Sossalla, Samuel Tobias

[["dc.bibliographiccitation.firstpage","347"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Annals of Thoracic and Cardiovascular Surgery"],["dc.bibliographiccitation.lastpage","351"],["dc.bibliographiccitation.volume","17"],["dc.contributor.author","Mirzaie, Masoud"],["dc.contributor.author","Fatehpur, Sheila"],["dc.contributor.author","Friedrich, Martin"],["dc.contributor.author","Sossalla, Samuel T."],["dc.contributor.author","Sohns, Christian"],["dc.contributor.author","Schoendube, Friedrich Albert"],["dc.contributor.author","Schmitto, Jan Dieter"],["dc.date.accessioned","2018-11-07T08:53:26Z"],["dc.date.available","2018-11-07T08:53:26Z"],["dc.date.issued","2011"],["dc.description.abstract","Objective: The present paper exemplary describes several severe stenoses of supraaortic branches with its symptoms and operative treatments. Methods: Eight patients, two female (68 +/- 5 y), six male (73 +/- 4 y), were retrospectively evaluated. Patients showed neurological signs as followed: recurring attacks of vertigo (80%), temporary paresis of extremity (20%), speech disorders (20%) and subclavian and/or carotic-steel-syndrome (15%). Seven patients have already been previously treated with revascularization of the supraaortic branches in the past. The surgical techniques used were thrombendarterectomy of the internal carotid artery, carotid-subclavian bypass and complex aortotruncal, aorto-carotid and aorto-subclavian-bypass. Results: One patient died nine days postoperatively due to myocardial infarction. Mean duration of stay on intensive care unit was 1.5 days. Mean duration of postoperative ventilation was six hours. Average duration of stay on normal ward was nine days. Conclusion: This study presents several complex reconstructions of supraaortic branches, which were indicated in cases with severe stenoses of supraaortic branches. Even though treatment strategies were complex the peri- and postoperative complication rates are quite low. These therapeutic strategies were necessary to avoid severe neurological complications in these patients."],["dc.identifier.doi","10.5761/atcs.oa.09.01432"],["dc.identifier.isi","000294510200005"],["dc.identifier.pmid","21881320"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/22408"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Medical Tribune Inc"],["dc.relation.issn","1341-1098"],["dc.title","Complex Reconstruction of Supraaortic Branches"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","European Journal of Heart Failure"],["dc.contributor.author","Pabel, Steffen"],["dc.contributor.author","Hamdani, Nazha"],["dc.contributor.author","Sossalla, Samuel"],["dc.date.accessioned","2021-04-14T08:29:26Z"],["dc.date.available","2021-04-14T08:29:26Z"],["dc.date.issued","2021"],["dc.identifier.doi","10.1002/ejhf.2091"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/82903"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.relation.eissn","1879-0844"],["dc.relation.issn","1388-9842"],["dc.title","A mechanistic rationale for the investigation of sodium–glucose co‐transporter 2 inhibitors in heart failure with preserved ejection fraction. Letter regarding the article ‘Baseline characteristics of patients with heart failure with preserved ejection fraction in the EMPEROR‐Preserved trial’"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","335"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Clinical Imaging"],["dc.bibliographiccitation.lastpage","341"],["dc.bibliographiccitation.volume","32"],["dc.contributor.author","Sohns, Christian"],["dc.contributor.author","Amarteifio, Erick"],["dc.contributor.author","Sossalla, Samuel T."],["dc.contributor.author","Heuser, Markus"],["dc.contributor.author","Obenauer, Silvia"],["dc.date.accessioned","2018-11-07T11:11:09Z"],["dc.date.available","2018-11-07T11:11:09Z"],["dc.date.issued","2008"],["dc.description.abstract","Aim: In this retrospective study, we assess the current role and future potential of computed tomography (CT) in the diagnostic algorithm of acute pulmonary embolism (PE). Materials and methods: Two hundred patients underwent 64-multidetector-row spiral CT of the chest, pelvis, and thigh for suspected PE. CT scans were reviewed, and the degree of contrast enhancement and the presence of PE and/or (deep) venous thrombosis were recorded. In the case of PE, the level of thrombus was noted as central, main, or lobar. If the scan yielded a positive result for thrombosis, intravenous localization was also determined. Patient age, length of admission, clinical course, clinical indication, and incidental findings were registered as well. Results: PE was detected in 60 of the 200 patients with a high clinical probability of having PE (30%). Thirty-four patients had a positive CT scan result for venous