Banxia-Houpu decoction diminishes iron toxicity damage in heart induced by chronic intermittent hypoxia.

CONTEXT: Obstructive sleep apnoea (OSA) causes chronic intermittent hypoxia (CIH), which results in mitochondrial dysfunction and generates reactive oxygen species (ROS) in the heart. Excessive free iron could accelerate oxidative damage, which may be involved in this process. Banxia-Houpu decoction (BHD) was reported to improve the apnoea hypopnoea index in OSA patients, but the specific mechanism was still unclear. OBJECTIVE: To investigate whether BHD could reduce CIH-induced heart damage by regulating iron metabolism and mitochondrial function. MATERIALS AND METHODS: C57BL/6N mice were randomly divided into control, CIH and BHD groups. Mice were exposed to CIH (21 - 5% O2, 20 times/h, 8 h/d) and administered BHD (3.51, 7.01 and 14.02 g/kg, intragastrically) for 21 d. Cardiac and mitochondrial function, iron levels, apoptosis and mitophagy were determined. RESULTS: BHD (7.01 g/kg) significantly improved cardiac dysfunction, pathological change and mitochondrial structure induced by CIH. BHD increased the Bcl-2/Bax ratio (1.4-fold) and inhibited caspase 3 cleavage in CIH mice (0.45-fold). BHD activated mitophagy by upregulating Parkin (1.94-fold) and PINK1 (1.26-fold), inhibiting the PI3K-AKT-mTOR pathway. BHD suppressed ROS generation by decreasing NOX2 (0.59-fold) and 4-HNE (0.83-fold). BHD reduced the total iron in myocardial cells (0.72-fold) and mitochondrial iron by downregulating Mfrn2 (0.81-fold) and MtFt (0.78-fold) proteins, and upregulating ABCB8 protein (1.33-fold). Rosmarinic acid, the main component of Perilla Leaf in BHD, was able to react with Fe2+ and Fe3+ in vitro. DISCUSSION AND CONCLUSIONS: These findings encourage the use of BHD to resist cardiovascular injury and provide the theoretical basis for clinical treatment in OSA patients.

Constrictive pericarditis in the setting of repeated chest trauma in a mixed martial arts fighter.

BACKGROUND: Constrictive pericarditis (CP) is characterized by scarring and loss of elasticity of the pericardium. This case demonstrates that mixed martial arts (MMA) is a previously unrecognized risk factor for CP, diagnosis of which is supported by cardiac imaging, right and left heart catheterization, and histological findings of dense fibrous tissue without chronic inflammation. CASE PRESENTATION: A 47-year-old Caucasian male former mixed martial arts (MMA) fighter from the Western United States presented to liver clinic for elevated liver injury tests (LIT) and a 35-pound weight loss with associated diarrhea, lower extremity edema, dyspnea on exertion, and worsening fatigue over a period of 6 months. Past medical history includes concussion, right bundle branch block, migraine headache, hypertension, chronic pain related to musculoskeletal injuries and fractures secondary to MMA competition. Involvement in MMA was extensive with an 8-year history of professional MMA competition and 13-year history of MMA fighting with recurrent trauma to the chest wall. The patient also reported a 20-year history of performance enhancing drugs including testosterone. Physical exam was notable for elevated jugular venous pressure, hepatomegaly, and trace peripheral edema. An extensive workup was performed including laboratory studies, abdominal computerized tomography, liver biopsy, echocardiogram, and cardiac magnetic resonance imaging. Finally, right and left heart catheterization-the gold standard-confirmed discordance of the right ventricle-left ventricle, consistent with constrictive physiology. Pericardiectomy was performed with histologic evidence of chronic pericarditis. The patient's hospital course was uncomplicated and he returned to NYHA functional class I. CONCLUSIONS: CP can be a sequela of recurrent pericarditis or hemorrhagic effusions and may have a delayed presentation. In cases of recurrent trauma, CP may be managed with pericardiectomy with apparent good outcome. Further studies are warranted to analyze the occurrence of CP in MMA so as to better define the risk in such adults.

Surgical Strategies for Cardiac Perforation After Catheter Ablation or Electrophysiology Study.

