The potential role of ferroptosis in COVID-19-related cardiovascular injury.

COVID-19, caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), emerged as a global health threat in 2019. An important feature of the disease is that multiorgan symptoms of SARS-CoV-2 infection persist after recovery. Evidence indicates that people who recovered from COVID-19, even those under the age of 65 years without cardiovascular risk factors such as smoking, obesity, hypertension, and diabetes, had a significantly increased risk of cardiovascular disease for up to one year after diagnosis. Therefore, it is important to closely monitor individuals who have recovered from COVID-19 for potential cardiovascular damage that may manifest at a later stage. Ferroptosis is an iron-dependent form of non-apoptotic cell death characterized by the production of reactive oxygen species (ROS) and increased lipid peroxide levels. Several studies have demonstrated that ferroptosis plays an important role in cancer, ischemia/reperfusion injury (I/RI), and other cardiovascular diseases. Altered iron metabolism, upregulation of reactive oxygen species, and glutathione peroxidase 4 inactivation are striking features of COVID-19-related cardiovascular injury. SARS-CoV-2 can cause cardiovascular ferroptosis, leading to cardiovascular damage. Understanding the mechanism of ferroptosis in COVID-19-related cardiovascular injuries will contribute to the development of treatment regimens for preventing or reducing COVID-19-related cardiovascular complications. In this article, we go over the pathophysiological underpinnings of SARS-CoV-2-induced acute and chronic cardiovascular injury, the function of ferroptosis, and prospective treatment approaches.

Non-invasive intradialytic percutaneous perfusion monitoring: a view to the heart through the skin.

Introduction: The life-sustaining treatment of hemodialysis (HD) induces recurrent and cumulative systemic circulatory stress resulting in cardiovascular injury. These recurrent insults compound preexisting cardiovascular sequalae leading to the development of myocardial injury and resulting in extremely high morbidity/mortality. This is largely a consequence of challenged microcirculatory flow within the myocardium (evidenced by detailed imaging-based studies). Currently, monitoring during HD is performed at the macrovascular level. Non-invasive monitoring of organ perfusion would allow the detection and therapeutic amelioration of this pathophysiological response to HD. Non-invasive percutaneous perfusion monitoring of the skin (using photoplethysmography-PPG) has been shown to be predictive of HD-induced myocardial stunning (a consequence of segmental ischemia). In this study, we extended these observations to include a dynamic assessment of skin perfusion during HD compared with directly measured myocardial perfusion during dialysis and cardiac contractile function. Methods: We evaluated the intradialytic microcirculatory response in 12 patients receiving conventional HD treatments using continuous percutaneous perfusion monitoring throughout HD. Cardiac echocardiography was performed prior to the initiation of HD, and again at peak-HD stress, to assess the development of regional wall motion abnormalities (RWMAs). Myocardial perfusion imaging was obtained at the same timepoints (pre-HD and peak-HD stress), utilizing intravenous administered contrast and a computerized tomography (CT)-based method. Intradialytic changes in pulse strength (derived from PPG) were compared with the development of HD-induced RWMAs (indicative of myocardial stunning) and changes in myocardial perfusion. Results: We found an association between the lowest pulse strength reduction (PPG) and the development of RWMAs (p = 0.03) and also with changes in global myocardial perfusion (CT) (p = 0.05). Ultrafiltration rate (mL/kg/hour) was a significant driver of HD-induced circulatory stress [(associated with the greatest pulse strength reduction (p = 0.01), a reduction in global myocardial perfusion (p = 0.001), and the development of RWMAs (p = 0.03)]. Discussion: Percutaneous perfusion monitoring using PPG is a useful method of assessing intradialytic hemodynamic stability and HD-induced circulatory stress. The information generated at the microcirculatory level of the skin is reflective of direct measures of myocardial perfusion and the development of HD-induced myocardial stunning. This approach for the detection and management of HD-induced cardiac injury warrants additional evaluation.

Very low risk of ST-elevation and non-ST-elevation myocardial infarction in patients with chest trauma.

