Creatine Kinase-myocardial Band Levels Research Articles

Assessment of cardiac parameters after the administration of nicorandil before primary percutaneous coronary intervention.

To assess cardiac troponin I and creatine kinase-myocardial band levels, electrocardiogram changes and major adverse cardiac events after treatment with nicorandil before primary percutaneous coronary intervention. The comparative, analytical study was conducted from October to November 2022 at the Pharmacology Department of Army Medical College, National University of Medical Sciences, Rawalpindi, Pakistan, in collaboration with the Rawalpindi Institute of Cardiology, Rawalpindi. The sample comprised ST-elevated myocardial infarction patients of either gender aged at least 30 years with an ejection fraction of at least 35% undergoing primary percutaneous coronary intervention. Participants were selected based on the above-mentioned inclusion and informed consent was taken before their enrolment in this research study. The sample was randomised into control group A receiving conventional acute coronary syndrome treatment, and intervention group B receiving nicorandil in addition to the conventional treatment. Cardiac troponin I and creatine kinase-myocardial band levels, electrocardiogram changes, and major adverse cardiac events noted and compared. Data was analysed using SPSS 26. Of the 140 patients, 70(50%) were in each of the 2 groups. In group B, 60(85.7%) patients achieved a completely settled ST segment on electrocardiogram compared to 25(35.7%) in group A (p=0.001). There was a significant inter-group difference with respect to cardiac troponin I value 6 hours after percutaneous coronary intervention and major adverse cardiac events (p<0.05), but creatine kinase-myocardial band level was no significantly different between the groups (p=0.761). Prophylactic use of nicorandil in ST-elevated myocardial infarction patients decreased the incidence of reperfusion injury.

Punicalagin attenuates isoproterenol-induced myocardial infarction through nuclear factor erythroid 2-related factor 2/silent information regulator transcript-1-mediated inhibition of inflammation and cardiac stress markers in experimental animal models.

Myocardial infarction (MI) is a significant global health issue and the leading cause of death. Myocardial infarction (MI) is characterized by events such as damage to heart cells and stress generated by inflammation. Punicalagin (PCN), a naturally occurring bioactive compound found in pomegranates, exhibits a diverse array of pharmacological effects against many disorders. This study aimed to assess the preventive impact of PCN, with its potential anti-inflammatory and antioxidant properties, on myocardial injury caused by isoproterenol (ISO) in rats and elucidate the possible underlying mechanisms. Experimental rats were randomly categorized into four groups: control group (fed a regular diet for 15 days), PCN group (orally administered PCN at 50 mg/kg body weight (b.w.) for 15 days), ISO group (subcutaneously administered ISO (85 mg/kg b.w.) on days 14 and 15 to induce MI), and PCN+ISO group (orally preadministered PCN (50 mg/kg b.w.) for 15 days and administered ISO (85 mg/kg b.w.) on days 14 and 15). The rat cardiac tissue was then investigated for cardiac marker, oxidative stress marker, and inflammatory marker expression levels. PCN prevented ISO-induced myocardial injury, suppressing the levels of creatine kinase-myocardial band, C-reactive protein, homocysteine, cardiac troponin T, and cardiac troponin I in the rats. Moreover, PCN treatment reversed (P<0.01) the ISO-induced increase in blood pressure, attenuated lipid peroxidation markers, and depleted both enzymatic and nonenzymatic markers in the rats. Additionally, PCN inhibited (P<0.01) ISO-induced overexpression of oxidative stress markers (p-38, p-c-Jun N-terminal kinase, and p-extracellular signal-regulated kinase 1), inflammatory markers (nuclear factor-kappa B, tumor necrosis factor-alpha, and interleukin-6), and matrix metalloproteinases and decreased the levels (P<0.01) of apoptosis proteins in the rats. Nuclear factor erythroid 2-related factor 2/silent information regulator transcript-1 (Nrf2/Sirt1) is a major cellular defense protein that regulates and scavenges oxidative toxic substances through apoptosis. Therefore, overexpression of Nrf2/Sirt1 to inhibit inflammation and oxidative stress is considered a novel target for preventing MI. PCN also significantly enhanced the expression of Nrf2/Sirt1 in ISO-induced rats. Histopathological analyses of cardiac tissue revealed that PCN treatment exhibited a protective effect on the heart tissue, mitigating damage. These findings show that by activating the Nrf2/Sirt1 pathway, PCN regulates oxidative stress, inflammation, and apoptosis, hence providing protection against ISO-induced myocardial ischemia.

Nicotinamide ribose ameliorates myocardial ischemia/reperfusion injury by regulating autophagy and regulating oxidative stress.