Catheter ablation is a treatment modality which has been increasingly used for cardiac arrhythmias. However, it is not complication-free, and cardiac perforation is one of its most life-threatening complications. As surgery is usually not the first-line treatment for this emergent episode, there were only very few sporadic surgical reports in the literature. This systemic review primarily aims to collect different surgical approaches for catheter-induced cardiac perforation to help surgeons manage this kind of uncommon and critical patients. Of the 452 initially screened articles, 22 studies (38 patients) were included in the systemic review. Of all the included patients, 84% (32/38) were found to have pericardial effusion acutely following catheter-related procedures, and 16% (6/38) experienced delayed-onset episodes. Regarding the surgical procedures, four patients underwent removal of clots only, eight patients underwent suture repair of the left ventricle (LV), nine patients underwent suture repair of the right ventricle (RV), five patients underwent suture repair of the LA, and four patients underwent sutureless repair of the LV and pulmonary vein (LV 1, RV 1, pulmonary vein 1). In addition to repair of perforation sites, the concomitant combined procedures included repair of intercostal vessels (complication of pericardiocentesis) for one patient, cryoablation for two patients, and maze procedure for one patient. For cardiac perforation following catheter ablation or electrophysiology study, although the majority of the patients are treated with pericardiocentesis and medical management at first, cardiovascular surgeons have to prepare to take over if the bleeding is persistent or if the cardiac tamponade is not relieved.

Qingyi decoction protects against myocardial injuries induced by severe acute pancreatitis.

BACKGROUND: We studied the protective effects of Qingyi decoction (QYD) (a Traditional Chinese Medicine) against severe acute pancreatitis (SAP)-induced myocardial infarction (MI). AIM: To study the function and mechanism of QYD in the treatment of myocardial injuries induced by SAP. METHODS: Ultrasonic cardiography, hematoxylin and eosin staining, immunohistochemistry, qRT-PCR, western blot, enzyme-linked immunosorbent assays, and apoptosis staining techniques were used to determine the effects of QYD following SAP-induced MI in Sprague-Dawley rats. RESULTS: Our SAP model showed severe myocardial histological abnormalities and marked differences in the symptoms, mortality rate, and ultrasonic cardiography outputs among the different groups compared to the control. The expression of serum cytokines [interleukin (IL)-1ß, IL-6, IL-8, IL-12, amyloid ß, and tumor necrosis factor-α] were significantly higher in the SAP versus QYD treated group (P < 0.05 for all). STIM1 and Orai1 expression in myocardial tissue extracts were significantly decreased post QYD gavage (P < 0.001). There was no significant histological difference between the 2-aminoethyl diphenylborinate inhibitor and QYD groups. The SAP group had a significantly higher apoptosis index score compared to the QYD group (P < 0.001). CONCLUSION: QYD conferred cardio-protection against SAP-induced MI by regulating myocardial-associated protein expression (STIM1 and Orai1).

Derangement of PaCO2 requires physician attention in acute carbon monoxide poisoning.

The objective was to describe the prevalence of derangement of the partial pressure of arterial carbon dioxide (PaCO2) and to determine the association between PaCO2 and adverse cardiovascular events (ACVEs) in carbon monoxide (CO)-poisoned patients. Additionally, we evaluated whether the derangement of PaCO2 was simply secondary to metabolic changes. This retrospective study included 194 self-breathing patients after CO poisoning with an indication for hyperbaric oxygen therapy and available arterial blood gas analysis at presentation and 6 h later. The incidence rate of hypocapnia at presentation after acute CO poisoning was 67.5%, and the mean PaCO2 during the first 6 h was 33 (31-36.7) mmHg. The most common acid-base imbalance in 131 patients with hypocapnia was primary respiratory alkalosis. The incidence rate of ACVEs during hospitalization was 50.5%. A significant linear trend in the incidence of ACVEs was observed across the total range of PaCO2 variables. In multivariate regression analysis, mean PaCO2 was independently associated with ACVEs (odds ratio 0.051; 95% confidence interval 0.004-0.632). PaCO2 derangements were common after acute CO poisoning and were not explainable as a mere secondary response to metabolic changes. The mean PaCO2 during the first 6 h was associated with ACVEs. Given the high incidence of ACVEs and PaCO2 derangement and the observed association between the mean PaCO2 and ACVEs, this study suggests that (1) PaCO2 should be monitored in the acute stage to predict and/or prevent ACVEs and (2) further investigation is needed to validate this result and explore the early manipulation of PaCO2 as a treatment strategy.

