Troponin Levels Research Articles

Association Between High Sensitivity Troponin Levels Following Pediatric Orthotopic Heart Transplantation and Intensive Care Unit Resource Utilization.

The utility of troponin levels, including high sensitivity troponin T (hs-TnT), after orthotopic heart transplant (OHT) is controversial. Conflicting data exist regarding its use as a marker of acute rejection. Few studies have examined possible associations of hs-TnT levels immediately after OHT with metrics of intensive care unit (ICU) resource utilization or risk of acute rejection. We performed a retrospective cohort chart review including all OHT recipients < 20years of age at our center between June 2019 and December 2022. Patients were divided into two groups based on supra- or sub-median initial hs-TnT levels (median 3462.5ng/L). Primary outcome was days requiring ICU-level care, secondary outcomes included days intubated, days requiring positive pressure ventilation (PPV), days on inotropic medications, actual ICU length of stay, Vasoactive Inotrope Scores (VIS) on postoperative days (POD) 0 through 7, and acute rejection at 30days and one year after OHT. Patients with higher hs-TnT required ICU level care for longer [13.5 (10-17.5) vs. 9.5 (8-12) days, p = 0.01] and spent more days intubated [6 (4-7) vs. 3 (3-5) days, p < 0.001], on PPV [9 (6-15) vs. 6 (5-8.5) days, p = 0.02], and on inotropes [11 (9-14) vs. 8 (7-11) days, p = 0.025]. VIS was only different between groups on POD7 [5 (3-7) vs. 3 (0-5), p = 0.04]. There was no difference in rejection between the groups. Higher hs-TnT immediately following pediatric OHT may predict higher ICU resource utilization, despite no difference in VIS, although it does not predict acute rejection in the first year after OHT.

Зв’язок рівня інтерлейкіну-6 з клінічним перебігом гострої тромбоемболії легеневої артерії

The aim – to investigate the possible influence of the level of interleukin-6 (IL-6) on the clinical course and remodeling of the right ventricle (RV) in patients with acute pulmonary embolism (PE).Materials and methods. 56 patients with a diagnosis of acute PE, confirmed by сomputed tomographic pulmonary angiography (CTPA), and in whom the level of IL-6 was determined, were studied. The patients were divided into two groups: 1 group with a normal IL-6 level (less than 5.9 pg/ml), 2 group with an elevated IL-6 level (more than 5.9 pg/ml). Clinical and anamnestic and laboratory-instrumental data were analyzed, statistical analysis of the resulting figures was carried out.Results and discussion. When comparing the groups depending on the level of IL-6, it was found that in group 1, not a single case of high-risk PE was recorded (p=0.052), while there was a significantly higher percentage of moderate-low-risk patients, p&lt;0.05. Patients in group 2 had a higher heart rate (p=0.0006), lower SBP (p=0.04) at admission, and a tendency to increase body mass index (p=0.089). In addition, in group 2, the average levels of leukocytes (p=0.046), d-dimer (p=0.007), CRP (p=0.004) were higher, and the level of lymphocytes (p=0.008) was lower than in group 1, and the trend was determined to an increase in neutrophils (p=0.07) and CPK MB (p=0.89) in the 2nd group. According to the ultrasound data, in group 2 there was more often the detection of thrombosis of the veins of the lower extremities (p=0.003), a significantly larger size of the RV (p=0.02), a tendency to increase the size of the right atrium (RA) and a higher level of systolic pulmonary pressure (p=0.068 ). Analysis of the CTPA showed a greater dilatation of the left LA (p=0.0297) and an increase in the LV/LV index (p=0.0072) in the 2nd group. Correlation analysis revealed an inverse connection with the level of SpO2 (p=0.03) and lymphocytes (p=0.0065), a direct connection with heart rate (p&lt;0.001), the ratio of LV/LV index (p=0.046), with the level of troponin I (p=0.014), D-dimer (p=0.026), leukocytes (p=0.026), neutrophils (0.038) and glucose (0.016), as well as the trend regarding the connection between the IL-6 level and the size of the RV according to echocardiography (p=0.07) and CPK MB level (p=0.086). The data of ROC analysis showed the connection of dilatation of the RV and Il-6 from the level of more than 7.65 pg/ml, with a sensitivity of the indicator of 90 %, specificity of 50 %.Conclusions. An Il-6 level increase is more common in elderly patients, patients with venous thrombosis of the lower extremities, tachycardia, hypotension, and with a greater risk of an adverse course during the hospital period. In 2 groups, a higher level of other markers of inflammation (leukocytes, CRP), larger sizes of the RV, a higher level of pulmonary artery pressure according to echocardiography and values of RV/LV according to CTPA results are observed. A direct connection between IL-6 level and heart rate, troponin level, D-dimer level, LV/LV ratio and inverse connection with saturation and lymphocyte level was established according to correlation analysis. Multivariate regression analysis established an independent connection between the IL-6 level and some laboratory (CPK MB, blood glucose) and echocardiographic parameters (RA, LV ESD, LV EDV, LV ESV, LV EF). The threshold level of Il-6, which is accompanied by dilatation of the RV according to Roc-analysis data, was determined.

