significant differences between the groups in the frequency of occurrence of all manifestations of arrhythmic syndrome, both initially and after therapy, however, in the main group, during treatment, the number of cases of ventricular arrhythmias in the form of group ventricular extrasystole and ventricular tachycardia bursts significantly decreased. During the period of inpatient treatment, all patients showed positive clinical dynamics: a decrease in the frequency and severity of angina attacks, a decrease and stabilization of blood pressure, an increase in exercise tolerance. Already on the third day of treatment with the use of the study drug Tivorel, relapses of anginal pain occurred less frequently (21.9 % of cases in the main group and 33.0 % in the control group). At the same time, there was a decrease in the need for the use of nitroglycerin and narcotic analgesics in order to relieve recurrent pain syndrome (23.1 % and 35.3 % of cases, respectively). In addition, on the third day after the development of AMI in patients of the main compared with the control, a lower incidence of atrioventricular blockade was recorded (4.3 % and 13.6 %, respectively). In the course of the analysis of the entire hospital period, it was found that in patients receiving Tivorel, atrioventricular blockades occurred almost 3 times less often than in the control group. The frequency of registration of ventricular extrasystole decreased on the 7th (34.1 %) and 10th days (45.7 %) of the disease.&#x0D; Conclusions. The use of the drug Tivorel (“Yuria-Pharm”) in addition to basic therapy helps to optimize the management of ACS patients without ST-segment elevation. With complex treatment with the use of the drug Tivorel, a faster regression of clinical manifestations of ACS is observed. The use of Tivorel in ACS therapy without ST-segment elevation stabilizes the patient’s condition and reduces the incidence of complications.

Relation of hs-CRP and Glycogen phosphorylase BB in Acute Myocardial Infarction Patients

Background: Inflammation has important role in the pathophysiology of atherosclerosis and acute myocardial infraction and hs-CRP is an inflammatory marker. GPBB is a marker of myocardial necrosis or myocardial ischmia i.e. the initial phase of AMI. The aim of this study was to know the levels of GPB and the relation between hs-CRP and GPBB in AMI patients. Materials & methods: This study was conducted in the Cardiology of J.A. Hospital and Department of biochemistry, G.R. Medical College, Gwalior. Patients were admitted with severe chest pain out of which 100 were included in this study. 50 normal healthy individuals were also selected. Blood samples were collected at the admission time for the analysis of hs-CRP and GPBB. All patients underwent thorough clinical examination and investigations. Estimation of GPBB and hs-CRP were done by ELISA method and other routine parameters done by enzymatic method. Results: The mean level of GPBB in patients was 46.92ng/mL while in controls it was 13.88ng/mL. The mean level of hs-CRP in patients was 4.38mg/L while in controls it was 1.34mg/L. There was highly significant difference of GPBB and hs-CRP in control group and AMI group. The finding of results showed that hs-CRP and GPBB was positively correlated. The levels of FBG, Triglyceride, Cholesterol, LDL, and VLDL were significantly increased and HDL was decreased in AMI group when compare controls. Conclusion: Our results demonstrate that there was positive correlation of hs-CRP and GPBB in AMI patients. So along with GPBB, hs-CRP is also additional marker of myocardial ischemia and AMI.

Evaluation of profilin 1 as a biomarker in myocardial infarction.

Profilin 1 (Pfn1) is likely to be involved in atherogenesis and myocardial infarction (MI). Clinical data on this subject are very limited. The aim of this study was to search for associations between serum Pfn1 and a number of parameters in MI patients: symptom onset to PCI time (OPT), myocardial necrosis markers, thrombolysis in myocardial infarction (TIMI) flow, antiplatelet drugs, heparin administration and typical atherosclerosis risk factors. We included patients with type 1 MI (according to the Third Universal Definition of Myocardial Infarction) who were able to precisely determine the time of symptom onset. Exclusion criteria involved conditions potentially altering platelet function. We screened 114 patients and included 65. We assessed serum Pfn1 in three time points: on admission (Pfn1_0), 24 hours post PCI (Pfn1_24) and 48 hours post PCI (Pfn1_48) and correlated it with OPT, cardiac necrosis markers (troponin T, CK, CKMB), TIMI flow in the infarct-related artery, pre-hospital P2Y12-antagonist and heparin administration and known atherosclerosis risk factors. Patients with a shorter OPT had higher Pfn1_0 (838.5 vs. 687.1 pg/ml, p=0.007). Patients with impaired coronary flow post PCI had lower Pfn1_24 (748.2 vs. 925.2 pg/ml, p=0.017) and Pfn1_48 (744.5 vs. 879.8, p=0.031. Pfn1_24 and Pfn1_48 were lower in patients who received a P2Y12 antagonist prior to hospital admission. Diabetic patients presented with lower Pfn1_0 concentrations. This is the first study assessing Pfn1 in type 1 MI patients in relation to the chosen parameters. Pfn1 may be a biochemical tool to objectify information on OPT in MI patients. We found an association between Pfn1 and post-PCI TIMI flow, antiplatelet drug administration and diabetes mellitus.

