Short-term exposure to ambient ozone associated with cardiac arrhythmias in healthy adults

Objective The exact biological mechanism whereby exposure to ambient ozone(O3)may contribute to clinical onset of cardiovascular events remains unclear.In this study,we aim to examine the impacts of O3 exposure on cardiac arrhythmias and potential pathways involved through autonomic dysfunction and myocardial injury.Methods Seventy-three non-smoking healthy adults were followed with 4 repeated measurements of 24-hour ambulatory arrhythmias,heart rate variability,ST-segment deviation,and blood pressure(BP)in Beijing,China,2014‒2016.Generalized additive mixed models coupled with distributed lag nonlinear models were constructed to evaluate the associations and potential interlinks between O3 exposure and outcome measurements.Results During the study period,24-hour average concentrations of ambient O3 were 47.4µg/m3(ranging from 1.0 to 165.9µg/m3).Increased risks of premature ventricular contraction and ventricular tachycardia were associated with interquartile range increases in O3 exposure during the last 5 days before each participant's clinic visit,with relative risks of 2.14(95%confidence interval[CI]:1.95 to 2.32)and 5.47(95%CI:3.51 to 7.43),respectively.Mediation analyses further showed that sympathetic activation,parasympathetic inhibition,and elevated BP levels,as well as heightened risks of ST-segment depression could mediate up to 47.74%of the risks of arrhythmias attributable to O3 exposure.Conclusion Our results suggest that short-term exposure to ambient O3 could prompt the genesis of arrhythmias partially through worsening autonomic function and myocardial burden.

Cardiac-targeted PIASy gene silencing mediates deSUMOylation of caveolin-3 and prevents ischemia/reperfusion-induced Na_(v)1.5 downregulation and ventricular arrhythmias

Background:Abnormal myocardial voltage-gated sodium channel 1.5(Nav1.5)expression and function cause lethal ventricular arrhythmias during myocardial ischemia–reperfusion(I/R).Protein inhibitor of activated STAT Y(PIASy)-mediated caveolin-3(Cav-3)small ubiquitin-related modifier(SUMO)modification affects Cav-3 binding to the Nav1.5.PIASy activity is increased after myocardial I/R,but it is unclear whether this is attributable to plasma membrane Nav1.5 downregulation and ventricular arrhythmias.Methods:Using recombinant adeno-associated virus subtype 9(AAV9),rat cardiac PIASy was silenced using intraventricular injection of PIASy short hairpin RNA(shRNA).After two weeks,rat hearts were subjected to I/R and electrocardiography was performed to assess malignant arrhythmias.Tissues from peri-infarct areas of the left ventricle were collected for molecular biological measurements.Results:PIASy was upregulated by I/R(P<0.01),with increased SUMO2/3 modification of Cav-3 and reduced membrane Nav1.5 density(P<0.01).AAV9-PIASy shRNA intraventricular injection into the rat heart down-regulated PIASy after I/R,at both mRNA and protein levels(P<0.05 vs.Scramble-shRNA+I/R group),decreased SUMO-modified Cav-3 levels,enhanced Cav-3 binding to Nav1.5,and prevented I/R-induced decrease of Nav1.5 and Cav-3co-localization in the intercalated disc and lateral membrane.PIASy silencing in rat hearts reduced I/R-induced fatal arrhythmias,which was reflected by a modest decrease in the duration of ventricular fibrillation(VF;P<0.05 vs.Scramble-shRNA+I/R group)and a significantly reduced arrhythmia score(P<0.01 vs.Scramble-shRNA+I/R group).The anti-arrhythmic effects of PIASy silencing were also evidenced by decreased episodes of ventricular tachycardia(VT),sustained VT and VF,especially at the time 5–10 min after ischemia(P<0.05 vs.Scramble-shRNA+IR group).Using in vitro human embryonic kidney 293 T(HEK293T)cells and isolated adult rat cardiomyocyte models exposed to hypoxia/reoxygenation(H/R),we confirmed that increased PIASy promoted Cav-3 modification by SUMO2/3 and Nav1.5/Cav-3 dissociation after H/R.Mutation of SUMO consensus lysine sites in Cav-3(K38R or K144R)altered the membrane expression levels of Nav1.5 and Cav-3 before and after H/R in HEK293T cells.Conclusions:I/R-induced cardiac PIASy activation increased Cav-3 SUMOylation by SUMO2/3 and dysregulated Nav1.5-related ventricular arrhythmias.Cardiac-targeted PIASy silencing mediated Cav-3 deSUMOylation and partially prevented I/R-induced Nav1.5 downregulation in the plasma membrane of cardiomyocytes,and subsequent ventricular arrhythmias in rats.PIASy was identified as a potential therapeutic target for life-threatening arrhythmias in patients with ischemic heart diseases.