Nicotinamide riboside (NR) has been reported to play a protective role in myocardial ischemia-reperfusion (I/R) injury when used in association with other drugs; however, the individual effect of NR is unknown. In the present study Evan's blue/triphenyl tetrazolium chloride staining, hematoxylin and eosin staining, echocardiography, western blotting, reverse transcription-quantitative PCR, and the detection of myocardial injury-associated markers and oxidative stress metabolites were used to explore the ability of NR to alleviate cardiac I/R injury and the relevant mechanisms of action. In a mouse model of I/R injury, dietary supplementation with NR reduced the area of myocardial ischemic infarction, alleviated pathological myocardial changes, decreased inflammatory cell infiltration and attenuated the levels of mitochondrial reactive oxygen species (ROS) and creatine kinase myocardial band (CK-MB). In addition, echocardiography suggested that NR alleviated the functional damage of the myocardium caused by I/R injury. In H9c2 cells, NR pretreatment reduced the levels of lactate dehydrogenase, CK-MB, malondialdehyde, superoxide dismutase and ROS, and reduced cell mortality after the induction of hypoxia/reoxygenation (H/R) injury. In addition, the results indicated NR activated sirt 1 via the upregulation of nicotinamide adenine dinucleotide (NAD+) and protected the cells against autophagy. The sirt 1 inhibitor EX527 significantly attenuated the ability of NR to inhibit autophagy, but had no significant effect on the ROS content of the H9c2 cells. In summary, the present study suggests that NR protects against autophagy by increasing the NAD+ content in the body via the sirt 1 pathway, although the sirt 1 pathway does not affect oxidative stress.

Anterior-wall and non-anterior-wall STEMIs do not differ in long-term mortality: results from the augsburg myocardial infarction registry.

Different ST-segment elevation myocardial infarction (STEMI) localizations go along with dissimilarities in the size of the affected myocardium, the causing coronary vessel occlusion, and the right ventricular participation. Therefore, this study aims to clarify if there is any difference in long-term survival between anterior- and non-anterior-wall STEMI. This study included 2,195 incident STEMI cases that occurred between 2009 and 2017, recorded by the population-based Augsburg Myocardial Infarction Registry, Germany. The study population comprised 1.570 men and 625 women aged 25-84 years at acute myocardial infarction. The patients were observed from the day of their first acute event with an average follow-up period of 4.3 years, (standard deviation: 3.0). Survival analyses and multivariable Cox regression analyses were performed to examine the association between infarction localizations and long-term all-cause mortality. Of the 2,195 patients, 1,118 had an anterior (AWS)- and 1,077 a non-anterior-wall-STEMI (NAWS). No significant associations of the STEMI localization with long-term mortality were found. When comparing AWS with NAWS, a hazard ratio of 0.91 [95% confidence interval: 0.75-1.10] could be calculated after multivariable adjustment. In contrast to NAWS, AWS was associated with a greater <28 day mortality, less current or former smoking and higher creatine kinase-myocardial band levels (CK-MB) and went along with a higher frequency of impaired left ventricular ejection fraction (<30%). Despite pathophysiological differences between AWS and NAWS, and identified differences in multiple clinical characteristics, no significant differences in long-term mortality between both groups were observed.

Troponin I, CK-MB, and inotropic score in hypoxic-ischemic encephalopathy and associated infant mortality

PurposeCardiovascular dysfunction is common in hypoxic-ischemic encephalopathy (HIE), which is one of the leading causes of multi-organ failure in neonates. We aimed to assess troponin I and creatine kinase myocardial band (CK-MB) levels, inotropic score (IS) in HIE patients, and their associations with HIE staging and mortality.MethodThe medical records of all HIE infants admitted to our unit between 2016 and 2018 were retrospectively analyzed. Demographic characteristics of the infants, seizures, anticonvulsive therapies, maximum inotrope doses, and the derived IS (dopamine dose [µg/kg/min] + dobutamine dose [µg/kg/min] + 100 × epinephrine dose [µg/kg/min]) and CK-MB and troponin-I levels obtained in the first six hours of life were compared according to HIE staging. Comparisons between survivors and non-survivors were made.ResultsThe study included data from 195 patients. Twenty-five patients were classified as stage 3, 116 as stage 2, and 54 as stage 1 HIE. Median Troponin-I, CK-MB level, and IS significantly differed by HIE staging (p < 0.01). The deceased infants had significantly higher median troponin I level [0.36 (0.02-3) vs. 0.16 (0.01–1.1) ng/ml; p = 0.006], median IS [20 (5-120) vs. 5 (5–10); p < 0.001], however, CK-MB values were comparable with survivors [129 (51–300) vs. 60.7 (31–300) ng/ml; p = 0.57]. The area under the curve was 0.93 for IS and 0.81 for Troponin I to predict mortality.ConclusionTroponin I, CK-MB, and IS could be successfully used as disease severity markers in HIE furthermore, troponin I and IS, are good predictors of mortality. These results need to be confirmed with larger prospective multi-center studies.