Clinical factors affecting left ventricular end-diastolic pressure in patients with acute ST-segment elevation myocardial infarction.

An association between left ventricular end-diastolic pressure (LVEDP) and outcomes of ischemic heart diseases has been reported. The present study aimed to investigate the LVEDP patterns and the effecting factors in patients with acute ST-segment elevation myocardial infarction (STEMI). A total of 515 STEMI patients receiving immediate percutaneous coronary intervention (PCI) were divided into two groups according to their LVEDP before left ventricular angiography: LVEDP of 15 mmHg or less (group A, n=145) and LVEDP above 15 mmHg (group B, n=370). Blood samples were collected before and within 24 hours after PCI, and an ultrasonic cardiogram was conducted to measure left ventricular ejection fraction (EF%) and to evaluate ventricular structure changes. The narrowness of each artery was measured with coronary angiography. In comparison with group A, patients in group B had a more infarction-related artery (IRA) descending branch and regional wall motion abnormality, a larger left atrial end-diastolic diameter (LAEDd) and a left ventricular end-diastolic diameter (LVEDd), a smaller EF%, a higher level of myocardial necrosis markers, and a higher heart failure rate. Furthermore, LVEDP level was found to be positively correlated with Gensini score, LAEDd, LVEDd, N-terminal pro b-type natriuretic peptide, troponin T, uric acid, creatine kinase (CK), CK myocardial band, low-density lipoprotein cholesterol and fasting blood glucose, and negatively correlated with glomerular filtration rate and EF%. LVEDP elevation has a higher incidence of heart failure and a higher risk of death, which is associated with the criminal blood vessels.

Coronavirus Disease 2019 and the Myocardium.

ResumoA infecção pelo coronavírus denominada COVID-19 promoveu crescente interesse de cardiologistas, emergencistas, intensivistas e pesquisadores, pelo estudo do acometimento miocárdico partindo de diferentes formas clínicas decorrentes de desmodulação imunoinflamatória e neuro-humoral.O acometimento miocárdico pode ser mínimo e apenas identificado a partir de alterações eletrocardiográficas, principalmente por aumento de troponinas cardíacas, ou no outro lado do espectro pelas formas de miocardite fulminante e síndrome de takotsubo.A descrição de provável miocardite aguda tem sido comumente apoiada pela observação da troponina elevada em associação com disfunção. A clássica definição de miocardite, respaldada pela biópsia endomiocárdica de infiltrado inflamatório é rara, e foi observada em um único relato de caso até o momento, não se identificando o vírus no interior dos cardiomiócitos.Assim, o fenômeno que se tem documentado é de injúria miocárdica aguda, sendo obrigatório afastar doença coronária obstrutiva a partir da elevação de marcadores de necrose miocárdica, associada ou não à disfunção ventricular, provavelmente associada à tempestade de citoquinas e outros fatores que podem sinergicamente promover lesão miocárdica, tais como hiperativação simpática, hipoxemia, hipotensão arterial e fenômenos trombóticos microvasculares.Fenômenos inflamatórios sistêmicos e miocárdicos após infecção viral estão bem documentados, podendo evoluir para remodelamento cardíaco e disfunção miocárdica. Portanto, será importante a cardiovigilância desses indivíduos para monitorar o desenvolvimento do fenótipo de miocardiopatia dilatada.A presente revisão apresenta os principais achados etiofisiopatológicos, descrição da taxonomia desses tipos de acometimento cardíaco e sua correlação com as principais formas clínicas do componente miocárdico presente nos pacientes na fase aguda de COVID-19.