Cardiac arrhythmias detection in an ECG beat signal using fast fourier transform and artificial neural network

Cardiac Arrhythmias shows a condition of abnor-mal electrical activity in the heart which is a threat to humans. This paper presents a method to analyze electrocardiogram (ECG) signal, extract the fea-tures, for the classification of heart beats according to different arrhythmias. Data were obtained from 40 records of the MIT-BIH arrhythmia database (only one lead). Cardiac arrhythmias which are found are Tachycardia, Bradycardia, Supraventricular Tachycardia, Incomplete Bundle Branch Block, Bundle Branch Block, Ventricular Tachycardia. A learning dataset for the neural network was obtained from a twenty records set which were manually classified using MIT-BIH Arrhythmia Database Directory and docu- mentation, taking advantage of the professional experience of a cardiologist. Fast Fourier transforms are used to identify the peaks in the ECG signal and then Neural Networks are applied to identify the diseases. Levenberg Marquardt Back-Propagation algorithm is used to train the network. The results obtained have better efficiency then the previously proposed methods.

Amiodarone Therapy for Cardiac Arrhythmias: Is It Associated with the Development of Cancers?

Amiodarone is used worldwide to treat cardiac arrhythmias, as well as highly symptomatic cases of atrial fibrillation. With this expanded use, especially following its 1985 United States Food and Drug Administration approval, and its use as a long-term therapy in common practice, reports of cancers temporarily related to amiodarone have begun to increase. Animal studies, several clinical trials, numerous case reports, and a population-based cohort study have suggested that cancers may be associated with amiodarone use. This review focuses on the ever increasing evidence in the literature that suggests amiodarone therapy, especially with long-term use, may increase the potential risk of cancer development. It also expresses the need for more definitive studies to be conducted to provide clinicians with a clear answer to this important question.

Diagnostic Dilemma of Intracardiac Mass: Tumor versus Thrombus-Case Series and Systematic Review

Background: The differential diagnosis for intracavitary cardiac masses is limited, typically including vegetations, tumors, or thrombi. Cardiac thrombi can often mimic cardiac tumors on imaging, creating a diagnostic challenge. Primary cardiac tumors are rare and usually benign, whereas most cardiac tumors result from metastases, commonly originating from malignancies in the breast, lung, or melanoma. Aim: This report highlights the importance of distinguishing various cardiac masses based on clinical presentations, clinical courses, and radiological features. Case Presentation: We describe two cases of cardiac masses with unique and diverse clinical features. Each case posed significant diagnostic challenges due to their distinct presentations and clinical progressions. Conclusion: These cases underscore the importance of considering both benign and metastatic origins in the differential diagnosis of intracavitary cardiac masses. Accurate differentiation between thrombi and tumors is crucial for appropriate management and treatment.