Cardiac perforation complicating cardiac electrophysiology procedures: value of angiography and use of a closure device to avoid cardiac surgery.

BACKGROUND: Computed tomography (CT) is used for the diagnosis of cardiac perforation (CP) although it has significant limitations. We report our experience with angiography to assist in the diagnosis and management of cardiac perforation during electrophysiology procedures. METHODS: Patients with suspected CP after pacemaker lead insertion (temporary = 2, permanent = 2) or during epicardial mapping/ablation (n = 2) were included. All patients underwent initial angiography with repeat study performed post-lead repositioning/withdrawal for the pacemaker cases. Patients with CP due to permanent pacing leads underwent CT comparison. RESULTS: In 4 pacemaker patients, temporary leads caused two acute perforations, permanent active fixation leads caused one subacute right ventricular perforation and one delayed right atrial perforation. CT overdiagnosed CP in one temporary pacemaker patient, and was non-diagnostic in an atrial lead perforation, whereas angiography was accurate in both. Angiography identified an active leak in atrial lead CP, guided percutaneous closure in one case and demonstrated sealing of perforation in all cases. In the 2 epicardial ablation cases, 1 patient underwent surgical repair after a persistent right ventricular perforation, but the other avoided surgery with novel use of an Amplazter® patent ductus arteriosus (PDA) closure device (Abbott, St Paul, MN, USA). CONCLUSIONS: Angiography may be more accurate than CT in the diagnosis of CP. Angiography is easy to perform, can be done acutely, reveals active leaks and can demonstrate sealing of perforations after percutaneous lead repositioning. Utilisation of a PDA closure device may avoid the need for surgery for RV perforation.

Utility of local atrial electrogram pattern for predicting left main coronary artery anatomical distance during mapping in the left pulmonary sinus of valsalva.

BACKGROUND: Ablation of right ventricular outflow tract (RVOT) ventricular arrhythmia (VA) within the left pulmonary sinus of Valsalva (LPSV) may increase the risk of left main coronary artery (LMCA) injury. PURPOSE: To delineate the anatomical characteristics between LMCA and LPSV and their association with atrial potential (AP) mapping in LPSV. METHODS: A total of 104 consecutive patients with RVOT-VA undergoing cardiac-gated computed tomography coronary angiography (CTCA) after ablation were retrospectively analyzed. RESULTS: The LMCA-LPSV anatomic relationship was classified into three types based on the CTCA measurements. Types 1 and 2 had a shorter LMCA-LPSV distance than that of type 3 (P < .001). The left atrial appendage (LAA)-LMCA distance and LAA-LPSV distance were associated with the incidence of AP in LPSV (odds ratio [OR] = 3.43, 95% confidence interval [CI]: 1.86-6.34, P < .001; OR = 1.196, 95% CI: 1.09-1.31, P < .001, respectively). Furthermore, the LMCA-LPSV distance showed a linear correlation with the LAA-LPSV distance (r2 = 0.93, P < .001). According to receiver operating characteristic (ROC) analysis, a LMCA-LPSV distance <5.4 mm could predict the possibility of AP during LPSV mapping (sensitivity 83%, specificity 81%, and area under the ROC curve 0.86). CONCLUSIONS: The presence of AP in the LPSV may be useful to predict a short distance from the LPSV to the LMCA and to identify patients at higher risk of LMCA injury. This information may contribute to efficient and safe ablation in this area but should be confirmed in future studies.

Hyperbaric therapy provides no benefit for skeletal muscle and respiratory function and accelerates cardiac injury in mdx mice.