SUN-913 A MEN-2a Syndrome Index Case Presenting with Adrenergic Crisis and Cardiogenic Shock Due to Bilateral Pheochromocytoma

Background: MEN-2A syndrome is commonly asymptomatic at diagnosis. Withal, pheochromocytoma presenting as cardiogenic shock is a recognized but exceptional occurrence. Case: A healthy 26-year-old female presented to the emergency department with precordial discomfort, headache and shortness of breath, starting that morning. She had a gum corrective surgery in the day before, was medicated with ibuprofen, pantoprazole and amoxicillin/clavulanic acid, and had previous history of migraine and smoking. Her blood pressure was high, and she had pulmonary edema and respiratory failure. ECG: sinus tachycardia, left axis deviation, and negative T wave in aVL. Analytically: leukocytosis, elevated myocardial necrosis markers (troponin I 1.29 ng/mL, normal < 0 ng/mL), and hyperlactacidemia. Transthoracic echocardiogram: severe left ventricular dysfunction, akinesia of the basal mid segments of all walls; image of thickening immediately above the aortic valvular plane. CT angiography: bilateral adrenal masses (9.2x9.2x10.8 cm on the right; 2.3x2.8x3.3 cm on the left), suggestive of pheochromocytoma. Cardiogenic shock led to patient transfer to our hospital for ECMO, in which she was maintained for 14 days. Pheochromocytoma was confirmed (normetanephrine 15689 µg/24h [normal < 390 µg/24h], metanephrine 15000 [normal < 320 µg/24h]) and adrenergic blockade initiated. Hospitalization complications and surgical risk delayed bilateral adrenalectomy to 1 month after admission. She initiated glucocorticoid and mineralocorticoid replacement, was transferred to the ward stable, and started a rehabilitation program before hospital discharge. Phosphocalcic metabolism was normal (PTH 38.7 pg/mL, normal 10–65 pg/mL). High calcitonin levels (87 pg/mL, normal <5 pg/mL) lead to the diagnosis of medullary thyroid carcinoma, followed by total thyroidectomy. MIBG showed “No foci of radiopharmaceutical overaptation related to norepinephrine transporter overexpression lesions.”, and genetic study revealed heterozygous variant c.1900T>C [p. (Cys634Arg)] in exon 11 of the RET gene, confirming suspicion of MEN-2A syndrome. As there was no family history of endocrine neoplasias, she was referred to genetic counselling for evaluation of family members. She maintains follow-up, currently treated with hydrocortisone 7.5 + 5 + 2.5 mg od, fludrocortisone 0.1 mg od, and levothyroxine 137 mcg, with improvement of functional capacity and general state (weight gain of 13 kg), recovery of left ventricular function, normal urinary metanephrines, and calcitonin < 2.0 pg/mL. Conclusions: To our knowledge, MEN-2A syndrome presenting with cardiogenic shock due to pheochromocytoma was not yet described. Knowledge of unusual presentations of rare syndromes is important to arise suspicion and improve differential diagnosis in life-threatening conditions as cardiogenic shock.

Hypotheses, rationale, design, and methods for prognostic evaluation of a randomized comparison between patients with coronary artery disease associated with ischemic cardiomyopathy who undergo medical or surgical treatment: MASS-VI (HF)

BackgroundIschemic cardiomyopathy and severe left ventricular dysfunction are well established to represent the main determinants of poor survival and premature death compared with preserved ventricular function. However, the role of myocardial revascularization as a therapeutic alternative is not known to improve the long-term prognosis in this group of patients. This study will investigate whether myocardial revascularization contributes to a better prognosis for patients compared with those treated with drugs alone and followed over the long term.MethodsThe study will include 600 patients with coronary artery disease associated with ischemic cardiomyopathy. The surgical or drug therapy option will be randomized, and the events considered for analysis will be all-cause mortality, nonfatal infarction, unstable angina requiring additional revascularization, and stroke. The events will be analyzed according to the intent-to-treat principle. Patients with multivessel coronary disease and left ventricular ejection fraction measurements of less than 35% will be included. In addition, myocardial ischemia will be documented by myocardial scintigraphy. Markers of myocardial necrosis will be checked at admission and after the procedure.DiscussionThe role of myocardial revascularization (CABG) in the treatment of patients with coronary artery disease and heart failure is not clearly established. The surgical option of revascularizing the myocardium is a procedure designed to reduce the load of myocardial hibernation in patients with heart failure caused by coronary artery disease. On the other hand, the assessment of myocardial viability is frequently used to identify patients with left ventricular ischemic dysfunction in which CABG may add survival benefit. However, the effectiveness of this option is uncertain. The great difficulty in establishing the efficacy of surgical intervention is based on the understanding of viability without ischemia. Thus, this study will include only patients with viable and truly ischemic myocardium to correct this anomaly.Trial registrationEvaluation of a randomized comparison between patients with coronary artery disease associated with ischemic cardiomyopathy submitted to medical or surgical treatment: MASS-VI (HF), ISRCTN77449548, Oct 10th, 2019 (retrospectively registered).