Elevated CK-MB levels are associated with adverse clinical outcomes in acute pancreatitis: a propensity score-matched study.

Cardiac injury, reflected by the measured concentrations of chemicals released from injured cardiac muscle, is common in acute pancreatitis (AP). However, there is no adequate evidence assessing the impact of cardiac injury on AP-related outcomes. Creatine kinase-myocardial band (CK-MB) mainly exists in the myocardium. Therefore, we sought to evaluate the relationship between the increase in CK-MB and the adverse clinical outcomes of AP. This propensity score-matched study analyzed AP patients admitted to the Department of Gastroenterology in the First Affiliated Hospital of Nanchang University from June 2017 to July 2022. Propensity score matching and multivariate logistic regression analysis were used to explore the relationship between CK-MB elevation and AP outcome variables. A total of 5,944 patients were screened for eligibility, of whom 4,802 were ultimately enrolled. Overall, 896 (18.66%) of AP patients had elevated (>24 U/ml) CK-MB levels, and 895 (99.89%) were paired with controls using propensity score matching. The propensity score-matched cohort analysis demonstrated that mortality (OR, 5.87; 95% CI, 3.89-8.84; P < 0.001), severe acute pancreatitis (SAP) (OR, 2.74; 95% CI, 2.23-3.35; P < 0.001), and infected necrotizing pancreatitis (INP) (OR, 3.40; 95% CI, 2.34-4.94; P < 0.001) were more frequent in the elevated CK-MB (>24 U/ml) group than in the normal CK-MB (≤ 24 U/ml) group. Using the multivariate logistic regression analysis, elevated CK-MB levels were independently associated with increased mortality (OR, 2.753, 95% CI, 2.095-3.617, P < 0.001), SAP incidence (OR, 2.223, CI, 1.870-2.643, P < 0.001), and INP incidence (OR, 1.913, 95% CI, 1.467-2.494, P < 0.001). CK-MB elevation was an independent risk factor for adverse clinical outcomes in AP patients. CK-MB elevation was significantly related to adverse outcomes in AP patients, which makes it a potentially useful laboratory parameter for predicting adverse clinical outcomes of AP.

Evaluation of the effect of oxidative stress on dynamics of cardiac biomarkers in Georgian elite athletes with overtraining syndrome

Abstract Funding Acknowledgements Type of funding sources: None. Background Training of professional athletes comprises of repetitive overloading to initiate structural and functional changes for favorable adaptation to the workouts, but with an inadequate recovery overloading may produce non-functional overreaching(NFO) and then overtraining syndrome(OTS). It is important to study chronic effects of exercises via responses of biomarkers for understanding of muscle fatigue and cardiac damage to identify athletes at risk of poor adaptation to training[3,4]. The purpose was to study the effects of oxidative stress on dynamics of cardiac biomarkers in Georgian elite athletes with OTS. Methods On the initial stage in 43 athletes(37 with NFO, 6 with OTS) study of relationship between oxidative stress and OTS revealed imbalance between oxidant production and antioxidant protection via attenuation of antioxidant capacity in athletes with OTS[1,2]. On the current stage of our study,in 43 NFO/OTS athletes and 40 age-matched controls without NFO/OTS pre-season serum creatine kinase myocardial band(CK-MB) and cardiac troponin I(cTnI) were measured, followed by in-season evaluation of the dynamic of their changes(HUMAN,Germany). In-season levels of CK-MB and cTnI were obtained 24hrs before strenuous sport-specific exercise of peak-season intensity, immediately after the work-load,after 6, 48,and 72hrs. Baseline and post-execise clinical assessment and transthoracic echocardiography(TTE) were performed in 6 and 48hrs after strenuous session(6 hrs corresponds to the time when cTnI is typically detectable in ischemic models;48 hrs-CK concentrations recovery time). Results Similar rising trend of CK-MB and cTnI levels was observed immediately after exercise, reaching peak values after 6hrs in all athletes, though, significantly greater in NFO/OTS athletes than in controls, and slightly exceeded reference range of cTnI (in NFO 0.128±0.092ng/ml, in OTS 0.137±0.061ng/ml). After 48hrs of recovery CK-MB and cTnI in NFO/OTS athletes were significantly higher than on entry, showing slower recovery,though normalized in 72hrs. TTE didn’t reveal any sustained alterations of systolic and diastolic functions, or clinically threatening myocardial damage, only minor diastolic changes due to adaptation to the post-exercise haemodynamic in OTS athletes(E/A pre-exercise:1.47±0.25, post-exercise:in 6hrs 1.06±0.14,in 48hrs 1.40±0.09,p&amp;lt;0,05). Elevated cardiac markers after strenuous exercise can be linked to increased cellular permeability and cardiac troponin leakage, amplified by oxidative stress existent in OTS athletes. Conclusions In our study intensive exercise caused transient increase of the CK-MB and cTnI in NFO/OTS athletes, without irreversible pathophysiological and clinical consequences, suggesting mostly benign cardiac involvement, though amplified by existent oxidative stress in athletes with OTS. Monitoring responses via alterations of biochemical parameters can be helpful to guide athletic training and prevent OTS.

