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ObjectiveAfter the brain and heart injuries were simulated by myocardial injury caused by acute cerebral ischemia， this study explored the mechanism of Naoxintong capsules in treating brain and heart injuries under cerebral ischemia state with Toll-like receptor （TLR） 2/TLR4 as the breakthrough point. MethodC57BL/6 male mice were randomly assigned into the sham operation， model， Naoxintong， and Ginaton groups. The middle cerebral artery occlusion （MCAO） method was used to establish a mouse model of cerebral ischemia. The neuroethological score， cerebral infarction area， cell apoptosis， ionized calcium-binding adaptor molecule 1 （IBA-1）-positive microglia proportion， and serum levels of N-terminal pro-brain natriuretic peptide （NT-proBNP）， creatine kinase-MB （CK-MB）， and lactic dehydrogenase （LDH） were determined to evaluate the pharmacodynamic effects of Naoxintong capsules on heart and brain injuries after cerebral ischemia in mice. Western blotting was employed to determine the expression of TLR2/TLR4 protein in the brain and heart of mice. ResultCompared with the sham operation group， the model group showed increased cerebral infarction area， neuroethological score， apoptosis rate， IBA-1-positive microglia proportion， and serum levels of NT-proBNP， CK-MB， and LDH （P<0.01）. Naoxintong capsules reduced the cerebral infarction area， neuroethological score， apoptosis rate， IBA-1-positive microglia proportion （P<0.01）， and serum NT-proBNP and CK-MB levels （P<0.05） in mice compared with the model group. Western blotting results showed that Naoxintong Capsules down-regulated the expression levels of TLR2 （P<0.05） in the brain and TLR2 （P<0.01） and TLR4 （P<0.05） in the heart. ConclusionCerebral ischemia can cause myocardial damage， reflecting the pathological process of cardiac injury after cerebral ischemia. Naoxintong capsules can mitigate brain and heart injuries after cerebral ischemia and achieve the simultaneous treatment of the brain and the heart， in which TLR2/TLR4 plays a role.
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Cardiac-resident macrophages (CRMs) play important roles in homeostasis, cardiac function, and remodeling. Although CRMs play critical roles in cardiac regeneration of neonatal mice, their roles are yet to be fully elucidated. Therefore, this study aimed to investigate the dynamic changes of CRMs during cardiac ontogeny and analyze the phenotypic and functional properties of CRMs in the promotion of cardiac regeneration. During mouse cardiac ontogeny, four CRM subsets exist successively: CX3CR1+CCR2-Ly6C-MHCII- (MP1), CX3CR1lowCCR2lowLy6C-MHCII- (MP2), CX3CR1-CCR2+Ly6C+MHCII- (MP3), and CX3CR1+CCR2-Ly6C-MHCII+ (MP4). MP1 cluster has different derivations (yolk sac, fetal liver, and bone marrow) and multiple functions population. Embryonic and neonatal-derived-MP1 directly promoted cardiomyocyte proliferation through Jagged-1-Notch1 axis and significantly ameliorated cardiac injury following myocardial infarction. MP2/3 subsets could survive throughout adulthood. MP4, the main population in adult mouse hearts, contributed to inflammation. During ontogeny, MP1 can convert into MP4 triggered by changes in the cellular redox state. These findings delineate the evolutionary dynamics of CRMs under physiological conditions and found direct evidence that embryonic and neonatal-derived CRMs regulate cardiomyocyte proliferation. Our findings also shed light on cardiac repair following injury.
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Cardiotoxicity induced by anticancer drug; doxorubicin (DOX) is a limiting factor for its prolonged use in chemotherapy. No effective drug is currently available to prevent DOX induced cardiomyopathy. Ganoderma lucidum is highly valued medicinal mushroom used in traditional medicine. Mycelia biomasses are considered as alternate sources of mushroom bioactive compounds. We examined the effect of bioactive extract of G. lucidum mycelia biomass (GLME) to prevent cardiotoxicity induced by DOX in rats using a cumulative dose 18 mg/kg body wt. GLME was administered to animals at doses of 250 and 500 mg/kg body wt. once daily for five days prior to DOX administration and continued for three more days. Animals were sacrificed 24 h after the last dose of drug. Activities of creatine kinase (CK), lactate dehydrogenase (LDH), endogenous antioxidant status, oxidative stress markers, electrocardiograph (ECG) and haematological parameters were evaluated. DOX administration drastically elevated CK, LDH, myocardial peroxidation and oxidative stress and significantly lowered endogenous antioxidant activity. GLME administration attenuated elevated levels of CK, LDH and oxidative stress and also ameliorated alterations in haematological and ECG parameters. Results revealed that bioactive extract of G. lucidum mycelia imparted significant protection against DOX induced cardiomyopathy suggesting the potential therapeutic significance of G. lucidum mycelia bioactives to alleviate DOX induced cardiomyopathy.
