Biochemical Markers Of Myocardial Damage Research Articles

Prognostic Value of Cardiac Troponin Release in Head Trauma Patients

Abstract Background Traumatic brain injury (TBI) is defined as damage to the brain sustained after the application of external physical force that causes temporary or permanent functional or structural damage to the brain. TBI stands as a major cause of death among youth in industrialized societies. Brain injury can be mild, moderate, and severe. Objective Myocardial dysfunction is frequently described as an underlying cause of mortality in traumatic brain injury (TBI) known as brain-cardiac link. The impact on prognosis of a disease remains uncertain. The present study aimed at investigating the correlation between serum cTnI levels as a biochemical marker of myocardial damage and morbidity, mortality of the patients with mild to moderate TBI. Patients and Methods This study was conducted to investigate the relationship between TBI and cTnI elevation, as well as the prognostic usefulness of this relationship and morbidity, mortality in patients with mild to moderate TBI. It has been claimed that there is a relationship between cardiac injury and mortality rate in TBI patients. Results In the present study, there was a non-significant relation between incidence of mortality and cause & type of injury among studied cases. This study revealed that there is significant relation between incidence of mortality and hospitalization characteristics (length of ICU stay, GCS, troponin level) among studied cases. However, there is a non-significant relation between incidence of mortality and length of hospital stay, AIS, GOS and troponin release. Results of binary logistic regression for prediction of mortality among studied cases were significant in GCS and troponin; however, were non-significant in length of ICU. Regarding validity of troponin in prediction of mortality among studied cases in the present study population, AUC of troponin was 0.912 (95% CI: 0.756-1.0) with cutoff point 0.265 (P < 0.001). Conclusion A non-significant relation was found between release of troponin and cause & type of injury among the studied cases. In addition, there was a non-significant relation between troponin level and mode & type of injury. Increased cTnI levels could be a predictor of mortality among patients with TBI.

Ранні маркери гострої доксорубіциніндукованої кардіотоксичності та механізми її розвитку

Arrhythmias and congestive heart failure, which pose the greatest risk of toxic cardiomyopathy, are the clinically limiting side effects of doxorubicin, the main highly active anticancer agent. The difficulty of early diagnosis of cardiomyopathy and timely detection of cardiac dysfunction associated with chemotherapy remains a significant medical problem. The aim of our study was to identify early signs of acute doxorubicin-induced cardiotoxicity in adult rats by assessing ECG changes and biochemical parameters. Acute cardiotoxicity was modelled by short-term intraperitoneal injection of doxorubicin at a total dose of 15 mg/kg. On the 5th day of the experiment, visual fluctuations of electrocardiogram (ECG) waveforms, duration and amplitude of the main teeth and intervals, as well as heart rate (HR) in the control and experimental groups of rats were studied to determine early ECG signs of cardiotoxicity. The most significant ECG changes were a doubling of the QT interval duration and significant ST-segment elevation in the rats of the experimental group. In experiments on isolated aortic rings, we demonstrated doxorubicin-induced disruption of both vascular relaxation and contraction mechanisms. The endothelium-dependent relaxation of vascular preparations of animals after administration of doxorubicin to acetylcholine (0.1 μmol/l) was 47% less than in the control group. The vascular ring contractions in rats under the influence of norepinephrine (10 μmol/l) were 59% lower than in control rats. After doxorubicin administration, oxidative stress developed against the background of cardiovascular disorders. Thus, the content of diene conjugates and malondialdehyde increased by 4 and 2.5 times, respectively. At the same time, in isolated cardiac mitochondria, the activity of inducible NO synthase increased 3.7-fold with a simultaneous significant 4.8-fold inhibition of constitutive NO synthase. An increase in the content of acute-phase biochemical parameters that are markers of damage, namely alanine aminotransferase (ALT), aspartate aminotransferase (AST) and creatine phosphokinase myocardial fraction (CPK MB) by 2.2, 1.4 and 1.5 times, respectively, was detected. Thus, the acute cardiotoxic effect of doxorubicin results in changes in the systolic-diastolic function of the left ventricle of the heart and its conduction, automaticity and contractility, as well as impaired relaxation and contraction of isolated preparations of the aorta against the background of increased activity of inducible and decreased constitutive NO synthesis, accompanied by oxidative stress and increased content of biochemical markers of myocardial damage.