A combination of Sophoraflavescens alkaloids and Panaxquinquefolium saponins attenuates coxsackievirus B3‑induced acute myocarditis in mice via NF‑κB signaling.

Timely treatment of viral myocarditis (VMC), a form of cardiac inflammation caused by viral infections, can reduce the occurrence of dilated cardiomyopathy and sudden death. Our previous study demonstrated the anti-inflammatory and anti-fibrotic effects of KX, a combination of Sophora flavescens alkaloids and Panax quinquefolium saponins, on an autoimmune myocarditis model in vivo. The present study explored the effects of KX on coxsackievirus B3 (CVB3)-induced acute VMC in mice. Mice were randomly divided into four groups: Control, VMC, KX-high (275 mg/kg) and KX-low (138 mg/kg). Mice in the VMC, KX-high and KX-low groups received injections of CVB3 to establish the VMC model, and those in the KX-high and KX-low groups also received KX by gavage (10 ml/kg) 2 h after virus injection until euthanasia was performed on day 7 or 21. Mice in the control group received an equal KX volume of purified water. The levels of lactate dehydrogenase (LDH), creatine kinase-myocardial band (CK-MB), cardiac troponin I (cTn-I), IL-1β, IL-6, TNF-α and high-sensitive C-reactive protein (hs-CRP) in mouse serum was measured using ELISA. Myocardial tissue structure and degree of injury were observed using hematoxylin and eosin staining. Western blotting and reverse transcription-quantitative PCR were performed to detect the expression levels of NF-κB pathway-related mRNA and protein in myocardial tissue. The results showed that the inflammation and myocardial damage levels of the mice in the VMC group were higher at 7 days than those at 21 days. At both 7 and 21 days, KX decreased the serum CK-MB, LDH, cTn-I, IL-6, TNF-α and hs-CRP levels, and inhibited NF-κB pathway-related mRNA and protein expression in the myocardium of mice. These findings indicated that KX may reduce the inflammatory response and attenuate the pathological damage in the acute and subacute phases of CVB3-induced VMC through the NF-κB pathway.

Analysis of Changes In Creatine Kinase Myocardial Band (CK-MB) And F2-Isoprostane Levels After A 30 Km Cycling Event In The Makassar Bike Community

This study aims to determine changes in levels of Creatine Kinase-Myocardial Band and F2-Isoprostane after a 30 km cycling event. This is a pre-experimental study on 30 subjects of male cyclists aged 30-60 years taken by purposive sampling method. The pretest was carried out the day before the 30 km cycling event, then the post-test was carried out 2 hours after the cycling event. Blood testing was done with an ELISA Kit. Data analysis using the Wilcoxon test showed significant changes in Creatine Kinase-Myocardial Band levels after a 30 km cycling event (p=0.003). Meanwhile, there was no significant change in F2-Isoprostane levels after the event (p=0.688). The results of the Spearman test showed that there was a correlation between changes in levels of creatine kinase-myocardial band with changes in levels of F2-Isoprostane (p=0.042).

Investigating the effect of myricetin against arsenic-induced cardiac toxicity in rats.

Arsenic intoxication is a serious health hazard worldwide. Its toxicity is associated with several disorders and health problems in humans. Recent studies revealed that myricetin has various biological effects, including anti-oxidation. The aim of this study is to investigate the protective effect of myricetin against arsenic-induced cardiotoxicity in rats. Rats were randomized to one of the following groups: control, myricetin (2mg/kg), arsenic (5mg/kg), myricetin (1mg/kg)+arsenic, and myricetin (2mg/kg)+arsenic. Myricetin was given intraperitoneally 30min before arsenic administration (5mg/kg for 10days). After treatments, the activity of lactate dehydrogenase (LDH) and the levels of aspartate aminotransferase (AST), creatine kinase myocardial band (CK-MB), lipid peroxidation (LPO), total antioxidant capacity (TAC), and total thiol molecules (TTM) were determined in serum samples and cardiac tissues. Also, histological changes in cardiac tissue were evaluated. Myricetin pretreatment inhibited arsenic-induced increase in LDH, AST, CK-MB, and LPO levels. Pretreatment with myricetin also enhanced the decreased TAC and TTM levels. In addition, myricetin improved histopathological alterations in arsenic-treated rats. In conclusion, the results of the present study demonstrated that treatment with myricetin prevented arsenic-induced cardiac toxicity at least in part by decreasing oxidative stress and restoring the antioxidant system.

