Acute post-streptococcal glomerulonephritis (APSGN) is the most common glomerulonephritis of childhood, and clinical presentation can vary widely. This case report presents an atypical manifestation of APSGN in an 8-year-old female patient with pleuritic chest pain and elevated troponin-I, despite lacking classical kidney symptoms. Imaging studies showed cardiomegaly and interstitial lung opacities. Further investigations revealed hematuria and proteinuria, and the diagnosis was confirmed through elevated antistreptolysin-O (ASO) titers and low complement 3 (C3) levels. The patient was successfully managed with fluid restriction, diuretics, and antihypertensives, resulting in the resolution of symptoms and normalization of laboratory values. This case highlights the significance of recognizing atypical manifestations of APSGN for ensuring prompt diagnosis and proper management in the pediatric population.

OBJECTIVE: It is unclear how serial high-sensitivity troponin-I (hsTnI) concentrations affect long-term prognosis in individuals with suspected acute coronary syndrome (ACS).
RESULTS: Subjects who underwent two hsTnI measurements (Siemens TnI Flex® Reagent) separated by 1-7 h, during a first-time hospitalization for myocardial infarction, unstable angina, observation for suspected myocardial infarction, or chest pain from 2012 through 2019, were identified through Danish national registries. Individuals were stratified per their hsTnI concentration pattern (normal, rising, persistently elevated, or falling) and the magnitude of hsTnI concentration change (<20%, >20-50%, or >50% in either direction). We calculated absolute and relative mortality risks standardized to the distributions of risk factors for the entire study population. A total of 20 609 individuals were included of whom 2.3% had died at 30 days, and an additional 4.7% had died at 365 days. The standardized risk of death was highest among persons with a persistently elevated hsTnI concentration (0-30 days: 8.0%, 31-365 days: 11.1%) and lowest among those with two normal hsTnI concentrations (0-30 days: 0.5%, 31-365 days: 2.6%). In neither case did relative hsTnI concentration changes between measurements clearly affect mortality risk. Among persons with a rising hsTnI concentration pattern, 30-day mortality was higher in subjects with a >50% rise compared with those with a less pronounced rise (2.2% vs. <0.1%).
CONCLUSIONS: Among individuals with suspected ACS, those with a persistently elevated hsTnI concentration consistently had the highest risk of death. In subjects with two normal hsTnI concentrations, mortality was very low and not affected by the magnitude of change between measurements.
In this Danish study of >20 000 individuals with suspected heart attack, we confirmed the clinical importance of drawing two consecutive blood samples for measurement of high-sensitivity troponin-I concentrations (a marker of damage to the heart): The risk of death was highest in persons with two elevated high-sensitivity troponin-I concentrations and lowest in those with two normal concentrations.Among persons who had a first normal and a subsequently elevated high-sensitivity troponin-I concentration, a >50% relative rise was associated with significantly higher risk of death at 30 days.

Myocardial infarction (MI) is a leading cause of death. Lipid-lowering interventions have been shown to decrease coronary events and mortality of MI and heart failure. In this investigation, we assessed the anti-hyperlipidemic effects of β-caryophyllene in isoproterenol-induced myocardial infarcted rats. β-Caryophyllene (20 mg/kg body weight) pre-and co-treatment was given to rats orally, daily, for 3 weeks. Isoproterenol (100 mg/kg body weight) was administered to rats to induce MI. The levels of serum cardiac troponins T and I, serum and heart total cholesterol, triglycerides, free fatty acids, and the levels of serum low-density and very low-density lipoprotein-cholesterols were augmented, and the level of serum high-density lipoprotein-cholesterol was lessened in myocardial infarcted rats. Further, the activity/levels of liver 3-hydroxy-3-methylglutaryl-coenzyme A reductase and plasma thiobarbituric acid reactive substances were amplified and the activity/levels of heart glutathione -S- transferase, vitamin C, and vitamin E were lessened by isoproterenol. A down-regulated expression of liver sterol regulatory element-binding protein-2 and liver low-density lipoprotein-receptor genes was observed by a reverse transcription-polymerase chain reaction study. Moreover, histopathology of Sudan III staining revealed an accumulation of fats in the heart of isoproterenol-induced rats. Nevertheless, β-caryophyllene pre-and co-treatment blocked alterations in all the parameters examined in isoproterenol-induced rats and inhibited the risk of MI. Moreover, the in vitro study revealed the potent free radical scavenging and antioxidant effects of β-caryophyllene. β-Caryophyllene\'s antioxidant and anti-hyperlipidemic properties are the possible mechanisms for the observed protective effects in this investigation.