A Comparative Study: Cardioprotective Effects of High-Intensity Interval Training Versus Ischaemic Preconditioning in Rat Myocardial Ischaemia-Reperfusion.

(1) Background: Years of research have identified ischemic preconditioning (IPC) as a crucial endogenous protective mechanism against myocardial ischemia-reperfusion injury, enhancing the myocardial cell's tolerance to subsequent ischemic damage. High-intensity interval training (HIIT) is promoted by athletes because it reduces exercise duration and improves metabolic response and cardiopulmonary function. Our objective was to evaluate and compare whether HIIT and IPC could reduce myocardial ischemia and reperfusion injury in rats. (2) Methods: Male Sprague-Dawley rats were divided into four groups: sham surgery, coronary artery occlusion (CAO), high-intensity interval training (HIIT), and ischemic preconditioning (IPC). The CAO, HIIT, and IPC groups experienced 40 min of coronary artery occlusion followed by 3 h of reperfusion to induce myocardial ischemia-reperfusion injury. Subsequently, the rats were sacrificed, and blood samples along with cardiac tissues were examined. The HIIT group received 4 weeks of training before surgery, and the IPC group underwent preconditioning before the ischemia-reperfusion procedure. (3) Results: The HIIT and IPC interventions significantly reduced the extent of the myocardial infarction size and the levels of serum troponin I and lactate dehydrogenase. Through these two interventions, serum pro-inflammatory cytokines, including TNF-α, IL-1β, and IL-6, were significantly decreased, while the anti-inflammatory cytokine IL-10 was increased. Furthermore, the expression of pro-apoptotic proteins PTEN, caspase-3, TNF-α, and Bax in the myocardium was reduced, and the expression of anti-apoptotic B-cell lymphoma 2 (Bcl-2) was increased, ultimately reducing cellular apoptosis in the myocardium. In conclusion, both HIIT and IPC demonstrated effective strategies with potential for mitigating myocardial ischemia-reperfusion injury for the heart.

Irisin protects against cardiac injury by inhibiting NLRP3 inflammasome-mediated pyroptosis during remodeling after infarction

This study aimed to explore the cardioprotective mechanism of irisin in the context of cardiac injury. Utilizing a myocardial infarction (MI) mouse model, we investigated the therapeutic potential of recombinant human irisin (rhIrisin) administered for 28 days post-infarction. The efficacy of irisin treatment was evaluated through echocardiographic assessment of cardiac function and serum analysis of myocardial injury markers. Our research provided novel insights into the impacts of irisin on the NLR Family Pyrin Domain Containing 3 (NLRP3) inflammasome activation and pyroptosis, assessed both in vivo in MI mice and in vitro in hypoxia/reoxygenation-treated H9C2 cells. Remarkably, irisin treatment significantly reduced levels of lactate dehydrogenase (LDH), creatine kinase-MB (CK-MB), and troponin I, indicating reduced myocardial injury. Echocardiography highlighted substantial improvements in left ventricular ejection fraction (LVEF), left ventricular fractional shortening (LVFS), and dimensions (LVIDd and LVIDs) in irisin-treated mice, underscoring enhanced cardiac function. Moreover, irisin was shown to significantly suppress the mRNA and protein expressions of key components involved in NLRP3 inflammasome pathway (NLRP3, ASC, caspase-1 (p20), and interleukin-18 (IL-18)) both in MI-induced mice and hypoxia/reoxygenation-treated cells. This study firstly reveals that the cardioprotective effect of irisin is mediated through the attenuation of NLRP3 inflammasome activation and pyroptosis, positioning irisin as a promising therapeutic agent for cardiac injury.