MINOCA due to vasospasm compared to other mechanisms: patients characteristics, evolution and prognosis

Abstract Introduction coronary vasospasm is a common cause of MINOCA (myocardial infarction with non-obstructive coronary arteries). The aim of this study is to compare characteristics and prognosis of patients (pts) with MINOCA due to vasospasm (MINOCA-V) vs those with MINOCA due to other causes (MINOCA-O). Methods we included all MINOCA pts between January 2015-December 2022. The definitions of MINOCA and vasospasm were based on European Clinical Guidelines. The diagnosis of vasospasm was made in the cath lab or with non-invasive bedside tests (ergonovine). The follow-up analysis included major adverse cardiovascular events (MACE: death from any cause, cardiovascular readmission, reinfarction and stroke). The median follow-up was 59.5 months [36-75]. Results there were a total of 120 MINOCA pts, of which 19 (16%) were MINOCA-V and 101 (84%) MINOCA-O (embolism, dissection, type II infarction, unknown). Regarding the clinical profile of MINOCA-V, they were fewer women (21 vs 49% p=0.03), younger (mean age 56±11 vs 63±15 p=0.03) and more smokers (78.9 vs 50.5% p=0.02). There were no significant differences in cocaine use (7.7 vs 5.5% p=0.75) or other baseline characteristics (Table 1). Not only there was a higher percentage of pts with ST elevation at admission in the vasospasm group (53 vs 12% p<0.01), but also they presented with a higher elevation of biochemical markers of myocardial damage (MMD), both troponin (125.11±203.8 vs 609.48±1661.2 ng/L,p<0.01) and CK (201±272.4 vs 338.75±384.3 U/L p=0.01). There were no significant differences in renal function (Cr 1.4±1.8 vs 1.1±1.5mg/dL p=0.15) and cholesterol levels (163.05±48 vs 172.6±65.7mg/dL p=0.99). The use of magnetic resonance imaging to complete diagnosis did not differ between both groups (26vs37% p=0.34), although it was more effective when approaching the etiology in MINOCA-O (0 vs 18%, p=0.04). The duration of admission was similar between both groups (6±4 days in MINOCA-V vs 5±4 in MINOCA-O, p=0.78). The treatment at discharge was different, being greater the use of nitrates (53vs10% p<0.01) and calcium antagonists (CA), both not dyhidropyridines (53 vs 7% p<0.01) and dihydropyridines (53 vs23% p=0.01) in MINOCA-V and less that of beta-blockers (BB) (0 vs 62% p<0.01) and acetylsalicylic acid (ASA) (32vs73% p<0.01). During follow-up, the evolution was similar in terms of mortality (HR 1.81 IC95%[0.33-10] p=0.2) and MACE (HR 1.76 IC95%[0.69-4.51] p=0.17). No differences were found in cardiovascular readmissions (HR 1.04 IC95%[0.35-3.07] p=0.29), stroke (no cases in both groups) and reinfarction (HR 1.3 IC95%[0.25-6.81] p=0.57). Conclusion we conclude that pts with MINOCA-V are more likely to be male, younger and smokers than MINOCA-O. They usually present with ST elevation and increased elevation of MMD. Treatment at discharge is different: with greater use of nitrates and CA and lower ASA and BB. The prognosis is similar in both groups with no significant differences in mortality or MACE.

Quantitative assessment of myocardial blood flow by dynamic single photon emission computed tomography: relationship with ECG changes and biochemical markers of damage in patients with acute myocardial infarction

Aim: To study the relationship of microcirculatory changes in coronary bed and electrocardiographic and laboratory signs of damage to myocardium in patients with acute myocardial infarction (AMI).Methods. The observational study included patients with newly emerged AMI. Depending on the ECG changes, the patients were divided into two groups: 1) with ST segment elevation (n = 75) (STEMI) and 2) without ST segment elevation (n = 44) (NSTEMI). All patients underwent electrocardiography, analysis of biochemical markers of myocardial damage, dynamic single photon emission computed tomography (SPECT) and myocardial perfusion imaging.Results. The study included 119 patients (age 62.5 ± 10.4 years, 63% men). STEMI patients had heavier perfusion defects at rest, 5.00 (3.00;9.00) and 0.00 (0.00;1.00), and after pharmacological stress test, 7.00 (5.00;13.00) and 2.50 (0.00;5.00), also they had more reduced stress myocardial blood flow (MBF), 1.09 (0.83;1.59) and 1.67 (1.36;2.46) ml/min/g, flow difference (FD), 0.36 (0.01;0.72) and 1.14 (0.63;1.72) ml/min/g, and myocardial flow reserve (MFR), 1.78 (1.11;2.19) and 2.57 (2.13;3.31), according to compared to NSTEMI patients. Correlation analysis revealed significant relationships between stress MBF and CPK after 24 hours and 4 days: r = –0.34 and r = = –0.31, troponin I upon admission and after 24 hours – r = –0.4 and r = –0.3; MFR and FD and troponin I upon admission – r = –0.41 and r = –0.41.Conclusion. Quantitative parameters of myocardial perfusion determined by early dynamic myocardial SPECT are associated with electrocardiographic changes and biochemical markers of myocardial damage and allow an adequate assessment of the severity of the disease in patients with AMI.