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@#BACKGROUND: Elevated troponin I (TnI) is common among trauma patients. TnI is an indicator of myocardial injury, but clinical diagnosis of blunt cardiac injury cannot be based solely on an increase in TnI. Therefore, this study aims to explore the changes and clinical significance of serum TnI in trauma patients. METHODS: The clinical data of consecutive trauma patients admitted to our trauma center between July 1, 2017 and July 31, 2020 were retrospectively analyzed. According to TnI levels within 24 hours of admission, patients were divided into the elevated and normal TnI groups. According to the TnI levels after 7 days of admission, a graph depicting a change in trend was drawn and then analyzed whether TnI was related to in-hospital mortality. RESULTS: A total of 166 patients (69 and 97 cases with elevated and normal TnI, respectively) were included in this study. The average hospital stay, intensive care time, mechanical ventilation time, and in-hospital mortality were higher in the elevated TnI group than in the normal TnI group (P<0.05). The TnI level of trauma patients gradually increased after admission and peaked at 48 hours (7.804±1.537 ng/mL). Subsequently, it decreased, and then recovered to normal within 7 days. However, 13 patients did not recover. Logistic regression analysis revealed that abnormal TnI at 7 days was independently related to in-hospital mortality. CONCLUSIONS: Trauma patients with elevated TnI levels may have a worse prognosis. Monitoring the changes in serum TnI is important, which can reflect the prognosis better than the TnI measured immediately after admission.
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Objective:To investigate the predictive value of serum D-dimer combined with myocardial injury markers on admission for early identification of high-risk patients with acute myocarditis.Methods:Patients hospitalized for acute myocarditis in China-Japan Friendship Hospital were retrospectively enrolled from 2010 to 2021. Patients were divided into the high D-dimer level group and low D-dimer level group according to the median value of D-dimer measured by immunoturbidimetry within 24 h of admission. In-hospital adverse events were defined as death, cardiogenic shock, malignant ventricular arrhythmia and new-onset heart failure. Multivariate logistic analysis was used to explore the independent predictors of in-hospital adverse events, and receiver operating characteristic curve was used to evaluate the predictive value.Results:A total of 106 patients were analyzed, including 52 high level D-dimer patients and 54 low level D-dimer patients, with an average age of (36±16) years, and 62.3% were male. Compared with the low D-dimer level group, patients in the high D-dimer level group had lower mean systolic blood pressure [(114±21) mmHg vs. (121±14) mmHg] and diastolic blood pressure [(71±13) mmHg vs. (76±10) mmHg], higher heart rate [(97±26) beats/min vs. (79±15) beats/min], higher C-reactive protein levels [6.82 (1.61, 20.05) mg/dL vs. 1.30 (0.13, 8.93) mg/dL] and creatinine levels [86.95 (67.63, 117.83) μmol/L vs. 68.80 (60.18, 81.93) μmol/L] on admission. The proportion of patients having QRS interval >120 ms on electrocardiogram was higher in high D-dimer level group (25.0% vs. 7.4%). There was no significant difference in patients with positive myocardial injury biomarkers between the two groups. The incidence of in-hospital adverse events was higher in the high D-dimer level group (67.3% vs. 22.2%, P<0.001). Multivariate logistic analysis showed that serum D-dimer levels and elevated myocardial injury markers on admission were independently associated with in-hospital adverse events. The area under the curve (AUC) of elevated serum D-dimer level on admission for predicting in-hospital adverse events was 0.781 (95% CI: 0.690-0.873), the sensitivity was 74.5%, and the specificity was 71.2%. When combined with positive cardiac biomarkers, the AUC was 0.831 (95% CI: 0.752-0.910) with a sensitivity of 80.9% and a specificity of 78.0%. Conclusions:Elevated D-dimer level on admission can predict the risk of in-hospital adverse events in patients with acute myocarditis. The combination of cardiac injury biomarkers can improve the predictive value.
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Objective:To study the protective effect and mechanism of paeoniflorin (pae) on myocardial injury in septic rats.Methods:Sprague-Dawley (SD) rats were randomly divided into 4 groups with 10 rats in each group. Rats were intraperitoneally injected with 1.4 ml normal saline and 1.4 ml 5% dimethyl sulfoxide (DMSO)solution independently in control group and DMSO group. Rats were intraperitoneally injected with 1.4 ml normal saline and 1.4 ml pae independently, then with 0.1 ml lipopolysaccharide (LPS) 1 hour later in sepsis group and pae group. Enzyme linked immunosorbent assay (ELISA) was used to detect serum cardiac troponin I (cTnI) levels and myocardial tissue tumor necrosis factor alpha (TNFα), interleukin(IL)-6, IL-1β, chemokine (C-X-C motif) ligand 1 (CXCL1), chemokine (C-X-C motif) ligand 2 (CXCL2), vascular cell adhesion molecule 1 (VCAM-1) levels. Evans blue (EB) method was used to detect the EB content of myocardial tissue. HE staining method was used to observe the pathological changes, real-time quantitative polymerase chain reaction (RT-qPCR) to detect mRNA expression levels of the above molecules, and Western-blot to detect vascular endothelium-cadherin (VE-cadherin), phosphorylated p38 mitogen-activated protein kinase (P-p38MAPK), phosphorylated Src protein (P-Src), Ras-Related C3 Botulinum Toxin Substrate 1 (Rac1) levels.Results:Compared with control group, cTnI level and the EB content in sepsis group increased significantly, and the myocardial inflammatory cell infiltration was obvious. The cTnI level and EB content in pae group were significantly reduced, and myocardial inflammatory cell infiltration was reduced [cTnI: (227.7±15.9)pg/ml vs. (312.9±17.9)pg/ml;EB: (13.2±2.3)μg/g vs. (23.8±2.9)μg/g; P<0.05]. Compared with control group, the levels of TNFα, IL-6, IL-1β, CXCL1, CXCL2, and VCAM-1 in sepsis group were increased. Compared with sepsis group, the above-mentioned molecular levels of pae group were significantly decreased [TNFα: (63.39±9.55)pg/ml vs. (126.54±19.17)pg/ml ;IL-6: (64.03±8.82)pg/ml vs. (85.60±9.52)pg/ml;IL-1β: (69.52±9.23)pg/ml vs. (130.45±15.10)pg/ml;CXCL1: (2 600.19±379.54)pg/ml vs. (4 903.89±533.42)pg/ml;CXCL2: (93.71±10.83)pg/ml vs. (127.24±13.92)pg/ml;VCAM-1: (112.22±13.49)pg/ml vs. (149.32±15.65)pg/ml, both P<0.05]. RT-qPCR results showed that the mRNA expressions of TNFα, IL-6, IL-1β, CXCL1, CXCL2 and VCAM-1 in the sepsis group were increased compared with the control group; Compared with sepsis group, the IL-6 mRNA (1.271±0.139 vs. 1.920±0.191, P<0.05), IL-1βmRNA (1.180±0.130 vs. 1.817±0.191, P<0.05), VCAM-1 mRNA (1.088±0.144 vs. 1.460±0.166, P<0.05) expression decreased significantly in the pae group. Compared with control group, the levels of P-p38MAPK and P-Src in sepsis group increased, and the level of VE-cadherin decreased. Compared with sepsis group, the levels of p38MAPK and P-p38MAPK in pae group were significantly decreased, and the level of VE-cadherin was increased (p38MAPK/β-actin: 1.125±0.078 vs. 1.520±0.164; P-p38MAPK protein: 1.639±0.133 vs. 2.112±0.222; both P<0.05). Conclusion:Paeoniflorin could improve the permeability of cardiac microvascular endothelium in sepsis rats and inhibit the secretion and expression of inflammation-related proteins and genes, which might be related to the inhibition of Src/VE-cadherin pathway by paeoniflorin.
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Objective:To assess the prognostic potential of post systolic shortening (PSS) on cardiac injury in the breast cancer patients after chemotherapy.Methods:This was a prospective cohort study in breast cancer patients after chemotherapy who were followed up to observe the risk of cardiac injury. A total of 69 female patients with HER-2 negative breast cancer were selected in the Fourth Hospital of Hebei Medical University from February to August 2019. The post-systolic strain index (PSI) of each segment of left ventricular myocardium after chemotherapy was obtained by two-dimensional speckle tracking echocardiography. PSI (%) was defined as follows: [(peak strain in cardiac cycle-peak strain in systole)/peak strain in cardiac cycle]×100%. PSS was regarded as meaningful if PSI >20%. End point was cardiac injury, which could be manifested as cardiotoxicity, cardiogenic death, myocardial infarction, unstable angina pectoris, and severe arrhythmias. Occurence of any above mentioned cardiac injuries was considered as end point event. According to the number of myocardial walls with PSS, the patients were divided into three groups: group A (no walls), group B (1 wall), and group C (≥2 walls). Additionally, the patients were also stratified according to tertiles of PSI: layer A (the first tertile), layer B (the second tertile), and layer C (the third tertile).Results:During a median follow-up of 18 months (Q 1=17 months, Q 3=18 months), 17 patients (24.64%) were diagnosed as having end point events. The risk of end point increased with the increase in the number of myocardial walls with PSS and the increase in PSI stratification.After adjusting for age, hypertension, systolic blood pressure, global longitudinal strain, and E peak of mitral early diastolic inflow velocity/average peak early diastolic mitral annular velocity e′ (E/e′), the association remained significant, (Per 1 increase in number of walls with PSS, hazard ratio, 1.96, P=0.007. Per 1% increase in PSI, hazard ratio, 1.44, P<0.001). In terms of predictive ability, the Harrell′s C index of PSS and of PSI was 0.70 and 0.73, respectively, both P<0.01, which indicated moderate accuracy. Conclusions:The presence of PSS in breast cancer patients after chemotherapy can provide independent prognostic information for the future occurrence of cardiac injury.
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Objective:To investigate the role and mechanism of sodium valproate (VPA) in cardiac and cerebral injuries after cardiopulmonary resuscitation (CPR) in pigs.Methods:Twenty-five healthy male domestic pigs, weighing (37±3) kg, were randomly divided into the sham group ( n=6), CPR group ( n=10), and CPR+VPA group ( n=9). Cardiac arrest was induced by alternating current delivered via a pacing catheter in the right ventricle and untreated for 9 min, and then CPR was performed for 6 min, in which this procedure was used to establish the animal model of cardiac arrest and CPR. At 5 min after resuscitation, a dose of 150 mg/kg of VPA was infused with a pump via the femoral vein in 1 h in the CPR+VAP group. At 1 h, 2 h, 4 h and 24 h after resuscitation, blood samples were drawn from the femoral vein, and then used to measure the serum concentrations of cardiac troponin I (cTnI), creatine kinase MB (CKMB), neuron specific enolase (NSE), and S100B protein (S100B) by ELISA. At 24 h after resuscitation, the animals were euthanized, and then tissue specimens in the left myocardium and brain cortex were rapidly harvested to detect the expression levels of C/EBP homologous protein (CHOP), caspase 12, and caspase 3 by Western blot, and the rate of apoptotic cells was detected by TUNEL. Continuous variables were compared with one way analysis of variance among the three groups. Results:(1) After resuscitation, cardiac and cerebral injury biomarkers including cTnI, CKMB, NSE, and S100B in serum were significantly increased in the CPR and CPR+VPA groups compared with the Sham group (all P<0.05). The serum concentrations of cTnI and NSE starting 1 h after resuscitation and the serum concentrations of CKMB and S100B starting 2 h after resuscitation were significantly decreased in the CPR+VPA group compared to the CPR group (all P<0.05). (2) Those proteins related to cell apoptosis mediated by endoplasmic reticulum stress, including CHOP, caspase 12, and caspase 3, were significantly increased, and meanwhile apoptosis index was markedly elevated after resuscitation in the CPR and CPR+VPA groups compared with the Sham group (all P<0.05). Nevertheless, the expression levels of CHOP, caspase 12, and caspase 3 were significantly decreased, and cell apoptosis was markedly reduced in the heart and brain after resuscitation in the CPR+VPA group compared to the CPR group (all P<0.05). Conclusions:VPA can alleviate cardiac and cerebral injuries after CPR in pigs, and its mechanism may be possibly related to the inhibition of cell apoptosis mediated by endoplasmic reticulum stress.