Phosphofructokinase mainly affects glycolysis and influences meat quality in postmortem meat

The aim of this study was to evaluate the comparative effects of hexokinase (HK), phosphofructokinase (PFK) and pyruvate kinase (PK) on glycolysis in postmortem meat. Three specific inhibitors were respectively added to postmortem lamb to produce a HK inhibition (HKI) group, a PFK inhibition (PFKI) group and a PK inhibition (PKI) group. Meat samples that assigned to these three groups and a control (CON) group were stored at 4 °C for 5 d. The results indicated that the activity of HK, PFK and PK were effectively restrained during storage. PFK activity was significantly correlated with lactate content (P < 0.05), but HK and PK activity showed a weak relationship with lactate content (P > 0.05). The myofibrillar fragmentation index of the PFKI and PKI groups were significantly lower than that of the CON and HKI groups (P < 0.05). The degradation levels of troponin T and desmin were the smallest in the PFKI group. The result of the myoglobin spectrum at 540 nm and 580 nm showed a decreasing level of oxymyoglobin after HK, PFK and PK inhibition. In conclusion, PFK showed a more dominant effect on glycolysis than HK and PK in postmortem muscle, which may provide a targeted strategy for meat quality regulation through glycolysis.

Genetic and clinical study of myeloperoxidase's association with coronary artery disease.

Unraveling myeloperoxidase's (MPO) correlation with coronary artery disease (CAD) and genetic variations, this study seeks to enhance diagnostic precision and therapeutic strategies. CAD patients were found to be older and more male than controls. Several clinical parameters, including glucose, total bilirubin, alkaline phosphatase, creatinine, and troponin levels, showed significant variations. Moreover, CAD patients had lower red cell distribution width (RDW%) and mean platelet volume (MPV) than controls. Serum MPO levels did not differ significantly between CAD patients and controls, and no correlation was found with other clinical parameters except for glucose, creatinine, and total bilirubin. The data suggest that serum MPO levels are not substantially related to CAD patients, as indicated by lower MPO levels in CAD patients compared to controls. While highlighting the potential of MPV and RDW% as predictors of severe atherosclerosis in CAD. Further research is needed to validate the diagnostic and prognostic value of RDW%, MPV, and MPO levels in CAD. 15092021-9-12. Registered 15 September 2021.

The first experience of the combined use of nitric oxide and molecular hydrogen for cardiac surgery in high-risk patients

The purpose of the study was to evaluate the effectiveness of myocardial protection with a combined supply of nitric oxide (NO) (40 ppm) and hydrogen (1.2 ppm) into the gas-air mixture delivery line of the cardiopulmonary bypass (CPB) machine during the entire period of CPB.Methods. The study included patients (n = 91) who had cardiac surgery under cardiopulmonary bypass and pharmacological cold cardioplegia. Patients were randomized into 3 groups. The Group 1 (n = 30) was control. Groups 2 (n = 28) and 3 (n = 33) received an isolated supply of NO (40 ppm) and a combined supply of NO (40 ppm) and hydrogen (1.2 ppm) into the extracorporeal IR circuit, respectively. During the postoperative period, clinical and functional indicators were studied (dynamics of myocardial contractile function according to ultrasound data); duration of artificial pulmonary ventilation (ALV); stay in the intensive care unit; hospital stay; mortality; level of marker of myocardial injury – troponin I (cTnI). Myocardial injury index (MII) was calculated to assess the degree of injury.Results. It was found that the level of cTnI in the postoperative period increased statistically significantly in all groups but was statistically significantly lower in Groups 2 and 3 compared to Group 1 at the end of the surgery and 12 and 24 hours after the surgery. Also, level of cTnI was statistically significantly lower in Group 3 at all stages of the study compared to Group 1 and after 12, 24 and 48 hours compared to Group 2. Statistically significantly lower MII values were revealed at all stages of the postoperative period in Group 3 compared with Groups 1 and 2. Changes in indicators of myocardial contractile function suggest an earlier and more complete recovery in Groups 2 and 3 (the changes were statistically significantly higher than that in Group 1). In Groups 2 and 3, the incidence of acute heart failure was statistically significantly lower (p = 0.046) compared to Group 1, according to Fisher’s exact test. There were no statistically significant differences in the incidence of acute respiratory and multiple organ failure in Groups 2 and 3 compared to Group 1. Also, patients of Groups 2 and 3 did not experience any complications in the early postoperative period. In Group 3, there was a statistically significant decrease in the duration of mechanical ventilation and stay in the intensive care unit after surgery compared to Group 2.Conclusion. Isolated supply of NO into the IR circuit has an additional cardioprotective effect, which is confirmed by statistically lower levels of troponin I and smaller changes in the indicators of myocardial contractile function during the postoperative period compared to standard technology. A more pronounced protective effect on the myocardium was shown with the combined supply of NO and molecular hydrogen to the IR circuit as seen by statistically lower levels of troponin I and MII in the postoperative period compared with the isolated supply of NO.

Cardiac Troponin Serum Concentration Measurement Is Useful Not Only in the Diagnosis of Acute Cardiovascular Events.

