Exposure to fine particulate matter (PM₂.₅) was associated with altered heart rate variability (HRV). However, whether blood pressure (BP) control and angiotensin II receptor blocker (ARB) treatment modifies the associations was seldom addressed. Therefore, we conducted a 3-phase panel study among 282 hypertensive subjects aged 35–74 years in four cities of China to address this issue. Real-time personal PM₂.₅ sampling and 24-h ambulatory electrocardiogram monitoring were performed repeatedly in 3 different seasons. Linear mixed-effects models were fitted overall and by control status of BP and ARB treatment to assess the associations between short-term PM₂.₅ exposure and HRV. The average hourly PM₂.₅ concentrations (Mean ± SD) ranged from 19.3 ± 18.2 μg/m³ to 99.4 ± 76.9 μg/m³ across study phases and cities. Generally, PM₂.₅ exposure was associated with decreased hourly and 24-h HRV. However, these adverse impacts were attenuated among patients with controlled BP (<140/90 mmHg). For each 10 μg/m³ increment in moving average of previous 2 days' (MA2d) PM₂.₅ exposure, 24-h SDNN (standard deviation of NN intervals) and rMSSD (root mean square of successive RR interval differences) decreased by 0.89% (95% CI: 0.19%–1.59%) and 2.98% (95% CI: 1.04%–4.89%) among patients with uncontrolled BP (≥140/90 mmHg), whereas no obvious declines were observed among those with controlled BP (Pdᵢffₑᵣₑₙcₑ = 0.007 and 0.022, respectively). Furthermore, ARB treatment alleviated or eliminated PM₂.₅-associated declines in hourly and 24-h HRV among those with uncontrolled BP. For instance, 24-h SDNN decreased by 1.31% (95% CI: 0.54%–2.07%) with a 10 μg/m³ increment in lag 2 days’ PM₂.₅ exposure in ARB nonusers, whereas no obvious changes were observed in ARB users (Pdᵢffₑᵣₑₙcₑ = 0.021). In conclusion, although PM₂.₅ exposure would decrease HRV, better BP control and ARB treatment could attenuate these adverse impacts, which provides supporting evidence for alleviating autonomic dysfunction of hypertension patients living in areas with high-level PM₂.₅.

Studies revealed long-term associations between noise exposure and cardiovascular health, but the underlying short-term mechanisms remain uncertain.To explore the concomitant and lagged short-term associations between personal exposure to noise and heart rate variability (HRV) in a real life setting in the Île-de-France region.The RECORD MultiSensor Study collected between July 2014 and June 2015 noise and heart rate data for 75 participants, aged 34–74 years, in their living environments for 7 days using a personal dosimeter and electrocardiography (ECG) sensor on the chest. HRV parameters and noise levels were calculated for 5-min windows. Short-term relationships between noise level and log-transformed HRV parameters were assessed using mixed effects models with a random intercept for participants and a temporal autocorrelation structure, adjusted for heart rate, physical activity (accelerometry), and short-term trends.An increase by one dB(A) of A-weighted equivalent sound pressure level (Leq) was associated with a 0.97% concomitant increase of the Standard deviation of normal to normal intervals (SDNN) (95% CI: 0.92, 1.02), of 2.08% of the Low frequency band power (LF) (95% CI: 1.97, 2.18), of 1.30% of the High frequency band power (HF) (95% CI: 1.17, 1.43), and of 1.16% of the LF/HF ratio (95% CI: 1.10, 1.23). The analysis of lagged exposures to noise adjusted for the concomitant exposure illustrates the dynamic of recovery of the autonomic nervous system. Non-linear associations were documented with all HRV parameters with the exception of HF. Piecewise regression revealed that the association was almost 6 times stronger below than above 65 Leq dB(A) for the SDNN and LF/HF ratio.Personal noise exposure was found to be related to a concomitant increase of the overall HRV, with evidence of imbalance of the autonomic nervous system towards sympathetic activity, a pathway to increased cardiovascular morbidity and mortality.