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Objective: To compare the cardioprotective efficacy of equimolar doses (50 mM/kg, p.o.) of phloretin and genistein against doxorubicin-induced cardiotoxicity in rats. Methods: Cardiotoxicity was induced in rats by intraperitoneal injection of 6 mg/kg doxorubicin on alternative days till the cumulative dose reached 30 mg/kg. This study included four treatment groups of rats (n=6): the control group (0.5% carboxymethyl cellulose solution-treated), the doxorubicin- treated group (0.5% carboxymethyl cellulose solution along with doxorubicin), the genistein-treated group (50 mM/kg/day; p.o. along with doxorubicin) and phloretin-treated group (50 mM/kg/day; p.o. along with doxorubicin). On the 10th day of dosing, rats were anesthetized for recording ECG, mean arterial pressure, and left ventricular function. Oxidative stress, nitric oxide levels, and inflammatory cytokines were estimated in the cardiac tissue. Cardiac function parameters (creatine kinase MB, lactate dehydrogenase, aspartate aminotransferase, and alanine transaminase) were estimated in the serum samples. Results: Phloretin treatment inhibited doxorubicin-induced oxidative stress and also reduced nitric oxide levels in cardiac tissues of rats. Phloretin administration attenuated doxorubicin- induced alterations in hemodynamic parameters (heart rate, mean arterial blood pressure, and left ventricular function) and suppressed the expression of pro-inflammatory cytokines. The cardiac injury markers like creatine kinase MB, lactate dehydrogenase, aspartate aminotransferase, and alanine transaminase were reduced by both genistein and phloretin. All these effects of phloretin were more prominent than genistein. Conclusions: Phloretin offers cardioprotection that is comparable to genistein, a clinically validated cardioprotectant against doxorubicin-induced cardiotoxicity. Further studies are needed to confirm and establish the therapeutic utility of phloretin as a chemopreventive adjuvant to doxorubicin chemotherapy.
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Blunt traumatic rupture of the heart carries a high mortality rate. Anatomical injuries have included the atrium, appendage and ventricle but injury to the left appendage has been reported very rarely. We present the case of a 71-year-old female who was a driver in a motor collision with major front-end damage where air bags were deployed. After being intubated and receiving pericardiocentesis for cardiac tamponade at an advanced critical care and emergency medical center, the patient was taken to our hospital and emergently to the operating room for exploration. There was brisk bleeding coming from a 2 cm laceration on the left atrial appendage. The injury was repaired using 4-0 polypropylene felt pledget-supported horizontal mattress sutures on the beating heart with the assistance of cardiopulmonary bypass. The present report describes this patient and our findings from a literature review.
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Objective:To investigate the role of Toll-like receptor 4 (TLR4) pathway on myocardial injury and cardiac dysfunction in septic rats.Methods:According to the random number table, 18 male Sprague-Dawley (SD) rats were divided into control group, lipopolysaccharide (LPS) group and TLR4 specific inhibitor TAK242 pretreatment group (TAK242+LPS group) with 6 rats in each group. The rat model of septic cardiac dysfunction was induced by intraperitoneal injection of LPS 15 mg/kg, and the control group was given the same amount of normal saline. The TAK242+LPS group was intraperitoneally given injection of TAK242 [it was injected intraperitoneally at a dose of 3 mg/kg and dissolved in 10% dimethyl sulfoxide (DMSO) and 90% corn oil according to the concentration of 0.2 g/L] 3 hours before LPS stimulation. The control group and LPS group were given the same amount of 10% DMSO and 90% corn oil. The cardiac function of rats in each group was examined by Doppler echocardiography 14 hours after injection of LPS. The blood of abdominal aorta was taken and the level of serum troponin (cTn) was measured by enzyme linked immunosorbent assay (ELISA). Myocardial tissue was harvested for hematoxylin-eosin (HE) staining, and the morphological changes of myocardial tissue were observed under light microscope. The mRNA expressions of interleukin-6 (IL-6) and tumor necrosis factor-α(TNF-α) in myocardial tissue were detected by real-time fluorescence quantitative polymerase chain reaction (qPCR). The protein expression of TLR4 in myocardial tissue was observed by immunohistochemical method. Western blotting was used to detect the levels of TLR4, nuclear factor-κB p65 (NF-κB p65) and its phosphorylation (p-NF-κB p65) in myocardial tissue.Results:① The cardiac function and myocardial injury: Doppler echocardiography showed that the levels of left ventricular end-diastolic volume (LVEDV) and left ventricular end-systolic volume (LVESV) in the LPS group were significantly higher than those in the control group, while left ventricular ejection fraction (LVEF) and left ventricular shortened fraction (LVFS) were significantly lower than those in the control group. The degeneration, necrosis and inflammatory cell infiltration of cardiomyocytes were found with light microscope in the LPS group, and the levels of serum cTn were significantly higher than those in the control group, indicating that LPS-induced sepsis could cause cardiac dysfunction and myocardial injury. TAK242 blocking TLR4 pathway had a protective effect on cardiac function and myocardium during sepsis. LVEDV and LVESV in the TAK242+LPS group were significantly lower than those