MicroRNA-331 and microRNA-151-3p as biomarkers in patients with ST-segment elevation myocardial infarction

We sought to analyse plasma levels of peripheral blood microRNAs (miRs) as biomarkers of ST-segment-elevation myocardial infarction (STEMI) due to type-1 myocardial infarction as a model situation of vulnerable plaque (VP) rupture. Samples of 20 patients with STEMI were compared both with a group of patients without angina pectoris in whom coronary angiogram did not reveal coronary atherosclerotic disease (no coronary atherosclerosis-NCA) and a group of patients with stable angina pectoris and at least one significant coronary artery stenosis (stable coronary artery disease-SCAD). This study design allowed us to identify miRs deregulated in the setting of acute coronary artery occlusion due to VP rupture. Based on an initial large scale miR assay screening, we selected a total of 12 miRs (three study miRs and nine controls) that were tested in the study. Two of the study miRs (miR-331 and miR-151-3p) significantly distinguished STEMI patients from the control groups, while ROC analysis confirmed their suitability as biomarkers. Importantly, this was observed in patients presenting early with STEMI, even before the markers of myocardial necrosis (cardiac troponin I, miR-208 and miR-499) were elevated, which suggests that the origin of miR-331 and miR-151-3p might be in the VP. In conclusion, the study provides two novel biomarkers observed in STEMI, which may be associated with plaque rupture.

CLINICAL CASE OF ACUTE MYOCARDIAL INFARCTION IN PATIENTS WITH MICROVASCULAR ANGINA

Purpose. To describe a clinical case of coronary burden without stenosing lesions of the main branches of the coronary arteries in a patient with microvascular angina with subsequent development of myocardial infarction with the formation of ischemic hypokinesis of the anterior-apical region of the left ventricle in the absence of elevated levels of serum markers of myocardial necrosis.Materials and methods. The study is based on a single clinical case. The object of the study is the patient in whom there were complaints of pressing pain localized behind the sternum and radiating to the left arm, accompanied by a mixed shortness of breath that occurred at rest, poorly stoped short-range nitrates and narcotic analgesics, sharp General weakness. Under primary inspection state of ailing average extent of gravity, consciousness clear, position active, skin integuments and visible mucous of clean, conventional painting. The patient was evaluated laboratory parameters, ECG, echo-cardiography (ECHO-kg), chest x-ray (OGK), coronary angiography (CAG), followed by transfer to the emergency Department of cardiology.Results. The conducted clinical and laboratory study revealed the presence of leukocytosis in the patient with the clinic of acute coronary syndrome, without increasing cardiospecific enzymes (CFC, CFC-MB, troponin test), as well as high activity of coagulogram indicators (fibrinogen, ACTV, rfmc). When conducting radiography of OGK in direct projection-congestive lungs, a picture of chronic bronchitis in combination with left ventricular myocardial hypertrophy.Conclusion. In the presented clinical case was described an example of development of microvascular lesions in coronary arteries in a patient with manifestation of acute coronary syndrome with severe prolonged chest pain and repolarization changes on ECG and without elevated levels of serum markers of myocardial necrosis, which probably leads to the definition of this state as fragile (or sharp) microvascular dysfunction with myocardial infarction.