Excimer laser coronary angioplasty versus manual aspiration thrombectomy in patients with ST-segment elevation myocardial infarction: analyzed by nuclear scintigraphy.

Clinical outcomes concerning the efficacy of excimer laser coronary angioplasty (ELCA) in real-world cases of acute myocardial infarction (MI) are limited. We evaluated and compared the impact of ELCA with manual aspiration thrombectomy on myocardial salvage and left ventricular (LV) systolic/diastolic function in patients with ST-segment elevation MI (STEMI) using nuclear scintigraphy. We enrolled 143 consecutive patients with STEMI treated with ELCA (63 patients) or manual aspiration thrombectomy (80 patients) between September 2016 and December 2020 in a single-center hospital. We evaluated the peak creatine kinase (CK)/ creatine kinase-myocardial band (CK-MB) levels and performed single-photon emission computed tomography (SPECT) analyses with Quantitative Gated SPECT and Quantitative Perfusion SPECT (Auto QUANT 7.2) at 3-10 days using 123I-BMIPP and 3 months following percutaneous coronary intervention using 99mTc-tetrofosmin to evaluate myocardial salvage and LV systolic/diastolic function. No significant difference was observed in the patient and periprocedural characteristics. Peak CK-MB level was significantly different between the groups (ELCA group, 190.0 [70.5-342.0] IU/L vs. aspiration group, 256.5 [157.0-354.8] IU/L, p = 0.047). Although no significant difference was observed in myocardial salvage, significant improvement in the LV ejection fraction (14.1 [6.2-19.8]% vs. 9.5 [3.9-15.3]%, respectively, p = 0.018) and peak emptying rate (-0.54 [-1.02-(-0.27)] mL/s vs. -0.38 [-0.76-(-0.05)] mL/s, respectively, p = 0.017) were detected. ELCA could suppress the myocardial deviation enzymes and potentially improve systolic function compared to manual aspiration thrombectomy in patients with STEMI.

The protective effect of curcumin on cardiac markers and fibrosis in abemaciclib-induced cardiac damage in rats.

Abemaciclib (ABE) is a cyclin-dependent kinase inhibitor used in combination with an antiestrogen in the treatment of breast cancer. In addition to the important therapeutic properties of this drug, its side effects are not fully known. In this study, we aimed to investigate the protective effect of curcumin (CUR) on cardiac damage caused by ABE administration. Forty rats were equally divided into control, dimethyl sulfoxide (150 µL), CUR (30 mg/kg/day), ABE (26 mg/kg/day), and ABE + CUR (26 mg/kg/day ABE and 30mg/kg/day CUR) groups (n = 8). Injections were administered daily for 28 days. Troponin-I, total cholesterol, and creatine kinase myocardial band (CK-MB) levels and cardiac fibrosis were higher in the ABE group than in the control group (p < 0.05), and were lower in the ABE + CUR group than in the ABE group (p < 0.05). The results showed that ABE administration can cause cardiac damage and increase cardiac fibrosis. However, they showed that coadministration of CUR with ABE could suppress increases in CK-MB, troponin-I, and total cholesterol levels and also cardiac fibrosis associated with cardiac damage. Therefore, we can infer that the subsequent administration of CUR ABE treatment can be used as a therapeutic strategy for preventing cardiac damage.

Clinical outcomes and characteristics of acute myocardial infarction patients with developing fever after percutaneous coronary intervention

The incidence of fever complicating percutaneous coronary intervention (PCI) is rare. However, little is known regarding the cause of fever after PCI. Therefore, this study aimed to determine the clinical characteristics of patients with acute myocardial infarction (AMI), with or without fever, after PCI. We enrolled a total of 926 AMI patients who underwent PCI. Body temperature (BT) was measured every 4 hours or 8 hours for 5 days after PCI. Patients were divided into two groups according to BT as follows: BT&lt;37.7°C (no-fever group) and BT ≥37.7°C (fever group). The 2 years clinical outcomes were compared subsequently. Fever after PCI was associated with higher incidence of major adverse cardiac events (MACE) (hazard ratio [HR], 1.56; 95% confidence interval [CI], 1.07-2.28; &lt;i&gt;P&lt;/i&gt;=0.021), all-cause death (HR, 2.32; 95% CI, 1.18-4.45; &lt;i&gt;P&lt;/i&gt;=0.014), cardiac death (CD) (HR, 2.57; 95% CI, 1.02-6.76; &lt;i&gt;P&lt;/i&gt;=0.049), and any revascularization (HR, 1.69; 95% CI, 1.02-2.81; &lt;i&gt;P&lt;/i&gt;=0.044) than without fever. In women, prior chronic kidney disease, lower left ventricular (LV) ejection fraction, higher LV wall motion score index, white blood cell count, peak creatine kinase-myocardial band level, and longer PCI duration were associated with fever after PCI. Procedures such as an intra-aortic balloon pump, extracorporeal membrane oxygenation, continuous renal replacement therapy, central and arterial line insertion, and cardiopulmonary resuscitation were related to fever after PCI. Fever after PCI in patients with AMI was associated with a higher incidence of MACE, all-cause death, CD, and any revascularization at the 2 years mark than in those without fever.