in the LPS group [LVEDV (μL): 71.25±21.16 vs. 118.01±11.89, LVESV (μL): 9.57±5.75 vs. 32.70±9.22, both P < 0.01]. LVEF and LVFS were significantly higher than those in the LPS group [LVEF: 0.868±0.075 vs. 0.722±0.095, LVFS: (59.88±8.46)% vs. (42.37±8.71)%, both P < 0.05]. Myocardial tissue injury was significantly reduced, and the serum cTn level was significantly lower than that in the LPS group (μg/L: 107.85±21.38 vs. 152.25±27.46, P < 0.05). ② Inflammatory parameters: the results of qPCR, Western blotting and immunohistochemistry showed that the mRNA expressions of IL-6 and TNF-α, the expression of TLR4 protein and the p-NF-κB p65/NF-κB p65 ratio in the LPS group were significantly higher than those in the control group, indicating that LPS-induced sepsis could activate the inflammatory response mediated by TLR4/NF-κB pathway in the heart. However, blocking the TLR4 pathway by TAK242 could inhibit the TLR4/NF-κB pathway and reduce the myocardial inflammation in septic rats. The mRNA expressions of IL-6 and TNF-α, the expression of TLR4 protein and the p-NF-κB p65/NF-κB p65 ratio in the TAK242+LPS group were significantly lower than those in the LPS group [IL-6 mRNA (2 -ΔΔCT): 10.44±3.30 vs. 107.50±29.48, TNF-α mRNA (2 -ΔΔCT): 2.38±0.68 vs. 3.77±0.56, TLR4 protein (TLR4/GAPDH): 0.39±0.01 vs. 0.58±0.04, p-NF-κB p65/NF-κB p65 ratio: 1.21±0.11 vs. 2.10±0.18, all P < 0.05]. Conclusion:TAK242 can protect LPS-induced cardiac dysfunction and myocardial injury by blocking the TLR4 mediated inflammatory response.
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Introduction: Penetrating ballistic cardiac injury is usuallyfatal before victim the gets any medical help. Retained intracardiac missile is a very rare entity and so far a very few caseshave been reported in the literature.Case report: We describe a young patient who presentedwith multiple life threatening pellet injuries involving chest,abdomen, and limbs. Patient had CT and echocardiographydocumented retained pellets in the heart with pericardialeffusion. Patient was managed successfully using conservativeapproach without any surgical intervention.Conclusion: this case highlights the importance of carefulmonitoring and conservative approach in such critically illpatients for a better outcome.
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Background: Penetrating cardiac injuries are rare and considered the most lethal of all trauma patients. Managing cardiac injuries is a great challenge for the trauma surgeons and the outcome of the treatment of such critical condition depends on the mechanism of injury, haemodynamic status of the patients at the time of presentation, heart chamber involved and other associated injuries. Materials and Methods: This is a prospective observational study of consecutive six patients with penetrating cardiac injuries from January 2015 to December 2019 treated in Regional Institute of Medical Sciences, Imphal, India. eFAST and CT scan of the chest were the main imaging methods used for diagnosis. All patients underwent tube thoracostomy for associated haemothorax in the emergency ward. Results: All the patients had penetrating cardiac injuries due to stabbing. Five (63.3%) patients presented with features of cardiac tamponade or with severe hypotension (systolic BP less than 80 mmHg) and one (16.7%) patient who was haemodynamically stable at the time of presentation had developed features of cardiac tamponade after 24 hours. Four patients had undergone emergency left anterolateral thoracotomy, one patient had undergone median sternotomy, and one patient underwent left anterolateral thoracotomy on the second day after admission. Conclusion: A high index of suspicion for cardiac trauma is extremely important in patients presented with penetrating thoracic injuries or upper abdominal injuries. Computed tomography of the chest can show the haemopericardium giving detailed information of associated pulmonary injury and hemothorax. Prompt diagnosis and early surgical intervention play a vital role to save these critically injured patients.
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A 55-year-old man was brought to our hospital with a knife penetrating his left anterior chest wall following a suicide attempt. Massive left hemothorax was identified on echocardiography ; however, there was no evidence of cardiac tamponade. After draining blood from the left thorax, computed tomography (CT) revealed that the tip of the knife had penetrated the left lung and reached the left pulmonary vein. In preparation for cardiopulmonary bypass, an emergency thoracotomy was scheduled with a plan to access the left lung and left pulmonary vein. The patient was transferred to the operating room, and the procedure was started with the patient in the supine position. During dissection of the femoral vessels, the patient suddenly developed hypotension. After surgical access to the heart was achieved via median sternotomy, a pericardiotomy was performed and cardiopulmonary bypass was established. A 50-mm stab wound was identified at the lateral wall of the left ventricle. The knife was removed, and the left ventricular wound was repaired. The lingular segment of the left lung was partially resected. The patient had no postoperative complications and was transferred to the referral hospital on postoperative day 25. This case report emphasizes the importance of taking appropriate measures for thoracotomy and cardiopulmonary bypass in patients with penetrating thoracic trauma with massive hemothorax, even in the absence of cardiac tamponade on imaging. We were able to successfully manage a life-threatening condition by taking appropriate measures.