КРУПНООЧАГОВЫЙ ИНФАРКТ МИОКАРДА И ОСТРОЕ ИШЕМИЧЕСКОЕ ПОВРЕЖДЕНИЕ ПОЧЕК

The aim of the study was to investigate specific clinical manifestations, homeostasis indices and parameters of the cardiovascular system in patients with acute ST-elevation myocardial infarction (STEMI) and acute ischemic kidney injury. Methods. 173 patients with STEMI participated in the study. The study group consisted of 111 patients with acute ischemic kidney injury associated with myocardial infarction (MI); 62 patients with MI and normal kidney function were enrolled in the comparison group. Clinical, anthropometric, laboratory, and instrumental diagnostic methods were used. Results. Compared with patients of the MI and normal kidney function group, those with MI and acute ischemic kidney injury had a higher average heart rate, required more prolonged vasopressor and/or inotropic therapy, and more frequently developed tachyarrhythmias with adverse prognostic impact and postinfarction aneurysms. The study revealed that patients of the MI and acute ischemic kidney injury group demonstrated more severe dilatation of the left ventricle (LV), more pronounced reduction in myocardial LV contractility according to echocardiography results; they developed multivessel coronary artery disease more frequently. Furthermore, patients of this group had a higher incidence of infarction-associated artery damage located in the proximal segments of major coronary arteries and more frequently developed thrombotic occlusion in the infarction-affected artery. Patients with MI and acute ischemic kidney injury had higher levels of inflammatory, myocardial necrosis, hemostasis and neurohormonal activation markers. Higher concentration of neutrophil gelatinase-associated lipocalin (uNGAL) was observed in patients with MI and acute ischemic kidney injury; moreover, in 14,1% of patients belonging to this group, elevated levels of this marker preceded the diagnostically significant increase in creatinine concentration and decrease in glomerular filtration rate. Conclusion. In patients with MI, the development of acute ischemic kidney injury was accompanied by more severe clinical manifestations, prognostically adverse indicators of early LV remodeling and coronary arteries disease, enhanced inflammatory processes and neuroendocrine system activity, as well as by elevated levels of myocardial necrosis and blood coagulation activity markers. The present study suggests applying uNGAL as an early marker of acute ischemic kidney injury in patients with MI.

P1769 Levels of serum markers of myocardial injury in patients with ST-elevation myocardial infarction correlate with global left ventricular longitudinal deformation

Abstract The aim of this study was to assess the correlation of levels of serum markers of myocardial injury with parameters of myocardial function assessed by 2D-speckle tracking echocardiography in patients with ST-elevation myocardial infarction (STEMI) Material and methods. The study group comprised 96 patients (69 male, mean age 58 ± 10 years) with first STEMI treated with successful primary percutaneous coronary intervention. Levels of serum markers of myocardial injury (troponin T and CKMB mass) were assessed on admission and then monitored during the hospitalization. 7-12 days after STEMI, all patients underwent resting 2D echocardiography with subsequent offline analysis using 2D speckle tracking algorithm. Measurements of left ventricular deformation included peak systolic longitudinal and transverse strain (SLS and STS) – maximal value before aortic valve closure, peak longitudinal and transverse strain (PLS and PTS) – including possible postsystolic contraction, systolic longitudinal and transverse strain rate (SLSR and STSR) at baseline. Results On admission median values (I – III quartile) of CKMB mass and troponin T were 20,0 ng/ml (6,3 – 59,0; range 1,9 – 475,3) and 0,25 ng/ml (0,06 – 1,04; range 0,01 – 11,2), respectively. Maximal values (I – III quartile) of CKMB mass and troponin T were 94,1 (28,0 – 215,7; range 3,2 – 500) and 3,29 (1,6 – 6,3; range 0,42 – 17,2), respectively. Statistically significant correlations were observed for the global values of the longitudinal strain parameters and the concentration of troponin T and CKMB mass (rs from 0.22 to 0.36). The strongest correlations were noted for the maximum serum level of troponin T. Among the best strain parameters was the global systolic longitudinal deflection (SLS). There was no statistically significant correlation between the parameters of transverse deformation and the concentrations of markers for myocardial necrosis. Conclusions Troponin T correlates with global left ventricular longitudinal deformation in patients with ST-elevation myocardial infarction.

Problems of differential diagnosis of acute coronary syndrome at prehospital stage in patients without ST segment elevation (literature review)

The article discusses the issues of prehospital diagnosis of acute coronary syndrome without ST segment elevation. A large number of errors that worsen the outcomes of the disease and the difficulties associated with the overload in patients with suspected acute coronary syndrome in emergency departments are indicated. The experience and prospects of studying the prehospital use of markers of myocardial necrosis are evaluated.

