Protección miocárdica

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Response of the human myocardium to ischemic injury and preconditioning: The role of cardiac and comorbid conditions, medical treatment, and basal redox status.

Jue, 04/06/2017 - 19:52
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Response of the human myocardium to ischemic injury and preconditioning: The role of cardiac and comorbid conditions, medical treatment, and basal redox status.

PLoS One. 2017;12(4):e0174588

Authors: Casós K, Ferrer-Curriu G, Soler-Ferrer P, Pérez ML, Permanyer E, Blasco-Lucas A, Gracia-Baena JM, Castro MA, Sureda C, Barquinero J, Galiñanes M

Abstract
BACKGROUND: The diseased human myocardium is highly susceptible to ischemia/reoxygenation (I/R)-induced injury but its response to protective interventions such as ischemic preconditioning (IPreC) is unclear. Cardiac and other pre-existing clinical conditions as well as previous or ongoing medical treatment may influence the myocardial response to I/R injury and protection. This study investigated the effect of both on myocardial susceptibility to I/R-induced injury and the protective effects of IPreC.
METHODS AND RESULTS: Atrial myocardium from cardiac surgery patients (n = 300) was assigned to one of three groups: aerobic control, I/R alone, and IPreC. Lactate dehydrogenase leakage, as a marker of cell injury, and cell viability were measured. The basal redox status was determined in samples from 90 patients. The response to I/R varied widely. Myocardium from patients with aortic valve disease was the most susceptible to injury whereas myocardium from dyslipidemia patients was the least susceptible. Tissue from females was better protected than tissue from males. Myocardium from patients with mitral valve disease was the least responsive to IPreC. The basal redox status was altered in the myocardium from patients with mitral and aortic valve disease.
CONCLUSIONS: The response of the myocardium to I/R and IPreC is highly variable and influenced by the underlying cardiac pathology, dyslipidemia, sex, and the basal redox status. These results should be taken into account in the design of future clinical studies on the prevention of I/R injury and protection.

PMID: 28380047 [PubMed - in process]

The Protective Effect of Apigenin on Myocardial Injury in Diabetic Rats mediating Activation of the PPAR-γ Pathway.

Mié, 04/05/2017 - 18:48
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The Protective Effect of Apigenin on Myocardial Injury in Diabetic Rats mediating Activation of the PPAR-γ Pathway.

Int J Mol Sci. 2017 Apr 04;18(4):

Authors: Mahajan UB, Chandrayan G, Patil CR, Arya DS, Suchal K, Agrawal YO, Ojha S, Goyal SN

Abstract
We substantiated the role of peroxisome proliferator-activated receptor-γ (PPAR-γ) activation in the protective effect of apigenin against the myocardial infarction (MI) in diabetic rats. Diabetes was induced by intraperitoneal administration of a single dose of streptozotocin (55 mg/kg). The study groups included diabetic rats receiving vehicle, apigenin (75 mg/kg/day, orally), GW9662 (1 mg/kg/day, intraperitoneally), and a combination of apigenin and GW9662 for 14 days. The MI was induced in all the study groups except the diabetic control group by subcutaneous injection of 100 mg/kg/day of isoproterenol on the two terminal days. The diabetes and isoproterenol-induced MI was evident as a reduction in the maximal positive and negative rate of developed left ventricular pressure and an increase in the left ventricular end-diastolic pressure. The activities of creatine kinase on myocardial bundle (CK-MB) and lactate dehydrogenase (LDH) were also reduced. Apigenin treatment prevented the hemodynamic perturbations, restored the left ventricular function and reinstated a balanced redox status. It protected rats against an MI by attenuating myonecrosis, edema, cell death, and oxidative stress. GW9662, a PPAR-γ antagonist reversed the myocardial protection conferred by apigenin. Further, an increase in the PPAR-γ expression in the myocardium of the rats receiving apigenin reinforces the role of PPAR-γ pathway activation in the cardioprotective effects of apigenin.

PMID: 28375162 [PubMed - in process]

Ventilation strategy has a major influence on remote ischaemic preconditioning in mice.

Mié, 04/05/2017 - 18:48
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Ventilation strategy has a major influence on remote ischaemic preconditioning in mice.

J Cell Mol Med. 2017 Apr 04;:

Authors: Davidson SM, He Z, Dyson A, Bromage DI, Yellon DM

Abstract
Whether oxygen should be administered acutely during ST-segment elevation myocardial infarction is debated. Despite this controversy, the possible influence of supplementary oxygen on animal models of ischaemia-reperfusion injury or cardioprotection is rarely considered. We used an in vivo mouse model of ischaemia and reperfusion to investigate the effect of ventilation with room air versus 100% oxygen. The coronary artery of anaesthetized mice was occluded for 40 min. followed by 2-hrs reperfusion. Infarct size was measured by tetrazolium staining and expressed as a percentage of area at risk, determined using Evan's blue. Unexpectedly, infarct size in mice ventilated with 100% oxygen was significantly smaller than in those ventilated with room air (33 ± 5% versus 46 ± 3%; n = 6; P < 0.01). We tested a standard protocol of 3 × 5 min. cycles of remote ischaemic preconditioning (RIPC) and found this was unable to protect mice ventilated with 100% oxygen. RIPC protocols using 2.5- or 10-min. occlusion were similarly ineffective in mice ventilated with oxygen. Similar disparate results were obtained with direct cardiac ischaemic preconditioning. In contrast, pharmacological protection using bradykinin administered at reperfusion was effective even in mice ventilated with 100% oxygen, reducing infarct size from 33 ± 5% to 21 ± 3% (n = 4-6; P < 0.01). Laser speckle contrast imaging of blood flow and direct pO2 measurements were made in the hindlimb, but these measurements did not correlate with protection. In conclusion, ventilation protocol can have a major influence on infarct size and ischaemic preconditioning protocols in mice.

PMID: 28374972 [PubMed - as supplied by publisher]

Loss of Nrf2 promotes rapid progression to heart failure following myocardial infarction.

Mié, 04/05/2017 - 18:48
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Loss of Nrf2 promotes rapid progression to heart failure following myocardial infarction.

Toxicol Appl Pharmacol. 2017 Mar 31;:

Authors: Strom J, Chen QM

Abstract
Nrf2 gene encodes a transcription factor regulating the expression of antioxidant and detoxification genes. We test here whether Nrf2 plays a role for cardiac protection during ischemic injury in an effort to establish Nrf2 as a target for cardiac protection therapies. Cardiac ischemia induced by the left anterior descending (LAD) coronary artery ligation results in myocardial infarction (MI). Young mice surviving MI show minimal signs of heart failure. Mice lacking Nrf2 experience an accelerated progression to heart failure that occurs within 10days following induction of MI. Nrf2 knockout (Nrf2 KO) mice have a survival rate similar to wild type (WT) mice at 24h after MI, but a significantly higher mortality rate within 10days after MI (50% vs 86%). Morphological examination revealed maladaptive remodeling, including cardiac hypertrophy and dilated left ventricle in Nrf2 KO mice, which were absent in WT mice. Measurements of cardiac function revealed increased left ventricular mass and decreases in cardiac output in Nrf2 KO mice. In addition, Nrf2 KO mice show biomarkers of heart failure, such as elevated levels of β-MHC, ANF, and BNP mRNA in the myocardium. These data support that Nrf2 plays an important role in protecting the myocardium from ischemic injury. Lack of Nrf2 leads to rapid development of heart failure.

PMID: 28373008 [PubMed - as supplied by publisher]

The gap junction modifier ZP1609 decreases cardiomyocyte hypercontracture following ischemia/reperfusion independent from mitochondrial connexin 43.

Mar, 04/04/2017 - 18:18
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The gap junction modifier ZP1609 decreases cardiomyocyte hypercontracture following ischemia/reperfusion independent from mitochondrial connexin 43.

Br J Pharmacol. 2017 Mar 30;:

Authors: Boengler K, Bulic M, Schreckenberg R, Schlueter KD, Schulz R

Abstract
BACKGROUND AND PURPOSE: Dysregulation of gap junction-mediated cell coupling contributes to development of arrhythmias and myocardial damage after ischemia/reperfusion (I/R). Connexin 43 (Cx43) is present at ventricular gap junctions and also in cardiomyocyte mitochondria. The dipeptide ZP1609 ((2S, 4R)-1-(2-aminoacetyl)-4-benzamidopyrrolidine-2-caboxylic acid) has antiarrhythmic properties and reduces infarct size when given at reperfusion. It is unclear, whether ZP1609 targets Cx43-containing mitochondria and impacts on cardiomyocyte hypercontracture following I/R.
EXPERIMENTAL APPROACH: The effects of ZP1609 on the function of mouse subsarcolemmal mitochondria (SSM, containing Cx43) and interfibrillar mitochondria (IFM, lacking Cx43) were studied. Also, isolated murine cardiomyocytes were subjected to simulated I/R without and with ZP1609 (applied during I/R or at the onset of reperfusion only) and the number of cardiomyocytes undergoing hypercontracture was quantified. Biochemical pathways targeted by ZP1609 in cardiomyocytes were analyzed.
KEY RESULTS: ZP1609 inhibited ADP-stimulated respiration and ATP production in SSM and IFM. ROS formation and calcium retention capacities in SSM and IFM were not affected by ZP1609, whereas potassium uptake was enhanced in IFM. The number of rod-shaped cardiomyocytes was improved by ZP1609 (10 μM) when administered either during I/R or reperfusion. ZP1609 altered the phosphorylation of proteins contributing to the protection against I/R injury.
CONCLUSIONS AND IMPLICATIONS: ZP1609 reduced mitochondrial respiration and ATP production, but enhanced potassium uptake of IFM. Additionally, ZP1609 reduced the extent of cardiomyocytes undergoing hypercontracture following I/R. The protective effect is independent from mitochondrial Cx43, since ZP1609 exerts the effects in function in Cx43-containing SSM and Cx43-naïve IFM.

PMID: 28369703 [PubMed - as supplied by publisher]

Usefulness of a thermoplastic breast bra for breast cancer radiotherapy : A prospective analysis.