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Objective To investigate the effects of therapeutic hypothermia (TH) on myocardial Ca2+/calmodulin-dependent protein kinase Ⅱ (CaMK Ⅱ) and cell autophagy after cardiopulmonary resuscitation (CPR) in swine.Methods Twenty healthy male domestic swine weighing 33-40 kg were randomly (random number) divided into 3 groups:sham group (n=4),CPR group (n=8) and TH group (n=8).Sham animals only underwent general preparation without experiencing cardiac arrest and resuscitation.The animal model was established by 8 min of electrically induced ventricular fibrillation and then 5 min CPR in the CPR and TH groups.Successful resuscitation was regarded as an organized rhythm with a mean arterial pressure of greater than 50 mmHg for 5 min or more.After successful resuscitation,body temperature was decreased to 33 ℃ by a cooling blanket and then maintained until 24 h post-resuscitation,and followed by a rewarming at a rate of 1 ℃/h for 5 h in the TH group.A normal temperature was maintained by the blanket throughout the experiment in the sham and CPR groups.At 6,12,24 and 30 h after resuscitation,the values of stroke volume (SV) and global ejection fraction (GEF) were measured by PiCCO,and meanwhile the serum concentrations of cardiac troponin Ⅰ (cTnI) were measured by ELISA assay and the serum activities of creatine kinase-MB (CK-MB) were evaluated by an automatic biochemical analyzer.At 30 h after resuscitation,the animals were sacrificed and left ventricular myocardium was obtained for the determination ofCaMK Ⅱ,microtubule-associated protein light chain 3 Ⅱ (LC3 Ⅱ) and p62 expressions by Western blot.The variables were compared with One way analysis of variance and then the Bonferroni test among the three groups.Results Compared with the sham group,myocardial dysfunction and injury after resuscitation were observed in the CPR and TH groups,which were indicated by decreased SV and GEF and also increased cTnI concentration and CK-MB activity in serum (all P＜0.05).Compared with the CPR group,the values of SV and GEF were significantly increased at 6 h after resuscitation,and serum cTnI concentration and CK-MB activity were significantly decreased starting 12 h after resuscitation in the TH group [SV (mL):25.0±6.9 vs 31.9±3.3 at 6 h,26.7±5.1 vs 34.6±3.7 at 12 h,28.8±3.3 vs 35.7±3.2 at 24 h,29.2±5.2 vs 36.7±3.3 at 30 h;GEF (％):17.1±2.7 vs 19.9±1.8 at 6 h,18.7±1.9 vs 21.6±1.8 at 12 h,19.3±2.3 vs 23.0±2.4 at 24 h,21.0±1.7 vs 23.7±1.7 at 30 h;cTnI (pg/mL):564±51 vs 466±56 at 12 h,534±38 vs 427±60 at 24 h,476±55 vs 375±46 at 30 h;CK-MB (U/L):803±164 vs 652±76 at 12 h,693±96 vs 557±54 at 24 h,633±91 vs 480±77 at 30 h,all P＜0.05].Tissue detection indicated that the expression of CaMK Ⅱ and LC3 Ⅱ were increased while the expression of p62 was decreased in post-resuscitation myocardium in the CPR and TH groups compared with the sham group (all P＜0.05).However,the expression of CaMK Ⅱ and LC3 Ⅱ were decreased and the expression of p62 was increased in postresuscitation myocardium in the TH group compared to the CPR group (CaMK Ⅱ:0.73±0.06 vs 0.58±0.05;LC3 Ⅱ:0.69±0.09 vs 0.50±0.07;p62:0.40±0.07 vs 0.68±0.14,all P＜0.05).Conclusion The mechanism of TH alleviating post-resuscitation myocardial dysfunction and injury may be related to the inhibition of CaMK Ⅱ expression and cell autophagy.
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Resumen: Introducción: La lesión renal aguda es común después de la cirugía cardiaca y está asociada con un incremento en la mortalidad. Los biomarcadores cardiacos son accesibles y pueden ayudar a predecir la lesión renal aguda (LRA). Objetivo: Investigar la utilidad diagnóstica de biomarcadores cardiacos para LRA en adultos operados de cirugía cardiaca. Material y métodos: Estudio de cohorte prospectivo en pacientes operados de cirugía cardiaca. Se midieron los siguientes biomarcadores cardiacos en las primeras seis horas del postoperatorio: péptido natriurético tipo B (BNP), troponina I ultrasensible (usTI), creatina fosfoquinasa (CPK), creatina fosfoquinasa MB (CPK-MB) y mioglobina. Resultados: De los 63 pacientes evaluados, 31 (49.2%) presentaron LRA. Los pacientes con LRA tuvieron niveles más elevados de BNP, usTI, CPK-MB y mioglobina, con significancia estadística. La mioglobina tuvo una muy buena área bajo la curva (AUC 0.81, IC 95% 0.66-0.95), seguida de usTI (AUC 0.71, IC 95% 0.58-0.92) y BNP (AUC 0.71 IC 95% 0.53-0.88) para detectar LRA. Los niveles de mioglobina ≥ 731 ng/mL tuvieron una buena razón de verosimilitud positiva (LR+ 7.73, IC 95% 1.04-57.24). El tiempo de circulación extracorpórea (CEC) (RM corregida de 6.11, IC 95% 1.55-9.55) y la elevación de mioglobina (RM corregida 1.00, IC 95% 1.00-1.10) fueron predictores independientes de LRA en el análisis multivariado. Conclusiones: Los niveles postoperatorios de biomarcadores cardiacos se encuentran significativamente más elevados en los pacientes con LRA. El tiempo de CEC y la elevación de mioglobina demostraron ser predictores independientes de LRA. Estos biomarcadores pueden ser adecuados para identificar pacientes con alto riesgo de LRA después de cirugía cardiaca.