Fabrication of Nanoformulation Containing Carvedilol and Silk Protein Sericin against Doxorubicin Induced Cardiac Damage in Rats.

Nanotechnology has emerged as an inspiring tool for the effective delivery of drugs to help treat Coronary heart disease (CHD) which represents the most prevalent reason for mortality and morbidity globally. The current study focuses on the assessment of the cardioprotective prospective ofanovel combination nanoformulation of sericin and carvedilol. Sericin is a silk protein obtained from Bombyx mori cocoon and carvedilol is a synthetic nonselective β-blocker. In this present study, preparation of chitosan nanoparticles was performed via ionic gelation method and were evaluated for cardioprotective activity in doxorubicin (Dox)-induced cardiotoxicity. Serum biochemical markers of myocardial damage play a substantial role in the analysis of cardiovascular ailments and their increased levels have been observed to be significantly decreased in treatment groups. Treatment groups showed a decline in the positivity frequency of the Troponin T test as well. The NTG (Nanoparticle Treated Group), CSG (Carvedilol Standard Group), and SSG (Sericin Standard Group) were revealed to have reduced lipid peroxide levels (Plasma and heart tissue) highly significantly at a level of p < 0.01 in comparison with the TCG (Toxic Control Group). Levels of antioxidants in the plasma and the cardiac tissue were also established to be within range of the treated groups in comparison to TCG. Mitochondrial enzymes in cardiac tissue were found to be elevated in treated groups. Lysosomal hydrolases accomplish a significant role in counteracting the inflammatory pathogenesis followed by disease infliction, as perceived in the TCG group. These enzyme levels in the cardiac tissue were significantly improved after treatment with the nanoformulation. Total collagen content in the cardiac tissue of the NTG, SSG, and CSG groups was established to be highly statistically significant at p < 0.001 as well as statistically significant at p < 0.01, respectively. Hence, the outcomes of this study suggest that the developed nanoparticle formulation is effective against doxorubicin-induced cardiotoxicity.

Кардіопротективний ефект інгаляційних анестетиків

На сьогодні є різниця між експериментальними даними на тваринах і клінічними результатами у пацієнтів кардіохірургічного і загальнохірургічного профілю. Протективна дія інгаляційних анестетиків ґрунтується на тих самих шляхах, що закладають основу захисту від ішемічного прекондиціонування. Наведено експериментальні дані щодо провідної ролі севофлурану й ізофлурану в активації мітохондріальних K+-каналів молекули аденозинтрифосфату аналогічно до того, що природним чином відбувається при ішемічному ураженні. Також в експерименті показано, що інгаляція севофлураном поліпшувала відновлення скоротливості міокарда до 67 % порівняно з 28 % у контрольній групі. Інший механізм кардіопротекції полягає у зміні активності мітохондріального переходу модуляції й активації цитокінів, що є ключовим внутрішньоклітинним сигнальним шляхом апоптозу. Наступний механізм кардіопротекції при використанні інгаляційних анестетиків — це зміна позаклітинного сигналу кіназ. Надано висновки клінічних досліджень щодо застосування інгаляційних анестетиків. Збереження мітохондріального споживання кисню вказує на кардіопротективний ефект внаслідок дії ізофлурану. Клінічні дослідження визначають, що сила стиснення шлуночків була значно поліпшена в групі севофлурану (з 53 до 85 %) і в групі десфлурану (з 53 до 86 %). Майбутні дослідження повинні оцінити найбільш оптимальний анестетик, його концентрацію та протокол для кращого кардіопротекторного ефекту.