Rationale for the ASSAIL-MI-trial: a randomised controlled trial designed to assess the effect of tocilizumab on myocardial salvage in patients with acute ST-elevation myocardial infarction (STEMI)

IntroductionInterleukin-6 (IL-6) may be involved in ischaemia-reperfusion injury and myocardial remodelling after myocardial infarction (MI). We have recently shown that IL-6 inhibition by tocilizumab attenuates systemic inflammation and troponin T-release...

OPERATIONALIZATION AND EARLY OUTCOMES OF A HIGH OBSERVATION CARDIAC UNIT FOR PATIENTS WITH LOWER GRACE RISK SCORES

Patients hospitalized with myocardial infarctions (MI) have been historically admitted to cardiovascular intensive care units (CICU); but, advances in coronary revascularization, pharmacotherapy, and high sensitivity markers for myocardial necrosis have contributed to a temporal reduction in MI morbidity and mortality. The GRACE score can accurately stratify the risk for in-hospital mortality in patients with MIs and studies have reported that 15-20% of admissions to the CICU have low-risk GRACE scores. Our previous retrospective work has reported no in-hospital deaths among patients with a GRACE score < 120 admitted to the CICU, yet little is known about the safety or potential cost savings of routinely triaging low risk ACS patients to a non-CICU environment. In a prospective case series after the opening in October, 2018 of a 4 bed high observation cardiac unit (HOC) with telemetry and a 4:1 nursing ratio at the Foothills Medical Centre, we followed patients admitted to the HOC through to hospital discharge. HOC admission criteria were a low-risk non-ST segment elevation MI (NSTEMI) or revascularized ST-segment elevation myocardial infarction (STEMI), defined as a GRACE score ≤ 120 or deemed clinically appropriate HOC admission by most responsible physician. Exclusion criteria included hemodynamic instability, ejection fraction < 40%, failed reperfusion, additional critical coronary stenoses of major vessels or complications related to percutaneous revascularization. The clinical outcomes of interest included in-hospital cardiac arrest, in-hospital mortality, and CICU admission. The economic outcome of interest was estimated cost savings. A total of 100 patients including 35 patients with STEMI and 65 with NSTEMI were admitted to the HOC. The mean GRACE score was 121 overall, 135 in STEMI patients and 114 in NSTEMI patients. The total HOC length of stay was 75 days in patients with STEMI and 194 days in patients with NSTEMI, respectively (Figure 1). There were no cardiac arrests and no in hospital deaths. A total of 2 patients were re-admitted to the CICU (Figure 1). Estimated CICU costs were $6,936/day and ward costs were $1,978/day. The estimated costs savings per 100 day HOC occupancy over CICU were $1,333,702. In an index cohort of 100 patients with MI and low GRACE scores admitted to an HOC, we observed no cardiac arrests or in-hospital deaths and a large potential savings to the health care system. These findings support the routine admission of low-risk patients with MI to low-intensity hospital telemetry wards thereby reducing critical care capacity strain and hospital costs.

The Value of Troponin T Level Change During Chemoradiation in Esophageal Cancer Patients

Cardiac adverse events are common in esophageal cancer patients who received chemoradiation (CRT). However, reliable marker is lacking to predict these cardiac events. Troponin T (TnT) is a marker of myocardial necrosis, which is widely used in diagnosis of acute coronary syndromes. The relationship between TnT level change during CRT and cardiac injury is unknown. We hypothesized that the TnT level change during CRT is associated with acute cardiac adverse events and long-term survival outcomes. We retrospectively reviewed 113 esophageal cancer patients who received definitive or neoadjuvant CRT from 2010-2016. All patients consented on a prospective blood collection protocol where samples are drawn at baseline before, once during, at the end of CRT, and at each follow up timepoints. Irradiation dose parameters for the whole heart and each chamber were recorded from the treatment plan. TnT levels were quantified using the Elecsys® TnT-high sensitive assay (Roche Diagnostic). TnT level change was defined as CRT end level divided by baseline level. Logistic regression was used to evaluate the correlation between TnT change and acute cardiac adverse events. Kaplan-Meier method was used to compare survival outcomes in different TnT level change groups. The median TnT level gradually increased from baseline, to mid treatment course, and at the end of CRT: 6.27, 8.56, and 10.63 pg/ml, respectively. The median TnT level change was 1.48 (IQR, 1.12-2.01). For the whole heart, left ventricle (LV), right ventricle (RV), and right atrium (RA), the dose distribution was different between IMRT and proton: IMRT mainly contributed to low dose level (<30Gy), while in high dose regions (>40Gy), proton using passive scattering approach had significantly higher dose than IMRT. The TnT level change was strongly correlated to LV and RV dose percentage from V5 to V50 in proton patients (p<0.01), but not in IMRT patients. Male, lower BMI and lower tumor location were associated with higher TnT increase, while TnT level change could not predict acute cardiac adverse events during CRT or postoperative cardiac complications. There was no significant correlation of TnT levels and survival outcomes. There was significant correlation of TnT levels and cardiac dose distribution in proton patients that was not seen in IMRT patients. Whether TnT level alterations with treatment could correlate with late cardiac events specifically in proton patients requires longer term follow up.