thrombosis (17%). Twenty-four of the 60 patients had proximal deep venous thrombosis (40%), and 2 patients had ann venous thrombosis (3%). Thirty-four of the 60 patients had without venous thrombosis (57%). Eight of the 200 patients had deep venous thrombosis without suspicion of PE (4%). The distribution of the proximal thrombi showed 15 in a central artery (25%), 13 in a main pulmonary artery (22%), and 32 in a lobar segmental artery (53%). There was diffuse allocation of the thrombus in all lobes. Furthermore, CT scan noted a total of 120 incidental findings. Conclusion: Our study indicates the potential clinical use of a diagnostic strategy for ruling out PE based on D-dimer testing and multidetector-row CT. A larger outcome study is needed before this approach can be adopted. (C) 2008 Elsevier Inc. All rights reserved."],["dc.identifier.doi","10.1016/j.clinimag.2008.01.028"],["dc.identifier.isi","000259211600001"],["dc.identifier.pmid","18760719"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/53366"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Inc"],["dc.relation.issn","1873-4499"],["dc.relation.issn","0899-7071"],["dc.title","64-multidetector-row spiral CT in pulmonary embolism with emphasis on incidental findings"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","179"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Current Heart Failure Reports"],["dc.bibliographiccitation.lastpage","186"],["dc.bibliographiccitation.volume","14"],["dc.contributor.author","Bengel, Philipp"],["dc.contributor.author","Ahmad, Shakil"],["dc.contributor.author","Sossalla, Samuel"],["dc.date.accessioned","2019-01-30T13:29:01Z"],["dc.date.available","2019-01-30T13:29:01Z"],["dc.date.issued","2017"],["dc.description.abstract","Over the last years, evidence is accumulating that enhanced late sodium current (INaL) in cardiac pathologies has fundamental consequences for cellular electrophysiology. This review discusses the underlying mechanisms of INaL-induced arrhythmias and the significance of INaL-inhibition as a possible therapeutic approach."],["dc.identifier.doi","10.1007/s11897-017-0333-0"],["dc.identifier.pmid","28455610"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/57422"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.relation.eissn","1546-9549"],["dc.title","Inhibition of Late Sodium Current as an Innovative Antiarrhythmic Strategy"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","642"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","ESC Heart Failure"],["dc.bibliographiccitation.lastpage","648"],["dc.bibliographiccitation.volume","5"],["dc.contributor.author","Mustroph, Julian"],["dc.contributor.author","Wagemann, Olivia"],["dc.contributor.author","Lücht, Charlotte M."],["dc.contributor.author","Trum, Maximilian"],["dc.contributor.author","Hammer, Karin P."],["dc.contributor.author","Sag, Can Martin"],["dc.contributor.author","Lebek, Simon"],["dc.contributor.author","Tarnowski, Daniel"],["dc.contributor.author","Reinders, Jörg"],["dc.contributor.author","Perbellini, Filippo"],["dc.contributor.author","Terracciano, Cesare"],["dc.contributor.author","Schmid, Christof"],["dc.contributor.author","Schopka, Simon"],["dc.contributor.author","Hilker, Michael"],["dc.contributor.author","Zausig, York"],["dc.contributor.author","Pabel, Steffen"],["dc.contributor.author","Sossalla, Samuel T."],["dc.contributor.author","Schweda, Frank"],["dc.contributor.author","Maier, Lars S."],["dc.contributor.author","Wagner, Stefan"],["dc.date.accessioned","2020-12-10T14:06:09Z"],["dc.date.available","2020-12-10T14:06:09Z"],["dc.date.issued","2018"],["dc.identifier.doi","10.1002/ehf2.12336"],["dc.identifier.issn","2055-5822"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/69797"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Empagliflozin reduces Ca/calmodulin-dependent kinase II activity in isolated ventricular cardiomyocytes"],["dc.title.alternative","Empagliflozin reduces CaMKII activity"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","280"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Clinical Imaging"],["dc.bibliographiccitation.lastpage","286"],["dc.bibliographiccitation.volume","32"],["dc.contributor.author","Sohns, Christian"],["dc.contributor.author","Heuser, Markus"],["dc.contributor.author","Sossalla, Samuel T."],["dc.contributor.author","Wolff, Hendrik"],["dc.contributor.author","Obenauer, Silvia"],["dc.date.accessioned","2018-11-07T11:13:19Z"],["dc.date.available","2018-11-07T11:13:19Z"],["dc.date.issued","2008"],["dc.description.abstract","Aim: In this retrospective study, we assess the current role and future potential of computed tomographic (CT) colonography as a viable alternative imaging tool for colorectal polyp detection and colon cancer screening. Materials and methods: Twenty patients have undergone virtual colonographic examinations with 64-multidetector-row spiral CT (MDCT), and three-dimensional images were created on a separate workstation that had the appropriate software for image processing. Images were reviewed by a radiologist, and anatomic division of the entire colon was used to locate the suspected lesions. Characteristics of bowel preparation, intracolonic, extracolonic, and incidental findings were noted, too. Results: Ten of the 20 patients (50%) had a positive CT colonography for polypoid lesions. Those lesions were distributed into the cecum (4 cases), colon ascendens (2 cases), colon descendens (2 cases), and sigma (2 cases). In 80%, bowel preparation was good, in 15% moderate, and in 5% inadequate. Furthermore, CT scan noted in total 20 incidental findings. Conclusion: CT colonography is currently a viable alternative imaging tool for colorectal polyp detection. There are several clinical situations where CT colonography may play an important role in patient care. These include for example evaluation of the colon after an incomplete conventional colonoscopic examination or evaluation in patients who are clinically unfit to undergo conventional colonoscopy. At centers where there is expertise in data acquisition and interpretation, CT colonography is being offered as a routine imaging examination. With continued improvements in bowel preparation, colonic distention, and CT colonography interpretation by sufficient numbers of radiologists this technology might have a substantial influence on colon cancer screening. (c) 2008 Elsevier Inc. All rights reserved."],["dc.identifier.doi","10.1016/j.clinimag.2008.01.001"],["dc.identifier.isi","000257908300006"],["dc.identifier.pmid","18603183"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/53863"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Inc"],["dc.relation.issn","0899-7071"],["dc.title","Current role and future potential of computed tomographic colonography for colorectal polyp detection and colon cancer screening - incidental findings"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","490"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","The Breast Journal"],["dc.bibliographiccitation.lastpage","497"],["dc.bibliographiccitation.volume","16"],["dc.contributor.author","Sohns, Christian"],["dc.contributor.author","Angic, Besim"],["dc.contributor.author","Sossalla, Samuel T."],["dc.contributor.author","Konietschke, Frank"],["dc.contributor.author","Obenauer, Silvia"],["dc.date.accessioned","2018-11-07T08:39:34Z"],["dc.date.available","2018-11-07T08:39:34Z"],["dc.date.issued","2010"],["dc.description.abstract","The object of this study was to assess the clinical usefulness of computer-assisted diagnosis (CAD) in the interpretation of early-research, benign and malignant mammograms in dependence on readers' experience with CAD. CAD was applied on digital mammograms of 303 patients who were divided into three groups: early-research (n = 103), benign (n = 102) and malignant group (n = 98). Mammograms were analyzed by three readers with different experience in evaluating mammograms (medical student, an assistant and an attending physician specifically trained in mammography). All images were presented accidentally with and without the influence of CAD and from different patient groups. The mammograms were classified according to BI-RADS classification. To evaluate readers' sensitivity and specificity with and without the application of the CAD system, ROC analysis and the corresponding area under the curve (AUC) were evaluated for each reader. Afterwards significant differences of the accuracy according to readers experience and according to the assistance of the CAD system were calculated. All readers have an account of accuracy by using CAD in both patient groups. The highest benefit has the student (10% increase of the AUC) followed by the resident (4%) and at least followed by the mammography fellow (3%). There are significant varieties of the accuracy in addiction to the readers' experience and to the examination method with and without CAD system. Patient group has not a significant influence to the elevation of accuracy by using the CAD. All three readers have nearly the same increase of AUC in the examinations of malignant and early-research group summarized and of the malignant group only. Finally, the increase of accuracy depends on the readers' experience. For all patient groups CAD-application causes a steeply increase of the ROC curve and consequently a gain of sensitivity."],["dc.identifier.doi","10.1111/j.1524-4741.2010.00963.x"],["dc.identifier.isi","000281667100006"],["dc.identifier.pmid","20642459"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/19028"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.relation.issn","1524-4741"],["dc.relation.issn","1075-122X"],["dc.title","Computer-assisted