FORENSIC-MEDICINE DETERMINATION OF ASPHICTIC STATE BY QUALITATIVE AND QUANTITATIVE INDICATORS OF TROPONIN I

The aim of the work was to determine the qualitative and quantitative content of the biochemical marker of myocardial damage (Troponin I) in the blood as a diagnostic criterion for asphyxia in cases of death from mechanical asphyxia. Material and methods of research. To determine the presence of an asphyxia, the indicators of the qualitative and quantitative content of Troponin I in the blood of 15 deceased were studied and analyzed, among which violent death was observed in 9 cases and non-violent in 6 cases. During the study, rapid tests were used for the qualitative detection of Troponin I; To determine the quantitative content of troponin I, we used a method based on enzyme-linked immunosorbent assay with subsequent statistical processing of the results using the MedStat package. Research results and their discussion. When conducting studies using express tests, the difference in the qualitative indicators of the biochemical marker Troponin I, depending on the causes and genesis of death: mechanical asphyxia, acute and chronic ischemic heart disease, was not found. Nevertheless, a difference was revealed in the quantitative indicators of the biochemical marker Troponin I, depending on the causes and genesis of death: mechanical asphyxia, acute and chronic ischemic heart disease at the significance level p = 0.008 (the average value of the quantitative content of Troponin I in the blood of deaths from mechanical ml ± 4.4 ng / ml; in the blood of those who died from acute and chronic ischemic heart disease 45.62 ng / ml ± 22.4 ng / ml). Conclusions. Thus, in the course of the studies, the inexpediency of determining the qualitative indicators of the biochemical marker Troponin I using express tests was proved and the expediency of using changes in the quantitative indicators of Troponin I to determine the asphyxia state in mechanical asphyxia and differential diagnosis of cases of violent death (mechanical asphyxia) was substantiated. death (acute and chronic ischemic heart disease), which makes it possible to increase the efficiency and reliability of forensic medical examinations.

Використання тропоніна І в якості біохімічного маркера для діагностики асфіктичного стану при механічній асфіксії

The purpose of the study was to determine the quantitative content of the biochemical marker of myocardial damage (subunits of the troponin complex: Troponin I) in the blood as a diagnostic criterion for asphyxia in mechanical asphyxia. Materials and methods. To determine the presence of asphyxia, the quantitative content of Troponin I in the blood of 12 dead people was studied and analyzed, among which violent death was observed in 7 cases and non-violent – in 5 cases. The study for biochemical detection of Troponin I used a method based on enzyme-linked immunosorbent assay followed by statistical processing of the results using the MedStat package. Results and discussion. Among the biochemical markers for the diagnosis of asphyxia in hanging and aspiration asphyxia, the most indicative is the determination of the quantitative content of Troponin I in the blood, which is also used in clinical practice to substantiate the diagnosis of cardiac pathology. Therefore, it is important to conduct a differential diagnosis of changes in quantitative indicators of biochemical markers depending on the cause and genesis of death. During the study of the quantitative content of Troponin I in the blood of those who died of mechanical asphyxia (hanging, aspiration asphyxia), it was found that the content of troponin I is from 140 ng/ml to 170 ng/ml. The quantitative content of Troponin I in the blood of those who died of acute and chronic coronary heart disease (control group) is from 10.1 ng/ml to 120 ng/ml. The average value of the quantitative content of Troponin I in two samples was found: in the blood of those who died of mechanical asphyxia – 156 ng/ml±4.4 ng/ml; in the blood of those who died of acute and chronic coronary heart disease – 45.62 ng/ml±22.4 ng/ml. The study revealed a difference in quantitative indicators of biochemical markers depending on the cause and genesis of death, found that the quantitative content of Troponin I in the blood of the dead from mechanical asphyxia (hanging, aspiration asphyxia) compared with the quantitative content of Troponin I in the blood of the dead with chronic coronary heart disease is higher, at the level of significance p=0.008. Conclusion. Thus, in the course of research, the feasibility of using changes in quantitative indicators of the biochemical marker Troponin I to determine the asphyxiation in violent death (mechanical asphyxia) and differential diagnosis in cases of non-violent death (acute and chronic coronary heart disease) was proved, which significantly increases efficiency and reliability of forensic medical examinations

Cardiotoxicity and multiorgan system failure caused by valproate poisoning

We report the case of severe valproate intoxication presenting as multiorgan failure. This is the first report to describe severe cardiac involvement, in which a 19-year-old woman developed atrial fibrillation, diffuse T wave inversion and QTc interval prolongation with elevated specific biochemical markers of myocardial damage. After 7 days of treatment, including supportive care, gastric lavage, activated charcoal, mannitol and hemodialysis, the patient recovered completely. After the poisoning there were no pathological echocardiographic changes and one month after discharge exercise stress testing did not provoke ischemia or arrhythmias.