Mar, 04/04/2017 - 18:18
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Usefulness of a thermoplastic breast bra for breast cancer radiotherapy : A prospective analysis.

Strahlenther Onkol. 2016 Sep;192(9):609-16

Authors: Piroth MD, Petz D, Pinkawa M, Holy R, Eble MJ

Abstract
BACKGROUND: Despite modern techniques, in some patients receiving whole breast radiotherapy (WBI) parts of the heart and the lung might receive doses which are nowadays considered relevant for the development of late morbidity. Our aim was to analyze the usefulness of a thermoplastic breast brassiere to reduce lung and heart doses.
PATIENTS AND METHODS: A total of 29 patients with left-sided and 16 patients with right-sided breast cancer treated with breast conserving surgery and WBI between 2012 and 2013 were included in a prospective study analyzing the effectiveness of a thermoplastic breast bra. WBI was performed using 3D tangential fields up to 50.4 Gy. Treatment planning was performed with and without bra. Several dosimetrical parameters were analyzed comparatively focusing on the heart and ipsilateral lung. For heart dose comparisons, subvolumes like the left anterior descending artery (LAD) and a defined apical region, so-called "apical myocardial territory" (AMT), were defined.
RESULTS: By using the bra, the mean lung dose was reduced by 30.6 % (left-sided cancer) and 29.5 % (right-sided; p < 0.001). The V20Gy for the left lung was reduced by 39.5 % (4.9 vs. 8.1 % of volume; p < 0.001). The mean and maximum heart doses were significantly lower (1.6 vs. 2.1 Gy and 30.7 vs. 39.3 Gy; p = 0.01 and p < 0.001), which also applies to the mean and maximum dose for the AMT (2.5 vs. 4.4 Gy and 31.0 vs. 47.2 Gy; p < 0.01 and p < 0.001). The mean and maximum dose for LAD was lower without reaching significance. No acute skin toxicities > grade 2 were observed.
CONCLUSION: By using a thermoplastic breast bra, radiation doses to the heart and especially parts of the heart apex and ipsilateral lung can be significantly lowered without additional skin toxicity.

PMID: 27287083 [PubMed - indexed for MEDLINE]

Cardioprotective effects of calcitonin gene-related peptide in isolated rat heart and in H9c2 cells via redox signaling.

Lun, 04/03/2017 - 18:10
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Cardioprotective effects of calcitonin gene-related peptide in isolated rat heart and in H9c2 cells via redox signaling.

Biomed Pharmacother. 2017 Mar 29;90:194-202

Authors: Tullio F, Penna C, Cabiale K, Femminò S, Galloni M, Pagliaro P

Abstract
The calcitonin-gene-related-peptide (CGRP) release is coupled to the signaling of Angeli's salt in determining vasodilator effects. However, it is unknown whether CGRP is involved in Angeli's salt cardioprotective effects and which are the mechanisms of protection. We aimed to determine whether CGRP is involved in myocardial protection induced by Angeli's salt. We also analyzed the intracellular signaling pathway activated by CGRP. Isolated rat hearts were pre-treated with Angeli's salt or Angeli's salt plus CGRP8-37, a specific CGRP-receptor antagonist, and subjected to ischemia (30-min) and reperfusion (120-min). Moreover, we studied CGRP-induced protection during oxidative stress (H2O2) and hypoxia/reoxygenation protocols in H9c2 cardiomyocytes. Cell vitality and mitochondrial membrane potential (ΔYm, MMP) were measured using MTT and JC-1 dyes. Angeli's salt reduced infarct size and ameliorated post-ischemic cardiac function via a CGRP-receptor-dependent mechanism. Pre-treatment with CGRP increased H9c2 survival upon challenging with either H2O2 (redox stress) or hypoxia/reoxygenation (H/R stress). Under these stress conditions, reduction in MMP and cell death were partly prevented by CGRP. These CGRP beneficial effects were blocked by CGRP8-37. During H/R stress, pre-treatment with either CGRP-receptor, protein kinase C (PKC) or mitochondrial KATP channel antagonists, and pre-treatment with an antioxidant (2-mercaptopropionylglycine) blocked the protection mediated by CGRP. In conclusion, CGRP is involved in the cardioprotective effects of Angeli's salt. In H9c2 cardiomyocytes, CGRP elicits PKC-dependent and mitochondrial-KATP-redox-dependent mechanisms. Hence, CGRP is an important factor in the redox-sensible cardioprotective effects of Angeli's salt.

PMID: 28364596 [PubMed - as supplied by publisher]

Pulmonary Protective Effect of Remote Ischaemic Preconditioning with Postconditioning in Patients Undergoing Cardiac Surgery.

Sáb, 04/01/2017 - 16:36
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Pulmonary Protective Effect of Remote Ischaemic Preconditioning with Postconditioning in Patients Undergoing Cardiac Surgery.

Heart Lung Circ. 2016 Oct;25(10):1039-40

Authors: Liu GP, Xue FS, Sun C, Yang GZ

PMID: 26935161 [PubMed - indexed for MEDLINE]

The impact of caffeine on connexin expression in the embryonic chick cardiomyocyte micromass culture system.