Cardiac troponin serum concentration is the primary marker used for the diagnosis of acute coronary syndrome. Moreover, the measurement of cardiac troponin concentration is important for risk stratification in patients with pulmonary embolism. The cardiac troponin level is also a general marker of myocardial damage, regardless of etiology. The purpose of this study is to conduct a literature review and present the most important information regarding the current state of knowledge on the cardiac troponin serum concentration in patients with chronic cardiovascular disease (CVD), as well as on the relationships between cardiac troponin serum concentration and features of subclinical cardiovascular dysfunction. According to research conducted to date, patients with CVDs, such as chronic coronary syndrome, chronic lower extremities' ischemia, and cerebrovascular disease, are characterized by higher cardiac troponin concentrations than people without a CVD. Moreover, the literature data indicate that the concentration of cardiac troponin is correlated with markers of subclinical dysfunction of the cardiovascular system, such as the intima-media thickness, pulse wave velocity, ankle-brachial index, coronary artery calcium index (the Agatston score), and flow-mediated dilation. However, further research is needed in various patient subpopulations and in different clinical contexts.

Mortality Predictors in Patients with Cardiovascular Involvement by COVID-19

Introduction: SARS-CoV-2 is a new coronavirus responsible for one of the most evident diseases today, COVID-19, registering approximately 419,000 deaths until 2020. Some risk factors for infection and mortality must be assessed in clinical and research scenarios, such as the presence of cardiovascular diseases, with clinical and laboratory alterations. Objective: Our study aims to analyze the association between clinical and laboratory data and in-hospital mortality in patients with cardiovascular involvement by COVID-19 in Brazil. Method: This is a retrospective, observational, single-center cohort study. The sample consisted of patients admitted to a reference hospital from July 2020 to April 2021. We included patients over 18 years of age, hospitalized with COVID-19 infection, who developed heart involvement identified by clinical or laboratory findings. Patients who were pregnant or had negative serological tests for COVID-19 were excluded. Clinical variables such as gender, age, comorbidities, medications used during hospitalization, chest computed-tomography findings, need for intensive care unit, need for mechanical ventilation, and need for intravenous vasoactive drugs were analyzed. The laboratory variables analyzed were: troponin, NT-proBNP and D-dimer levels. The endpoint of the study was in-hospital death. Statistical analysis of the collected data was performed using Pearson&amp;apos;s Chi-square test, Student&amp;apos;s T test; p values &amp;lt; 0.05 were considered statistically significant. Results: 139 patients were included, and 30 (21.58%) patients died during hospitalization. The group that evolved to death, compared to the discharge group, was older (71 vs 65 years; p = 0.03), had more pleural effusion on chest computed-tomography (36% vs 17%; p = 0.023), had higher troponin levels (40% vs 20%; p = 0.02), more need for intensive care (83% vs 52%; p = 0.002), orotracheal intubation (83% vs 26%; p = 0.001), use of norepinephrine (76% vs 18%; p = 0.001), use of dobutamine (16% vs 4%; p = 0.023), and use of unfractioned heparin (46% vs 21%; p = 0.005). Conclusion: Advanced age was significantly associated with in-hospital death. In radiological patterns, despite the high incidence of ground-glass opacities, pleural effusion was the only finding associated with mortality. Increased troponin levels, but not NT-proBNP or D-dimer, was associated with in-hospital mortality. The need for norepinephrine and dobutamine, in addition to Intensive Care Unit admission and orotracheal Intubation, were also more frequent in the group that presented death during hospitalization, as wells as the use of unfractionated heparin rather than enoxaparin.

Colchicine alleviates myocardial ischemia-reperfusion injury in mice by activating AMPK

To investigate the protective effect of colchicine against myocardial ischemia-reperfusion injury (I/R) and explore the underlying mechanism. H9C2 cells exposed to hypoxia/reoxygenation (H/R) were treated with 3 nmol/L colchicine, after which the changes in cell viability were assessed using MTT assay, and AMPK phosphorylation, the expressions of NOX4, NRF2, SOD2, BAX, Bcl-2, and cleaved caspase-3 were detected with Western blotting. Male C57BL/6 mice were randomized into sham operation, I/R, I/R+colchicine, and I/R+colchicine+dorsomorphin (DSMP) groups. After the treatments, myocardial expressions of p-AMPK/AMPK, 8-OHdG, cleaved caspase-3, mitochondrial BAX (Mito-BAX), and cytoplasmic cytochrome C (Cyt-Cyto C) were examined and cardiac functions, infarct area, ATP content, and serum levels of lactic dehydrogenase (LDH) and cardiac troponin T (cTnT) levels were assessed. In H9C2 cells, H/R exposure significantly reduced AMPK phosphorylation and expressions of NRF2, SOD2, and Bcl-2, lowered cell viability, and up-regulated the expressions of NOX4, BAX, and cleaved caspase-3 (P < 0.05), and these changes were obviously alleviated by colchicine treatment (P < 0.05). In the mouse models, myocardial I/R injury significantly reduced myocardial AMPK phosphorylation level, ATP content, and expressions of NRF2, SOD2 and Bcl-2, caused cardiac function impairment, enhanced NOX4, Mito-BAX, Cyt-Cyto C, BAX, 8-OHdG, and cleaved caspase-3 expressions, and increased infarct area and serum LDH and cTnT levels (P < 0.05). Colchicine treatment significantly reversed the damaging effects of I/R (P < 0.05), but its protective effects was obviously antagonized by DSMP (P < 0.05). Colchicine alleviates myocardial I/R injury and protects cardiac function in mice by reducing myocardial oxidative stress and apoptosis via activating AMPK.