The clinical significance of procedural myocardial infarction in stable ischemic heart disease patients and implications for interpretation of Ischemia trial a registry analysis

Abstract Background The definition, incidence, and clinical significance of procedural myocardial infarction (MI) remains controversial. Interpretations from landmark trials such as “Ischemia” was found to be sensitive to the definition of procedural MI used (1). Purpose Evaluation of the incidence of procedural MIs in our institution according to the standard definitions of Society of Cardiovascular Angiography &amp; Intervention (SCAI) (2), Fourth Universal Definition of Myocardial Infarction (UDMI) (3) and Ischemia trial (4) and whether they predicted major adverse cardiovascular events (MACE) to validate clinical relevance of these definitions. Moreover, the study also explored the possibility whether HS-troponin alone could predict MACE thereby simplifying the definition of procedural MIs in the context of its wide-spread availability and its role as a standard biochemical marker of myocardial damage. Methods We analysed ECGs, coronary angiograms and next day HS troponin-I results on consecutive patients who underwent elective percutaneous coronary intervention for stable Ischaemic Heart Disease during 2014–2018. Primary outcome was MACE including death, MI, stent thrombosis and need for repeat revascularisation within 12 months from index procedure. Results We treated 909 patients with a mean age of 67.5 years and 78.4% were males. The proportion of patients in our cohort that met the troponin-based definition of procedural MI based on the Ischemia trial, SCAI and 4th UDMI were 10.1%, 6.3% and 25.1%. Occurrence of procedural MI according to these standard definitions were not predictive of MACE at 1 year (8.1% v 8.7% p=0.8; 11.1% v 8.5% p=0.5; 10.2% v 8.1%, p=0.3) (Table 1). The one-year MACE rate in the entire cohort was 8.5%. MACE rates were steady at troponin I levels below 2000 ng/L after which was there was a significant increase in MACE rates to 13.2% at troponin &amp;gt;2500, 19.1% for troponin levels &amp;gt;5000 and 33.3% for troponin&amp;gt;10,000 ng/L. Conclusions Procedural MI according to the Ischemia Trial definition was not predictive of MACE at 1 year, whereas troponin elevations above 2000 ng/L were associated with higher incidence of MACE in our cohort. These findings have significant implications for the interpretation of the Ischemia Trial. Moreover, potential of HS-troponin I level as a stand-alone and clinically relevant criteria for procedural MIs may be explored. Funding Acknowledgement Type of funding sources: None.

Indications to coronary artery bypass graft angiography in the early postoperative period

Aim. To determine indications to emergency coronary artery bypass angiography.Methods. 7,616 medical records of patients with coronary artery disease who underwent isolated CABG in the period from 2012 to 2019 at the Federal Center for Cardiovascular Surgery were reviewed. Of them, 103 (1.35%) patients underwent emergency coronary artery bypass graft angiography in the early postoperative period to verify signs of myocardial damage. Patients were assigned to two groups based on angiographic findings and selected treatment strategy. Out of 75 patients, 57 patients from Group 1 had no severe angiographic signs of occlusive changes of the grafts and native arteries. But 18 patients reported failed graft and required conservative management. Group 2 (n = 28) included patients who had failed coronary artery bypass grafts according to angiography findings. 20 patients underwent endovascular treatment, and 8 patients underwent repeated surgery. The control group included 30 patients (0.39%) without any signs of ischemic myocardial damage. Intraoperative flow was assessed as well as postoperative electrocardiographic and echocardiographic records. Biochemical markers of myocardial damage were measured.Results. Blood flow velocity was less than 20 ml/min, and the pulsatility index exceeded 3.0 according to the intraoperative flow assessment of coronary artery bypass grafts with impaired blood flow according to angiography findings. There was no relationship found between ischemic changes according to ECG, ECHO-CG, and angiographic findings. Significant differences were found in troponin I levels between Group 1 (patients with coronary artery graft dysfunction) and the control group (Group 3) at all time intervals (1, 6, 12, 24 and 48 hours).Conclusion. The predictors of failed coronary artery bypass grafts in the early postoperative period allowed identifying indications to emergency angiography.

Aloin alleviates doxorubicin-induced cardiotoxicity in rats by abrogating oxidative stress and pro-inflammatory cytokines.