Sáb, 04/01/2017 - 16:36
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The impact of caffeine on connexin expression in the embryonic chick cardiomyocyte micromass culture system.

J Appl Toxicol. 2016 07;36(7):903-13

Authors: Ahir BK, Pratten MK

Abstract
Cardiomyocytes are electrically coupled by gap junctions, defined as clusters of low-resistance multisubunit transmembrane channels composed of connexins (Cxs). The expression of Cx40, Cx43 and Cx45, which are present in cardiomyocytes, is known to be developmentally regulated. This study investigates the premise that alterations in gap junction proteins are one of the mechanisms by which teratogens may act. Specifically, those molecules known to be teratogenic in humans could cause their effects via disruption of cell-to-cell communication pathways, resulting in an inability to co-ordinate tissue development. Caffeine significantly inhibited contractile activity at concentrations above and including 1500 μm (P < 0.05), while not affecting cell viability and total protein, in the embryonic chick cardiomyocyte micromass culture system. The effects of caffeine on key cardiac gap junction protein (Cx40, Cx43 and Cx45) expression were analysed using immunocytochemistry and in-cell Western blotting. The results indicated that caffeine altered the expression pattern of Cx40, Cx43 and Cx45 at non-cytotoxic concentrations (≥2000 μm), i.e., at concentrations that did not affect total cell protein and cell viability. In addition the effects of caffeine on cardiomyocyte formation and function (contractile activity score) were correlated with modulation of Cxs (Cx40, Cx43 and Cx45) expression, at above and including 2000 μm caffeine concentrations (P < 0.05). These experiments provide evidence that embryonic chick cardiomyocyte micromass culture may be a useful in vitro method for mechanistic studies of perturbation of embryonic heart development. Copyright © 2015 John Wiley & Sons, Ltd.

PMID: 26304238 [PubMed - indexed for MEDLINE]

A genome-wide trans-ethnic interaction study links the PIGR-FCAMR locus to coronary atherosclerosis via interactions between genetic variants and residential exposure to traffic.

Jue, 03/30/2017 - 14:47
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A genome-wide trans-ethnic interaction study links the PIGR-FCAMR locus to coronary atherosclerosis via interactions between genetic variants and residential exposure to traffic.

PLoS One. 2017;12(3):e0173880

Authors: Ward-Caviness CK, Neas LM, Blach C, Haynes CS, LaRocque-Abramson K, Grass E, Dowdy ZE, Devlin RB, Diaz-Sanchez D, Cascio WE, Miranda ML, Gregory SG, Shah SH, Kraus WE, Hauser ER

Abstract
Air pollution is a worldwide contributor to cardiovascular disease mortality and morbidity. Traffic-related air pollution is a widespread environmental exposure and is associated with multiple cardiovascular outcomes such as coronary atherosclerosis, peripheral arterial disease, and myocardial infarction. Despite the recognition of the importance of both genetic and environmental exposures to the pathogenesis of cardiovascular disease, studies of how these two contributors operate jointly are rare. We performed a genome-wide interaction study (GWIS) to examine gene-traffic exposure interactions associated with coronary atherosclerosis. Using race-stratified cohorts of 538 African-Americans (AA) and 1562 European-Americans (EA) from a cardiac catheterization cohort (CATHGEN), we identify gene-by-traffic exposure interactions associated with the number of significantly diseased coronary vessels as a measure of chronic atherosclerosis. We found five suggestive (P<1x10-5) interactions in the AA GWIS, of which two (rs1856746 and rs2791713) replicated in the EA cohort (P < 0.05). Both SNPs are in the PIGR-FCAMR locus and are eQTLs in lymphocytes. The protein products of both PIGR and FCAMR are implicated in inflammatory processes. In the EA GWIS, there were three suggestive interactions; none of these replicated in the AA GWIS. All three were intergenic; the most significant interaction was in a regulatory region associated with SAMSN1, a gene previously associated with atherosclerosis and B cell activation. In conclusion, we have uncovered several novel genes associated with coronary atherosclerosis in individuals chronically exposed to increased ambient concentrations of traffic air pollution. These genes point towards inflammatory pathways that may modify the effects of air pollution on cardiovascular disease risk.

PMID: 28355232 [PubMed - in process]

Cardioprotection with halogenated gases: how does it occur?

Jue, 03/30/2017 - 14:47
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Cardioprotection with halogenated gases: how does it occur?