Diagnosis in Full-field Digital Mammography-Results in Dependence of Readers Experiences"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1262"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Journal of Clinical Investigation"],["dc.bibliographiccitation.lastpage","1274"],["dc.bibliographiccitation.volume","123"],["dc.contributor.author","Luo, Min"],["dc.contributor.author","Guan, Xiaoqun"],["dc.contributor.author","Luczak, Elizabeth D."],["dc.contributor.author","Lang, Di"],["dc.contributor.author","Kutschke, William"],["dc.contributor.author","Gao, Zhan"],["dc.contributor.author","Yang, Jinying"],["dc.contributor.author","Glynn, Patric"],["dc.contributor.author","Sossalla, Samuel"],["dc.contributor.author","Swaminathan, Paari D."],["dc.contributor.author","Weiss, Robert M."],["dc.contributor.author","Yang, Baoli"],["dc.contributor.author","Rokita, Adam G."],["dc.contributor.author","Maier, Lars S."],["dc.contributor.author","Efimov, Igor R."],["dc.contributor.author","Hund, Thomas J."],["dc.contributor.author","Anderson, Mark E."],["dc.date.accessioned","2018-11-07T09:27:39Z"],["dc.date.available","2018-11-07T09:27:39Z"],["dc.date.issued","2013"],["dc.description.abstract","Diabetes increases oxidant stress and doubles the risk of dying after myocardial infarction, but the mechanisms underlying increased mortality are unknown. Mice with streptozotocin-induced diabetes developed profound heart rate slowing and doubled mortality compared with controls after myocardial infarction. Oxidized Ca2+/calmodulin-dependent protein kinase II (ox-CaMKII) was significantly increased in pacemaker tissues from diabetic patients compared with that in nondiabetic patients after myocardial infarction. Streptozotocin-treated mice had increased pacemaker cell ox-CaMKII and apoptosis, which were further enhanced by myocardial infarction. We developed a knockin mouse model of oxidation-resistant CaMKII delta (MM-VV), the isoform associated with cardiovascular disease. Streptozotocin-treated MM-VV mice and WT mice infused with MitoTEMPO, a mitochondrial targeted antioxidant, expressed significantly less ox-CaMKII, exhibited increased pacemaker cell survival, maintained normal heart rates, and were resistant to diabetes-attributable mortality after myocardial infarction. Our findings suggest that activation of a mitochondrial/ox-CaMKII pathway contributes to increased sudden death in diabetic patients after myocardial infarction."],["dc.identifier.doi","10.1172/JCI65268"],["dc.identifier.isi","000315749400036"],["dc.identifier.pmid","23426181"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/30588"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/105"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.notes.submitter","Najko"],["dc.relation","SFB 1002: Modulatorische Einheiten bei Herzinsuffizienz"],["dc.relation","SFB 1002 | A03: Bedeutung CaMKII-abhängiger Mechanismen für die Arrhythmogenese bei Herzinsuffizienz"],["dc.relation.issn","0021-9738"],["dc.relation.workinggroup","RG L. Maier (Experimentelle Kardiologie)"],["dc.relation.workinggroup","RG Sossalla (Kardiovaskuläre experimentelle Elektrophysiologie und Bildgebung)"],["dc.title","Diabetes increases mortality after myocardial infarction by oxidizing CaMKII"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","673"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","European Journal of Heart Failure"],["dc.bibliographiccitation.lastpage","680"],["dc.bibliographiccitation.volume","8"],["dc.contributor.author","Schillinger, Wolfgang"],["dc.contributor.author","Teucher, Nils"],["dc.contributor.author","Christians, Claus"],["dc.contributor.author","Kohlhaas, Michael"],["dc.contributor.author","Sossalla, Samuel"],["dc.contributor.author","Van Nguyen, Phuc"],["dc.contributor.author","Schmidt, Albrecht G."],["dc.contributor.author","Schunck, Ortwin"],["dc.contributor.author","Nebendahl, Klaus"],["dc.contributor.author","Maier, Lars S."],["dc.contributor.author","Zeitz, Oliver"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.date.accessioned","2017-09-07T11:52:27Z"],["dc.date.available","2017-09-07T11:52:27Z"],["dc.date.issued","2006"],["dc.description.abstract","We investigated the hypothesis that increased intracellular [Na+](i) in heart failure contributes to preservation of SR Ca2+ load which may become particularly evident at slow heart rates. [Na+]i in SBFI-loaded myocytes from rabbits with pacing-induced heart failure (PHF) was significantly higher at each frequency as compared to Sham-operated animals. Furthermore, PHF rabbits demonstrated reduced SR Ca2+-ATPase protein levels (-37%, p < 0.04) but unchanged Na+/Ca2+ exchanger protein levels. At 0.25 Hz, isometric