[ { "key": "CCCR6ZRF", "version": 1, "library": { "type": "group", "id": 7574, "name": "AMC Heart Center", "links": { "alternate": { "href": "https://www.zotero.org/groups/amc_heart_center", "type": "text/html" } } }, "links": { "self": { "href": "https://api.zotero.org/groups/7574/items/CCCR6ZRF", "type": "application/json" }, "alternate": { "href": "https://www.zotero.org/groups/amc_heart_center/items/CCCR6ZRF", "type": "text/html" } }, "meta": { "createdByUser": { "id": 8053, "username": "jssgdejong", "name": "", "links": { "alternate": { "href": "https://www.zotero.org/jssgdejong", "type": "text/html" } } }, "creatorSummary": "Bhuiyan et al.", "parsedDate": "2009-05", "numChildren": 0 }, "data": { "key": "CCCR6ZRF", "version": 1, "itemType": "journalArticle", "title": "Clinical and genetic analysis of long QT syndrome in children from six families in Saudi Arabia: are they different?", "creators": [ { "creatorType": "author", "firstName": "Zahurul A", "lastName": "Bhuiyan" }, { "creatorType": "author", "firstName": "Safar", "lastName": "Al-Shahrani" }, { "creatorType": "author", "firstName": "Ayman S", "lastName": "Al-Khadra" }, { "creatorType": "author", "firstName": "Saleh", "lastName": "Al-Ghamdi" }, { "creatorType": "author", "firstName": "Khalaf", "lastName": "Al-Khalaf" }, { "creatorType": "author", "firstName": "Marcel M A M", "lastName": "Mannens" }, { "creatorType": "author", "firstName": "Arthur A M", "lastName": "Wilde" }, { "creatorType": "author", "firstName": "Tarek S", "lastName": "Momenah" } ], "abstractNote": "Congenital long QT syndrome (LQTS) is an inherited cardiac arrhythmia disorder characterized by prolongation of the QT interval; patients are predisposed to ventricular tachyarrhythmias and fibrillation leading to recurrent syncope or sudden cardiac death. We performed clinical and genetic studies in six Saudi Arabian families with a history of sudden unexplained death of children. Clinical symptoms, ECG phenotypes, and genetic findings led to the diagnosis of LQT1 in two families (recessive) and LQT2 in four families (three recessive and one dominant). Onset of arrhythmia was more severe in the recessive carriers and occurred during early childhood in all recessive LQT1 patients. Arrhythmia originated at the intrauterine stages of life in the recessive LQT2 patients. LQT1, causing mutation c.387-5 T > A in the KCNQ1 gene, and LQT2, causing mutation c.3208 C > T in the KCNH2 gene, are presumably founder mutations in the Assir province of Saudi Arabia. Further, all LQTS causing mutations detected in this study are novel and have not been reported in other populations.", "publicationTitle": "Pediatric Cardiology", "publisher": "", "place": "", "date": "May 2009", "volume": "30", "issue": "4", "section": "", "partNumber": "", "partTitle": "", "pages": "490-501", "series": "", "seriesTitle": "", "seriesText": "", "journalAbbreviation": "Pediatr Cardiol", "DOI": "10.1007/s00246-008-9377-y", "citationKey": "", "url": "http://www.ncbi.nlm.nih.gov/pubmed/19184172", "accessDate": "2009-11-12T22:53:09Z", "PMID": "", "PMCID": "", "ISSN": "1432-1971", "archive": "", "archiveLocation": "", "shortTitle": "Clinical and genetic analysis of long QT syndrome in children from six families in Saudi Arabia", "language": "", "libraryCatalog": "NCBI PubMed", "callNumber": "", "rights": "", "extra": "PMID: 19184172", "tags": [ { "tag": "Adolescent", "type": 1 }, { "tag": "Child", "type": 1 }, { "tag": "Child, Preschool", "type": 1 }, { "tag": "Death, Sudden, Cardiac", "type": 1 }, { "tag": "Female", "type": 1 }, { "tag": "Humans", "type": 1 }, { "tag": "Infant", "type": 1 }, { "tag": "Long QT Syndrome", "type": 1 }, { "tag": "Male", "type": 1 }, { "tag": "Pedigree", "type": 1 }, { "tag": "Saudi Arabia", "type": 1 } ], "collections": [], "relations": {}, "dateAdded": "2009-11-12T22:53:09Z", "dateModified": "2009-11-12T22:53:09Z" } }, { "key": "XTF2B7ZT", "version": 1, "library": { "type": "group", "id": 7574, "name": "AMC Heart Center", "links": { "alternate": { "href": "https://www.zotero.org/groups/amc_heart_center", "type": "text/html" } } }, "links": { "self": { "href": "https://api.zotero.org/groups/7574/items/XTF2B7ZT", "type": "application/json" }, "alternate": { "href": "https://www.zotero.org/groups/amc_heart_center/items/XTF2B7ZT", "type": "text/html" } }, "meta": { "createdByUser": { "id": 8053, "username": "jssgdejong", "name": "", "links": { "alternate": { "href": "https://www.zotero.org/jssgdejong", "type": "text/html" } } }, "creatorSummary": "van der Bilt et al.", "parsedDate": "2009-02-17", "numChildren": 0 }, "data": { "key": "XTF2B7ZT", "version": 1, "itemType": "journalArticle", "title": "Impact of cardiac complications on outcome after aneurysmal subarachnoid hemorrhage: a meta-analysis", "creators": [ { "creatorType": "author", "firstName": "I A C", "lastName": "van der Bilt" }, { "creatorType": "author", "firstName": "D", "lastName": "Hasan" }, { "creatorType": "author", "firstName": "W P", "lastName": "Vandertop" }, { "creatorType": "author", "firstName": "A A M", "lastName": "Wilde" }, { "creatorType": "author", "firstName": "A", "lastName": "Algra" }, { "creatorType": "author", "firstName": "F C", "lastName": "Visser" }, { "creatorType": "author", "firstName": "G J E", "lastName": "Rinkel" } ], "abstractNote": "Impact of cardiac complications after aneurysmal subarachnoid hemorrhage (SAH) remains controversial. We performed a meta-analysis to assess whether EKG changes, myocardial damage, or echocardiographic wall motion abnormalities (WMAs) are related to death, poor outcome (death or dependency), or delayed cerebral ischemia (DCI) after SAH. METHODS: Articles on cardiac abnormalities after aneurysmal SAH that met predefined criteria and were published between 1960 and 2007 were retrieved. We assessed the quality of reports and extracted data on patient characteristics, cardiac abnormalities, and outcome measurements. Poor outcome was defined as death or dependence by the Glasgow Outcome Scale (dichotomized at < or = 3) or the modified Rankin scale (dichotomized at > 3). If studies used another dichotomy or another outcome scale, we used the numbers of patients with poor outcome provided by the authors. We calculated pooled relative risks (RRs) with corresponding 95% confidence intervals for the relation between cardiac abnormalities and outcome measurements. RESULTS: We included 25 studies (16 prospective) with a total of 2,690 patients (mean age 53 years; 35% men). Mortality was associated with WMAs (RR 1.9), elevated troponin (RR 2.0) and brain natriuretic peptide (BNP) levels (RR 11.1), tachycardia (RR 3.9), Q waves (RR 