Control of cardiac excitability and arrhythmias by microRNAs

Recent studies revealing the important roles of microRNAs（miRNAs） in regulating expression of ion channel genes have opened up a research field for extending and deepening our investi- gation into the cardiac excitability and the associated arrhythmogenesis.Cardiac excitability,the fundamental property of the cardiac myocytes,defines the cardiac conduction,repolarization,automaticity,intracellular calcium handling,and their regional heterogeneity. Our previous and ongoing studies and the work from other laboratories have demonstrated the significant involvement of miRNAs in regulating every aspects of cardiac excitability.We have found earlier that the muscle-specific miRNA miR-1 boosts up the arrhythmogenic potential through targeting gap junction channel connexin 43 in myocardial infarction.A subsequent study revealed that miR-1 can also cause arrhythmias by impairing Ca2+ handling by targeting phosphatase.We then identified another muscle-specific miRNA miR-133 promotes abnormal QT prolongation by repressing HERG K+ channel expression in diabetic cardiomyopathy. Subsequently,we discovered that both miR- 1 and miR-133 are involved in the reexpression of pacemaker channels HCN2/HCN4 to enhance abnormal automaticity in cardiac hypertrophy.Recently, we further identified miR-328 as an important determinant for atrial fibrillation（AF） and the associated adverse atrial electrical remodeling via targeting L-type Ca2+ channels.While all the above-mentioned miRNAs are proarrhythmic,we have newly identified for the first time a natural antiarrhythmic miRNA miR-26.We found that all three members of the miR-26 family is downregulated in their expression in AF tissues and this downregulation increases AF vulnerability as a result of removal of an endogenous antiarrhythmic factor.miR-26 downregulation shortens atrial action potential favoring AF by increasing inward rectifier K+ current（IK1） density. This is caused by an upregulation of Kir2.1 K+ channel subunit due to derepression of its encoding gene KCNJ2 as we have validated KCNJ2 as a target gene for miR-26.Administration of a LNA-modified antimiR-26 antisense through tail vein injection increases AF vulnerability as indicated by increased number of mice with AF induction by intracardiac pacing.And this effect is blunted by co-injection of either an adenovirus vector carrying miR-26 precursor sequence or a LNA-modified miR-26 mimic to specifically target KCNJ2.We further discovered that the activity of NFAT transcription factor is enhanced in AF which represses the transcription of miR-26. We characterized the promoter region of the host genes of all three members of the miR-26 miRNA family and identified a common cis-acting element for NFAT binding.Thus,our study unraveled a novel miRNA signaling pathway AF NFAT miR-26 KC-NJ2 /Kir2.1/IK1 AF as a positive feedback loop favoring AF and the remodeling process.

Approach to cardiac masses: Thinking inside and outside the box

In this editorial we comment on the article by Huffaker et al,published in the current issue of the World Journal of Clinical Cases.Cardiac masses encompass a broad range of lesions,potentially involving any cardiac structure,and they can be either neoplastic or non-neoplastic.Primitive cardiac tumors are rare,while metastases and pseudotumors are relatively common.Cardiac masses frequently pose significant diagnostic and therapeutic challenges.Multimodality imaging is fundamental for differential diagnosis,treatment,and surgical planning.In particular cardiac magnetic resonance(CMR)is currently the gold standard for noninvasive tissue characterization.CMR allows evaluation of the relationship between the tumor and adjacent structures,detection of the degree of infiltration or expansion of the mass,and prediction of the possible malignancy of a mass with a high accuracy.Different flow charts of diagnostic work-up have been proposed,based on clinical,laboratory and imaging findings,with the aim of helping physicians approach the problem in a pragmatic way(“thinking inside the box”).However,the clinical complexity of cancer patients,in particular those with rare syndromes,requires a multidisciplinary approach and an open mind to go beyond flow charts and diagnostic algorithms,in other words the ability to“think outside the box”.

Cardiac arrhythmias and cardiac arrest related to mushroom poisoning: A case report