Aloin, an anthraquinone present in the aloe species, possesses antiangiogenic, chemopreventive and antioxidant properties. It exerts cytotoxicity against breast cancer and ovarian cancer cell lines. These properties of aloin project it as a chemopreventive adjuvant to anticancer chemotherapy. We evaluated the effect of concurrent oral administration of aloin against doxorubicin (DOX)-induced cardiotoxicity in rats. The protective effects of aloin against DOX-induced toxicity were evident as a statistically significant inhibition ofa rise in the biochemical markers of myocardial damage including lactate dehydrogenase (LDH), creatinine kinase-myocardial band (CK-MB), alanine aminotransferase (ALT), and aspartate aminotransferase (AST). Aloin dose dependently inhibited the DOX-induced changes in ECG like increased ST-height and prolonged QT interval. It protected heart against the lipid peroxidation and restored the levels of antioxidative defenses: reduced glutathione, catalase and superoxide dismutase. Aloin prominently reduced the levels of proinflammatory cytokines- TNF-α, IL-1β and IL-6. Notably, the significant protective effects of aloin were evident even atthe strikingly lower doses of 1 and 5mg/kg per day. Our results highlight the necessity to further investigate the chemopreventive effects of aloin against other chemotherapeutic agents.

D-dimer Düzeyi Koroner Arter Baypas Cerrahisinden Sonra İskemi/Reperfüzyon Hasarının Bir Bulgusudur

Introduction: Myocardial Ischaemia-Reperfusion (I-R) injury produces a spectrum of clinical cardiovascular outcomes after cardiac surgery. The pathogenesis of I-R injury is complex and involves the activation and amplification of several systemic and local proinflammatory pathways. The process of restoring blood flow to the ischaemic myocardium can induce injury and paradoxically reduce the beneficial effects of myocardial reperfusion. The objective of this study was to determine the correlation between cardiac markers such as the Mb fraction of the creatine kinase (CK-MB), troponin I (cTnI) and D-dimer levels as a marker of myocardial injury secondary to I-R injury after coronary artery bypass surgery. Patients and Methods: Herein, a prospective study was designed that included 50 consecutive coronary artery bypass grafting (CABG) patients. Pre and postoperative blood samples were taken due to study protocol and such markers as Mb fraction of the creatine kinase (CK-MB), troponin I (cTnI) and D-dimer were measured. Results: All three markers were significantly elevated in postoperative blood samples. The D-dimer level reached its peak at the first and another peak at 12th hour postoperatively. However, the peak serum values of CK-MB and cTnI occurred at 6th and 12th hour, respectively. Conclusion: We demonstrated that D-dimer levels as a marker of generated thrombin during reperfusion correlated with other well-known biochemical markers of myocardial damage in the postoperative period. In other words, D-dimer levels may stand as a marker of I-R-induced myocardial damage.

Biochemical markers of myocardium damage in children with cardiomyopathy.

The article presents the results of studies of 104 patients with cardiomyopathy hospitalized in the cardiorheumatological departments of the Republican Specialized Scientific and Practical Medical Center of Pediatrics in Tashkent and the Republican Children's Multidisciplinary Medical Center of the Republic of Karakalpakstan. An analysis of the results of the study showed that in children with cardiomyopathy there is an increase in the level of tissue (LDH, CPK) and cardiospecific (CPK-MB) enzymes, regardless of the region of residence and the form of the disease, which indicate myocardial dysfunction. Therefore, these enzymes can be regarded as highly specific biochemical markers of myocardial damage, and an increase in their activity can be used as criteria for the diagnosis of heart disease. Of the biochemical parameters, a reliable prognostic criterion for the development and outcome of cardiomyopathy is a progressive increase in the level of endothelin with increasing duration of the disease.

1273Efficacy and safety of prehabilitation before coronary artery bypass grafting