2.9), ST-segment depression (RR 2.1), T-wave abnormalities (RR 1.8), and bradycardia (RR 0.6). Poor outcome was associated with elevated troponin (RR 2.3) and creatine kinase MB (CK-MB) levels (RR 2.3) and ST-segment depression (RR 2.4). Occurrence of DCI was associated with WMAs (RR 2.1), elevated troponin (RR 3.2), CK-MB (RR 2.9), and BNP levels (RR 4.5), and ST-segment depression (RR 2.4). All RRs were significant. CONCLUSION: Markers for cardiac damage and dysfunction are associated with an increased risk of death, poor outcome, and delayed cerebral ischemia after subarachnoid hemorrhage. Future research should establish whether these cardiac abnormalities are independent prognosticators and should be directed toward pathophysiologic mechanisms and potential treatment options.", "publicationTitle": "Neurology", "publisher": "", "place": "", "date": "Feb 17, 2009", "volume": "72", "issue": "7", "section": "", "partNumber": "", "partTitle": "", "pages": "635-642", "series": "", "seriesTitle": "", "seriesText": "", "journalAbbreviation": "Neurology", "DOI": "10.1212/01.wnl.0000342471.07290.07", "citationKey": "", "url": "http://www.ncbi.nlm.nih.gov/pubmed/19221297", "accessDate": "2009-11-12T22:53:02Z", "PMID": "", "PMCID": "", "ISSN": "1526-632X", "archive": "", "archiveLocation": "", "shortTitle": "Impact of cardiac complications on outcome after aneurysmal subarachnoid hemorrhage", "language": "", "libraryCatalog": "NCBI PubMed", "callNumber": "", "rights": "", "extra": "PMID: 19221297", "tags": [ { "tag": "Adult", "type": 1 }, { "tag": "Clinical Trials as Topic", "type": 1 }, { "tag": "Female", "type": 1 }, { "tag": "Heart Diseases", "type": 1 }, { "tag": "Humans", "type": 1 }, { "tag": "Male", "type": 1 }, { "tag": "Middle Aged", "type": 1 }, { "tag": "Risk Factors", "type": 1 }, { "tag": "Subarachnoid Hemorrhage", "type": 1 }, { "tag": "Treatment Outcome", "type": 1 } ], "collections": [], "relations": {}, "dateAdded": "2009-11-12T22:53:02Z", "dateModified": "2009-11-12T22:53:02Z" } }, { "key": "B79IREGG", "version": 1, "library": { "type": "group", "id": 7574, "name": "AMC Heart Center", "links": { "alternate": { "href": "https://www.zotero.org/groups/amc_heart_center", "type": "text/html" } } }, "links": { "self": { "href": "https://api.zotero.org/groups/7574/items/B79IREGG", "type": "application/json" }, "alternate": { "href": "https://www.zotero.org/groups/amc_heart_center/items/B79IREGG", "type": "text/html" } }, "meta": { "createdByUser": { "id": 8053, "username": "jssgdejong", "name": "", "links": { "alternate": { "href": "https://www.zotero.org/jssgdejong", "type": "text/html" } } }, "creatorSummary": "Meregalli et al.", "parsedDate": "2009-03", "numChildren": 0 }, "data": { "key": "B79IREGG", "version": 1, "itemType": "journalArticle", "title": "Type of SCN5A mutation determines clinical severity and degree of conduction slowing in loss-of-function sodium channelopathies", "creators": [ { "creatorType": "author", "firstName": "Paola G", "lastName": "Meregalli" }, { "creatorType": "author", "firstName": "Hanno L", "lastName": "Tan" }, { "creatorType": "author", "firstName": "Vincent", "lastName": "Probst" }, { "creatorType": "author", "firstName": "Tamara T", "lastName": "Koopmann" }, { "creatorType": "author", "firstName": "Michael W", "lastName": "Tanck" }, { "creatorType": "author", "firstName": "Zahurul A", "lastName": "Bhuiyan" }, { "creatorType": "author", "firstName": "Frederic", "lastName": "Sacher" }, { "creatorType": "author", "firstName": "Florence", "lastName": "Kyndt" }, { "creatorType": "author", "firstName": "Jean-Jacques", "lastName": "Schott" }, { "creatorType": "author", "firstName": "J", "lastName": "Albuisson" }, { "creatorType": "author", "firstName": "Philippe", "lastName": "Mabo" }, { "creatorType": "author", "firstName": "Connie R", "lastName": "Bezzina" }, { "creatorType": "author", "firstName": "Herve", "lastName": "Le Marec" }, { "creatorType": "author", "firstName": "Arthur A M", "lastName": "Wilde" } ], "abstractNote": "BACKGROUND: Patients carrying loss-of-function SCN5A mutations linked to Brugada syndrome (BrS) or progressive cardiac conduction disease (PCCD) are at risk of sudden cardiac death at a young age. The penetrance and expressivity of the disease are highly variable, and new tools for risk stratification are needed. OBJECTIVES: We aimed to establish whether the type of SCN5A mutation correlates with the clinical and electrocardiographic phenotype. METHODS: We studied BrS or PCCD probands and their relatives who carried a SCN5A mutation. Mutations were divided into 2 main groups: missense mutations (M) or mutations leading to premature truncation of the protein (T). The M group was subdivided according to available biophysical properties: M mutations with 90% (M(inactive)) peak I(Na) reduction were analyzed separately. RESULTS: The study group was composed of 147 individuals with 32 different mutations. No differences in age and sex distribution were found between the groups. Subjects carrying a T mutation had significantly more syncopes than those with an M(active) mutation (19 of 75 versus 2 of 35, P = .03). Also, mutations associated with drastic peak I(Na) reduction (T and M(inactive) mutants) had a significantly longer PR interval, compared with M(active) mutations. All other electrocardiographic parameters were comparable. After drug provocation testing, both PR and QRS intervals were significantly longer in the T and M(inactive) groups than in the M(active) group. CONCLUSION: In loss-of-function SCN5A channelopathies, patients carrying T and M(inactive) mutations develop a more severe phenotype than those with M(active) mutations. This is associated with more severe conduction disorders. This is the first time that genetic data are proposed for risk stratification in BrS.", "publicationTitle": "Heart Rhythm: The Official Journal of the Heart Rhythm Society", "publisher": "", "place": "", "date": "Mar 2009", "volume": "6", "issue": "3", "section": "", "partNumber": "", "partTitle": "", "pages": "341-348", "series": "", "seriesTitle": "", "seriesText": "", "journalAbbreviation": "Heart Rhythm", "DOI": "10.1016/j.hrthm.2008.11.009", "citationKey": "", "url": "http://www.ncbi.nlm.nih.gov/pubmed/19251209", "accessDate": "2009-11-12T22:52:54Z", "PMID": "", "PMCID": "", "ISSN": "1556-3871", "archive": "", "archiveLocation": "", "shortTitle": "", "language": "", "libraryCatalog": "NCBI PubMed", "callNumber": "", "rights": "", "extra": "PMID: 19251209", "tags": [ { "tag": "Adult", "type": 1 }, { "tag": "Arrhythmias, Cardiac", "type": 1 }, { "tag": "Brugada Syndrome", "type": 1 }, { "tag": "Codon, Terminator", "type": 