BACKGROUND Mushroom exposure is a global health issue.The manifestations of mushroom poisoning (MP) may vary.Some species have been reported as rhabdomyolytic,hallucinogenic,or gastrointestinal poisons.Critical or even fatal MPs are mostly attributable to Amanita phalloides,with the development of severe liver or renal failure.Myocardial injury and even cases mimicking ST-segment elevation myocardial infarction (STEMI) have been previously reported,while cardiac arrhythmia or cardiac arrest is not commonly seen.CASE SUMMARY We report a 68-year-old woman with MP who suffered from delirium,seizure,long QT syndrome on electrocardiogram (ECG),severe cardiac arrhythmias of multiple origins,and cardiac arrest.She was intubated and put on blood perfusion.Her kidney and liver functions were intact;creatine kinase-MB was mildly elevated,and then fell within normal range during her hospital stay.We sent the mushrooms she left for translation elongation factor subunit 1α,ribosomal RNA gene sequence,and internal transcribed spacer sequence analyses.There were four kinds of mushrooms identified,two of which were found to be toxic.CONCLUSION This is the first time that we found cardiac toxicity caused by Panaeolus subbalteatus and Conocybe lactea,which were believed to be toxic to the liver,kidney,and brain.We suggest that intensive monitoring and ECG follow-up are essential to diagnose prolonged QT interval and different forms of tachycardia in MP patients,even without the development of severe liver or renal failure.The mechanisms need to be further investigated and clarified based on animal experiments and molecular signal pathways.

Heart rate-adjusted PR as a prognostic marker of long-term ventricular arrhythmias and cardiac death in ICD/CRT-D recipients

Objective To evaluate the PR to RR interval ratio (PR/RR,heart rate-adjusted PR) as a prognostic marker for long-term ventricular arrhythmias and cardiac death in patients with implantable cardioverter defibrillator (ICDs) and cardiac resynchronization therapy with defibrillators (CRT-D).Methods We retrospectively analyzed data from 428 patients who had an ICD/CRT-D equipped with home monitoring.Baseline PR and RR interval data prior to ICD/CRT-D implantation were collected from standard 12-lead electrocardiograph,and the PR/RR was calculated.The primary endpoint was appropriate ICD/CRT-D treatment of ventricular arrhythmias (VAs),and the secondary endpoint was cardiac death.Results During a mean follow-up period of 38.8 ± 10.6 months,197 patients (46%) experienced VAs,and 47 patients (11%) experienced cardiac death.The overall PR interval was 160 ± 40 ms,and the RR interval was 866 ± 124 ms.Based on the receiver operating characteristic curve,a cut-off value of 18.5% for the PR/RR was identified to predict VAs.A PR/RR ≥ 18.5% was associated with an increased risk of VAs [hazard ratio (HR)= 2.243,95% confidence interval (CI)= 1.665–3.022,P < 0.001) and cardiac death (HR = 2.358,95%CI = 1.240–4.483,P = 0.009) in an unadjusted analysis.After adjustment in a multivariate Cox model,the relationship remained significant among PR/RR ≥ 18.5%,VAs (HR = 2.230,95%CI = 1.555–2.825,P < 0.001) and cardiac death (HR = 2.105,95%CI = 1.101–4.025,P = 0.024.Conclusions A PR/RR ≥ 18.5% at baseline can serve as a predictor of future VAs and cardiac death in ICD/CRT-D recipients.

Spontaneous type 1 pattern, ventricular arrhythmias and sudden cardiac death in Brugada Syndrome： an updated systematic review and meta-analysis

Brugada syndrome （BrS） is primary electrical disorder characterized by ST segment elevation with right bundle branch block morphology in patients with apparent structurally normal hearts, It predisposes affected individuals to ventricular tachycardia/fibrillation （VT/VF） and sudden cardiac death （SCD）.A number of studies have identified risk factors that are associated with a more malignant course of disease. These include male gender, syncope, a spontaneous type 1 ECG pattern, family history of SCD, family history of Brugada syndrome,

Cardiac arrest, stony heart, and cardiopulmonary resuscitation: An updated revisit