Hexafluoropropylene oxide dimer acid (HFPO-DA) is a perfluorooctanoic acid (PFOA) substitute. In the current study, potential developmental cardiotoxicity and hepatotoxicity following HFPO-DA exposure in chicken embryo has been investigated, focusing on the roles of peroxisome proliferator activated receptor alpha (PPARα), the major molecular target in PFOA-induced toxicities. HFPO-DA was exposed to fertile chicken eggs via air cell injection, morphology and function of the target organs (heart and liver) in hatchlings were investigated with histopathology and electrocardiography, and the serum levels of HFPO-DA had been measured with quadrupole-time of flight liquid chromatograph-mass spectrometer (Q-TOF LC/MS). Additionally, lentivirus-mediated in ovo PPARα silencing was used to assess the roles of PPARα in HFPO-DA induced developmental toxicities. The results indicated that developmental exposure to HFPO-DA induced developmental cardiotoxicity, including thinned right ventricular wall and elevated heart rates, similar to those observed with PFOA exposure, as well as developmental hepatotoxicity in the form of steatosis. Silencing of PPARα alleviated such effects, suggesting participation of PPARα in HFPO-DA induced developmental toxicities in chicken embryo. Moreover, enhanced expression of PPARα downstream genes, cluster of differentiation 36 (CD36) and enoyl-CoA hydratase and 3-hydroxyacyl CoA dehydrogenase (EHHADH), were observed in HFPO-DA exposed animal heart tissues, which can be abolished by PPARα silencing. On the other hand, liver-type fatty acid binding protein (L-FABP) and CD36 expression were effectively enhanced in exposed liver tissues, but not EHHADH, suggesting differential mechanism of toxicity in heart and liver tissues. In summary, developmental exposure to HFPO-DA induced developmental cardiotoxicity and hepatotoxicity in hatchling chickens similar to PFOA, and PPARα still participates in such toxicities, with some differential downstream gene regulations in different organs. Further investigation on HFPO-DA-induced developmental toxicities is guaranteed.

Diesel exhaust (DE) had been associated with cardiopulmonary toxicity and developmental toxicity. However, neonatal very early-in-life exposure had not been extensively studied previously. To investigate the potential effects of neonatal very early-in-life exposure to DE, a brand-new chicken embryo in ovo exposure model had been established, with which the cardiopulmonary effects of DE exposure via air cell infusion at embryonic day 18/19 (ED18/19) were assessed in hatchling chicks post-hatch 0-, 1-, or 2-weeks. Heart rates were assessed with electrocardiography. Cardiac and pulmonary morphologies were investigated with histopathological methods. Cardiopulmonary effects were explored with immunohistochemistry for alpha smooth muscle actin (alpha-SMA). In further investigations, the expression levels of phosphorylated AhR, serum levels of TGF-β1, phosphorylated SMAD2/3 and phosphorylated p38MAPK were assessed in the lung tissues. Significantly elevated heart rates, increased right ventricular wall thickness and cardiac collagen deposition were observed in the hearts of exposed hatchling chicks. Significantly increased collagen deposition as well as increased vascular alpha-SMA layer thickness/decreased cavity area were observed in exposed animal lungs. These effects persisted up to two weeks post-hatch. Mechanistic studies revealed elevated phosphorylated AhR expression levels in 0-week and 1-week chicken lungs, while phosphorylated SMAD2/3 levels significantly increased in 0-week chicken lungs but decreased in 2-week chicken lungs following DE exposure. Phosphorylation of p38MAPK did not remarkably increase until 2-week post-hatch. In summary, the novel chicken neonatal very early-in-life exposure model effectively exposed the chicken embryos during the neonatal initial breathing, resulting in cardiopulmonary toxicity, which is associated with AHR, TGF-β1 and MAPK signaling.