BACKGROUND: The goal of this study was to evaluate any association between blunt chest trauma and occurrence of ST-elevation myocardial infarction and non-ST-elevation myocardial infarction. METHODS: Data from the National Inpatient Sample (NIS) database from 2010-2014, of patients over the age of 40, hospitalized for blunt chest trauma (ICD 959.11), with STEMI or NSTEMI, was used in this study. We performed a chi-squared test to analyze this association. We also performed a multivariant analysis adjusting for race, gender, and age. RESULTS: We found that there is not an increased risk of STEMI/NSTEMI following blunt chest trauma, P > 0.05. We also found no correlation between STEMI or NSTEMI and chest trauma after adjusting for race, gender, and age. For STEMI after adjustments in 2010 (P=0.52), 2011 (P=0.19), 2012 (P=0.60), 2013 (P=0.88), and 2014 (P=0.14). For NSTEMI adjustments in 2010 (P=0.03), 2011 (P=0.06), 2012 (P=0.01), 2013 (P=0.21), and 2014 (P=0.03). CONCLUSION: Both ST-elevation myocardial infarction and non-ST-elevation myocardial infarction were not significantly associated with blunt chest trauma.

PM2.5 induces alterations in gene expression profile of platelet-derived extracellular vesicles and mediates cardiovascular injury in rats.

Platelet-derived extracellular vesicles (P-EVs), as the most abundant vesicles in blood, have been proven to play cardinal roles in cardiovascular injury. RNAs (especially miRNAs) carried by P-EVs can be transferred to the receptor, which plays a critical role in regulating vascular endothelial function. PM2.5 is one of the most well-known risk factors that cause cardiovascular disease. Therefore, the objective of the current study was to explore whether exposure to PM2.5 would alter the gene expression profile of P-EVs, and to further elucidate the role of RNAs (especially miRNAs) carried by P-EVs in cardiovascular injury induced by PM2.5 exposure. P-EVs were isolated from the platelet-rich plasma which was exposed and unexposed to PM2.5, and the differentially expressed target genes were evaluated using whole-transcriptome gene sequencing. Rats were treated with P-EVs under different exposure conditions (a protein concentration of 50 µg/mL) and an equal volume of normal saline. The pathological damage of the thoracic aorta and cardiac tissue was evaluated and the coagulation function of the rats was detected. The differentially expressed genes were shown to be mainly concentrated in inflammation, angiogenesis, and apoptosis-related pathways. Moreover, P-EVs extracted from PM2.5-exposed plasma had the potential to trigger an inflammatory response, impair vascular endothelial function, disrupt the normal coagulation process, and promote a prothrombotic state. Our study indicated that PM2.5 induces cardiovascular injury in rats by interfering with the gene expression of P-EVs. It will provide new targets for studying the mechanism involved in PM2.5-induced cardiovascular injury.

Sudden-Onset Paraplegia: A Unique Presentation of Acute Aortic Dissection (AD).

Aortic dissection (AD) is a rare but deadly diagnosis that emergency medicine physicians must consider in a wide variety of patient presentations. This case report describes a 42-year-old male bull rider who developed acute-onset bilateral lower extremity paralysis and loss of sensation. He was later found to have a type A Stanford AD during his emergency department evaluation.

Heme oxygenase-1 protects against PM2.5 induced endothelial dysfunction through inhibition of HIF1α.

PM2.5 has been accepted as a strong risk factor for cardiovascular diseases. Activation of the renin-angiotensin system (RAS) has been proved to be a key factor in triggering vascular endothelial dysfunction upon PM2.5 exposure in our previous reports. In the current study, we observed the concurrent induction of hemoxygenase (HO)- 1 and RAS components (ANGII and AT1R) expression both in the vascular endothelial cell lines and in rat lung tissue after PM2.5 exposure. Furthermore, HO-1 inhibited RAS activation by suppressing the expression and activity of HIF1α, the upstream transcriptional activator of ANGII and AT1R. In addition, HO-1 blocked significantly increased the release of cell adhesion molecules and chemokines (VCAM-1, E-Selectin, P-Selectin, IL-8, MCP-1) that drive monocyte-endothelium adhesion, along with the enhanced the generation of oxidative stress response mediators in the vascular endothelium. These data together indicate that PM2.5 induced HO-1 upregulation functions as a self-defense response to antagonize endothelial dysfunction by inhibiting HIF1α-mediated RAS activation. Targeting endogenous protective pathway might be helpful to protect from PM2.5-induced cardiovascular injury.