BACKGROUND: Plasma concentrations of cardiac troponins increase in healthy individuals after strenuous training, but the response to lower exercise intensities has not been characterized.
OBJECTIVE: To determine whether exercise at moderate intensity significantly increases plasma cardiac troponins measured with different assays in healthy recreational athletes.
METHODS: Twenty-four self-reported healthy volunteers were instructed to complete three 60-min bouts of treadmill running at variable intensities: High-intensity training (HIT) including a maximal exercise test and an anaerobic threshold test followed by training at 80%-95% of maximum heart rate (HRmax ), Moderate-intensity training (MIT) at 60%-75% of HRmax , and Low-intensity training (LIT) at 45%-55% of HRmax . Blood samples were collected before and at 2, 4, and 6 h after HIT and 4 h after MIT and LIT. Troponin I and T were measured in plasma samples with assays from Abbot, Siemens, and Roche.
RESULTS: Plasma troponins measured with all assays were significantly increased compared to baseline after HIT but not after LIT. After HIT, the fraction of all participants with one or more values above the assay-specific 99th percentiles ranged from 13% to 61%. The biomarker criteria for acute myocardial injury were met after HIT for troponin T in 75% of female participants having no clinical evidence of coronary artery disease.
CONCLUSIONS: High-intensity, but not moderate- or low-intensity, training for 60 min induced a potentially clinically significant increase in plasma cardiac troponins in healthy volunteers. Results exceeding the population 99th percentiles were most frequent with the troponin T assay.

UNASSIGNED: An acute ST-elevation myocardial infarction (STEMI) is a serious cardiovascular condition with a high risk of morbidity and mortality. Irisin is adipomyokine that is associated with various health conditions. In post-STEMI, elevated serum irisin levels are associated with more adverse cardiovascular events.
UNASSIGNED: The purpose of this study was to investigate associations between the serum irisin levels and acute MI (AMI) and whether irisin may be a useful biomarker for severity of AMI in patients with STEMI. Possible correlations between serum irisin and cardiac troponin-I (cTi) levels were investigated.
UNASSIGNED: A total of 90 subjects (46 control subjects and 44 STEMI patients) were included in the study. Besides demographic data, presence of diabetes mellitus and hypertension, electrocardiography (ECG) findings, blood biochemistry, cardiac biomarkers (cTi) and serum irisin levels were examined.
UNASSIGNED: Significantly lower heart rate (HR) and significantly higher ST-elevation and QTc interval were detected in ECG recordings in STEMI patients (p < 0.05). Serum irisin levels were significantly lower in STEMI patients compared to the control subjects (p < 0.001). The decrease in the serum irisin levels was significantly correlated with the increase in cTi levels, as well as increased QTc (p < 0.05). The sensitivity and specificity of irisin were found to be 93% and 78%, respectively.
UNASSIGNED: Decreased irisin levels were found to be highly predictive in STEMI. In patients with STEMI, the serum irisin levels were associated with cTi levels and QTc, suggesting that irisin is a promising biomarker for AMI cases.

BACKGROUND: Homocysteine (Hcy) is involved in various methylation processes, and its plasma level is increased in cardiac ischemia. Thus, we hypothesized that levels of homocysteine correlate with the morphological and functional remodeling of ischemic hearts. Thus, we aimed to measure the Hcy levels in the plasma and pericardial fluid (PF) and correlate them with morphological and functional changes in the ischemic hearts of humans.
METHODS: Concentration of total homocysteine (tHcy) and cardiac troponin-I (cTn-I) of plasma and PF were measured in patients undergoing coronary artery bypass graft (CABG) surgery (n = 14). Left-ventricular (LV) end-diastolic diameter (LVED), LV end-systolic diameter (LVES), right atrial, left atrial (LA) area, thickness of interventricular septum (IVS) and posterior wall, LV ejection fraction (LVEF), and right ventricular outflow tract end-diastolic area (RVOT EDA) of CABG and non-cardiac patients (NCP; n = 10) were determined by echocardiography, and LV mass was calculated (cLVM).
RESULTS: Positive correlations were found between Hcy levels of plasma and PF, tHcy levels and LVED, LVES and LA, and an inverse correlation was found between tHcy levels and LVEF. cLVM, IVS, and RVOT EDA were higher in CABG with elevated tHcy (>12 µM/L) compared to NCP. In addition, we found a higher cTn-I level in the PF compared to the plasma of CABG patients (0.08 ± 0.02 vs. 0.01 ± 0.003 ng/mL, p < 0.001), which was ~10 fold higher than the normal level.
CONCLUSIONS: We propose that homocysteine is an important cardiac biomarker and may have an important role in the development of cardiac remodeling and dysfunction in chronic myocardial ischemia in humans.