Duchenne muscular dystrophy (DMD) is a uniformly fatal condition of striated muscle wasting resulting in premature death from respiratory and/or cardiac failure. Symptomatic therapy has prolonged survival by limiting deaths resulting from respiratory insufficiency, but there is currently no effective therapy for most patients with DMD. This grim prognosis has led patients and their families to seek unproven therapeutic approaches. One such approach is the use of hyperbaric therapies, which 14% of DMD patients self-report using. The primary goal of this study was to determine if intermittent hyperbaric exposure altered the muscle function of the mdx mouse, a genetic model of DMD. To do this, mdx mice were exposed to three daily 90-minute 1.3 atmosphere hyperbaric exposures for 4 weeks. Skeletal muscle, respiratory, and cardiac function were assessed in treated and untreated wild type and dystrophic mice. The results of these studies find that hyperbaric and hyperoxic approaches resulted in increased cardiac fibrosis in dystrophic mice and no beneficial effects on the functional parameters measured. These data suggest that these oxygen-based therapies are unlikely to provide therapeutic benefit to DMD patients.

Evaluating the protective potency of Acacia hydaspica R. Parker on histological and biochemical changes induced by Cisplatin in the cardiac tissue of rats.

BACKGROUND: Increase oxidative trauma is the main cause behind Cisplatin (CP) induced cardiotoxicity which restricts its clinical application as anti-neoplastic prescription. Acacia hydaspica is a natural shrub with diverse bioactivities. Acacia hydaspica ethyl acetate extract (AHE) ameliorated drug-induced cardiotoxicity in animals with anti-oxidative mechanisms. Current study aimed to evaluate the protective potential of A. hydaspica against cisplatin-induced myocardial injury. METHODS: Rats were indiscriminately distributed into six groups (n = 6). Group 1: control; Groups 2: Injected with CP (7.5 mg/kg bw, i.p, single dose) on day 16; Group 3: Treated for 21 days with AHE (400 mg/kg b.w, oral); Group 4: Received CP injection on day 16 and treated with AHE for 5 days post injection; Group 5: Received AHE (400 mg/kg b.w/day, p.o.) for 21 days and CP (7.5 mg/kg b.w., i.p.) on day 16; Group 6: Treated with silymarin (100 mg/kg b.w., p.o.) after 1 day interval for 21 days and CP injection (7.5 mg/kg b.w., i.p.) on day 16. On 22nd day, the animals were sacrificed and their heart tissues were removed. Cisplatin induced cardiac toxicity and the influence of AHE were evaluated by examination of serum cardiac function markers, cardiac tissue antioxidant enzymes, oxidative stress markers and histology. RESULTS: CP inoculation considerably altered cardiac function biomarkers in serum and diminished the antioxidant enzymes levels, while increased oxidative stress biomarkers in cardiac tissues AHE treatment attenuated CP-induced deteriorations in creatine kinase (CK), Creatine kinase isoenzymes MB (CK-MB), cardiac Troponin I (cTNI) and lactate dehydrogenase (LDH) levels and ameliorated cardiac oxidative stress markers as evidenced by decreasing lipid peroxidation, H2O2 and NO content along with augmentation in phase I and phase II antioxidant enzymes. Additionally, CP inoculation also induced morphological alterations which were ameliorated by AHE. In pretreatment group more significant protection was observed compared to post-treatment group indicating preventive potential of AHE. The protective potency of AHE was comparable to silymarin. CONCLUSION: Results demonstrate that AHE attenuated CP induce cardiotoxicity. The polyphenolic metabolites and antioxidant properties of AHE might be responsible for its protective influence.

Percutaneous Management of Left Atrial Appendage Perforation: Keep Calm and Think Fast.

Left atrial appendage (LAA) perforation is a possible complication not only after release of the closure device, but also during the diagnostic phase due to sheath positioning in the LAA. We present an 83-year-old woman with permanent atrial fibrillation and high thromboembolic and bleeding risk who was admitted for elective percutaneous LAA closure. During angiographic study, she suddenly became hypotensive. Heart perforation with leakage of contrast in the pericardial space was evident and imaging confirmed cardiac tamponade. Rapid release of the closure device and pericardial evacuation allowed the operators to successfully manage the cardiac tamponade and avoid a surgical option.

Effect of intralipid on myocardial injury during valve replacement surgery with concomitant radiofrequency ablation: A randomized controlled trial.