Individualized Perioperative Hemodynamic Management Using Hypotension Prediction Index Software and the Dynamics of Troponin and NTproBNP Concentration Changes in Patients Undergoing Oncological Abdominal Surgery.

Abdominal oncologic surgeries pose significant risks due to the complexity of the surgery and patients' often weakened health, multiple comorbidities, and increased perioperative hazards. Hypotension is a major risk factor for perioperative cardiovascular complications, necessitating individualized management in modern anesthesiology. This study aimed to determine the dynamics of changes in troponin and NTproBNP levels during the first two postoperative days in patients undergoing major cancer abdominal surgery with advanced hemodynamic monitoring including The AcumenTM Hypotension Prediction Index software (HPI) (Edwards Lifesciences, Irvine, CA, USA) and their association with the occurrence of postoperative cardiovascular complications. A prospective study was conducted, including 50 patients scheduled for abdominal cancer surgery who, due to the overall risk of perioperative complications (ASA class 3 or 4), were monitored using the HPI software. Hypotension was qualified as at least one ≥ 1 min episode of a MAP < 65 mm Hg. Preoperatively and 24 and 48 h after the procedure, the levels of NTproBNP and troponin were measured, and an ECG was performed. We analyzed data from 46 patients and found that 82% experienced at least one episode of low blood pressure (MAP < 65 mmHg). However, the quality indices of hypotension were low, with a median time-weighted average MAP < 65 mmHg of 0.085 (0.03-0.19) mmHg and a median of 2 (2-1.17) minutes spent below MAP < 65 mmHg. Although the incidence of perioperative myocardial injury was 10%, there was no evidence to suggest a relationship with hypotension. Acute kidney injury was seen in 23.9% of patients, and it was significantly associated with a number of episodes of MAP < 50 mmHg. Levels of NTproBNP were significantly higher on the first postoperative day compared to preoperative values (285.8 [IQR: 679.8] vs. 183.9 [IQR: 428.1] pg/mL, p < 0.001). However, they decreased on the second day (276.65 [IQR: 609.4] pg/mL, p = 0.154). The dynamics of NTproBNP were similar for patients with and without heart failure, although those with heart failure had significantly higher preoperative concentrations (435.9 [IQR: 711.15] vs. 87 [IQR: 232.2] pg/mL, p < 0.001). Patients undergoing laparoscopic surgery showed a statistically significant increase in NTproBNP. This study suggests that advanced HPI monitoring in abdominal cancer surgery effectively minimizes intraoperative hypotension with no significant NTproBNP or troponin perioperative dynamics, irrespective of preoperative heart failure.

Comparison of Arctic Front Advance Pro and POLARx cryoballoons for ablation therapy of atrial fibrillation: an intraprocedural analysis.

Cryoballoon (CB) ablation has become a popular method for pulmonary vein isolation (PVI) in atrial fibrillation (AF) treatment. This study aimed to compare the intraprocedural ablation characteristics of two cryoballoons, Arctic Front Advance Pro™ (AFA-Pro, Medtronic) and POLARx™ (Boston Scientific). In this retrospective single-center study, 230 symptomatic paroxysmal or persistent AF patients underwent CB ablation with either AFA-Pro or POLARx. Propensity-score matching resulted in two cohorts of 114 patients each. Baseline and procedural characteristics were comparable between both CBs. POLARx achieved lower minimal temperatures (e.g., left superior pulmonary vein, LSPV: AFA-Pro - 49.0°C vs. POLARx - 59.5°C) and lower temperatures at time-to-isolation (TTI). Additionally, POLARx reached lower temperatures faster, as evidenced by lower temperatures after 40 and 60s, and a larger mean temperature change between 20 and 40s. POLARx also had a greater area under the curve below 0°C and a longer thawing phase. Both CBs achieved comparable high rates of final PV-isolation. TTI, minimal esophagus temperature, and first-pass isolation rates were similar between groups. Periprocedural complications, including phrenic nerve injuries, were comparable. Troponin levels in the left atrium were elevated with both systems. Values and change in troponin were numerically higher in the POLARx group (delta troponin: AFA-Pro 36.3 (26.4, 125.4) ng/L vs. POLARx 104.9 (49.5, 122.2) ng/L), p = 0.077). AFA-Pro and POLARx are both highly effective and safe CB systems for PVI. POLARx exhibited significant faster and lower freezing characteristics, and numerically higher troponin levels might indicate greater myocardial injury. However, these differences did not translate into improved performance, procedural efficiency, or safety.