Influence of the cardio-ankle vascular index on chronic-phase left ventricular dysfunction after ST-segment elevation myocardial infarction.

This study aimed to investigate the possible influence of arterial stiffness assessed by the cardio-ankle vascular index (CAVI) on chronic-phase left ventricular dysfunction in patients with ST-segment elevation myocardial infarction (STEMI). A total of 208 consecutive patients with first STEMI (age, 64 ± 11 years; 86% men) who underwent reperfusion therapy within 12 h of onset were enrolled. We analysed arterial stiffness by measuring CAVI in a stable phase after admission and performed two-dimensional echocardiography at baseline and 7 months' follow-up. Subsequently, we assessed left ventricular global longitudinal strain (LV-GLS) to evaluate left ventricular function. A total of 158 (75.9%) patients underwent baseline cardiac magnetic resonance (CMR). We estimated left ventricular infarct size by measuring peak levels of creatine kinase-myocardial band (CK-MB), and CMR-late gadolinium enhancement (LGE). On the basis of the median CAVI value, the patients were allocated into high CAVI (CAVI ≥ 8.575) and low CAVI (CAVI < 8.575) groups. The groups showed no statistically significant differences in LV-GLS at baseline (-13.5% ± 3.1 vs. -13.9% ± 2.7%, P = 0.324). However, LV-GLS was significantly worse in the high CAVI group than in the low-CAVI group at 7 months (-14.0% ± 2.9 vs. -15.6% ± 3.0%, P < 0.001). Stratified by CAVI and peak CK-MB or LGE, the four groups showed significant differences in LV-GLS at 7 months after STEMI (both P < 0.001). Multivariate linear regression analysis with the forced inclusion model showed that CAVI was an independent predictor of LV-GLS at 7 months ( P = 0.015). CAVI early after STEMI onset was significantly associated with chronic-phase LV-GLS. In addition, combining CAVI with CK-MB or LGE improves its predictive ability for evaluation of chronic-phase LV-GLS. Thus, the arterial stiffness assessment by CAVI was an important factor related to chronic-phase left ventricular dysfunction after the first STEMI.

Pharmacokinetics of tildipirosin in horses after intravenous and intramuscular administration and its potential muscle damage

Tildipirosin is a novel semisynthetic macrolide antibiotic exclusively used in veterinary practice to treat respiratory infections. There are no pharmacokinetic or safety information available regarding the use of tildipirosin after intramuscular administration in horses. Thus, the objective of this work was to determine the disposition kinetics of tildipirosin after intravenous (IV) and intramuscular (IM) administration in horses and its potential muscle damage and cardiotoxicity. Six mature, Spanish-breed horses were used in a crossover study with a washout period of 30 days. Tildipirosin (18%) was administered at single doses by IV (2 mg/kg) and IM (4 mg/kg) routes. Tildipirosin plasma concentrations were determined by HPLC assay with ultraviolet detection. Muscle damage and inflammation were assessed by creatine kinase (CK) and haptoglobin (Hp), respectively. Creatine kinase myocardial band (CK-MB) and troponin (Tn) were used to evaluate cardiotoxicity. Tildipirosin in horses reached peak concentrations (Cmax = 1.13 μg/mL) at 0.60 h (tmax) after IM administration with an absolute bioavailability of 109.2%. Steady-state volume of distribution and clearance were 3.31 ± 0.57 L/kg and 0.22 ± 0.02 L/h/kg, respectively. Tildipirosin did not cause cardiotoxicity since CK-MB and Tn basal levels were not significantly different from those obtained after several days post-administration. Mild local reactions were observed after IM administration. This local inflammation was associated with mild myolysis (CK 239–837 UI/L), which was detectable for 48 h. In brief, tildipirosin could help to treat respiratory infections in horses because it showed extensive distribution, high bioavailability and did not provoke general adverse reactions.

Combination of Sophora flavescens alkaloids and Panax quinquefolium saponins modulates different stages of experimental autoimmune myocarditis via the NF-κB and TGF-β1 pathways.