Abstract Purpose To evaluate the effectiveness and safety of high intensity prehabilitation included in the routine preoperative management of patients with coronary artery disease (CAD) for elective on-pump coronary artery bypass grafting (CABG). Methods 38 male patients with stable CAD referred to on-pump CABG who either underwent prehabilitation or not were assigned into two study groups. Group 1 patients (n=20, the mean age 61.5 years [55; 64] underwent high intensity treadmill exercises. Group 2 patients (n=18, the mean age 62.0 years [56; 65]) underwent routine preoperative management without prehabilitation. Treadmill exercises in Group 1 patients were performed under hemodynamic control and ECG monitoring. The training power of a workout was calculated based on cardiopulmonary exercise test (CPET) performed before preoperative exercises, and was estimated as 80% of the maximal power obtained during the exercise test. Adenosine loading single-photon emission computed tomography (SPECT) was used to measure the parameters of myocardial perfusion before preoperative exercises and on days 5–7 after CABG in both study groups. Biochemical markers of myocardial damage (troponin I, NT-proBNP) were measured before the training session, after it and then in the postoperative period to assess the safety of the prehabilitation program. In-hospital postoperative complications were recorded and analyzed. Results Both study groups were comparable in the main clinical and demographic parameters, intraoperative clinical parameters as well as in preoperative CPET and SPECT results. There were no cases of complications during prehabilitation. The analysis of myocardial perfusion parameters demonstrated that patients who had undergone prehabilitation had significantly higher accumulation of radiopharmaceuticals than those in the control group in basal segments (74.9±3.98% vs. 70.3±7.40% p=0.04), middle (86.7±5.24% vs. 79.6±10.43%, p=0.03) and apical (85.8±5.03% vs. 79.0±8,67%, p=0.02) myocardium. The stress-induced ischemia (SDS) was less pronounced in Group 1 compared to Group 2 (0 scores and 0.9±0.53 scores, respectively, p=0.04). Myocardial perfusion defect significantly decreased during the infusion of adenosine (SSS) (p=0.013), as well as the SDS index (p=0.018) in the prehabilitation group after CABG compared with the baseline. Both groups had similar serum troponin I levels within the normal range before and after CABG. NT-pro BNP levels significantly increased in the postoperative period in patients who did not undergo prehabilitation (p=0.003). Patients who underwent prehabilitation had a significantly lower incidence of the in-hospital postoperative complications compared to patients without exercise trainings (p=0.002). Conclusion The inclusion of high intensity preoperative exercises in the routine preoperative management of patients referred to elective CABG is safe and effective method of cardioprotection improving surgical outcomes.

The Zingiber officinale Roscoe Reduces Chest Pain on Patients Undergoing Coronary Angioplasty: A Clinical Trial

Introduction: Evidence from animal studies suggests that Zingiber officinale (ginger) may help prevent ischemia–reperfusion injury (IRI) in heart. The aim of the present study was to investigate the effect of ginger on inducing preconditioning on patients undergoing angioplasty. Methods: Thirty-four patients, referred for elective angioplasty, were randomly divided into the control (17 patients) and ginger groups (17 patients). Subjects in the experimental group were provided 250 mg ginger powder in Zintoma capsules per day for 10 days, whereas those in the control group received placebo. The patients underwent percutaneous transluminal coronary angioplasty (PTCA) (One 45-second balloon inflation and 2 minutes reperfusion). Chest pain scores were assessed immediately after angioplasty and cardiac injury biomarkers were assessed 12 hours later. Results: The average pain score during the balloon inflation in the ginger group was significantly lower than the control group (2.1±1 versus 3.8±1.5, P = 0.04). Troponin I was elevated in both groups after angioplasty, but there was not any significant difference between groups in this regard (P = 0.12 and 0.10, respectively). Conclusion: The use of ginger reduces chest pain during coronary angioplasty but its effect on the release of biochemical markers of myocardial damage is obscure.

Pharmacological screening of substances with cardioprotective effect in the group of 3-oxypyridine derivatives

Introduction: The search for new compounds with antihypoxic and cardioprotective effects among 3-oxypyridine derivatives is promising.&#x0D; Research objectives: To study the anti-hypoxic and cardioprotective effects of 3-oxypyridine derivatives.&#x0D; Materials and methods: The search for compounds with an antihypoxic effect was carried out on blood leukocytes of rats in in vitro. To simulate hypoxia, Oil for Tissue Culture (SAGE) was used, 500 µl of which was applied into wells over a growth medium in order to block gas exchange. The cardioprotective effect of 3-oxypyridine derivatives was studied in the model of coronary-occlusive myocardial infarction (30 minutes of ischemia, 90 minutes of reperfusion). The level of troponin I (Tn I) was determined as a biochemical marker of myocardial damage.&#x0D; Results and discussion: In the in vitro experiments, when culting white blood cells, the lead compound in the group of 3-oxypyridine derivatives was identified under code LKhT 21–16, which increases the number of viable cells in the presence of hypoxia, surpassing the reference drugs. When confirming the chemical structure of the lead compound, LHT 21–16, a high sensitivity of the NMR spectroscopy method was revealed.&#x0D; In studying the cardioprotective activity in the model of coronary-occlusive myocardial infarction compound LHT 21–16 exerted a marked cardioprotective effect when reducing the size of the necrotic zone and the level of biochemical marker Tn I.&#x0D; Conclusions: 3-oxypiridine derivatives have antihypoxic and cardioprotective effects, which shows in a high number of surviving cells in the presence of hypoxia in the in vitro model, a reduced size of the necrotic zone and a reduced level of Tn I in the coronary-occlusive myocardial infarction.