Role of the ubiquitin-proteasome system in the sarcopenic-like phenotype induced by CCL5/RANTES.

Sarcopenia is characterized by reduced muscle strength and mass and a decline in muscle fiber diameter and amount of sarcomeric proteins. Sarcopenia involves the activation of the ubiquitin-proteasome system (UPS). MuRF-1 and atrogin-1 are E3 ubiquitin ligases belonging to UPS, leading to proteolysis mediated by the PSMB 5, 6, and 7 subunits of 20S proteasome. CCL5/RANTES induces a sarcopenic-like effect in muscle cells. The present work explored the impact of CCL5 on UPS components and the influence of UPS on its sarcopenic-like effect. We demonstrated that CCL5 increased MuRF-1 and atrogin-1 protein levels and mRNA levels of subunits PSMB 5, 6, and 7. We used the MG132 inhibitor to elucidate the role of the 20S proteasome in the CCL5-induced sarcopenic-like effect. This inhibitor prevented the decrease in troponin and MHC protein levels and partially prevented the reduction in the diameter of single-isolated FDB muscle fibers induced by CCL5. These findings indicate that CCL5 actively modulates the UPS. Moreover, our results show the direct participation of UPS in the sarcopenic-like phenotype induced by CCL5.

Outcome of Primary Percutaneous Coronary Intervention for STEMI due to Stent Thrombosis

Background: Stent thrombosis (ST) is a critical complication following percutaneous coronary intervention (PCI), contributing significantly to morbidity and mortality in patients with ST-elevation myocardial infarction (STEMI). Advances in drug-eluting stent technology and antiplatelet therapy have mitigated, but not eliminated, the risk of ST. The management of STEMI due to ST in resource-limited settings remains a challenging endeavor, necessitating a comprehensive evaluation of treatment outcomes. Objective: To assess the mortality rates and clinical outcomes following primary PCI in patients with STEMI attributed to stent thrombosis in a resource-constrained setting, and to analyze the association of mortality with patient age and TIMI flow grade post-PCI. Methods: This quasi-experimental study was conducted at Lady Reading Hospital, Peshawar, from July to December 2023. A total of 150 patients presenting with STEMI due to ST and undergoing PCI were included. Diagnostic measures included electrocardiography, troponin levels, echocardiography, and angiography to assess left ventricular function and stent thrombosis. The procedures were performed by experienced interventional cardiologists, followed by standard post-procedure management. Data analysis was performed using SPSS version 25, focusing on mortality rates, the association of mortality with patient age, and TIMI flow grades. Results: Among the 150 patients studied, mortality was observed in 36 cases (24%). The mean age of patients who died was 48.33 years (SD = 14.267), compared to 42.47 years (SD = 12.618) for survivors, with a significant association between age and mortality (P = 0.02). Analysis of TIMI flow grade post-PCI revealed a strong correlation with mortality; patients with TIMI flow grades I and II exhibited higher mortality rates, with a highly significant P value of 0.0001. Conclusion: The study highlights a significant mortality rate among patients with STEMI due to stent thrombosis undergoing primary PCI in a resource-limited setting. Advanced age and lower TIMI flow grades post-PCI were significantly associated with increased mortality. These findings underscore the necessity for vigilant post-PCI monitoring and tailored management strategies to improve clinical outcomes in this high-risk population.

Clinical Biochemistry of Serum Troponin.

Accurate measurement and interpretation of serum levels of troponin (Tn) is a central part of the clinical workup of a patient presenting with chest pain suspicious for acute coronary syndrome (ACS). Knowledge of the molecular characteristics of the troponin complex and test characteristics of troponin measurement assays allows for a deeper understanding of causes of false positive and false negative test results in myocardial injury. In this review, we discuss the molecular structure and functions of the constituent proteins of the troponin complex (TnT, TnC, and TnI); review the different isoforms of Tn and where they are from; survey the evolution of clinical Tn assays, ranging from first-generation to high-sensitivity (hs); provide a primer on statistical interpretation of assay results based on different clinical settings; and discuss potential causes of false results. We also summarize the advances in technologies that may lead to the development of future Tn assays, including the development of point of care assays and wearable Tn sensors for real-time continuous measurement.