1 }, { "tag": "Death, Sudden, Cardiac", "type": 1 }, { "tag": "Female", "type": 1 }, { "tag": "Heart Conduction System", "type": 1 }, { "tag": "Humans", "type": 1 }, { "tag": "Male", "type": 1 }, { "tag": "Middle Aged", "type": 1 }, { "tag": "Muscle Proteins", "type": 1 }, { "tag": "Mutation", "type": 1 }, { "tag": "Mutation, Missense", "type": 1 }, { "tag": "Phenotype", "type": 1 }, { "tag": "Risk Assessment", "type": 1 }, { "tag": "Sodium Channel Blockers", "type": 1 }, { "tag": "Sodium Channels", "type": 1 } ], "collections": [], "relations": {}, "dateAdded": "2009-11-12T22:52:54Z", "dateModified": "2009-11-12T22:52:54Z" } }, { "key": "M3ZPK8RI", "version": 1, "library": { "type": "group", "id": 7574, "name": "AMC Heart Center", "links": { "alternate": { "href": "https://www.zotero.org/groups/amc_heart_center", "type": "text/html" } } }, "links": { "self": { "href": "https://api.zotero.org/groups/7574/items/M3ZPK8RI", "type": "application/json" }, "alternate": { "href": "https://www.zotero.org/groups/amc_heart_center/items/M3ZPK8RI", "type": "text/html" } }, "meta": { "createdByUser": { "id": 8053, "username": "jssgdejong", "name": "", "links": { "alternate": { "href": "https://www.zotero.org/jssgdejong", "type": "text/html" } } }, "creatorSummary": "Kléber et al.", "parsedDate": "1986-01", "numChildren": 0 }, "data": { "key": "M3ZPK8RI", "version": 1, "itemType": "journalArticle", "title": "Changes in conduction velocity during acute ischemia in ventricular myocardium of the isolated porcine heart", "creators": [ { "creatorType": "author", "firstName": "A G", "lastName": "Kléber" }, { "creatorType": "author", "firstName": "M J", "lastName": "Janse" }, { "creatorType": "author", "firstName": "F J", "lastName": "Wilms-Schopmann" }, { "creatorType": "author", "firstName": "A A", "lastName": "Wilde" }, { "creatorType": "author", "firstName": "R", "lastName": "Coronel" } ], "abstractNote": "Conduction velocities along longitudinal (vL) and transverse (vT) fiber axes were determined in isolated porcine hearts from subepicardial activation patterns that were produced by local stimulation and measured with a multiterminal electrode. In some of the experiments extracellular [K+] ([K+]o) and transmembrane potentials were recorded. During normal perfusion vL and vT were (cm/sec) 50.08 +/- 2.13, (SE) and 21.08 +/- 0.97. After 3 to 5 min of global ischemia, vL and vT decreased to approximately 30 and 13 cm/sec. Before the occurrence of total inexcitability propagation became time dependent 2: 1 block developed and centrifugal spread from the stimulus site was partially blocked at short intervals and was normal at long intervals. This suggested that slowed conduction was dependent on spatial nonuniformities of recovery from excitability. Slowing of conduction during ischemia was not explained by accumulation of [K+]o alone, because vL and vT at a given [K+]o were lower during ischemia than during perfusion with elevated K+. In hearts perfused at 20 mM [K+]o \"slow responses\" were produced by addition of epinephrine (2.5 X 10(-5)M). Resting membrane potentials of slow responses were significantly lower than of depressed action potentials during ischemia. The values vL and vT of slow responses (10 and 5 cm/sec) were much lower than the lowest values during ischemia (20 and 10 cm/sec). This indicates that slow conduction in ischemia is associated with depressed action potentials initiated by a partially inactivated rapid Na+ inward current. The time dependence of nonuniform propagation and the relatively high conduction velocities explain two major characteristics of reentrant tachycardias in acute ischemia: the large diameters of reentrant circuits and the beat-to-beat changes in localization of conduction block.", "publicationTitle": "Circulation", "publisher": "", "place": "", "date": "Jan 1986", "volume": "73", "issue": "1", "section": "", "partNumber": "", "partTitle": "", "pages": "189-198", "series": "", "seriesTitle": "", "seriesText": "", "journalAbbreviation": "Circulation", "DOI": "", "citationKey": "", "url": "http://www.ncbi.nlm.nih.gov/pubmed/3940667", "accessDate": "2009-11-12T22:50:49Z", "PMID": "", "PMCID": "", "ISSN": "0009-7322", "archive": "", "archiveLocation": "", "shortTitle": "", "language": "", "libraryCatalog": "NCBI PubMed", "callNumber": "", "rights": "", "extra": "PMID: 3940667", "tags": [], "collections": [], "relations": {}, "dateAdded": "2009-11-12T22:50:49Z", "dateModified": "2009-11-12T22:50:49Z" } }, { "key": "NN7IQRUA", "version": 1, "library": { "type": "group", "id": 7574, "name": "AMC Heart Center", "links": { "alternate": { "href": "https://www.zotero.org/groups/amc_heart_center", "type": "text/html" } } }, "links": { "self": { "href": "https://api.zotero.org/groups/7574/items/NN7IQRUA", "type": "application/json" }, "alternate": { "href": "https://www.zotero.org/groups/amc_heart_center/items/NN7IQRUA", "type": "text/html" } }, "meta": { "createdByUser": { "id": 8053, "username": "jssgdejong", "name": "", "links": { "alternate": { "href": "https://www.zotero.org/jssgdejong", "type": "text/html" } } }, "creatorSummary": "Wilde and Kléber", "parsedDate": "1986-02", "numChildren": 0 }, "data": { "key": "NN7IQRUA", "version": 1, "itemType": "journalArticle", "title": "The combined effects of hypoxia, high K+, and acidosis on the intracellular sodium activity and resting potential in guinea pig papillary muscle", "creators": [ { "creatorType": "author", "firstName": "A A", "lastName": "Wilde" }, { "creatorType": "author", "firstName": "A G", "lastName": "Kléber" } ], "abstractNote": "Several reports have shown that electrical and ionic changes occurring in acute myocardial ischemia can be closely mimicked by exposure of tissue to hypoxic, acid-, and glucose-free solutions at elevated [K+]o. In the present work, this approach was chosen to distinguish between the combined effects of hypoxia, substrate withdrawal, and acidosis, and the effects of two different levels of [K+]o (4.7 mM and 11.5 mM) on intracellular sodium activity and resting membrane potential. Measurements were made with microelectrodes in isolated guinea pig papillary muscles. In normoxia at 4.7 mM [K+]o, intracellular sodium activity was 7.5 mM (+/- 1.9 mM, SD) during stimulation at 1 Hz. Combined hypoxia, substrate withdrawal, and acidosis increased intracellular sodium activity significantly, by 3-4 mM in 4.7 mM [K+]o and by approximately 2 mM in 11.5 mM [K+]o, after 9-10 minutes. Increasing [K+]o in normoxic solution decreased intracellular sodium activity by 1.9 mM (+/- 1.3 mM, SD). The transition from normal (4.7 mM [K+]o) Tyrode's solution to \"ischemic solution\" (hypoxia, acidosis, substrate withdrawal, 11.5 mM [K+]o) was associated with a small initial increase and a subsequent decrease of intracellular sodium activity. The steady state level after 12 minutes was not significantly different from the level in normal Tyrode's solution. The secondary decrease of intracellular sodium activity coincided with the gradual development of inexcitability and was absent in quiescent preparations. Combined hypoxia, acidosis, and glucose-withdrawal produced a depolarization by 7-10 mV at 4.7 mM and at 11.5 mM [K+]o, probably reflecting cellular potassium loss and extracellular potassium accumulation in the restricted extracellular space.