BACKGROUND: This study aimed to evaluate the effect of intralipid postconditioning (ILPC) on myocardial damage in patients undergoing valve replacement surgery with concomitant radiofrequency ablation (RFA) for atrial fibrillation (AF). METHODS: Randomized patient and assessor-blind controlled trial conducted in adult patients undergoing valve replacement surgery with concomitant RFA. Sixty-nine patients were randomly assigned to ILPC group (n = 34) or control group (n = 35): ILPC group received an intravenous infusion of 20% intralipid (2 mL/kg) just 10 minutes before aortic cross-unclamping, and control group received an equivalent volume of normal saline. Serum cardiac troponin-T (cTnT) and creatine kinase-MB (CK-MB) was measured before surgery and at 4, 12, 24, 48, and 72 hours after surgery. The primary endpoints were the 72-hour area under the curve (AUC) for cTnT and CK-MB. RESULTS: The total 72-hour AUC of cTnT (P = .33) and CK-MB (P = .52) were comparable between 2 groups. The left ventricle ejection fraction at discharge (P = .011) was higher in the ILPC group than that in the control group, while the AF recurrence did not differ significantly between 2 groups. CONCLUSIONS: There was no observed beneficial effect of ILPC on myocardial injury documented by the cardiac biomarkers in patients undergoing valve replacement surgery with concomitant RFA, and the effect of intralipid against myocardial I/R injury is undetectable within the background of massive biomarker release following ablation owing to localized myocardial necrosis. Besides, there are no other published data about the cardioprotective role of intralipid in patients undergoing this procedure and benefits of this protection need further studies to validate.

Protective effect of the extract of Yi-Qi-Fu-Mai preparation on hypoxia-induced heart injury in mice.

Yi-Qi-Fu-Mai (YQFM) is extensively used clinically to treat cardiovascular diseases in China. To explore the anti-hypoxia effect of the extract of YQFM preparation (EYQFM), the EYQFM (1.4, 2.8, and 5.5 g·kg(-1)·d(-1)) was assessed for its heart-protective effect in a chronic intermittent hypoxia (CIH) animal model (oxygen pressure 7%-8%, 20 min per day) for 28 days of treatment. Betaloc (0.151 6 g·kg(-1)·d(-1)) was used as a positive control. The histopathological analyses of heart in CIH mice were conducted. Several cardiac state parameters, such as left ventricular ejection fractions (EF), stroke volume (SV), expression of creatine kinase (CK), lactate dehydrogenase (LDH), superoxide dismutase (SOD), and malondialdehyde (MDA) were measured. The results showed that treatment with EYQFM markedly reversed swelling of the endothelial cells and vacuolization in the heart when compared with the model group. Further study demonstrated that EYQFM significantly improved ventricular myocardial contractility by increasing EF and SV. In addition, EYQFM inhibited the activity of CK, LDH, decreased the level of MDA and improved SOD activity. The results demonstrated that EYQFM significantly improved the tolerability of myocardium to hypoxia and ameliorated the cardiac damage in the CIH model.

Ventricular arrhythmias near the distal great cardiac vein: challenging arrhythmia for ablation.

BACKGROUND: Catheter ablation for ventricular arrhythmia (VA) near the distal great cardiac vein (GCV) is often challenging, and data are limited. METHODS AND RESULTS: Analysis was performed in 30 patients (19 men; age, 52.8±15.5 years) who underwent catheter ablation for focal VA (11 ventricular tachycardia and 19 premature contractions) with early activation in the GCV (36.7±8.0 ms pre-QRS). Angiography in 27 patients showed earliest GCV site within 5 mm of a coronary artery in 20 (74%). Ablation was performed in the GCV in 15 patients and abolished VA in 8. Ablation was attempted at adjacent non-GCV sites in 19 patients and abolished VA in 5 patients (4 from the left ventricular endocardium and 1 from the left coronary cusp); all success had VA with an initial r wave in lead I and activation ≤7 ms after the GCV (GCV-non-GCV interval). In 13 patients, percutaneous epicardial mapping was performed, but because of adjacent coronaries only 2 received radiofrequency application with VA elimination in 1. Surgical cryoablation was performed in 3 patients and abolished VA in 2. Overall acute success was achieved in 16 (53%) patients. After a median of 2.8 months, 13 patients remained free of VA. Major complications occurred in 4 patients, including coronary injury requiring stenting. CONCLUSIONS: Ablation for this arrhythmia is challenging and often limited by the adjacent coronary vessels. Success of anatomically guided endocardial ablation may be identified by a short GCV-non-GCV interval and r wave in lead I.