The post-resuscitation period is recognized as the main predictor of cardiopul-monary resuscitation(CPR)outcomes.The first description of post-resuscitation syndrome and stony heart was published over 50 years ago.Major manifestations may include but are not limited to,persistent precipitating pathology,systemic ischemia/reperfusion response,post-cardiac arrest brain injury,and finally,post-cardiac arrest myocardial dysfunction(PAMD)after successful resuscitation.Why do some patients initially survive successful resuscitation,and others do not?Also,why does the myocardium response vary after resuscitation?These ques-tions have kept scientists busy for several decades since the first successful resuscitation was described.By modifying the conventional modalities of resu-scitation together with new promising agents,rescuers will be able to salvage the jeopardized post-resuscitation myocardium and prevent its progression to a dismal,stony heart.Community awareness and staff education are crucial for shortening the resuscitation time and improving short-and long-term outcomes.Awareness of these components before and early after the restoration of circulation will enhance the resuscitation outcomes.This review extensively addresses the underlying pathophysiology,management,and outcomes of post-resuscitation syndrome.The pattern,management,and outcome of PAMD and post-cardiac arrest shock are different based on many factors,including in-hospital cardiac arrest vs out-of-hospital cardiac arrest(OHCA),witnessed vs unwitnessed cardiac arrest,the underlying cause of arrest,the duration,and protocol used for CPR.Although restoring spontaneous circulation is a vital sign,it should not be the end of the game or lone primary outcome;it calls for better understanding and aggressive multi-disciplinary interventions and care.The development of stony heart post-CPR and OHCA remain the main challenges in emergency and critical care medicine.

Phoneutria Spider Toxins Target Channels Involved in Cardiac Arrhythmias, Ischemia and Pain

Toxins isolated from the venom of the spider Phoneutria nigriventer either inhibit or activate a vast number of targets, such as ion channels, with high selectivity and affinity. PhTx3-1 toxin is a selective blocker of IA currents of K^＋ channels, and PhTx3-3 and PhTx3-4 are calcium channel blockers of the P/Q-type calcium channels. The spider neurotoxin PhTx3-6 reversibly and non-specifically inhibits high-voltage-activated Ca^2＋ channels with varying potency （N 〉 R 〉 P/Q 〉 L） in heterologous and native systems. There has been a huge increase in the range of medical disorders involving ionic channels, and blockers of these channels have potential as therapeutic agents. The mechanism of action of each toxin family is different; thus, each needs to be evaluated for its therapeutic potential. This review will focus on peptide toxins purified from the venom of the spider Phoneutria nigriventer that are currently being evaluated in preclinical tests as possible drugs for the treatment of pain, cardiac arrhythmias and ischemia.

Cell and gene therapy for arrhythmias： Repair of cardiac conduction damage

Action potentials generated in the sinoatrial node （SAN） dominate the rhythm and rate of a healthy human heart. Subsequently, these action potentials propagate to the whole heart via its conduction system. Abnormalities of impulse generation and/or propagation in a heart can cause arrhythmias. For example, SAN dysfunction or conduction block of the atrioventricular node can lead to serious bradycardia which is currently treated with an implanted electronic pacemaker. On the other hand, conduction damage may cause reentrant tachyarrhythmias which are primarily treated pharmacologically or by medical device-based therapies, including defibrillation and tissue ablation. However, drug therapies sometimes may not be effective or are associated with serious side effects. Device-based therapies for cardiac arrhythmias, even with well developed technology, still face inadequacies, limitations, hardware complications, and other challenges. Therefore, scientists are actively seeking other alternatives for antiarrhythmic therapy. In particular, cells and genes used for repairing cardiac conduction damage/defect have been investigated in various studies both in vitro and in vivo. Despite the complexities of the excitation and conduction systems of the heart, cell and gene-based strategies provide novel alternatives for treatment or cure of cardiac arrhythmias. This review summarizes some highlights of recent research progress in this field.