force was similar in cardiac trabeculae from PHF rabbits as compared to control (PHF, 3.6 +/- 1.3; Sham, 4.4 +/- 0.6 mN/mm(2)). Rapid cooling contractures (RCCs) were unchanged indicating preserved SR Ca2+ load at this frequency. In Sham, isometric twitch force increased with rising frequencies to 29.0 +/- 2.8 mN/mm(2) at 3.0 Hz (p < 0.05) as compared to 0.25 Hz. RCCs showed a parallel increase by 186 +/- 47% (p < 0.01). In PHF, frequency-dependent increase in force (15.8 +/- 4.7 mN/mm(2) at 3.0 Hz) and RCCs (increase by 70 +/- 40%) were significantly blunted. Thus, in PHF in rabbits SR Ca2+ load is preserved at low frequencies despite decreased SR Ca2+-ATPase expression. This may result from [Na+](i)-dependent changes in Na+/Ca2+ exchanger activity. (c) 2006 European Society of Cardiology. Published by Elsevier B.V All rights reserved."],["dc.identifier.doi","10.1016/j.ejheart.2006.01.013"],["dc.identifier.gro","3143598"],["dc.identifier.isi","000242383300002"],["dc.identifier.pmid","16540370"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/1130"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Elsevier Science Bv"],["dc.relation.issn","1388-9842"],["dc.title","High intracellular Na+ preserves myocardial function at low heart rates in isolated myocardium from failing hearts"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","32"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Journal of Molecular and Cellular Cardiology"],["dc.bibliographiccitation.lastpage","43"],["dc.bibliographiccitation.volume","45"],["dc.contributor.author","Sossalla, Samuel"],["dc.contributor.author","Wagner, Stefan"],["dc.contributor.author","Rasenack, Eva C. L."],["dc.contributor.author","Ruff, Hanna"],["dc.contributor.author","Weber, Sarah L."],["dc.contributor.author","Schoendube, Friedrich A."],["dc.contributor.author","Tirilomis, Theodor"],["dc.contributor.author","Tenderich, Gero"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Belardinelli, Luiz"],["dc.contributor.author","Maier, Lars S."],["dc.date.accessioned","2017-09-07T11:48:16Z"],["dc.date.available","2017-09-07T11:48:16Z"],["dc.date.issued","2008"],["dc.description.abstract","The goal of this study was to test the hypothesis that the novel anti-ischemic drug ratiolazine, which is known to inhibit late I-Na, could reduce intracellular [Na+](i) and diastolic [Ca2+](i) overload and improve diastolic function. Contractile dysfunction in human heart failure (HF) is associated with increased [Na+](i) and elevated diastolic [Ca2+](i). Increased Na influx through voltage-gated Na+ channels (late I-Na) has been suggested to contribute to elevated [Na+](i) in HF. In isometrically contracting ventricular muscle strips from end-stage failing human hearts, ranolazine (10 mu mol/L) did not exert negative inotropic effects on twitch force amplitude. However, ranolazine significantly reduced frequency-dependent increase in diastolic tension (i.e., diastolic dysfunction) by similar to 30% without significantly affecting sarcoplasmic reticulum (SR) Ca2+ loading. To investigate the mechanism of action of this beneficial effect of ranolazine on diastolic tension, Anemonia sulcata toxin II (ATX-II, 40 nmol/L) was used to increase intracellular Na+ loading in ventricular rabbit myocytes. ATX-II caused a significant rise in [Na+](i) typically seen in heart failure via increased late I-Na. In parallel, ATX-II significantly increased diastolic [Ca2+](i). In the presence of ranolazine the increases in late I-Na, as well as [Na+](i) and diastolic [Ca2+](i) were significantly blunted at all stimulation rates without significantly decreasing Ca2+ transient amplitudes or SR Ca2+ content. In summary, ranolazine reduced the frequency dependent increase in diastolic tension without having negative inotropic effects on contractility of muscles from end-stage failing human hearts. Moreover, in rabbit myocytes the increases in late I-Na, [Na+](i) and [Ca2+](i) caused by ATX-II, were significantly blunted by ranolazine. These results suggest that ratiolazine may be of therapeutic benefit in conditions of diastolic dysfunction due to elevated [Na+](i) and diastolic [Ca2+](i). (C) 2008 Elsevier Inc. All rights reserved."],["dc.identifier.doi","10.1016/j.yjmcc.2008.03.006"],["dc.identifier.gro","3143272"],["dc.identifier.isi","000257543800004"],["dc.identifier.pmid","18439620"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/767"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Academic Press Ltd- Elsevier Science Ltd"],["dc.relation.eissn","1095-8584"],["dc.relation.issn","0022-2828"],["dc.title","Ranolazine improves diastolic dysfunction in isolated myocardium from failing human hearts - Role of late sodium current and intracellular ion accumulation"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]