OBJECTIVE: In this study, cardiac biomarkers, blood parameters, electrocardiography (ECG), and echocardiography were investigated in children with carbon monoxide (CO) poisoning, and the diagnostic value of these parameters was investigated.
METHODS: The demographical, clinical, and laboratory data of children aged 0-18 years who were admitted to the pediatric emergency department due to CO poisoning between January 2019 and January 2022 were retrospectively scanned from medical records. The patients were divided into two groups as troponin-I positive and troponin-I negative.
RESULTS: There were 107 children aged 0-18 years (average age, 10.46 ± 5.77 years; 51% female) with CO poisoning. There were 13 patients with troponin-I positive myocardial injury. Troponin-I was positive in 3 patients whose carboxyhemoglobin (COHb) level was below 2% at the time of admission. In one patient, troponin-I, which was normal at admission, increased by the 24th hour of hospitalization. Hyperbaric oxygen therapy was given due to headache in one patient, although the COHb level of that patient was below 25%. An NT-proBNP level of ≥ 219.5 ng/L predicted the development of troponin-I positivity with a sensitivity of 70% and a specificity of 86.7% (AUC, 0.967 (0.58-0.994); p = 0.017). White blood cell (WBC), neutrophil, neutrophil-to-lymphocyte ratio (NLR), immature granulocyte (IG), and IG% levels were found to be significantly higher in the troponin-positive patient group. DISCUSSION AND CONCLUSION: NT-proBNP has been shown to be an early diagnostic marker for myocardial dysfunction. Additionally, when cardiac markers are not available, full blood parameters may assist clinicians for patient treatment and referral.

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.

Haematological parameters obtained from the full blood count, such as neutrophil-to-lymphocyte ratio (NLR), are cost-effective tests which have been shown to be predictive of the prognosis of many diseases. We aimed to evaluate certain haematological parameters and cardiac biomarkers to test whether they could predict cardiac involvement by COVID-19 infection.
This retrospective study included patients aged 1 month to 18 years having a positive COVID-19 PCR test but no comorbidity, who were admitted to the paediatric emergency department between 15 March 2020 and 1 February 2021.
There were 292 COVID-19 PCR-positive patients, 12 MIS-C patients and 70 healthy controls. A receiver operator characteristic curve analysis was performed to predict MIS-C in patients with COVID-19 infection. An NLR value of ≥5.03 could predict MIS-C with a sensitivity of 66.7% and a specificity of 91.6%; a proBNP value of ≥329.5 ng/L with a sensitivity of 91.7% and a specificity of 95.6%; a CKMB value of ≥2.95 μg/L with a sensitivity of 100% and a specificity of 77.7%; and a troponin-I value of ≥0.03 μg/L with a sensitivity of 75% and a specificity of 99.2%. A logistic regression analysis showed that an NLR value of ≥5.03 increased the risk of MIS-C 19.3 fold; a proBNP value of ≥329.5 ng/L increased the risk 238 fold; and a troponin-I value of ≥0.03 μg/L increased the risk 60 fold.
At the time of admission, parameters such as proBNP, troponin-I and NLR can predict the development of MIS-C in COVID-19 patients with high sensitivity and specificity.

The growing burden of myocardial infarction (MI) becomes a major global health issue that is accountable for considerable mortality worldwide. Hence, it is obligatory to develop a new treatment for MI having lesser side effects. Cardiac hypertrophy, oxidative stress, and inflammatory pathways play crucial roles in the pathogenesis of MI. This investigation established the anti-cardiac hypertrophic, antioxidant, anti-inflammatory, and myocardial infarct size limiting effects of valencene. Rats were induced MI by isoproterenol (100 mg/kg body weight) and then treated with valencene and cardiac sensitive markers, cardiac hypertrophy, oxidative stress, markers of inflammation, nuclear factor- κB inflammatory pathway, and myocardial infarct size was estimated/determined. The serum cardiac diagnostic markers, cardiac hypertrophy, conjugated dienes, markers of inflammation, pro-inflammatory cytokines, and myocardial infarct size were significantly (P < 0.05) increased by isoproterenol. Further, antioxidant enzymes and anti-inflammatory cytokine gene were significantly (P < 0.05) decreased in the heart. The 2, 3, 5-triphenyl tetrazolium chloride dye staining revealed a larger infarct size. Moreover, histological results of myocardial infarcted rat\'s cardiac tissue revealed separation of cardiac muscle fibers, necrosis, and inflammatory cells. Post-treatment with valencene (12 mg/kg body weight) orally, daily, for two weeks to isoproterenol-induced myocardial infarcted rats reversed all above said structural, biochemical, molecular, and histological parameters investigated, by its anti-cardiac hypertrophic, antioxidant, anti-inflammatory, and myocardial infarct size limiting effects. Thus, valencene is a potential candidate for inhibiting cardiac hypertrophy, oxidative stress, nuclear factor- κB inflammatory pathway, and myocardial infarct size and exhibited cardioprotection in MI.