(ABSTRACT TRUNCATED AT 250 WORDS)", "publicationTitle": "Circulation Research", "publisher": "", "place": "", "date": "Feb 1986", "volume": "58", "issue": "2", "section": "", "partNumber": "", "partTitle": "", "pages": "249-256", "series": "", "seriesTitle": "", "seriesText": "", "journalAbbreviation": "Circ. Res", "DOI": "", "citationKey": "", "url": "http://www.ncbi.nlm.nih.gov/pubmed/3948342", "accessDate": "2009-11-12T22:50:47Z", "PMID": "", "PMCID": "", "ISSN": "0009-7330", "archive": "", "archiveLocation": "", "shortTitle": "", "language": "", "libraryCatalog": "NCBI PubMed", "callNumber": "", "rights": "", "extra": "PMID: 3948342", "tags": [], "collections": [], "relations": {}, "dateAdded": "2009-11-12T22:50:47Z", "dateModified": "2009-11-12T22:50:47Z" } }, { "key": "HM3FFHCA", "version": 1, "library": { "type": "group", "id": 7574, "name": "AMC Heart Center", "links": { "alternate": { "href": "https://www.zotero.org/groups/amc_heart_center", "type": "text/html" } } }, "links": { "self": { "href": "https://api.zotero.org/groups/7574/items/HM3FFHCA", "type": "application/json" }, "alternate": { "href": "https://www.zotero.org/groups/amc_heart_center/items/HM3FFHCA", "type": "text/html" } }, "meta": { "createdByUser": { "id": 8053, "username": "jssgdejong", "name": "", "links": { "alternate": { "href": "https://www.zotero.org/jssgdejong", "type": "text/html" } } }, "creatorSummary": "Kleber and Wilde", "parsedDate": "1986-10", "numChildren": 0 }, "data": { "key": "HM3FFHCA", "version": 1, "itemType": "journalArticle", "title": "Regulation of intracellular sodium ions in acute reversible myocardial ischemia--a perspective", "creators": [ { "creatorType": "author", "firstName": "A G", "lastName": "Kleber" }, { "creatorType": "author", "firstName": "A A", "lastName": "Wilde" } ], "abstractNote": "", "publicationTitle": "Journal of Molecular and Cellular Cardiology", "publisher": "", "place": "", "date": "Oct 1986", "volume": "18 Suppl 4", "issue": "", "section": "", "partNumber": "", "partTitle": "", "pages": "27-30", "series": "", "seriesTitle": "", "seriesText": "", "journalAbbreviation": "J. Mol. Cell. Cardiol", "DOI": "", "citationKey": "", "url": "http://www.ncbi.nlm.nih.gov/pubmed/3023645", "accessDate": "2009-11-12T22:50:46Z", "PMID": "", "PMCID": "", "ISSN": "0022-2828", "archive": "", "archiveLocation": "", "shortTitle": "", "language": "", "libraryCatalog": "NCBI PubMed", "callNumber": "", "rights": "", "extra": "PMID: 3023645", "tags": [], "collections": [], "relations": {}, "dateAdded": "2009-11-12T22:50:46Z", "dateModified": "2009-11-12T22:50:46Z" } }, { "key": "6BEC8JPQ", "version": 1, "library": { "type": "group", "id": 7574, "name": "AMC Heart Center", "links": { "alternate": { "href": "https://www.zotero.org/groups/amc_heart_center", "type": "text/html" } } }, "links": { "self": { "href": "https://api.zotero.org/groups/7574/items/6BEC8JPQ", "type": "application/json" }, "alternate": { "href": "https://www.zotero.org/groups/amc_heart_center/items/6BEC8JPQ", "type": "text/html" } }, "meta": { "createdByUser": { "id": 8053, "username": "jssgdejong", "name": "", "links": { "alternate": { "href": "https://www.zotero.org/jssgdejong", "type": "text/html" } } }, "creatorSummary": "Wilensky et al.", "parsedDate": "1986-11", "numChildren": 0 }, "data": { "key": "6BEC8JPQ", "version": 1, "itemType": "journalArticle", "title": "The subendocardial border zone during acute ischemia of the rabbit heart: an electrophysiologic, metabolic, and morphologic correlative study", "creators": [ { "creatorType": "author", "firstName": "R L", "lastName": "Wilensky" }, { "creatorType": "author", "firstName": "J", "lastName": "Tranum-Jensen" }, { "creatorType": "author", "firstName": "R", "lastName": "Coronel" }, { "creatorType": "author", "firstName": "A A", "lastName": "Wilde" }, { "creatorType": "author", "firstName": "J W", "lastName": "Fiolet" }, { "creatorType": "author", "firstName": "M J", "lastName": "Janse" } ], "abstractNote": "Isolated preparations of rabbit interventricular septum were perfused through the coronary arteries with oxygenated Tyrode's solution and placed in a tissue bath where they were superfused as well. Transmembrane potentials were simultaneously recorded from the subendocardium with two flexibly mounted microelectrodes, one from a superficial cell, and the other from a deep cell. Ischemia was produced by stopping coronary flow while superfusion with oxygenated Tyrode's solution was maintained. After a 7 to 12 min ischemic period, the preparation was fixed by coronary perfusion with fixative while the microelectrodes remained in place. After fixation, the microelectrodes were withdrawn. Appropriate tissue blocks were cut in 4 micron serial sections and the microelectrode track was followed until the tip position was identified. Transmembrane potentials during ischemia were divided into two categories: \"border zone\" potentials (resting membrane potential [RMP] 73 +/- 3 mVe, action potential amplitude [APA] 81 +/- 13 mV, action potential duration [APD] 116 +/- 48 msec, n = 12) and \"ischemic\" potentials (RMP 53 +/- 4 mV, APA 44 +/- 11 mV, APD 102 +/- 42 msec, n = 8). Ischemic potentials were recorded from cells at depths greater than 560 micron below the endocardial surface and border zone potentials were recorded in a layer at between 130 and 650 micron below the surface. In a separate series of experiments, extracellular concentrations of K+ and pH were measured with ion-sensitive electrodes at different depths and, after a 10 min period of ischemia, part of the septum was placed in liquid nitrogen to allow determination of phosphocreatine (PC) levels in successive 50 to 100 micron layers. After 10 min of ischemia, extracellular K+ gradually increased from 4 to 9 mM in endocardium to a depth of 600 micron, pH fell from 7.4 to 6.6 over the same distance, and PC decreased to very low, stable levels at only 800 micron. It is concluded that in the first 10 min of acute