Chronic cardiac inflammation and fibrosis can progress into severe forms of cardiomyopathy. Sophora flavescens alkaloids (KuShen) have been previously reported to exert anti-inflammatory effects, whereas Panax quinquefolium saponins (XiYangShen) has been shown to alleviate cardiac fibrosis. Therefore, the potential effects of their combination (KX) on different stages of autoimmune myocarditis were investigated in the present study. Mice were randomly divided into the following four groups: Control; experimental autoimmune myocarditis (EAM); KX-High (275 mg/kg); and KX-Low (138 mg/kg). A 21-day and a 60-day EAM model was established through multi-site subcutaneous injections of cardiac myosin mixed with complete Freund's adjuvant on days 0, 7, 21 and 42. Mice in the High and Low KX groups were treated by gavage (10 ml/kg) daily from day 0 (1 day before treatment) until sacrifice (day 21 or 60). Mice in the control and EAM groups received an equivalent volume of distilled water. The levels of lactate dehydrogenase (LDH), creatine kinase-myocardial band (CK-MB), cardiac troponin I (cTn-I), IL-1β, IL-6, TNF-α, TGF-β1, collagen type I (Col Ⅰ) and collagen type III (Col Ⅲ) were measured by ELISA in the mouse myocardial tissues or serum. Myocardial tissue structure and extent of fibrosis were visualized using H&E and Masson's staining. Western blotting and immunohistochemistry were used to measure the expression levels NF-κB and TGF-β1 pathway proteins in the myocardial tissues. The degree of inflammation in the 21-day EAM model was found to be significantly higher compared with that in the 60-day EAM model. KX significantly reduced the inflammatory response at 21 days by decreasing the expression levels of CK-MB, LDH, cTn-I, IL-1β, IL-6, TNF-α and TGF-β-activated kinase 1-binding protein 1/NF-κB pathway proteins. Myocardial fibrosis in the 60-day EAM model was also significantly worse compared with that in the 21-day EAM model. However, fibrosis was significantly delayed by treatment with KX. In addition, KX significantly decreased the expression levels of TGF-β1, Smad2, Smad4, Col I and Col III. Therefore, these data suggest that KX is beneficial for treating myocarditis by targeting multiple pathways.

Comparisons of High Intensity Interval Training and Continuous Training on Metabolomic Alteration and Cardiac Function in Male Adolescent Rats.

Background: Comparisons between high intensity interval training (HIIT) and continuous training (CT) regarding improvements of adolescents’ cardiac function are scarce and the preferred intensity for cardiac improvement with restricted myocardial damage remains unknown. This study conducted a 4-weeks training in male adolescent rats under moderate (MI) or high intensity (HI) HIIT and CT programs, aiming to discover and compare exercise-induced myocardial adaptations towards these two training methods. Methods: 39 male adolescent Sprague-Dawley rats (aged 4 weeks) were randomly assigned to high intensity HIIT (HI-HIIT, n = 8), moderate intensity HIIT (MI-HIIT, n = 8), high intensity CT (HI-CT, n = 8), moderate intensity CT (MI-CT, n = 8) and sedentary control (SC, n = 7) groups. Rats in training groups were trained for 4 weeks and echocardiography was performed at baseline and after the final training. Serum creatine kinase myocardial band (CK-MB), cardiac troponin T (cTn-T) and untargeted metabolomics analysis were measured from blood samples collected 24 h after the final training. Results: HIIT groups had greater cardiac output improvement than CT groups while no significant difference was found between the HI-HIIT and the MI-HIIT groups. HI-CT group showed higher serum CK-MB and cTn-T levels compared to MI-HIIT, MI-CT and control groups. Untargeted metabolomics analysis identified eleven HI-HIIT-related metabolites, five MI-HIIT-related metabolites and two HICT-related metabolites. The majority of the identified metabolites were phospholipid-related. Phosphatidylglyceride 18 level was significantly different between the HI-CT and MI-CT groups, and was negatively associated with cTn-T in CT groups. Conclusion: HIIT and CT improve cardiac function of adolescent rats while the HIIT demonstrates better improvement and less myocardial damage. High and moderate training intensities in HIIT exert similar cardiac benefits. HI-CT induced myocardial damage might be associated with serum phospholipids.

A randomized, placebo-controlled, double-blind trial to evaluate efficacy and safety of Shen-Yuan-Dan capsules, a traditional Chinese medicine, for treatment of peri-procedure myocardial injury following percutaneous coronary intervention