A Rat Model of Adenine-induced Chronic Renal Failure Complicated with Cardiovascular Disease / 中国实验方剂学杂志

ObjectiveTo explore the preparation method of a rat model of adenine-induced chronic renal failure complicated with cardiovascular disease by investigating the effect of different time points of adenine gastric lavage on general vital signs， biochemical indicators， and cardiac and renal tissue structure and function of model rats. MethodRats in the model group were administered adenine at 150 mg·kg-1·d-1 by gavage for 16 weeks， while those in the normal group were given an equal volume of 0.5% carboxymethyl cellulose sodium solution by gavage. At weeks 5， 13， 17， 24-hour urinary protein quantification （24 h-UTP）， biochemical indicators， cardiac ultrasound， and changes in cardiac and renal tissue structure and function were measured in both the model and normal groups. Blood pressure was measured at weeks 5 and 13 in both groups. Weekly changes in body weight were recorded， and general conditions of the rats were observed daily. Result① Compared with the normal group， the model group showed a significant decrease in body weight （P<0.05）. ② Rats in the model group exhibited a significant increase in urine volume， and proteinuria appeared at week 13. ③ Compared with the normal group， the model group showed significant differences in triglyceride （TG）， total cholesterol （TC）， creatinine （Cr）， blood urea nitrogen （BUN）， blood potassium， and blood phosphorus at week 5 （P<0.05）， which increased gradually over time. At week 17， uric acid levels were significantly elevated （P<0.05）， and blood calcium levels were reduced at the end of week 17 （P<0.01）. ④ Compared with the normal group， the model group showed a significant increase in blood pressure at week 5 （P<0.05）， which progressively worsened. ⑤ There was no statistically significant difference in left ventricular wall thickness between the model and normal groups at week 5， but a significant difference was observed at week 13 （P<0.05）. ⑥ Fibrosis appeared in the kidneys of rats in the model group at week 5 and gradually worsened， while obvious fibrosis occurred around the cardiovascular system at week 13 as compared with the results in the normal group. ⑦ In the proximal tubular epithelial cells of the model group， there was an increasing presence of high-density rhomboid needle-shaped crystals， damaged cell membrane integrity， increased cell spacing， increased lysosomes， increased mitochondrial proliferation， denser mitochondrial cristae， and outer mitochondrial membrane. ⑧ Compared with the rats in the normal group， rats in the model group exhibited depressed spirits， significantly reduced activity， hunched posture， dry fur， pale ears and toes， swollen cheeks， increased nocturnal urination， and dark and viscous blood. ConclusionAdenine by gavage at 150 mg·kg-1·d-1 for 12 weeks can be used to establish a rat model of chronic renal failure complicated with cardiovascular disease， which can be used for the prevention and treatment research on chronic renal failure and its associated cardiovascular complications. The syndrome of adenine-induced rat model of chronic renal failure belongs to the deficiency of spleen and kidney， turbidity and stasis obstruction， and can be used to study the mechanisms of warming and tonifying the spleen and kidney， resolving stasis， and eliminating turbidity in the treatment of chronic renal failure.

Case report: Right coronary artery rupture-A rare complication of cardiopulmonary resuscitation.

An 8-month-old female experienced a life-threatening right coronary artery rupture resulting from cardiopulmonary resuscitation (CPR) 1 week after corrective surgery for Tetralogy of Fallot (TOF). Emergency exploratory thoracotomy was performed due to uncorrectable hemorrhagic shock. During exploration, active bleeding was detected in the anterior branch of the right ventricular coronary artery. After the repair, the patient's condition improved. Coronary artery rupture is an extremely rare complication of CPR. Here, we present a case that provides new reflections and warnings to clinicians.

Cardiovascular injury and clinical features of multisystem inflammatory syndrome in children (MIS-C) related to Covid-19 in Vietnam.