Drug Des Devel Ther. 2017;11:837-849

Authors: Guerrero-Orriach JL, Escalona Belmonte JJ, Ramirez Fernandez A, Ramirez Aliaga M, Rubio Navarro M, Cruz Mañas J

Abstract
Numerous studies have studied the effect of halogenated agents on the myocardium, highlighting the beneficial cardiac effect of the pharmacological mechanism (preconditioning and postconditioning) when employed before and after ischemia in patients with ischemic heart disease. Anesthetic preconditioning is related to the dose-dependent signal, while the degree of protection is related to the concentration of the administered drug and the duration of the administration itself. Triggers for postconditioning and preconditioning might have numerous pathways in common; mitochondrial protection and a decrease in inflammatory mediators could be the major biochemical elements. Several pathways have been identified, including attenuation of NFκB activation and reduced expression of TNFα, IL-1, intracellular adhesion molecules, eNOS, the hypercontraction reduction that follows reperfusion, and antiapoptotic activating kinases (Akt, ERK1/2). It appears that the preconditioning and postconditioning triggers have numerous similar paths. The key biochemical elements are protection of the mitochondria and reduction in inflammatory mediators, both of which are developed in various ways. We have studied this issue, and have published several articles on cardioprotection with halogenated gases. Our results confirm greater cardioprotection through myocardial preconditioning in patients anesthetized with sevoflurane compared with propofol, with decreasing levels of troponin and N-terminal brain natriuretic peptide prohormone. The difference between our studies and previous studies lies in the use of sedation with sevoflurane in the postoperative period. The results could be related to a prolonged effect, in addition to preconditioning and postconditioning, which could enhance the cardioprotective effect of sevoflurane in the postoperative period. With this review, we aim to clarify the importance of various mechanisms involved in preconditioning and postconditioning with halogenated gases, as supported by our studies.

PMID: 28352158 [PubMed - in process]

TIEG1 deficiency confers enhanced myocardial protection in the infarcted heart by mediating the Pten/Akt signalling pathway.

Jue, 03/30/2017 - 14:47
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TIEG1 deficiency confers enhanced myocardial protection in the infarcted heart by mediating the Pten/Akt signalling pathway.

Int J Mol Med. 2017 Feb 13;:

Authors: Cen M, Hu P, Cai Z, Fang T, Zhang J, Lu M

Abstract
The transforming growth factor (TGF)-β-inducible early gene-1 (TIEG1) plays a crucial role in modulating cell apoptosis and proliferation in a number of diseases, including pancreatic cancer, leukaemia and osteoporosis. However, the functional role of TIEG1 in the heart has not been fully defined. In this study, we first investigated the role of TIEG1 in ischaemic heart disease. For in vitro experiments, cardiomyocytes were isolated from both TIEG1 knockout (KO) and wile-type (WT) mice, and the apoptotic ratios were evaluated after a 48‑h ischaemic insult. A cell proliferation assay was performed after 7 days of incubation under normoxic conditions. In addition, the angiogenic capacity of endothelial cells was determined by tube formation assay. For in vivo experiments, a model of myocardial infarction (MI) was established using both TIEG1 KO and WT mice. Echocardiography was performed at 3 and 28 days post-MI, whereas the haemodynamics test was performed 28 days post-MI. Histological analyses of apoptosis, proliferation, angiogenesis and infarct zone assessments were performed using terminal deoxynucleotidyltransferase-mediated dUTP nick-end labelling (TUNEL) staining, BrdU immunostaining, α-smooth muscle actin (α-SMA)/CD31 immunostaining and Masson's trichrome staining, respectively. Changes in the expression of related proteins caused by TIEG1 deficiency were confirmed using both reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and western blot analysis. Our results demonstrated that the absence of TIEG1 prevented cardiomyocytes from undergoing apoptosis and promoted higher proliferation; it stimulated the proliferation of endothelial cells in vitro and in vivo. Improved cardiac function and less scar formation were observed in TIEG1 KO mice, and we also observed the altered expression of phosphatase and tensin homolog (Pten), Akt and Bcl-2/Bax, as well as vascular endothelial growth factor (VEGF). On the whole, our findings indicate that the absence of TIEG1 plays a cardioprotective role in ischaemic heart disease by promoting changes in Pten/Akt signalling.

PMID: 28350070 [PubMed - as supplied by publisher]

The future is now: neuroprotection during cardiopulmonary resuscitation.

Mié, 03/29/2017 - 14:45
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The future is now: neuroprotection during cardiopulmonary resuscitation.

Curr Opin Crit Care. 2017 Mar 24;:

Authors: Moore JC, Bartos JA, Matsuura TR, Yannopoulos D

Abstract
PURPOSE OF REVIEW: Survival with favorable neurological function after cardiac arrest remains low. The purpose of this review is to identify recent advances that focus on neuroprotection during cardiopulmonary resuscitation (CPR).
RECENT FINDINGS: Multiple strategies have been shown to enhance neuroprotection during CPR. Brain perfusion during CPR is increased with therapies such as active compression decompression CPR and intrathoracic pressure regulation that improve cardiac preload and decrease intracranial pressure. Head Up CPR has been shown to decrease intracranial pressure thereby increasing cerebral perfusion pressure and cerebral blood flow. Sodium nitroprusside enhanced CPR increases cerebral perfusion, facilitates heat exchange, and improves neurologic survival in swine after cardiac arrest. Postconditioning has been administered during CPR in laboratory settings. Poloxamer 188, a membrane stabilizer, and ischemic postconditioning have been shown to improve cardiac and neural function after cardiac arrest in animal models. Postconditioning with inhaled gases protects the myocardium, with more evidence mounting for the potential for neural protection.
SUMMARY: Multiple promising neuroprotective therapies are being developed in animal models of cardiac arrest, and are in early stages of human trials. These therapies have the potential to be bundled together to improve rates of favorable neurological survival after cardiac arrest.