ischemia, an endocardial border zone exists of 40 to 60 cell layers in which transmembrane potentials are affected relatively little by ischemia. Within this electrophysiologic border zone extracellular K+ was lower than 9 mM, pH was higher than 6.6, and tissue content of PC was not lower than 40% of normal. In layers deeper than 600 micron, with further development of a metabolic gradient, action potentials became markedly depressed. This electrophysiologic inhomogeneity within the ischemic subendocardium could be a factor in arrhythmogenesis during the first minutes of ischemia.", "publicationTitle": "Circulation", "publisher": "", "place": "", "date": "Nov 1986", "volume": "74", "issue": "5", "section": "", "partNumber": "", "partTitle": "", "pages": "1137-1146", "series": "", "seriesTitle": "", "seriesText": "", "journalAbbreviation": "Circulation", "DOI": "", "citationKey": "", "url": "http://www.ncbi.nlm.nih.gov/pubmed/3769171", "accessDate": "2009-11-12T22:50:44Z", "PMID": "", "PMCID": "", "ISSN": "0009-7322", "archive": "", "archiveLocation": "", "shortTitle": "The subendocardial border zone during acute ischemia of the rabbit heart", "language": "", "libraryCatalog": "NCBI PubMed", "callNumber": "", "rights": "", "extra": "PMID: 3769171", "tags": [], "collections": [], "relations": {}, "dateAdded": "2009-11-12T22:50:44Z", "dateModified": "2009-11-12T22:50:44Z" } }, { "key": "IS8GMWAI", "version": 1, "library": { "type": "group", "id": 7574, "name": "AMC Heart Center", "links": { "alternate": { "href": "https://www.zotero.org/groups/amc_heart_center", "type": "text/html" } } }, "links": { "self": { "href": "https://api.zotero.org/groups/7574/items/IS8GMWAI", "type": "application/json" }, "alternate": { "href": "https://www.zotero.org/groups/amc_heart_center/items/IS8GMWAI", "type": "text/html" } }, "meta": { "createdByUser": { "id": 8053, "username": "jssgdejong", "name": "", "links": { "alternate": { "href": "https://www.zotero.org/jssgdejong", "type": "text/html" } } }, "creatorSummary": "de Bakker et al.", "parsedDate": "1988-03", "numChildren": 0 }, "data": { "key": "IS8GMWAI", "version": 1, "itemType": "journalArticle", "title": "Reentry as a cause of ventricular tachycardia in patients with chronic ischemic heart disease: electrophysiologic and anatomic correlation", "creators": [ { "creatorType": "author", "firstName": "J M", "lastName": "de Bakker" }, { "creatorType": "author", "firstName": "F J", "lastName": "van Capelle" }, { "creatorType": "author", "firstName": "M J", "lastName": "Janse" }, { "creatorType": "author", "firstName": "A A", "lastName": "Wilde" }, { "creatorType": "author", "firstName": "R", "lastName": "Coronel" }, { "creatorType": "author", "firstName": "A E", "lastName": "Becker" }, { "creatorType": "author", "firstName": "K P", "lastName": "Dingemans" }, { "creatorType": "author", "firstName": "N M", "lastName": "van Hemel" }, { "creatorType": "author", "firstName": "R N", "lastName": "Hauer" } ], "abstractNote": "In this report we describe electrophysiologic and histologic findings in hearts and endocardially resected preparations from patients with sustained ventricular tachycardias in the chronic phase of myocardial infarction. We recorded simultaneously from 64 endocardial sites during tachycardia in 72 patients that were operated on for medically intractable ventricular tachycardias. Two other patients underwent heart transplantation, and mapping was performed on the explanted isolated heart connected to a Langendorff perfusion set-up. During operation 139 tachycardias with different morphologies could be induced. Although the majority of evidence supports the concept of a reentrant mechanism for these tachycardias, we found that 105 tachycardias appeared to arise at a focal area of less than 1.4 cm2. In only three cases macroreentry around the infarction scar could be detected. Of 21 tachycardias in which the \"origin\" appeared to be focal, earliest subendocardial activation was preceded by discrete electrograms of low amplitude (presystolic activity). In three tachycardias presystolic activity was detected at several sites, permitting reconstruction of its route. Histology of the endocardial resected preparation in one of these cases revealed separate zones of viable myocardial fibers in areas in which presystolic activity was recorded. These zones were located intramurally and subendocardially, supporting the concept that reentry occurred via isolated bundles of surviving myocytes at the border of the infarct and the larger subendocardial muscle mass. Conduction velocity through the isolated tracts was on the order of 25 cm/sec. Similar reentrant pathways were found in the two isolated hearts. Extracellular and intracellular recordings were made from 20 endocardial preparations that were excised from areas in which tachycardia originated. Preparations were superfused in a tissue bath. These experiments showed that action potentials were usually close to normal, but occasionally action potentials with reduced amplitude and slow upstrokes were found. In addition, there were cells that exhibited both fast and slow upstrokes, depending on the direction of the wavefront. Histology of seven resected preparations and the isolated hearts showed subendocardially as well as intramurally located zones of viable myocardium. Fractionation of extracellular electrograms and slow conduction were found in areas where surviving muscle fibers and strands of fibrous tissue were interwoven, and in zones where muscle fibers were oriented in parallel but isolated by strands of connective tissue.(ABSTRACT TRUNCATED AT 400 WORDS)", "publicationTitle": "Circulation", "publisher": "", "place": "", "date": "Mar 1988", "volume": "77", "issue": "3", "section": "", "partNumber": "", "partTitle": "", "pages": "589-606", "series": "", "seriesTitle": "", "seriesText": "", "journalAbbreviation": "Circulation", "DOI": "", "citationKey": "", "url": "http://www.ncbi.nlm.nih.gov/pubmed/3342490", "accessDate": "2009-11-12T22:50:42Z", "PMID": "", "PMCID": "", "ISSN": "0009-7322", "archive": "", "archiveLocation": "", "shortTitle": "Reentry as a cause of ventricular tachycardia in patients with chronic ischemic heart disease", "language": "", "libraryCatalog": "NCBI PubMed", "callNumber": "", "rights": "", "extra": "PMID: 3342490", "tags": [], "collections": [], "relations": {}, "dateAdded": "2009-11-12T22:50:42Z", "dateModified": "2009-11-12T22:50:42Z" } }, { "key": "VBM7M64K", "version": 1, "library": { "type": "group", "id": 7574, "name": "AMC Heart