BACKGROUND: This study aimed to describe the cardiovascular injury and clinical features of multisystem inflammatory syndrome in children (MIS-C) related to coronavirus disease 2019 (COVID-19) in Ho Chi Minh City, Vietnam. METHODS: This was a retrospective cohort study of children with MIS-C (from September 1, 2021 to February 28, 2022) in Children's Hospital 1, Ho Chi Minh City. Demographics, clinical history, significant underlying conditions, clinical manifestations, laboratory investigations, and medical management were analyzed. RESULTS: A total of 76 patients were included (median age, 5.9 years old, 2 months-16 years). The male/female ratio was 1.6/1. Most patients (75/76) had no previous medical conditions. The mean time from acute severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection to symptom onset was 39 days. During an acute SARS-CoV-2 infection, these patients are either asymptomatic or mildly symptomatic. In addition to fever, gastrointestinal symptoms were also prominent, as observed in our study, with 75%, 73.7%, and 72.3% of patients presenting with abdominal pain, vomiting, and loose stools, respectively. The levels of inflammatory markers increased upon admission and returned to normal levels after treatment. Echocardiography revealed decreased myocardial contractility and coronary injury in 16 (21.1%) and 32 (42.1%) patients, respectively. Most cases (72/76) had no fever within 3 days of intravenous immunoglobulin (IVIG) and methylprednisolone treatment. No deaths occurred in this study. The mean duration of hospitalization was 7.2 days. CONCLUSION: Cardiovascular involvement was observed in approximately 53.9% of the patients. Anti-inflammatory treatment with IVIG and methylprednisolone had a favorable short-term outcome. However, long-term follow-up studies on post-discharge MIS-C cases are needed to make appropriate treatment recommendations in the acute phase.

Cardiovascular Damage in COVID-19: What We Know Two Years Later.

PURPOSE OF THE REVIEW: The Coronavirus disease 2019 (COVID-19) pandemic has profoundly influenced cardiological clinical and basic research in the past two years. In the present review, we summarize the current knowledge on myocardial involvement in COVID-19, providing an overview on the incidence, the pathogenetic mechanisms, and the clinical implications of cardiac injury in this setting. RECENT FINDINGS: The possibility of heart involvement in patients with COVID-19 has received great attention since the beginning of the pandemic. After more than two years, several steps have been taken in understanding the mechanisms and the incidence of cardiac injury during COVID-19 infection. Similarly, studies globally have clarified the implications of co-existing heart disease and COVID-19. Severe COVID-19 infection may be complicated by myocardial injury. To date, a direct damage from the virus has not been demonstrated. The presence of myocardial injury should be systematically assessed for a prognostication purpose and for possible therapeutic implications.

The Underlying Cardiovascular Mechanisms of Resuscitation and Injury of REBOA and Partial REBOA.

Introduction: Resuscitative Endovascular Balloon Occlusion of the Aorta (REBOA) is used for aortic control in hemorrhagic shock despite little quantification of its mechanism of resuscitation or cardiac injury. The goal of this study was to use pressure-volume (PV) loop analysis and direct coronary blood flow measurements to describe the physiologic changes associated with the clinical use of REBOA. Methods: Swine underwent surgical and vascular access to measure left ventricular PV loops and left coronary flow in hemorrhagic shock and subsequent placement of occlusive REBOA, partial REBOA, and no REBOA. PV loop characteristics and coronary flow are compared graphically with PV loops and coronary waveforms, and quantitatively with measures of the end systolic and end pressure volume relationship, and coronary flow parameters, with accounting for multiple comparisons. Results: Hemorrhagic shock was induced in five male swine (mean 53.6 ± 3.6 kg) as demonstrated by reduction of stroke work (baseline: 3.1 vs. shock: 1.2 L*mmHg, p < 0.01) and end systolic pressure (ESP; 109.8 vs. 59.6 mmHg, p < 0.01). ESP increased with full REBOA (178.4 mmHg; p < 0.01), but only moderately with partial REBOA (103.0 mmHg, p < 0.01 compared to shock). End systolic elastance was augmented from baseline to shock (1.01 vs. 0.39 ml/mmHg, p < 0.01) as well as shock compared to REBOA (4.50 ml/mmHg, p < 0.01) and partial REBOA (3.22 ml/mmHg, p = 0.01). Percent time in antegrade coronary flow decreased in shock (94%-71.8%, p < 0.01) but was rescued with REBOA. Peak flow increased with REBOA (271 vs. shock: 93 ml/min, p < 0.01) as did total flow (peak: 2136, baseline: 424 ml/min, p < 0.01). REBOA did not augment the end diastolic pressure volume relationship. Conclusion: REBOA increases afterload to facilitate resuscitation, but the penalty is supraphysiologic coronary flows and imposed increase in LV contractility to maintain cardiac output. Partial REBOA balances the increased afterload with improved aortic system compliance to prevent injury.