Effect of cardiac rehabilitation care after coronary intervention on cardiac function recovery and negative mood in patients with myocardial infarction

BACKGROUND Cardiovascular disease,particularly myocardial infarction(MI)profound impact on patients'quality of life and places a substantial burden on the healthcare and economy systems.Developments in medical technology have led to the emer-gence of coronary intervention as an essential method for treating MI.AIM To assess the effects of cardiac rehabilitation care on cardiac function recovery and negative emotions in MI after coronary intervention.METHODS This study included a total of 180 patients with MI during the period from June 2022 to July 2023.Selected patients were divided into two groups:An observation group,which receiving cardiac rehabilitation care;a control group,which re-ceiving conventional care.By comparing multiple observation indicators such as cardiac function indicators,blood pressure,exercise tolerance,occurrence of adverse cardiac events,and negative emotion scores between the two groups of patients.All the data were analyzed and compared between two groups.RESULTS There were 44 males and 46 females in the observation group with an average age of 36.26±9.88 yr;there were 43 males and 47 females in the control group,with an average age of 40.87±10.5 yr.After receiving the appropriate postoperative nursing measures,the results of the observation group showed significant improvement in several indicators compared with the control group.Indicators of cardiac function,such as left ventricular end-diastolic internal diameter and left ventricular ejection fraction were significantly better in the observation group than in the control group(P<0.05).Exercise endurance assessment showed that the 6-minute walking test distance was significantly increased in the patients of the observation group(P<0.01).In addition,the incidence of adverse cardiac events was significantly lower in the observation group,and negative mood scores were significantly reduced(P<0.05).CONCLUSION Cardiac rehabilitation care after coronary intervention has a significant positive impact on functional recovery.This emphasizes the importance of cardiac rehabilitation care to improve patient recovery.

Overall approaches to cardiac tumors:Still an unsolved enigma?

Cardiac tumors are neoplasms involving heart structures at any level,meaning the myocardium,valves,and cardiac chambers.When considering cardiac masses,it is not uncommon for surgeons to be surprised when they diagnose one.The real incidence of this complex group of diseases has been explored only after cardiac diagnostic tools became more appropriate.Despite differential diagnosis being relevant,surgical indication is usually requested for all malignant cardiac tumors and also for many types of benign tumors.The development of cardiac imaging techniques,therefore,has been the key point for a better understanding of the history of cardiac tumors and especially of the relevance of surgical indication in such conditions.Systematic and combined applications of echocardiography,cardiac computed tomography and magnetic resonance allow in the majority of case a clear definition of the nature of a newly discovered cardiac mass.The presence of a Li-Fraumeni syndrome seems to be the trigger aspect in accelerating the propensity of developing a cardiac tumor.Despite the revolutionary usefulness of the cardiac imaging techniques available,it is still considered a hazard to diagnose a malignant cardiac mass just with radiological imaging;the mainstay of the final diagnosis stands in surgical excision of the mass and histopathological report.

Cardiac rehabilitation after cardiac surgery:An important underutilized treatment strategy

Physical inactivity remains in high levels after cardiac surgery,reaching up to 50%.Patients present a significant loss of functional capacity,with prominent muscle weakness after cardiac surgery due to anesthesia,surgical incision,duration of cardiopulmonary bypass,and mechanical ventilation that affects their quality of life.These complications,along with pulmonary complications after surgery,lead to extended intensive care unit(ICU)and hospital length of stay and significant mortality rates.Despite the well-known beneficial effects of cardiac rehabilitation,this treatment strategy still remains broadly underutilized in patients after cardiac surgery.Prehabilitation and ICU early mobilization have been both showed to be valid methods to improve exercise tolerance and muscle strength.Early mobilization should be adjusted to each patient’s functional capacity with progressive exercise training,from passive mobilization to more active range of motion and resistance exercises.Cardiopulmonary exercise testing remains the gold standard for exercise capacity assessment and optimal prescription of aerobic exercise intensity.During the last decade,recent advances in healthcare technology have changed cardiac rehabilitation perspectives,leading to the future of cardiac rehabilitation.By incorporating artificial intelligence,simulation,telemedicine and virtual cardiac rehabilitation,cardiac surgery patients may improve adherence and compliance,targeting to reduced hospital readmissions and decreased healthcare costs.