PMID: 28346232 [PubMed - as supplied by publisher]

Patient- and lesion-tailored algorithm of endovascular treatment for arterial occlusive disease of extracranial arteries supplying the brain: safety of the treatment at 30-day follow-up.

Mié, 03/29/2017 - 14:45
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Patient- and lesion-tailored algorithm of endovascular treatment for arterial occlusive disease of extracranial arteries supplying the brain: safety of the treatment at 30-day follow-up.

Postepy Kardiol Interwencyjnej. 2017;13(1):53-61

Authors: Latacz P, Simka M, Brzegowy P, Janas P, Kazibudzki M, Pieniążek P, Ochała A, Popiela T, Mrowiecki T

Abstract
INTRODUCTION: Although surgical endarterectomy remains the treatment of choice for carotid artery stenosis, stenting plays an important role as an alternative treatment modality, especially in high-risk patients. The actual safety profile associated with stenting procedures is probably better than that reported by randomized controlled trials.
AIM: To assess the safety of stent implantations in extracranial arteries supplying the brain, and also to identify risk factors associated with this procedure.
MATERIAL AND METHODS: This was a post hoc analysis, with 30-day follow-up. We analyzed the results of treatment of 372 patients who underwent 408 procedures, 197 such procedures in asymptomatic, and 211 in symptomatic individuals. Stenting procedures were performed using a technique and armamentarium which were tailored to the type and anatomy of lesions.
RESULTS: There were 6 (1.5%) strokes, including 2 (0.5%) major strokes, 1 ipsi- and 1 contralateral, and 4 (1.0%) minor strokes. In asymptomatic patients there was 1 (0.3%) minor stroke. Transient ischemic attacks occurred in 5 (1.2%) patients. There were 2 (0.5%) non-STEMI myocardial infarctions and 2 (0.5%) non-stroke related fatalities. Risk factors of these adverse events were diabetes mellitus, lesions localized in a tortuous segment of the artery, embolic material in the filter and bilateral stenoses of carotid arteries. Additional risk factors in asymptomatic patients were renal impairment and advanced coronary artery disease; and in symptomatic patients, grade 3 arterial hypertension, dislipidemia, cigarette smoking and lesions requiring predilatation.
CONCLUSIONS: Stenting procedures of extracranial arteries supplying the brain, which are tailored to the type and anatomy of lesions, seem to be relatively safe.

PMID: 28344618 [PubMed - in process]

Hyperbaric Oxygen Preconditioning Provides Preliminary Protection Against Doxorubicin Cardiotoxicity.

Mié, 03/29/2017 - 14:45
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Hyperbaric Oxygen Preconditioning Provides Preliminary Protection Against Doxorubicin Cardiotoxicity.

Acta Cardiol Sin. 2017 Mar;33(2):150-155

Authors: Tezcan O, Karahan O, Alan M, Ekinci C, Yavuz C, Demirtas S, Ekinci A, Caliskan A

Abstract
BACKGROUND: Doxorubicin (DOX) is generally recognized to have important cardiotoxic side effects. Studies are contradictory about the interaction between hyperbaric oxygen (HBO2) therapy and doxorubicin-induced cardiomyotoxicity. Recent data suggests that HBO2 therapy can lead to preconditioning of myocardium while generating oxidative stress. Herein we have investigated the effect of HBO2 therapy in a DOX-induced cardiomyocyte injury animal model.
METHODS: Twenty-one rats were divided into three equal groups as follows: 1) Group 1 is a control group (without any intervention), used for evaluating the basal cardiac structures and determining the normal value of cardiacs and serum oxidative markers; 2) Group 2 is the doxorubicin group (single dose i.p. 20 mg/kg doxorubicin) for detecting the cardiotoxic and systemic effects of doxorubicin; 3) Group 3 is the doxorubicin and HBO2 group (100% oxygen at 2.5 atmospheric for 90 minutes, daily), for evaluating the effect of HBO2 in doxorubicin induced cardiotoxicity. At the end of the protocols, the hearts were harvested and blood samples (2 ml) were obtained.
RESULTS: The doxorubicin treated animals (Group 2) had increased oxidative stress markers (both cardiac and serum) and severe cardiac injury as compared to the basal findings in the control group. Nevertheless, the highest cardiac oxidative stress index was detected in Group 3 (control vs. Group 3, p = 0.01). However, histological examination revealed that cardiac structures were well preserved in Group 3 when compared with Group 2.
CONCLUSIONS: Our results suggest that HBO2 preconditioning appears to be protective in the doxorubicin-induced cardiotoxicity model. Future studies are required to better elucidate the basis of this preconditioning effect of HBO2.

PMID: 28344418 [PubMed - in process]

Urolithin A alleviates myocardial ischemia/reperfusion injury via PI3K/Akt pathway.

Mié, 03/29/2017 - 14:45
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Urolithin A alleviates myocardial ischemia/reperfusion injury via PI3K/Akt pathway.