Early and long-term outcomes of re-sternotomy for aortic valve replacement with patent coronary artery grafts.

OBJECTIVE: The aim was to evaluate early and long-term outcomes of re-sternotomy for aortic valve replacement (AVR) with previous patent coronary artery grafts. METHODS: Data for re-sternotomy for AVRs (group 1 isolated AVR, group 2 AVR with concomitant procedure) were collected (2000-2019). Logistic regression analysis was performed to identify predictors of in-hospital mortality and postoperative composite outcome (in-hospital death, transient ischemic attack/stroke, renal failure requiring new hemofiltration, deep sternal wound infection, re-exploration for bleeding/tamponade and length of stay >30 days). Survival curves were compared using log-rank test Cox proportion hazards model was used for predictors of long-term survival. RESULTS: Total 178 patients were included (groups 1-90 patients, group 2-88 patients). Mean age was 75 ± 4 years and mean log EuroSCORE was 17 ± 12% (15 ± 8% - group 1 vs. 19 ± 14% - group 2, p = 0.06). Mean follow-up was 6.3 ± 4.4 years. Cardiovascular injury occurred in 12%. Left internal mammary artery was most commonly injured. In-hospital mortality was 7.8% (5% - group 1 vs. 10.2% - group 2, p = 0.247). NYHA class III-IV, perioperative intra-aortic balloon pump and cardiovascular injury were independent predictors of in-hospital mortality (hazard ratio: 13.33, 95% confidence interval: 2.04-83.33, p = 0.007). Survival was significantly worse with cardiovascular injury at re-sternotomy up to 5 years (46% vs. 67%, p = 0.025) and postoperative complications (p = 0.023). Survival was significantly lower than age-matched first-time AVR and UK population. CONCLUSIONS: Long-term survival is significantly impaired by cardiovascular injury and perioperative complications of re-sternotomy.

Consensus Guidelines for the Prevention and Management of Periprocedural Complications of Transcatheter Patent Ductus Arteriosus Closure with the Amplatzer Piccolo Occluder in Extremely Low Birth Weight Infants.

Transcatheter closure of patent ductus arteriosus (PDA) in premature infants is a feasible, safe, and an effective alternative to surgical ligation and may be performed with an implant success rate of 97%. Major procedural complications related to transcatheter PDA closure in extremely low birth weight (ELBW) infants are relatively infrequent (< 3%) ,but may be associated with a fatality if not optimally managed. Operators performing transcatheter PDA closures should be knowledgeable about these potential complications and management options. Prompt recognition and treatment are often necessary to avoid serious consequences. With strict guidelines on operator training, proctoring requirements, and technical refinements, transcatheter PDA closure in ELBW infants can be performed safely with low complication rates. This article summarizes the consensus guidelines put forward by a panel of physicians for the prevention and management of periprocedural complications of transcatheter PDA closure with the Amplatzer Piccolo Occluder in ELBW infants.

[Impact of cardiovascular metabolic diseases on COVID-19: review of recent progress].

The high comorbidity between cardiovascular and metabolic diseases (CVMD) and coronavirus disease 2019 (COVID-19) and the consequent high mortality and the potential risk of cardiovascular damage have brought great challenges to the clinical diagnosis and treatment of the condition. The latest studies found that advanced age, immune function defects, inflammatory factor storms and oxidative stress damage all potentially contribute to the high comorbidity of the two. Direct virus invasion, myocardial oxygen supply and demand imbalance and vascular endothelial and coagulation dysfunction may be important mechanisms for cardiovascular injury in COVID-19 patients. In addition, the expression level of ACE2 (the cell membrane receptor of SARS-CoV-2) in various organs and the peripheral blood not only mediates the direct invasion and damage of the organs, but also participates in regulation of the balance of systematic inflammation and oxidative stress, thus affecting the susceptibility and outcomes of the patients. Herein we review the recent research progress in the comorbidity between COVID-19 and CVMD and explore the mechanisms of cardiovascular damage caused by SARS-CoV-2, thus to provide a theoretical basis for the clinical diagnosis and treatment of COVID-19 with underlying CVMD.

Cardiovascular injuries during COVID-19 infection: A PROCESS-compliant case series from the Eastern Morocco.