Endothelial dysfunction and cardiovascular risk in post-COVID-19 patients after 6- and 12-months SARS-CoV-2 infection.

SARS-CoV-2 infection causes severe endothelial damage, an essential step for cardiovascular complications. Endothelial-colony forming cells (ECFCs) act as a biomarker of vascular damage but their role in SARS-CoV-2 remain unclear. The aim of this study was to assess whether the number of ECFCs and angiogenic biomarkers remained altered after 6 and 12-months post-infection and whether this imbalance correlated with the presence of long-COVID syndrome and other biological parameters measured. Seventy-two patients were recruited at different time-points after overcoming COVID-19 and thirty-one healthy controls. All subjects were matched for age, gender, BMI, and comorbidities. ECFCs were obtained from peripheral blood and cultured with specific conditions. The results confirm the presence of a long-term sequela in post-COVID-19 patients, with an abnormal increase in ECFC production compared to controls (82.8% vs. 48.4%, P < 0.01) that is maintained up to 6-months (87.0% vs. 48.4%, P < 0.01) and 12-months post-infection (85.0% vs. 48.4%, P < 0.01). Interestingly, post-COVID-19 patients showed a significant downregulation of angiogenesis-related proteins compared to controls indicating a clear endothelial injury. Troponin, NT-proBNP and ferritin levels, markers of cardiovascular risk and inflammation, remained elevated up to 12-months post-infection. Patients with lower numbers of ECFC exhibited higher levels of inflammatory markers, such as ferritin, suggesting that ECFCs may play a protective role. Additionally, long-COVID syndrome was associated with higher ferritin levels and with female gender. These findings highlight the presence of vascular sequela that last up to 6- and 12-months post-infection and point out the need for preventive measures and patient follow-up.

Impact of prolonged exposure to occasional and regular waterpipe smoke on cardiac injury, oxidative stress and mitochondrial dysfunction in male mice.

Regular waterpipe smoking (Reg-WPS) is well recognized for its deleterious effect on the heart. However, there is a paucity of experimental studies on the impact of occasional waterpipe smoking (Occ-WPS), also known as nondaily smoking, versus Reg-WPS on cardiac homeostasis, and the mechanisms underlying these effects. Hence, we aimed, in the present study, to investigate the effect of Occ-WPS (30min/day, 1day/week) versus Reg-WPS (30min/day, 5days/week) for 6months on systolic blood pressure (SBP), cardiac injury, oxidative markers, chemokines, proinflammatory cytokines, DNA damage and mitochondrial function compared with air (control) exposed mice. Our results show that SBP was increased following exposure to either Occ-WPS or Reg-WPS compared with air-exposed mice. Moreover, we found that only Reg-WPS induced a significant elevation in the levels of troponin I, brain natriuretic peptide, lactate dehydrogenase, and creatine phosphokinase. However, the atrial natriuretic peptide (ANP) was significantly increased in both Occ-WPS and Reg-WPS groups. Compared with air-exposed mice, the levels of lipid peroxidation, reduced glutathione and monocyte chemoattractant protein-1 were only significantly augmented in the Reg-WPS. However, catalase, superoxide dismutase, and CXCL1 were significantly increased in both Occ-WPS and Reg-WPS. The concentrations of the adhesion molecules E-selectin, vascular cell adhesion molecule-1, and intercellular adhesion molecule-1 were solely elevated in the heart of mice exposed to Reg-WPS. Similarly, the concentrations of interleukin-1β and tumor necrosis factor α were only significantly augmented in the Reg-WPS. However, both Occ-WPS and Reg-WPS triggered significant augmentation in the levels of IL17 and DNA damage compared to the control groups. Furthermore, while Occ-WPS induced a slight but statistically insignificant elevation in the concentrations of mammalian targets of rapamycin and nuclear factor erythroid-derived 2-like 2 (Nrf2) expression, Reg-WPS exposure increased their levels substantially, in addition to p53 and mitochondrial complexes II & III, and IV activities compared with air-exposed mice. In conclusion, our findings show that while the long-term Occ-WPS exposure induced an elevation of SBP, ANP, antioxidant enzymes, IL17, CXCL1, and cardiac DNA damage, Reg-WPS exposure was consistently associated with the elevation of SBP and occurrence of cardiac damage, inflammation, oxidative stress, DNA damage and mitochondrial dysfunction.

Analysis of Age-Specific Predictors of Mortality in Patients with Coronavirus Disease 2019.