Diabetes is a clinical condition that is associated with insulin deficiency and hyperglycemia. Cardiomyopathy, retinopathy, neuropathy, and nephropathy are well known complications of the elevated blood glucose. Diabetic cardiomyopathy is a clinical disorder that is associated with systolic and diastolic dysfunction along with cardiac fibrosis, inflammation, and elevated oxidative stress. In this study, diabetes was induced by intraperitoneal injection of streptozotocin (STZ) 50 mg/kg. We determined the plasma levels of cardiac troponin-T (cTnT) and creatinine kinase MB (CK-MB) by ELISA. Diabetic rats showed abnormal cardiac architecture and increased collagen production. Significant elevation in ST-segment, prolonged QRS, and QT-intervals and increased ventricular rate were detected. Additionally, diabetic rats showed a prolongation in P wave duration and atrial tachyarrhythmia was observed. Plasma levels of cTnT and CK-MB were elevated. In conclusion, these electrocardiographic changes (elevated ST-segment, prolonged QT interval, and QRS complex, and increased heart rate) along with histopathological changes and increased collagen formation could be markers for the development of diabetic cardiomyopathy in rats.

The study aimed at assessing the diagnostic ability of advanced electrocardiogram (ECG) analysis to predict the levels of NT-proBNP and Troponin I. ECG and the blood NT-proBNP and Troponin I were taken from 50 acutely carbon monoxide poisoned patients and 21 control subjects matched with age and sex. The severity of the studied cases was classified into mild, moderate, and severe using clinical classification. ECG parameters (RR interval, corrected QT (QTc) interval, P wave dispersion (Pwd)), and cardiac biomarkers (NT-proBNP and Troponin I) were significantly higher in cases than in control (p= 0.015, 0.008, 0.002, <0.001, and <0.001 respectively). Cut-off values resulted from combined ROC curves analysis can predict blood Troponin I more than 0.05 ng/ml and NT-proBNP more than 125 pg/ ml (with 88% and 84% accuracy respectively). In addition, two regression equations were developed using all studied ECG parameters to predict Troponin I and NT-proBNP (with 68% and 43% accuracy respectively). RR average, PR average, QRS average, QTd, QTc, and Pwd could be used to predict Troponin I and NT-proBNP levels with good accuracy in carbon monoxide poisoning patients.

Copper deficiency (CuD) is a common mineral disorder in ruminants, which causes histomorphological changes in the heart due to disturbances in copper-dependent metalloenzymes. However, alterations in the measurable cardiac parameters during CuD have not been studied in ruminants, especially in goats. Therefore, the current study aimed to investigate longitudinally the potential role of electrocardiography (ECG) and echocardiography to detect the CuD-induced cardiac damage at different time intervals and concomitantly highlighting the impact of CuD on specific hemato-biochemical parameters and histological cardiac disruption in goats. Eight Shiba goats were included and divided into two equal groups; copper adequate (CuA) as a control and copper-deficient (CuD) that supplemented with copper-chelating agents (sulfur 3 g/kg DM and molybdenum 40 mg/kg DM). The hemato-biochemical analysis, ECG assessment at the base apex lead, and right-side echocardiography were performed just before the experimental onset (T0), and later on at two-time intervals after existing of CuD, at the fifth (T5) and seventh (T7) months. Necropsy and histopathological examination of the heart were performed at the end of the experiment. In the CuD group, the heart dimensions at T5 and T7 showed significant increase in QRS duration, ST-segment duration, the left atrial area in systole, left ventricular diameter and volume in diastole, stroke volume, and cardiac output compared with CuA (P < 0.05). Also, myocardial degeneration, necrosis, and fibrosis were evidenced with a concurrent increase of plasma creatine kinase, lactate dehydrogenase, aspartate aminotransferase, and cardiac troponin I (P < 0.05). In conclusion, CuD disturbs hemato-biochemical parameters and results in myocardial damage and cardiac dilatation that increases some ECG and echocardiographic parameters without development of systolic dysfunction. The ECG and echocardiography can potentially detect cardiac changes in long-lasting CuD in goats.