Abstract: Introduction: Acute kidney injury is common after cardiac surgery and is associated with postoperative mortality. Cardiac biomarkers are more accessible and can help predict acute kidney injury. Objectives: To investigate the relationship between cardiac biomarkers with acute kidney injury (AKI) postoperatively in adults undergoing cardiac surgery. Material and methods: Prospective cohort study in post-operated cardiac surgery adults. We measured the following cardiac biomarkers in the first 6 hours of the postoperative period: B-type natriuretic peptide (BNP), ultrasensitive troponin I (USTI), creatine phosphokinase (CPK), creatine phosphokinase MB (CPK-MB) and myoglobin. Results: Of the 63 patients evaluated, 31 (49.2%) presented AKI. Patients with AKI had significantly higher levels of BNP, usTI, CPK-MB, and myoglobin. Myoglobin had a good area under the curve (AUC 0.81, 95% CI 0.66-0.95), followed by usTI (AUC 0.71, 95% CI 0.58-0.92) and BNP (AUC 0.71 95% CI 0.53-0.88) to detect AKI. Myoglobin levels ≥ 731 ng/mL had a positive likelihood ratio (7.73, 95% CI 1.04-57.24). The time of extracorporeal circulation (adjusted odds-ratio 6.11, 95% CI 1.55 to 9.55) and myoglobin elevation (Adjusted odds-ratio 1.00, 95% CI 1.00 to 1.01) were independent predictors of AKI. Conclusions: The postoperative levels of cardiac biomarkers are significantly higher in patients with AKI. Extracorporeal circulation (CCE) time and myoglobin elevation were shown to be predictors of AKI. These biomarkers may be suitable for identifying patients at high risk for AKI after cardiac surgery.
Resumo: Introdução: A lesão renal aguda é comum após cirurgia cardíaca e está associada a um aumento da mortalidade. Os biomarcadores cardíacos são acessíveis e podem ajudar a prever a lesão renal aguda (LRA). Objetivo: Investigar a utilidade diagnóstica de biomarcadores cardíacos para LRA em pacientes submetidos à cirurgia cardíaca. Materiais e métodos: Estudo de coorte prospectivo em pacientes submetidos à cirurgia cardíaca. Os seguintes biomarcadores cardíacos foram medidos nas primeiras 6 horas de pós-operatório: peptídeo natriurético tipo B (BNP), troponina I ultrassensível (usTI), creatinofosfoquinase (CPK), creatinofosfoquinase MB (CPK-MB) e mioglobina. Resultados: Dos 63 pacientes avaliados 31 (49.2%) apresentaram LRA. Pacientes com LRA apresentaram níveis mais elevados de BNP, usTI, CPK-MB e mioglobina, com significância estatística. A mioglobina teve uma área sob a curva adecuada (AUC 0.81, IC 95% 0.66-0.95), seguida por usTI (AUC 0.71, IC 95% 0.58-0.92) e BNP (AUC 0.71 IC 95% 0.53-0.88) para detectar LRA. Os níveis de mioglobina ≥ 731 ng/mL tiveram razão de verossimilhança positiva (LR + 7.73, IC 95% 1.04-57.24). O tempo de circulação extracorpórea (CEC) (RM corrigida de 6.11, IC 95% 1.55-9.55) e elevação da mioglobina (RM corrigida 1.00, IC 95% 1.00-1.10) foram preditores independentes de LRA na análise multivariada. Conclusão: Os níveis pós-operatórios de biomarcadores cardíacos são significativamente maiores em pacientes com LRA. O tempo da CEC e a elevação da mioglobina demonstraram ser preditores independentes de LRA. Esses biomarcadores podem ser adequados para identificar pacientes com alto risco de LRA após cirurgia cardíaca.