Diagnostic re-classification and prognostic risk stratification of patients with acute chest pain.

Unstable angina and myocardial infarction are prevalent manifestations of acute coronary artery disease, combined in the term ‘acute coronary syndromes’. The introduction of sensitive markers for myocardial necrosis has led to confusion regarding the distinction between small myocardial infarctions and ‘true’ unstable angina, and the application of ever more sensitive markers has accelerated the pace at which patients with unstable angina are being re-classified to non-ST-segment elevation myocardial infarction. But in how many patients with acute chest pain is myocardial ischaemia really the cause of their symptoms? Numerous studies have shown that most have <5 ng/l high-sensitivity cardiac troponin, and that their prognosis is excellent (event rate <0.5% per year), incompatible with ‘impending infarction’. This marginalisation of patients with unstable angina pectoris should lead to the demise of this diagnosis. Without unstable angina, the usefulness of the term acute coronary syndromes may be questioned next. It is better to abandon the term altogether and revert to the original diagnosis of thrombus-related acute coronary artery disease, myocardial infarction. A national register should be the next logical step to monitor and guide the application of effective therapeutic measures and clinical outcomes in patients with myocardial infarction.

High admission glucose levels predict worse short-term clinical outcome in non-diabetic patients with acute myocardial infraction: a retrospective observational study

BackgroundPatients with acute myocardial infarction (AMI) often accompanied by admission hyperglycemia, which usually predicts a poor clinical outcomes for non-diabetes mellitus. Appropriate cut-point to identify high risk individuals in these patients remains controversial.MethodsOne thousand six hundred ninety-eight non-diabetes AMI patients in this retrospective study were divided into 3 groups according to admission glucose levels (euglycemia group≤140 mg/dL, moderate hyperglycemia group 141–179 mg/dL, severe hyperglycemia group≥180 mg/dL). The primary endpoint of this study was all-cause in-hospital mortality rate. In-hospital motality related risk factors was analyzed by multivariate binary logistic regression analyses.ResultsAll myocardial necrosis markers and Log NT-proBNP in severe hyperglycemia group were significantly higher than those in the other 2 groups. Logistic regression showed that independent predictors of the in-hospital mortality rate in non-diabetic patients with AMI were age (OR = 1.057, 95% CI 1.024–1.091, P < 0.001), logarithm of the N-terminal pro-brain natriuretic peptide (OR = 7.697, 95% CI 3.810–15.550, P < 0.001), insufficient myocardial reperfusion (OR = 7.654, 95% CI 2.109–27.779, P < 0.001), percutaneous coronary intervention (OR = 0.221, 95% CI 0.108–0.452, P < 0.001) and admission glucose (as categorical variable). Patients with moderate hyperglycemia (OR = 1.186, 95% CI 0.585–2.408, P = .636) and severe hyperglycemia (OR = 4.595, 95% CI 1.942–10.873, P = 0.001) had a higher all-cause in-hospital mortality rate compared with those with euglycemia after AMI in non-diabetic patients.ConclusionsThe all-cause in-hospital mortality risk increases remarkably as admission glucose levels elevated in non-diabetic patients with AMI, especially in patients with admission glucose levels ≥180 mg/dL. Severe admission hyperglycemia could be regarded as prospective high-risk marker for non-diabetic AMI patients.