Previous studies have shown that exposure to particulate matter (PM) increased variety of health problems, particularly cardiovascular diseases leading to premature mortality. The cardiac effects of particulate matter containing PM₁₀ include increased infarct size, decreased heart function, and increased arrhythmias in experimental ischemia-reperfusion models in rats. The aim of this study was to evaluate the effects of particles with an aerodynamic diameter smaller than 10 μm (PM₁₀) on isolated-rat heart and also to determine the efficacy of gallic acid (GA) as a preventive agent in oxidative damage. The healthy rats were divided into 8 equal groups which served as, control, GA, PM₁₀ (0.5, 2.5, and 5 mg/kg), and PM₁₀+GA groups. PM₁₀ administered into the lungs via the trachea in two stages with 48-h interval. After all experiments, the electrocardiogram was recorded. Then, the hemodynamic parameters and ventricular arrhythmias in rat isolated-hearts were assessed using Langendorff apparatus and according to the Lambeth conventions. In addition, the inflammation and oxidative stress factors in cardiac tissues were evaluated in all groups. The obtained results showed that the exposure to PM caused to decrease in cardiac hemodynamic and electrocardiogram parameters. Also, in PM₁₀ rat groups, the IL-6, TNF-α, and oxidative stress parameters were increased. Gallic acid preserved the value of cardiac parameters and inflammation in rat hearts. In summary, we added a novel therapeutic effect of gallic acid for cardiac dysfunction induced by particulate matter. These findings could be related to antioxidant and antiinflammation properties and the obtained results suggest that natural antioxidant like gallic acid could be a therapeutic agent in prevention and management of health issues in the polluted areas of the world.

Novel soil remediation equipment based on electro-kinetic geosynthetics (EKG) was developed for in situ isolation of metals from paddy soil. Two mutually independent field plot experiments A and B (with and without electric current applied) were conducted. After saturation using ferric chloride (FeCl₃) and calcium chloride (CaCl₂), soil water drainage capacity, soil cadmium (Cd) removal performance, energy consumption as well as soil residual of iron (Fe) and chloride (Cl) were assessed. Cadmium dissolved in the soil matrix and resulted in a 100% increase of diethylenetriamine-pentaacetic acid (DTPA) extracted phyto-available Cd. The total soil Cd content reductions were 15.20% and 26.58% for groups A and B, respectively, and electric field applications resulted in a 74.87% increase of soil total Cd removal. The electric energy consumption was only 2.17 kWh/m³ for group B. Drainage by gravity contributed to > 90% of the overall soil dewatering capacity. Compared to conventional electro-kinetic technology, excellent and fast soil water drainage resulted in negligible hydrogen ion (H⁺) and hydroxide ion (OH⁻) accumulation at nearby electrode zones, which addressed the challenge of anode corrosion and cathode precipitation of soil metals. External addition of FeCl₃ and CaCl₂ caused soil Fe and Cl residuals and led to 4.33–7.59% and 139–172% acceptable augments in soil total Fe and Cl content, correspondingly, if compared to original untreated soils. Therefore, the novel soil remediation equipment developed based on EKG can be regarded as a promising new in situ technology for thoroughly isolating metals from large-scale paddy soil fields.

In this study, cardiac and locomotor activities of signal crayfish Pacifastacus leniusculus were investigated under exposure to a range of natural (i.e., odors of conspecific crayfish, predatory fish, food, and injured conspecific) and one chemical (i.e., disinfectant chloramine-T) stimuli. Crayfish locomotion was simultaneously initiated with an increase in heart rate only when affected by chloramine-T, while locomotor response was delayed in all cases (or was not manifested at all by some specimens) when disturbed by the natural stressors. The heart rate differences measured before and during the stimulation were arranged as follows: odor of conspecific crayfish (9.2 ± 7.1%) < predator (18.4 ± 13%) < food (33.5 ± 15.7%) < chloramine-T (41.1 ± 14.7%) < injured conspecific (51.8 ± 28.4%). Analysis of the peculiarities of crayfish heartbeat under exposure to the tested stimuli revealed complex cardiac responses as was previously observed by an electrocardiography approach, that is, a slowed heart rate followed by a delayed increase. Evaluation of the intrinsic parameters of crayfish bioindicators remains essential due to the possibility of detection of the substantial ethological responses even in motionless animals. The role and appropriateness of signal crayfish as a bioindicator of water quality is discussed; they seem to be an applicable species for this task due to their sufficient sensitivity and broad availability. In addition to providing a better understanding of stereotypic crayfish behaviors induced by common and chemical stressors, the results of this study may serve as reference data for the evaluation of crayfish suitability for water quality tests.