BackgroundPeri-procedural myocardial injury (PMI) is a common complication of percutaneous coronary intervention (PCI), which cannot be entirely avoided using available treatments. The findings of earlier research have shown that Shen-Yuan-Dan (SYD) capsules, a traditional Chinese medicine, can potentially alleviating PMI. This study aimed to confirm further this hypothesis in a rigorous, well-designed randomized controlled study. MethodsOur clinical trial was randomized, double-blinded, and placebo-controlled. A total of 181 patients with unstable angina (UA) undergoing elective PCI were randomized to pretreatment with SYD or a placebo under the basis of conventional treatment; 87 patients were pretreated with SYD (4 capsules, 3 times a day, with a further 4 capsules 2 h before PCI) 3 days before the procedure, and 94 patients were given a placebo. No patients received reloading statins before PCI, and SYD or placebo was maintained for 1 month after PCI. The primary endpoint was the incidence of PMI. The secondary endpoint was calculating the incidence rate of all 30-day major adverse cardiovascular events (all-cause mortality, non-fatal myocardial infarction, unplanned revascularization). The safety outcomes, including abnormalities in electrocardiogram and serum biochemical examinations caused by drug use, were also tested. ResultsThe levels of creatine kinase-myocardial band (CK-MB) in both the SYD and placebo groups were increased at 4 h and 24 h after PCI compared with before the procedure (P < 0.05). The incidence rate of PMI in the SYD group (10.3 %) was lower than that in the placebo group (34 %) (absolute difference, 23.7 % [95 % CI, 11.7–34.8 %], P < 0.01). After taking SYD, the relative risk reduction (RRR) and absolute risk reduction (ARR) were 69.7 % and 24.3 %, respectively; further, number needed to treat (NNT) was 4.2. The 30-day major adverse cardiovascular event (MACE) rate was not statistically different between the SYD and placebo groups (6.9 % vs. 9.6 %, P = 0.352). There were no abnormal situations during the trial. ConclusionThese findings showed that pretreatment with SYD could safely reduce the incidence rate of PMI in patients with UA undergoing elective PCI. Further study on the effects of SYD and how it can improve adverse cardiovascular events outcomes is needed.

Correlation of Vitamin D levels with markers of bone metabolism in COVID-19 patients

Introduction: Low serum Vitamin D levels are common in orthopedic patients in India. Low serum Vitamin D levels are implicated in COVID-19 worsening the illness. With this background, we assessed serum Vitamin D levels in COVID-19 patients presenting to us and correlated them with other markers of bone metabolism and systemic immune response. Materials and Methods: A cross-sectional analytical study was done on 107 COVID-19 patients. The sample was taken for serum calcium, serum Vitamin D, serum phosphate, bone-specific alkaline phosphatase (ALP), serum parathyroid hormone, creatine phosphokinase (CPK), CPK myocardial band (MB), serum protein, C-reactive protein, erythrocyte sedimentation rate, and hemoglobin in these patients. The levels were correlated with each other to assess their relations in COVID-19 patients. Results: One hundred out of 107 patients had low serum Vitamin D levels. In these patients, serum lactate dehydrogenase and serum ALP levels were high, and creatine kinase MB levels were low. The illness was found more in diabetic/hypertensive and rheumatoid arthritis patients. The values and findings correlate with increased disease activity and osteopenia with no obvious muscular injury. Conclusion: Managing Vitamin D deficiency (VDD) has been taken up as a major step in COVID-19 affection. The markers of bone metabolism and their correlation with serum Vitamin D were equivocal in COVID-19-affected and not affected Indian populations. The risk of infection has been more in diabetic, hypertensive, and rheumatoid arthritis patients, all of whom were also suffering from VDD.

Akut koroner sendromlarda sistemik immün-inflamasyon indeksi ve yüksek duyarlılıklı kardiyak troponin T

Aim: Acute coronary syndromes (ACSs) are classified as ST-segment elevated myocardial infarction (STEMI), non-ST-segment elevated myocardial infarction (NSTEMI) and unstable angina pectoris (USAP). Cardiac troponins constitute the cornerstone biomarkers for the laboratory diagnosis of ACS. In this study, we aimed to investigate whether systemic immune-inflammation index (SII) is associated with peak cardiac troponin T (TnT) levels in ACS.Methods: Consecutive patients with ACS whose coronary angiography was performed were included in the present study (n=397). Admission SII was determined as platelet count x neutrophil count/lymphocyte count. Serum levels of cardiac enzymes, including high-sensitivity TnT and creatine kinase-myocardial band (CK-MB), were measured at the time of admission and repeated daily during patients’ hospital stay.Results: Patients were categorized as namely STEMI (n=92) and NSTEMI/USAP (n=141). The findings obtained in this study showed that the median of SII levels was higher in STEMI than NSTEMI/USAP at a significant level. Correlation analysis of SII with various clinical and laboratory parameters demonstrated a significant correlation with C-reactive protein, peak CK-MB (r=0.52, p&amp;lt;0.001), peak TnT (r=0.49, p&amp;lt;0.001) and left ventricular ejection fraction (r= -0.48, p&amp;lt;0.001). Multivariate linear regression analysis identified age and log-SII (Beta Coefficient: 1.29, 95% Confidence Interval: 0.93-1.66, p&amp;lt;0.001) as independent predictors of peak TnT levels.Conclusion: SII is an independent predictor of peak TnT levels and significantly correlates with peak CK-MB levels in patients with ACS. SII significantly and inversely correlates with left ventricular systolic functions.