Center", "links": { "alternate": { "href": "https://www.zotero.org/groups/amc_heart_center", "type": "text/html" } } }, "links": { "self": { "href": "https://api.zotero.org/groups/7574/items/VBM7M64K", "type": "application/json" }, "alternate": { "href": "https://www.zotero.org/groups/amc_heart_center/items/VBM7M64K", "type": "text/html" } }, "meta": { "createdByUser": { "id": 8053, "username": "jssgdejong", "name": "", "links": { "alternate": { "href": "https://www.zotero.org/jssgdejong", "type": "text/html" } } }, "creatorSummary": "Wilde et al.", "parsedDate": "1988-10", "numChildren": 0 }, "data": { "key": "VBM7M64K", "version": 1, "itemType": "journalArticle", "title": "Catecholamine release and potassium accumulation in the isolated globally ischemic rabbit heart", "creators": [ { "creatorType": "author", "firstName": "A A", "lastName": "Wilde" }, { "creatorType": "author", "firstName": "R J", "lastName": "Peters" }, { "creatorType": "author", "firstName": "M J", "lastName": "Janse" } ], "abstractNote": "The relation between the release of endogenous catecholamines and the rise in extracellular potassium concentration [( K+]0) was studied during global ischemia in the isolated perfused rabbit heart. An increase in release of catecholamines was observed only after ischemic periods longer than 10 min. In agreement with other studies, [K+]0 initially rose until a plateau phase was established after 8 min. During this phase [K+]0 actually decreased in several hearts. In these hearts, lactate release was larger (116.9 +/- 22.4 mumol/g dry wt, n = 5) than in hearts in which no decrease in [K+]0 was observed (83.3 +/- 16.0 mumol/g dry wt, n = 6). Blockade of the alpha- and beta-adrenoceptors by phentolamine (5 x 10(-6) M) and propranolol (10(-6) M), respectively, prevented the decrease in [K+]0. These findings show that the secondary decrease in [K+]0 is associated with increased glycolytic flux. Moreover, catecholamines are a prerequisite for this decrease and are frequently observed between 8 and 15 min of ischemia.", "publicationTitle": "Journal of Molecular and Cellular Cardiology", "publisher": "", "place": "", "date": "Oct 1988", "volume": "20", "issue": "10", "section": "", "partNumber": "", "partTitle": "", "pages": "887-896", "series": "", "seriesTitle": "", "seriesText": "", "journalAbbreviation": "J. Mol. Cell. Cardiol", "DOI": "", "citationKey": "", "url": "http://www.ncbi.nlm.nih.gov/pubmed/3216399", "accessDate": "2009-11-12T22:50:39Z", "PMID": "", "PMCID": "", "ISSN": "0022-2828", "archive": "", "archiveLocation": "", "shortTitle": "", "language": "", "libraryCatalog": "NCBI PubMed", "callNumber": "", "rights": "", "extra": "PMID: 3216399", "tags": [], "collections": [], "relations": {}, "dateAdded": "2009-11-12T22:50:39Z", "dateModified": "2009-11-12T22:50:39Z" } }, { "key": "GGICQIUS", "version": 1, "library": { "type": "group", "id": 7574, "name": "AMC Heart Center", "links": { "alternate": { "href": "https://www.zotero.org/groups/amc_heart_center", "type": "text/html" } } }, "links": { "self": { "href": "https://api.zotero.org/groups/7574/items/GGICQIUS", "type": "application/json" }, "alternate": { "href": "https://www.zotero.org/groups/amc_heart_center/items/GGICQIUS", "type": "text/html" } }, "meta": { "createdByUser": { "id": 8053, "username": "jssgdejong", "name": "", "links": { "alternate": { "href": "https://www.zotero.org/jssgdejong", "type": "text/html" } } }, "creatorSummary": "Wilde et al.", "parsedDate": "1989", "numChildren": 0 }, "data": { "key": "GGICQIUS", "version": 1, "itemType": "journalArticle", "title": "Glibenclamide inhibition of ATP-sensitive K+ channels and ischemia-induced K+ accumulation in the mammalian heart", "creators": [ { "creatorType": "author", "firstName": "A A", "lastName": "Wilde" }, { "creatorType": "author", "firstName": "D", "lastName": "Escande" }, { "creatorType": "author", "firstName": "C A", "lastName": "Schumacher" }, { "creatorType": "author", "firstName": "D", "lastName": "Thuringer" }, { "creatorType": "author", "firstName": "M", "lastName": "Mestre" }, { "creatorType": "author", "firstName": "J W", "lastName": "Fiolet" } ], "abstractNote": "", "publicationTitle": "Pflügers Archiv: European Journal of Physiology", "publisher": "", "place": "", "date": "1989", "volume": "414 Suppl 1", "issue": "", "section": "", "partNumber": "", "partTitle": "", "pages": "S176", "series": "", "seriesTitle": "", "seriesText": "", "journalAbbreviation": "Pflugers Arch", "DOI": "", "citationKey": "", "url": "http://www.ncbi.nlm.nih.gov/pubmed/2506522", "accessDate": "2009-11-12T22:50:38Z", "PMID": "", "PMCID": "", "ISSN": "0031-6768", "archive": "", "archiveLocation": "", "shortTitle": "", "language": "", "libraryCatalog": "NCBI PubMed", "callNumber": "", "rights": "", "extra": "PMID: 2506522", "tags": [], "collections": [], "relations": {}, "dateAdded": "2009-11-12T22:50:38Z", "dateModified": "2009-11-12T22:50:38Z" } }, { "key": "72TQF9A4", "version": 1, "library": { "type": "group", "id": 7574, "name": "AMC Heart Center", "links": { "alternate": { "href": "https://www.zotero.org/groups/amc_heart_center", "type": "text/html" } } }, "links": { "self": { "href": "https://api.zotero.org/groups/7574/items/72TQF9A4", "type": "application/json" }, "alternate": { "href": "https://www.zotero.org/groups/amc_heart_center/items/72TQF9A4", "type": "text/html" } }, "meta": { "createdByUser": { "id": 8053, "username": "jssgdejong", "name": "", "links": { "alternate": { "href": "https://www.zotero.org/jssgdejong", "type": "text/html" } } }, "creatorSummary": "de Bakker et al.", "parsedDate": "1990-06", "numChildren": 0 }, "data": { "key": "72TQF9A4", "version": 1, "itemType": "journalArticle", "title": "Ventricular tachycardia in the infarcted, Langendorff-perfused human heart: role of the arrangement of surviving cardiac fibers", "creators": [ { "creatorType": "author", "firstName": "J M", "lastName": "de Bakker" }, { "creatorType": "author", "firstName": "R", "lastName": "Coronel" }, { "creatorType": "author", "firstName": "S", "lastName": "Tasseron" }, { "creatorType": "author", "firstName": "A A", "lastName": "Wilde" }, { "creatorType": "author", "firstName": "T", "lastName": "Opthof" }, { "creatorType": "author", "firstName": "M J", "lastName": "Janse" }, { "creatorType": "author", "firstName": "F J", "lastName": "van Capelle" }, { "creatorType": "author", "firstName": "A E", "lastName": "Becker" }, { "creatorType": "author", "firstName": "G", "lastName": "Jambroes" } ], "abstractNote": "Electrophysiologic and histologic studies were performed on Langendorff-perfused human hearts from patients who underwent heart transplantation because of extensive infarction. In nine hearts, 15 sustained ventricular tachycardias could be induced