Biochem Biophys Res Commun. 2017 Mar 23;:

Authors: Tang L, Mo Y, Li Y, Zhong Y, He S, Zhang Y, Tang Y, Fu S, Wang X, Chen A

Abstract
Ischemia/reperfusion (I/R) induces additional damage to the restoration of blood flow to ischemic myocardium. This study examined the effects of urolithin A (UA) on myocardial injury of ischemia/reperfusion in vivo and vitro and explored its underlying mechanisms. Mice were subjected to myocardial ischemia followed by reperfusion. Cells were subjected to hypoxia followed by reoxygenation. UA alleviated hypoxia/reoxygenation (H/R) injury in myocardial cells, reduced myocardial infarct size and cell death in mice after ischemia/reperfusion. Meanwhile, UA enhanced antioxidant capacity in cardiomyocytes following hypoxia/reoxygenation. UA reduced myocardial apoptosis following ischemia/reperfusion. The protection of UA was abolished by LY294002, a PI3K/Akt-inhibitor. These results demonstrated that UA alleviates myocardial ischemia/reperfusion injury probably through PI3K/Akt pathway.

PMID: 28343995 [PubMed - as supplied by publisher]

Aqueous extract from leaf of Artocarpus altilis provides cardio-protection from isoproterenol induced myocardial damage in rats: Negative chronotropic and inotropic effects.

Mié, 03/29/2017 - 14:45
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Aqueous extract from leaf of Artocarpus altilis provides cardio-protection from isoproterenol induced myocardial damage in rats: Negative chronotropic and inotropic effects.

J Ethnopharmacol. 2017 Mar 22;:

Authors: Nwokocha C, Palacios J, Simirgiotis MJ, Thomas J, Nwokocha M, Young L, Thompson R, Cifuentes F, Paredes A, Delgoda R

Abstract
ETHNOPHARMACOLOGICAL RELEVANCE: The leaves of Artocarpus altilis (Parkinson ex F.A.Zorn, Fosberg) (Moraceae) are used in the management of hypertension; this study assessed the cardio-protective effects of the leaf extract on isoproterenol (ISO) induced myocardial damage in rats.
MATERIAL AND METHODS: Twenty (20) adult male Sprague-Dawley rats (175-230g) were divided into 5 groups. Group 1 (Control), 2 (AA) received 50mg/Kg Artocarpus altilis (AA) only; 3 (ISO) received 85mg/Kg ISO only; 4 (ISO+AA/50) and 5 (ISO+AA/100) received 50 and 100mg/Kg AA respectively for 6 days, after induced with ISO twice (85mg/Kg) at a 24-hour period. Blood pressure readings were taken before and after the administering of ISO using the tail cuff method. ECG was performed on anaesthetized rats. Cardiac contractility was measured in isolated right atrial muscles. Assessment of myocardial infarct (MI) size, heart/body weight ratio, biochemical, hematological and histo-morphological parameters were conducted at the end of seven days. An aqueous extract from leaves of A. altilis was analyzed for organic compounds using UHPLC mass spectrometry.
RESULTS: ISO induced myocardial damage through an elevation of the heart rate (HR), infarct size and ECG distortions. Treatment with AA significantly (p˂0.05) reduced heart/body weight ratio (49%), MI (96%), HR (27%), sympathovagal imbalance (36%) and serum cardiac biomarkers (AST, LDH, HDL, triglycerides and CCK) caused by ISO. AA decreased the beat frequency of isolated right atrium (11%) cause by ISO, an action similar to propranolol (beta-adrenergic antagonist; 20%), but showed no significant changes in the QTc intervals of the ECG (suggesting no cardio-toxic drug-herb interactions), Thirty nine compounds were detected using high resolution LC-MS analysis (HPLC-Orbitrap-APCI-MS) in the extract. Pure compounds, as gallic acid and rutin, presented a higher negative chronotropic effect, similar to propranolol.
CONCLUSION: Oral administration of aqueous extract of Artocarpus artilis has cardio-protective functions in myocardial injury, in part, by decreasing the HR, reduced contractility and infarct size. These findings may explain the cardio-protective use of A. altilis in traditional medicine.

PMID: 28342858 [PubMed - as supplied by publisher]

Effect of the human therapeutic drug diltiazem on the haematological parameters, histology and selected enzymatic activities of rainbow trout Oncorhynchus mykiss.

Mié, 03/29/2017 - 14:45
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Effect of the human therapeutic drug diltiazem on the haematological parameters, histology and selected enzymatic activities of rainbow trout Oncorhynchus mykiss.