The compound Chinese medicine "Kang Fu Ling" protects against high power microwave-induced myocardial injury.

BACKGROUND: The prevention and treatment of Microwave-caused cardiovascular injury remains elusive. This study investigated the cardiovascular protective effects of compound Chinese medicine "Kang Fu Ling" (KFL) against high power microwave (HPM)-induced myocardial injury and the role of the mitochondrial permeability transition pore (mPTP) opening in KFL protection. METHODS: Male Wistar rats (100) were divided into 5 equal groups: no treatment, radiation only, or radiation followed by treatment with KFL at 0.75, 1.5, or 3 g/kg/day. Electrocardiography was used to Electrophysiological examination. Histological and ultrastructural changes in heart tissue and isolated mitochondria were observed by light microscope and electron microscopy. mPTP opening and mitochondrial membrane potential were detected by confocal laser scanning microscopy and fluorescence analysis. Connexin-43 (Cx-43) and endothelial nitric oxide synthase (eNOS) were detected by immunohistochemistry. The expression of voltage-dependent anion channel (VDAC) was detected by western blotting. RESULTS: At 7 days after radiation, rats without KFL treatment showed a significantly lower heart rate (P<0.01) than untreated controls and a J point shift. Myocyte swelling and rearrangement were evident. Mitochondria exhibited rupture, and decreased fluorescence intensity, suggesting opening of mPTP and a consequent reduction in mitochondrial membrane potential. After treatment with 1.5 g/kg/day KFL for 7 d, the heart rate increased significantly (P<0.01), and the J point shift was reduced flavorfully (P<0.05) compared to untreated, irradiated rats; myocytes and mitochondria were of normal morphology. The fluorescence intensities of dye-treated mitochondria were also increased, suggesting inhibition of mPTP opening and preservation of the mitochondrial membrane potential. The microwave-induced decrease of Cx-43 and VDAC protein expression was significantly reversed. CONCLUSION: Microwave radiation can cause electrophysiological, histological and ultrastructural changes in the heart. KFL at 1.5 g/kg/day had the greatest protective effect on these cardiovascular events. mPTP plays an important role in the protective effects of KFL against microwave-radiation-induced myocardial injury.

Contact-force recovery can predict cardiac perforation during radiofrequency ablation.

BACKGROUND: During radiofrequency ablation (RFA), the ability to know whether a steam pop has led to cardiac perforation (CP) would be of profound clinical significance. We aimed to determine whether catheter contact-force characteristics can predict whether a steam pop during RFA causes CP. METHODS: We used a 7.5F Thermocool® Smarttouch™ force-sensing catheter (Biosense Webster Inc., Diamond Bar, CA, USA) to perform open-chest left atrial RFA under direct visualization in four sheep. We measured the contact force and its direction every 50 ms during RFA. At each steam pop, we noted whether CP occurred. We then analyzed the contact-force signals to determine whether specific features predicted the presence (+) or absence (-) of CP. RESULTS: A total of 24 steam pops occurred; 10 were CP+ and 14 were CP-. At the time of CP+ and CP- events, the contact force was 50 ± 25 and 40 ± 15 g, respectively (P = 0.146). All steam-pop events were associated with a rapid drop-off in contact force, but 10 of the 14 CP- events showed an immediate contact-force rebound, whereas none of the CP+ events did. This rebound presumably occurred as the catheter tip resumed contact with the left atrial wall. The average contact-force rebound equaled 80-100% of the contact-force drop-off. CONCLUSIONS: The ability to measure catheter contact force during RFA is a valuable asset, as contact-force recovery may be used to predict CP. Further studies are warranted to validate our findings in the clinical setting.