NILAI DIAGNOSTIK UJI TROPONIN I KUANTITATIF METODE IMMUNOKROMATOGRAFI

Cardiac troponins are the most sensitive and specific biochemical markers of myocardial damage but there is no standardization of WHO for cardiac troponin I, resulting in a variability for diagnostic value. It is necessary to determine diagnostic value for a new kitof troponin I. To evaluate a new quantitative immunochromatography assay for troponin I at a various cut off level. A cross sectionalstudy was conducted in 64 patients with acute myocardial infarction (AMI) and 55 non-AMI as control from February to September2007. The level of cardiac troponin I (cTnI) was measured and determined it diagnostic value at a various cut off level. The sensitivity,specificity, PPV and NPV of this assay were 91%, 91%, 92% and 89% at cut off level of 1,0 ng/ml (according to the kit), respectively.The cut off of cTnI were divided into five levels: 0.8, 1.0, 1.2, 1.5, and 2.0 with the area under curve were 0.923, 0.908, 0.912, and0.897, respectively. The sensitivity were 94%, 91%, 86%, 81% and 72%, respectively, the specificity were 91%, 91%, 96%, 98% and98%, respectively. This rapid diagnostic test is sensitive and specific to diagnose an acute coronary syndromes.

Učestalost akutnog koronarnog sindroma i anksioznosti kod pacijenata koji se žale na bol u grudima

Introduction: In triage of patients in general and ambulance clinics and ambulance services, patients who report for chest pain are treated as emergency cases and are a priority in relation to other patients. Aim: Determine the importance of priority care for patients with chest pain and timely selection of these patients in relation to myocardial damage and fear of it. Methodology: In the period from 01.03.2017. until 01.03.2018. On the occasion of the medical check-up for chest pain, 121 patients were examined. Everyone was treated as an emergency. They had prioritized care, an auscultatory and electrocardiographic examination, in order to further determine the coronary state of the laboratory laboratory analysis of biochemical markers of myocardial damage within the emergency response service. The data were obtained by a retrospective study using electronic card of these patients. Data processing was used for hi-square statistics and Pirson's correlation. Results: Of the total number of patients (121) who reported for chest pain, 42 or 36.52% of them were diagnosed with acute coronary syndrome. In 67 and 58.26% of respondents no acute coronary syndrome was found, and in 6 subjects, which make up 5.22% of the total percentage of patients, the disease ended with a flight outcome in the next year. Six respondents did not appear again for an examination in this clinic, but with their chosen physician and were further excluded from the research in the future. Conclusion: In this study, we observed the frequency of anxiety and acute coronary syndrome in patients who complain of chest pain. It can be concluded that in the group where acute coronary syndrome has not been diagnosed, and who have checked for fear due to excessive fear of several women, in the other two groups with diagnosed acute coronary syndrome and the aquatic outcome of several men.

Combination Therapy With Coenzyme Q10 and Trimetazidine in Patients With Acute Viral Myocarditis

Acute viral myocarditis is an inflammatory disease with global impact. Although it may resolve spontaneously, its course is not easily predicted, and there is a paucity of specific treatment options available with proven efficacy. Coenzyme Q10 (CQ10) and trimetazidine possess antioxidant and antiinflammatory effects. We examined the therapeutic efficacy of these agents in acute viral myocarditis both individually and in combination. Patients were blinded and randomized to receive CQ10 (n = 42), trimetazidine (n = 39), or CQ10 + trimetazidine (n = 43) treatment. Serum inflammatory and oxidative stress marker and myocardial enzyme levels, and heart function were measured. Both CQ10 and trimetazidine decreased inflammatory and oxidative stress biomarker levels compared with baseline measurements. However, combination therapy with CQ10 and trimetazidine showed a significantly more powerful effect not only on markers of inflammation and oxidative stress, but also on left ventricular systolic function and troponin, compared with either treatment alone. This study confirmed the beneficial effect of CQ10 and trimetazidine individually, but demonstrated a superior effect of combining the therapies on cardiac left ventricular ejection fraction, and biochemical markers of myocardial damage in acute viral myocarditis.