Chemosphere. 2016 Aug;157:57-64

Authors: Steinbach C, Burkina V, Schmidt-Posthaus H, Stara A, Kolarova J, Velisek J, Randak T, Kroupova HK

Abstract
Diltiazem is a pharmaceutical belonging to a group of calcium channel blockers (CCB) that is widely used in the treatment of angina pectoris and hypertension. The objective of the present study was to assess the effect of diltiazem on rainbow trout (Oncorhynchus mykiss). Juvenile trout were exposed for 21 and 42 days to three nominal concentrations of diltiazem: 0.03 μg L(-1) (environmentally relevant concentration), 3 μg L(-1), and 30 μg L(-1) (sub-lethal concentrations). The number of mature neutrophilic granulocytes was significantly increased by 450 and 400% in fish exposed to 3 μg L(-1) and 30 μg L(-1) diltiazem compared to the control, respectively. Antioxidant enzyme activity was affected in liver and gills of fish exposed to all tested concentrations of diltiazem but the changes were mostly transient and not concentration dependent. Creatine kinase activity was markedly increased (ranging from 520 to 845%) at all tested diltiazem concentrations at the end of the exposure indicating muscle and/or kidney damage. The highest concentration was associated with histological changes in heart, liver, and kidney. These alterations can be attributed to the effects of diltiazem on the cardiovascular system, similar to those observed in the human body, as well as to its metabolism. At the environmentally relevant concentration, diltiazem was found to induce some alterations in the blood, gills, and liver of fish, indicating its potential for adverse effects on non-target organisms in the aquatic environment.

PMID: 27208646 [PubMed - indexed for MEDLINE]

Transcarotid Artery Revascularization With Flow Reversal.

Lun, 03/27/2017 - 08:50
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Transcarotid Artery Revascularization With Flow Reversal.

J Endovasc Ther. 2017 Apr;24(2):265-270

Authors: Alpaslan A, Wintermark M, Pintér L, Macdonald S, Ruedy R, Kolvenbach R

Abstract
PURPOSE: To report a study evaluating the safety and efficacy of stenting via direct carotid access with flow reversal using the ENROUTE Transcarotid Neuroprotection System.
METHODS: Between March 2009 and June 2012, 75 patients (mean age 72.6 years; 45 men) underwent carotid artery stenting with the ENROUTE System; the majority of patients (63, 84%) were asymptomatic. The primary safety endpoint was the composite of major stroke, myocardial infarction, or death at 30 days. Efficacy outcomes included acute device success, procedure success, and tolerance to flow reversal. Fifty-six (74.7%) patients underwent diffusion-weighted magnetic resonance imaging (DW-MRI) before and after the procedure to assess the development of new ischemic brain lesions.
RESULTS: Acute device and procedure success were achieved in 68 (90.6%) patients. The reverse flow circuit was established in 71 (94.6%) patients; only 5 patients demonstrated transient intolerance to flow reversal that did not interfere with completion of the procedure. The mean time on flow reversal was 19.1 minutes. In the DW-MRI substudy, 10 (17.9%) of 56 patients had ipsilateral new white lesions with a mean volume of 0.17 mL. At 30 days, no major stroke, myocardial infarction, or death occurred; 1 patient had experienced a minor stroke that was adjudicated as not related to either the device or procedure.
CONCLUSION: Results of the PROOF study demonstrate the safety and efficacy of transcarotid revascularization with the ENROUTE Transcarotid Neuroprotection System.

PMID: 28335706 [PubMed - in process]

Custodiol versus cold Calafiore for elective cardiac arrest in isolated aortic valve replacement: a propensity-matched analysis of 7263 patients†.

Dom, 03/26/2017 - 05:30
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Custodiol versus cold Calafiore for elective cardiac arrest in isolated aortic valve replacement: a propensity-matched analysis of 7263 patients†.

Eur J Cardiothorac Surg. 2017 Mar 03;:

Authors: Hoyer A, Lehmann S, Mende M, Noack T, Kiefer P, Misfeld M, Bakhtiary F, Mohr FW

Abstract
OBJECTIVES: This study was designed to assess the impact of crystalloid cardioplegia (CCP) and blood cardioplegia (BCP) on short- and long-term outcome after isolated aortic valve replacement (AVR).
METHODS: A total of 7263 patients undergoing AVR at our institution between November 1994 and June 2015 were identified. CCP (Custodiol ® ) was used in 83% ( n  = 5998) and intermittent cold BCP in 1007 patients (14%). For 4790 patients, propensity scores were calculated from baseline data, risk factors, comorbidities and characteristics of the disease, resulting in 825 pairs. The primary outcome was operative mortality (OM).
RESULTS: There was no significant difference in OM between CCP and BCP cohorts [33 of 825 (4.0%) vs 35 of 825 (4.2%), P  = 0.90]. The incidence of postoperative complications was comparable between both groups. Long-term survival was also not different between CCP and BCP (log-rank test: P  = 0.9). Multiple Cox regression analysis demonstrated that mortality was significantly affected by renal function ( P  < 0.001), logistic EuroSCORE ( P  < 0.001), male sex ( P  = 0.005) and diabetes ( P  = 0.037). Patients with reduced left ventricular ejection fraction ≤30% showed improved survival when receiving BCP intraoperatively [odds ratio: 2.28 (1.12-4.63); P  = 0.03].
CONCLUSIONS: CCP and BCP provide equivalent outcome after isolated AVR. However, BCP seems to be beneficial for patients with reduced left ventricular ejection fraction.

PMID: 28329384 [PubMed - as supplied by publisher]