Effects of systematic cardiac rehabilitation training in elderly patients with unstable angina following cardiac stent implantation

BACKGROUND Coronary stent implantation is usually used to treat unstable angina to alleviate stenosis or occlusion,promoting blood flow restoration and alleviating symptoms such as myocardial ischemia.And postoperative cardiac rehabilitation is essential for enhancing recovery and prognosis.Nevertheless,conventional rehabilitation lacks specificity,particularly for elderly patients with multiple comorbidities and poor compliance,rendering it less effective.AIM To investigate the effects of systematic cardiac rehabilitation training in elderly patients with unstable angina following coronary stenting intervention.METHODS A retrospective enrollment was conducted comprising fifty-four elderly patients with unstable angina pectoris who underwent systematic cardiac rehabilitation training after receiving coronary intervention as the rehabilitation group,while fifty-three elderly patients who received basic nursing and rehabilitation guidance measures after coronary intervention were assigned to the control group.Differences in Seattle Angina Questionnaire scores,survival quality(SF-36)scores,cardiopulmonary exercise function assessment index,echocardiographic cardiac function index,and adverse cardiovascular events were compared between the two groups.RESULTS After intervention,the rehabilitation group observed greater VO2 Max,maximum metabolic equivalent,eft ventricular ejection fraction,left ventricular end-diastolic diameter and smaller left ventricular end-systolic diameter.And the rehabilitation group observed greater scores of physical activity limitation,stable angina pectoris,treatment satisfaction,and SF-36 score.The incidence of adverse cardiovascular events in the two groups,showed no significant difference.CONCLUSION Systematic cardiac rehabilitation following coronary stenting in elderly patients with unstable angina pectoris can enhance cardiac function recovery,consequently enhancing both quality of life and cardiopulmonary exercise tolerance.

Hypoxia-preconditioned bone marrow-derived mesenchymal stem cells protect neurons from cardiac arrest-induced pyroptosis

Cardiac arrest can lead to severe neurological impairment as a result of inflammation,mitochondrial dysfunction,and post-cardiopulmonary resuscitation neurological damage.Hypoxic preconditioning has been shown to improve migration and survival of bone marrow–derived mesenchymal stem cells and reduce pyroptosis after cardiac arrest,but the specific mechanisms by which hypoxia-preconditioned bone marrow–derived mesenchymal stem cells protect against brain injury after cardiac arrest are unknown.To this end,we established an in vitro co-culture model of bone marrow–derived mesenchymal stem cells and oxygen–glucose deprived primary neurons and found that hypoxic preconditioning enhanced the protective effect of bone marrow stromal stem cells against neuronal pyroptosis,possibly through inhibition of the MAPK and nuclear factor κB pathways.Subsequently,we transplanted hypoxia-preconditioned bone marrow–derived mesenchymal stem cells into the lateral ventricle after the return of spontaneous circulation in an 8-minute cardiac arrest rat model induced by asphyxia.The results showed that hypoxia-preconditioned bone marrow–derived mesenchymal stem cells significantly reduced cardiac arrest–induced neuronal pyroptosis,oxidative stress,and mitochondrial damage,whereas knockdown of the liver isoform of phosphofructokinase in bone marrow–derived mesenchymal stem cells inhibited these effects.To conclude,hypoxia-preconditioned bone marrow–derived mesenchymal stem cells offer a promising therapeutic approach for neuronal injury following cardiac arrest,and their beneficial effects are potentially associated with increased expression of the liver isoform of phosphofructokinase following hypoxic preconditioning.

Cardiac arrhythmias

920643 Insight into the mechanism of tor-sade de points (TDP) induced by cesiumchloride. SHEN Jianbing (沈坚冰), et al. Res-Sect, Cardivasc Dis, 1st Affili Hosp, Suzhou MedColl, 215006. Chin J Intern Med 1992; 31(7):

A contradictory phenomenon of thicken pericardium and cardiac compression without inferior vena cava dilation:sign of IVC escape

A 77-year-old female presented with shortness of breath and tightness of chest was admitted.Her past medical history included hypertension and she has been taking nifedipine regularly.Two years before,she was diagnosed with pericardial effusion(Figure 1)and had pericardiocentesis drainage.On physical examination,her blood pressure was 151/100 mm-Hg and her pulse rate was 91 beats/min.