We investigated predictors of mortality, including demographic, clinical, and laboratory parameters, in hospitalized patients with coronavirus disease 2019 (COVID-19) pneumonia. This retrospective, single-center study included 651 consecutive Turkish adults who had been admitted to the emergency department with a diagnosis of COVID-19. We recorded the demographic, clinical, and laboratory parameters of the patients. The patients were divided into two groups: patients aged ≥65 years and patients aged <65 years. The predictors of mortality for hospitalized COVID-19 patients were evaluated. The study included 651 patients (354 [54.4%] men and 297 [45.6%] women; mean age, 56.40 ± 15.70 years). The most common comorbidities were hypertension (37.6%), diabetes mellitus (28.9%), and coronary artery disease (CAD) (16.1%). The overall mortality rate was 10.6% (n = 69); the mortality rate was higher in men than in women. Advanced age; chronic renal failure (CRF); prolonged activated partial thromboplastin time; high serum neutrophil and platelet counts; high C-reactive protein to albumin (CRP/albumin) ratio; and high levels of albumin, lactate dehydrogenase (LDH), and high-sensitivity troponin I (TnI-hs) were independent predictors of mortality in all age groups. Multivariate logistic regression analysis showed that chronic obstructive pulmonary disease (COPD), high serum platelet count, high CRP/albumin ratio, and high levels of albumin, TnI-hs, and D-dimer were independent predictors of mortality in patients aged <65 years. Conversely, advanced age, CAD, CRF, and high levels of serum CRP and LDH were independent predictors of mortality in patients aged ≥65 years.

N-phenyl and N-benzyl substituted succinimides: Preclinical evaluation for their antihypertensive effect and underlying mechanism

The study was designed to investigate the antihypertensive potential of 2-(2, 5-dioxo-1-phenylpyrrolidin-3-yl)-3-(4-isopropylphenyl)-2-methylpropanal (Comp-1) and 2-(1-benzyl-2,5-dioxopyrrolidin-3-yl)-3-(4-isopropylphenyl)-2-methylpropanal (Succ-5) in rats. The study results showed that, just like nifedipine (the standard reference drug), the test compounds, Comp-1 (at doses of 15 and 20 mg/kg) and Succ-5 (at a dose of 20 mg/kg) had significant antihypertensive effect against deoxycorticosterone acetate-salted rats. The test compounds maintained the level of cardiac markers troponin I and creatinine kinase myocardial bands (CK-MB) in serum, and modulate the oxidative stress markers Glutathione s-transferase (GST) activity, reduced glutathione (GSH), catalase levels, and lipid peroxidation (LPO). These compounds also reduced the expression of inflammatory markers, including cyclooxygenase-2 (COX-2) and tumor necrosis factor alpha (TNF-α) in heart tissues. Furthermore, in the ex-vivo study, the test substances relaxed the contractions induced by phenylephrine (PE) and potassium (K+). Vasodilation was endothelium-independent because the test substances showed nearly the same effect in aortic rings with intact endothelium, denuded endothelium, and with L-NAME pretreatment. The test compounds shifted the calcium curve to the right, i.e., contraction was inhibited and decreased the maximal response. This study demonstrated the antihypertensive, anti-inflammatory, antioxidant, and vasodilate effects of the test compounds. In addition, the results supported the phenomenon of calcium channel blockades responsible for vasodilation.

Complexity of coronary artery disease and the release of cardiac biomarkers after CABG.

In patients with complex coronary artery disease (CAD) undergoing cardiac surgery, myocardial protection might be impaired due to microvascular obstruction, resulting in myocardial injury and subsequent biomarker release. Therefore, this study investigated the correlation between the complexity of CAD, reflected by the SYNTAX Score, and the release of cardiac biomarkers after CABG. In a consecutive series of 919 patients undergoing isolated CABG SYNTAX scores I and II were calculated to assess the complexity of CAD. Levels of high sensitivity cardiac troponin T (hs-cTnT) and creatine kinase-myocardial band (CK-MB) were routinely measured once before and serially after surgery. Patients were divided into tertiles according to their SYNTAX Scores I and II. Spearman correlations and regression models were performed to measure the degree of association between the release of hs-cTnT and CK-MB and the SYNTAX Scores. Patients with a higher SYNTAX Score I had more comorbidities reflected in a higher EuroSCORE II. Preoperatively, higher levels of cardiac biomarkers were found in patients with higher SYNTAX Score II. No correlation was observed between hs-cTnT, CK-MB and SYNTAX Score I or II. Regression models did not show any association between cardiac biomarkers and the complexity of CAD. The complexity of CAD is not associated with the release of cardiac biomarkers after CABG. Factors influencing postoperative biomarker release need to be elucidated in future trials to include postoperative biomarker release into risk stratification models predicting outcome after cardiac surgery.