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Objective: To investigate the cardiovascular reflex induced by the activation of cardiac transient receptor potential vanillic acid receptor 1(TRPV1), the central location of reflex and its peripheral neurotransmitters of the rats, and to elucidate the central and peripheral neural mechanisms of cardiovascular reflex mediated by TRPV1 receptor. Methods: A total of 60 healthy male SD rats were randomly divided into control group, ido-RTX group, atropine group, immunofluorescence group and nerve tract tracking group; there were 12 rats in each group. Pericardial intubation was performed in the rats in various groups after anesthesia. The changes of heart rates and blood pressures of the rats in control group, ido-RTX group and atropine group were observed by arterial intubation. The tissue samples were collected 1 h after intropericardial injection of capsaicin in imunofluorescence group, and the co-expression of c-Fos positive neurons induced by capsaicin and cholinesterase positive neurons in the medulla oblongata was observed by immunofluorescence technigue. Intraopericardial injected carbonyl cyanine fluorescent dye (Dil) was used as retrograde tracer in nerve tract group, and the distribution of Dil positive cells in the medulla oblongata was observed by fluorescence microscope 1 week later. Results: The blood pressure and heart rate of the rats in control group were decreased significantly after intrapericardial injection of capsaicin of the rats in control group (P0. 05); after intrapericardial injection of capsaicin, the number of c-Fos positive neurons in nucleus tractus solitarii, dorsal motor nucleus of vagus and nucleus ambiguous of medulla oblongata was increased significantly (P<0. 05); most of these neurons were cholinesterase positive neurons; after intrapericardial injection of Dil, a large number of red fluorescent labeled neurons and nerve endings appeared in the nucleus tractus solitarii, dorsal motor nucleus of vagus and nucleus ambiguous. Conclusion: Intrapericardial injection of capsaicin can selectively activate the TRPV1 receptors in the heart, increase the excitability of cholinergic neurons in the cardiovascular center of the medulla oblongata, increase the peripheral release of acetylcholine, and produce an inhibitory effect on the cardiovascular activity by activating the M receptor.
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Objective To explore the early diagnosis,therapeutic methods and efficacy for blunt cardiac injury (BCI).Methods All BCI patients from September 2003 t9 August 2018 were studied retrospectively in respect of sex,age,cause of injury,diagnostic methods,therapeutic procedures,and outcome.The patients were divided into two groups:nonoperative group (n=305) and operative group (n=43).The two groups were compared and analyzed.Results Totally 348 BCI patients accounted for 18.3％ of 1 903 patients with blunt thoracic injury (BTI),and the mortality rate was 10.1％.The main cause of injury was traffic accident with an incidence of 48.3％.The diagnostic methods included electrocardiogram (ECG),enzymes and troponin I,echocardiography,and CT scanning,or confirmed by emergency thoracatomy.In the nonoperative group,patients were mainly myocardial contusion,with a mortality rate of 6.9％.In the operative group,patients were mainly cardiac rupture and pericardial hernia,and the mortality was 32.6％.The incidence of negative ECG between the two groups was not significantly different (16.7％ vs 11.6％,P＞0.05).The incidence of shock and mortality in the operative group were significantly higher than those in the the nonoperative group (P＜0.01).The number of death directly resulted from BCI in the operative group was greater than that in the nonoperative group (P＜0.05).Conclusions For BTI patients,BCI must be highly suspected,and necessary examinations should be given.To manage myocardial contusion without surgery,it is necessary to protect the heart,alleviate edema of myocardium,and control arrhythmia with drugs.To deal with those patients requiring operation,early recognition and expeditious thoracotomy are essential.
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Objective: Intestinal absorption liquid as medicine carriers, one or more kinds of traditional Chinese medicine protecting cardiac injury in Naoxintong capsule will be found through separation and combination of prescription. This study also can expand protecting mechanisms of Naoxintong capsule. Method: Naoxintong intestinal absorption liquids of single, combination and total prescription were prepared. H9c2 cell line exposed to H2O2 was established. Cell survival rate was determined with methyl thiazolyl tetrazolium(MTT). Cell apoptosis rate was examined by Annexin Ⅴ-FITC/PI staining with a flow cytometer. Aquaporin1(AQP1) expression was detected by Western blot. One or more kinds of traditional Chinese medicine in Naoxintong capsule which exerted protective effect from cardiac injury were screened through separation and combination of prescription. Result: As compared with control group, the protein expression level of AQP1 was significantly increased(PPPPPPConclusion: Naoxintong capsule acts as a protective role in myocardial injury through decreasing AQP1 expression and inhibiting cell apoptosis. Salviae Miltiorrhizae Radix et Rhizoma, Pheretima, Scorpio are important components in Naoxintong capsule.
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Objective@#To explore the early diagnosis, therapeutic methods and efficacy for blunt cardiac injury (BCI).@*Methods@#All BCI patients from September 2003 to August 2018 were studied retrospectively in respect of sex, age, cause of injury, diagnostic methods, therapeutic procedures, and outcome. The patients were divided into two groups: nonoperative group (n=305) and operative group (n=43). The two groups were compared and analyzed.@*Results@#Totally 348 BCI patients accounted for 18.3% of 1 903 patients with blunt thoracic injury (BTI), and the mortality rate was 10.1%. The main cause of injury was traffic accident with an incidence of 48.3%. The diagnostic methods included electrocardiogram (ECG), enzymes and troponin I, echocardiography, and CT scanning, or confirmed by emergency thoracatomy. In the nonoperative group, patients were mainly myocardial contusion, with a mortality rate of 6.9%. In the operative group, patients were mainly cardiac rupture and pericardial hernia, and the mortality was 32.6%. The incidence of negative ECG between the two groups was not significantly different (16.7% vs 11.6%, P>0.05). The incidence of shock and mortality in the operative group were significantly higher than those in the the nonoperative group (P<0.01). The number of death directly resulted from BCI in the operative group was greater than that in the nonoperative group (P<0.05).@*Conclusions@#For BTI patients, BCI must be highly suspected, and necessary examinations should be given. To manage myocardial contusion without surgery, it is necessary to protect the heart, alleviate edema of myocardium, and control arrhythmia with drugs. To deal with those patients requiring operation, early recognition and expeditious thoracotomy are essential.