BACKGROUND: To date, more than 105,805,951 cases of COVID-19 have been diagnosed including 2,312,278 deaths. Many patients have cardiovascular risk-factors and/or co-morbidities and a lot of them developed de novo heart conditions during the active or the post-infectious phase of the infection. A number of studies tried to demonstrate an association between poor prognostic outcomes and cardiovascular comorbidities and related damages, but the quality of current evidence is still weak. PATIENTS AND METHODS: The aim of this single-center report is to describe the prevalence of cardiac injuries among our COVID-19 patients, to explore their association with survival outcomes and to demonstrate the medical care provided in our real-world setting. Our study included 610 COVID-19 patients admitted to the intensive care unit of our university hospital of whom13.77% (n = 84) presented cardiovascular injuries and which we included in this case series. RESULTS: The average age of our patients was 65 years (27-90). 60 were men (71.42%) while 24 were women (28.55%). Their average BMI was 29.7 kg/m2. Among them, 50 had a pulmonary embolism (59.52%), 12 patients had a myocardial infarction (14.28%), 10 presented pericarditis (11.9%) and 3 developed myocarditis (3.57%). There were 6 cases of ischemia (7.14%), 2 cases of stroke (2.38%), and 1 case of decompensated heart failure (1.19%). Among our patients, 46.42% had diabetes, 32.14% had a high blood pressure, 13.09% had a chronic renal failure and 14.28% had a history of ischemic heart disease. 14 patients (16.66%) had an elevated troponin with higher levels than 1000 ng/mL. The D-dimer value was high in almost all patients (80.95%). Lung damage from COVID-19 was extensive in 27.38%, severe in 32.14%, and critical in 40.47% of enrolled cases. CT chest angiography, ECG, and cardiac ultrasound were performed to the paraclinical confirmatory exploration of cardiac damages of these patients. Medical care was based on isolation, azithromycin, vitamin C, zinc, vitamin D, salicylic acid, dexamethasone followed with methylprednisolone, and anticoagulation for all hospitalized patients. Tocilizumab was indicated for 17 patients with hyperferritinemia (20.23% of patients). The initial respiratory care of our patients required oxygen therapy using nasal cannula (7.14%) high concentration masks (33.33%), high flow nasal cannula treatment (11.9%), non-invasive ventilation (NIV) (5.95%), and mechanical ventilation (41.66%). Thrombolysis was performed in three subjects with myocardial infarction and 2 underwent angioplasty with placement of an active stent at the proximal interventricular anterior artery, which all were successful. Three massive pulmonary embolisms died despite adequate treatment. Colchicine and salicylic acid were administered for pericarditis cases. Thromboprophylaxis was indicated for all patients and was reinforced if a venous thrombotic episode was confirmed. Patients with limb ischemia underwent surgical treatment. Among the 84 patients included in our cohort, 34 (40.47%) died in intensive care unit and 50 (59.52%) had a favorable evolution. CONCLUSION: Cardiovascular involvement during COVID-19 should not be neglected and are associated with severe outcomes.

Cardiovascular disease in patients with COVID-19: evidence from cardiovascular pathology to treatment.

The coronavirus disease-2019 (COVID-19) caused by the novel coronavirus severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) has rapidly developed into a global pneumonia pandemic. Cardiovascular disease is the major comorbidity of COVID-19 patients and is closely related to the severity of COVID-19. SARS-CoV-2 infection can directly or indirectly cause a series of cardiac complications, including acute myocardial injury and myocarditis, heart failure and cardiac arrest, arrhythmia, acute myocardial infarction, cardiogenic shock, Takotsubo cardiomyopathy, and coagulation abnormalities. Intensive research on the SARS-CoV-2-associated cardiovascular complications is urgently needed to elucidate its exact mechanism and to identify potential drug targets, which will help to formulate effective prevention and treatment strategies. Hence, this review will summarize recent progress regarding the effects of COVID-19 on the cardiovascular system and describe the underlying mechanism of cardiovascular injury caused by SARS-CoV-2.

Electroimmunodetection of cardiac C-reactive protein for determining myocardial Injury.

C-reactive protein (CRP) is an acute phase reactant to be a marker of inflammation and has been correlated with the cardiac injury. An immunoassay was performed using anti-human CRP antibody on an InterDigitated electrode (IDE) sensor to determine and specify CRP concentration for diagnosing the condition of myocardial inflammation. To promote the detection, gold nanoparticle (GNP) was seeded on the aminated-IDE surface. Anti-CRP was hitched on the GNP-seeded surface and identified the abundance of CRP. The limit of quantification was found as 100 fM, and the higher current response was noticed by increasing CRP concentrations with the sensitivity at 1 pM. Furthermore, CRP-spiked human serum did not interfere the determination of CRP and increased the current response, indicating suitability for a real-life sample. Similarly, the control experiments with nonimmune antibody Troponin I are not showing the definite current responses, proving the selective identification of CRP. This method of diagnosing is needful to determine the cardiovascular injury at the right time.

The Role of NLRP3 Inflammasome in Radiation-Induced Cardiovascular Injury.

The increasing risk of long-term adverse effects from radiotherapy on the cardiovascular structure is receiving increasing attention. However, the mechanisms underlying this increased risk remain poorly understood. Recently, the nucleotide-binding domain and leucine-rich-repeat-containing family pyrin 3 (NLRP3) inflammasome was suggested to play a critical role in radiation-induced cardiovascular injury. However, the relationship between ionizing radiation and the NLRP3 inflammasome in acute and chronic inflammation is complex. We reviewed literature detailing pathological changes and molecular mechanisms associated with radiation-induced damage to the cardiovascular structure, with a specific focus on NLRP3 inflammasome-related cardiovascular diseases. We also summarized possible therapeutic strategies for the prevention of radiation-induced heart disease (RIHD).

Neurohormones, inflammatory mediators, and cardiovascular injury in the setting of heart failure.

Neurohormones and inflammatory mediators have effects in both the heart and the peripheral vasculature. In patients with heart failure (HF), neurohormonal activation and increased levels of inflammatory mediators promote ventricular remodeling and development of HF, as well as vascular dysfunction and arterial stiffness. These processes may lead to a vicious cycle, whereby arterial stiffness perpetuates further ventricular remodeling leading to exacerbation of symptoms. Although significant advances have been made in the treatment of HF, currently available treatment strategies slow, but do not halt, this cycle. The current treatment for HF patients involves the inhibition of neurohormonal activation, which can reduce morbidity and mortality related to this condition. Beyond benefits associated with neurohormonal blockade, other strategies have focused on inhibition of inflammatory pathways implicated in the pathogenesis of HF. Unfortunately, attempts to target inflammation have not yet been successful to improve prognosis of HF. Further work is required to interrupt key maladaptive mechanisms involved in disease progression.

The protective effects of selenium supplementation on ambient PM2.5-induced cardiovascular injury in rats.

Substantial epidemiological and experimental studies have shown that ambient fine particulate matter (PM2.5) exposure can lead to myocardial damage in human and animal through the mechanism of inflammation and oxidative stress. The purpose of the current study was to investigate whether selenium yeast (SeY) supplementation could prevent cardiovascular injury caused by PM2.5 in rats. Fifty-six Sprague-Dawley rats were randomly divided into seven groups: saline control group; solvent control group, low-, middle-, and high-dose Se pretreatment groups, PM2.5 exposure group, and high-dose Se control group. The rats were pretreated with different concentration of dietary SeY for 28 days, then were exposed to PM2.5 by intratracheal instillation every other day, a total of three times. The levels of inflammatory markers (tumor necrosis factor-alpha (TNF-α), interleukin-1beta (IL-1ß), soluble intercellular adhesion molecule-1 (sICAM-1), and oxidative responses-related indicators total antioxidant capacity (T-AOC), total superoxide dismutase (T-SOD), glutathione peroxidase (GSH-Px), and malondialdehyde (MDA) were measured in blood and myocardium of the left ventricle. The results showed that although PM2.5 caused a decrease of T-AOC, T-AOD, and GSH-Px and increase of MDA and sICM-1, pretreatment with SeY induced a dose-dependent increase in these anti-oxidative indicators and a decrease in oxidative indicators. In addition, the levels of TNF-α and IL-1ß in Se pretreatment groups were significantly lower than that in PM2.5 exposure group. The results indicated that Se supplementation could effectively prevent cardiovascular inflammation and oxidative stress induced by PM2.5. The results also indicated that the nutritional supplementation might be an effective way to protecting people's health from air pollution.