by programmed stimulation. In all hearts, mapping of epicardial and endocardial electrical activity during tachycardia was carried out. Histologic examination of the infarcted area between the site of latest activation of one cycle and the site of earliest activation of the next cycle revealed zones of viable myocardial tissue. In two hearts in which the time gap between latest and earliest activation was small, surviving myocardial tissue constituted a continuous tract that traversed the infarct. In three other hearts in which the time gap was large, surviving tissue consisted of parallel bundles that coursed separately over a few hundred micrometers, then merged into a single bundle and finally branched again. The direction of the fibers within the bundles was perpendicular to the direction of the activation front in that area. A similar type of inhomogeneous anisotrophy and activation delay was found in an infarcted papillary muscle removed from one of the explanted hearts and studied in a tissue bath during basic stimulation. Histologic examination of this preparation revealed that the delay was caused by a zigzag route of activation over branching and merging bundles of surviving myocytes separated by connective tissue.", "publicationTitle": "Journal of the American College of Cardiology", "publisher": "", "place": "", "date": "Jun 1990", "volume": "15", "issue": "7", "section": "", "partNumber": "", "partTitle": "", "pages": "1594-1607", "series": "", "seriesTitle": "", "seriesText": "", "journalAbbreviation": "J. Am. Coll. Cardiol", "DOI": "", "citationKey": "", "url": "http://www.ncbi.nlm.nih.gov/pubmed/2345240", "accessDate": "2009-11-12T22:50:37Z", "PMID": "", "PMCID": "", "ISSN": "0735-1097", "archive": "", "archiveLocation": "", "shortTitle": "Ventricular tachycardia in the infarcted, Langendorff-perfused human heart", "language": "", "libraryCatalog": "NCBI PubMed", "callNumber": "", "rights": "", "extra": "PMID: 2345240", "tags": [], "collections": [], "relations": {}, "dateAdded": "2009-11-12T22:50:37Z", "dateModified": "2009-11-12T22:50:37Z" } }, { "key": "WWIPG3PC", "version": 1, "library": { "type": "group", "id": 7574, "name": "AMC Heart Center", "links": { "alternate": { "href": "https://www.zotero.org/groups/amc_heart_center", "type": "text/html" } } }, "links": { "self": { "href": "https://api.zotero.org/groups/7574/items/WWIPG3PC", "type": "application/json" }, "alternate": { "href": "https://www.zotero.org/groups/amc_heart_center/items/WWIPG3PC", "type": "text/html" } }, "meta": { "createdByUser": { "id": 8053, "username": "jssgdejong", "name": "", "links": { "alternate": { "href": "https://www.zotero.org/jssgdejong", "type": "text/html" } } }, "creatorSummary": "Wilde et al.", "parsedDate": "1990-10", "numChildren": 0 }, "data": { "key": "WWIPG3PC", "version": 1, "itemType": "journalArticle", "title": "Potassium accumulation in the globally ischemic mammalian heart. A role for the ATP-sensitive potassium channel", "creators": [ { "creatorType": "author", "firstName": "A A", "lastName": "Wilde" }, { "creatorType": "author", "firstName": "D", "lastName": "Escande" }, { "creatorType": "author", "firstName": "C A", "lastName": "Schumacher" }, { "creatorType": "author", "firstName": "D", "lastName": "Thuringer" }, { "creatorType": "author", "firstName": "M", "lastName": "Mestre" }, { "creatorType": "author", "firstName": "J W", "lastName": "Fiolet" }, { "creatorType": "author", "firstName": "M J", "lastName": "Janse" } ], "abstractNote": "We investigated the contribution of opening of the ATP-sensitive K+ channel to extracellular accumulation of K+ during ischemia with the use of glibenclamide, a specific blocker of this K+ channel. To characterize the electrophysiological effects of glibenclamide during metabolic inhibition (by either application of dinitrophenol or hypoxia) we performed patch-clamp studies in isolated membrane patches of guinea pig myocytes and in intact guinea pig myocytes and studied action potential parameters in isolated superfused guinea pig papillary muscle. We studied the effect of glibenclamide on extracellular accumulation of K+ and H+ in isolated retrogradely perfused globally ischemic hearts of rat, guinea pig, and rabbit. Experimental evidence is presented that supports the conclusions that glibenclamide 1) effectively blocks open K+ATP channels, 2) reverses the dinitrophenol-induced increase of the outward current and prevents the hypoxia-induced shortening of the action potential, 3) decreases the rate of K+ accumulation during the first minutes of ischemia in stimulated hearts, an effect which was entirely absent in quiescent hearts, and 4) does not influence the rate and extent of ischemia-induced extracellular acidification.", "publicationTitle": "Circulation Research", "publisher": "", "place": "", "date": "Oct 1990", "volume": "67", "issue": "4", "section": "", "partNumber": "", "partTitle": "", "pages": "835-843", "series": "", "seriesTitle": "", "seriesText": "", "journalAbbreviation": "Circ. Res", "DOI": "", "citationKey": "", "url": "http://www.ncbi.nlm.nih.gov/pubmed/2119912", "accessDate": "2009-11-12T22:50:33Z", "PMID": "", "PMCID": "", "ISSN": "0009-7330", "archive": "", "archiveLocation": "", "shortTitle": "", "language": "", "libraryCatalog": "NCBI PubMed", "callNumber": "", "rights": "", "extra": "PMID: 2119912", "tags": [], "collections": [], "relations": {}, "dateAdded": "2009-11-12T22:50:33Z", "dateModified": "2009-11-12T22:50:33Z" } }, { "key": "KERIBFSV", "version": 1, "library": { "type": "group", "id": 7574, "name": "AMC Heart Center", "links": { "alternate": { "href": "https://www.zotero.org/groups/amc_heart_center", "type": "text/html" } } }, "links": { "self": { "href": "https://api.zotero.org/groups/7574/items/KERIBFSV", "type": "application/json" }, "alternate": { "href": "https://www.zotero.org/groups/amc_heart_center/items/KERIBFSV", "type": "text/html" } }, "meta": { "createdByUser": { "id": 8053, "username": "jssgdejong", "name": "", "links": { "alternate": { "href": "https://www.zotero.org/jssgdejong", "type": "text/html" } } }, "creatorSummary": "Wilde and Kléber", "parsedDate": "1991-05", "numChildren": 0 }, "data": { "key": "KERIBFSV", "version": 1, "itemType": "journalArticle", "title": "Effect of norepinephrine and heart rate on intracellular sodium activity and membrane potential in beating guinea pig ventricular muscle", "creators": [ { "creatorType": "author", "firstName": "A A", "lastName": "Wilde" }, { "creatorType": "author", "firstName": "A G", "lastName": "Kléber" } ], "abstractNote": "The effect of 3 microM norepinephrine (NE) on intracellular sodium activity (aiNa) and resting membrane potential was studied by continuous intracellular recordings with a conventional and an ion-selective microelectrode. The electrodes were impaled simultaneously in small (diameter, 0.3 mm) superfused trabeculae of the beating guinea pig ventricle at 37 degrees C. In the absence of NE, changes of the beating rate produced an increase of aiNa by 1.5 +/- 0.17 mM (from 0 to 1 Hz) and 1.9 +/- 0.47 mM (from 0 to 2 Hz). In the presence of NE, there was a very small significant increase of aiNa during constant stimulation (1 Hz) and at at [K+]o of 4.7 and 11.5 mM. After 7 minutes of exposure, aiNa increased by 0.5 +/- 0.19 mM (mean +/- SEM, n = 4) at [K+]o of 4.7 mM and by 0.5 +/- 0.22 (n = 6) at [K+]o of 11.5 mM. Resting membrane potential became more positive by 1 mV at both levels of [K+]o. The effect of NE became also clearly manifest from the configurational changes of action potentials (profound increase in plateau height and duration). Stimulation of the Na(+)-K+ pump by NE became manifest from the changes of resting membrane potential and aiNa after abrupt cessation of stimulation. The magnitude and the rate of the decrease in aiNa and the initial rate of hyperpolarization were significantly greater in the presence of NE than in its absence.(ABSTRACT TRUNCATED AT 250 WORDS)", "publicationTitle": "Circulation Research", "publisher": "", "place": "", "date": "May 1991", "volume": "68", "issue": "5", "section": "", "partNumber": "", "partTitle": "", "pages": "1482-1489", "series": "", "seriesTitle": "", "seriesText": "", "journalAbbreviation": "Circ. Res", "DOI": "", "citationKey": "", "url": "http://www.ncbi.nlm.nih.gov/pubmed/2019003", "accessDate": "2009-11-12T22:50:30Z", "PMID": "", "PMCID": "", "ISSN": "0009-7330", "archive": "", "archiveLocation": "", "shortTitle": "", "language": "", "libraryCatalog": "NCBI PubMed", "callNumber": "", "rights": "", "extra": "PMID: 2019003", "tags": [], "collections": [], "relations": {}, "dateAdded": "2009-11-12T22:50:30Z", "dateModified": "2009-11-12T22:50:30Z" } }, { "key": "IM9PVXKA", "version": 1, "library": { "type": "group", "id": 7574, "name": "AMC Heart Center", "links": { "alternate": { "href": "https://www.zotero.org/groups/amc_heart_center", "type": "text/html" } } }, "links": { "self": { "href": "https://api.zotero.org/groups/7574/items/IM9PVXKA", "type": "application/json" }, "alternate": { "href": "https://www.zotero.org/groups/amc_heart_center/items/IM9PVXKA", "type": "text/html" } }, "meta": { "createdByUser": { "id": 8053, "username": "jssgdejong", "name": "", "links": { "alternate": { "href": "https://www.zotero.org/jssgdejong", "type": "text/html" } } }, "creatorSummary": "Hauer et al.", "parsedDate": "1991-07", "numChildren": 0 }, "data": { "key": "IM9PVXKA", "version": 1, "itemType": "journalArticle", "title": "Ventricular tachycardia after in vivo DC shock ablation in dogs. Electrophysiologic and histologic correlation", "creators": [ { "creatorType": "author", "firstName": "R N", "lastName": "Hauer" }, { "creatorType": "author", "firstName": "J M", "lastName": "de Bakker" }, { "creatorType": "author", "firstName": "A A", "lastName": "de Wilde" }, { "creatorType": "author", "firstName": "W", "lastName": "Straks" }, { "creatorType": "author", "firstName": "J T", "lastName": "Vermeulen" }, { "creatorType": "author", "firstName": "M J", "lastName": "Janse" } ], "abstractNote": "BACKGROUND. DC shock catheter ablation for the treatment of ventricular tachycardia (VT) may induce VT episodes that disappear within days. METHODS AND RESULTS. A 30-J cathodal shock was delivered to the endocardial left ventricular wall in 15 closed-chest dogs. All dogs had VT during the first day after ablation. Eleven of these dogs were studied on the first day. Extensive epicardial and endocardial activation mapping in vivo, in Langendorff-perfused hearts, and in tissue blocks in a tissue bath localized the site of origin of VT to subendocardial Purkinje fibers in a border zone surrounding the central necrotic ablation lesion. Intracellular recording showed that this zone consisted of a subendocardial superficial layer (SSL) of cells with abnormal characteristics, a resting membrane potential (RMP) of -58 +/- 11 mV (mean +/- SD), and an action potential amplitude (APA) of 61 +/- 20 mV. In addition, the steepness of phase 0 of the action potential was markedly reduced. In three dogs abnormal automaticity was found in a very small area. Immediately below the SSL, cells were normal with an RMP of -78 +/- 5 mV and an APA of 107 +/- 8 mV. Histology confirmed a thin SSL with edematous and necrotic cells, hemorrhage, and infiltration. The other four dogs were studied at 1 week after ablation when VT was absent. Microelectrode impalement in the SSL was either impossible or showed nearly normal action potential characteristics. Histological examination showed a markedly thickened fibrotic subendocardial layer at places where impalement was impossible. Normal subendocardium was found in other areas of the border zone. CONCLUSIONS. Our results indicate that VT after DC shock ablation originates from cells with abnormal automaticity in the superficial subendocardial border zone around the central ablation lesion. Within 1 week edematous and necrotic cells in this border zone are replaced by a fibrotic layer, and this transition is associated with the disappearance of VT.", "publicationTitle": "Circulation", "publisher": "", "place": "", "date": "Jul 1991", "volume": "84", "issue": "1", "section": "", "partNumber": "", "partTitle": "", "pages": "267-278", "series": "", "seriesTitle": "", "seriesText": "", "journalAbbreviation": "Circulation", "DOI": "", "citationKey": "", "url": "http://www.ncbi.nlm.nih.gov/pubmed/2060100", "accessDate": "2009-11-12T22:50:28Z", "PMID": "", "PMCID": "", "ISSN": "0009-7322", "archive": "", "archiveLocation": "", "shortTitle": "", "language": "", "libraryCatalog": "NCBI PubMed", "callNumber": "", "rights": "", "extra": "PMID: 2060100", "tags": [], "collections": [], "relations": {}, "dateAdded": "2009-11-12T22:50:28Z", "dateModified": "2009-11-12T22:50:28Z" } }, { "key": "GENKG3T8", "version": 1, "library": { "type": "group", "id": 7574, "name": "AMC Heart Center", "links": { "alternate": { "href": "https://www.zotero.org/groups/amc_heart_center", "type": "text/html" } } }, "links": { "self": { "href": "https://api.zotero.org/groups/7574/items/GENKG3T8", "type": "application/json" }, "alternate": { "href": "https://www.zotero.org/groups/amc_heart_center/items/GENKG3T8", "type": "text/html" } }, "meta": { "createdByUser": { "id": 8053, "username": "jssgdejong", "name": "", "links": { "alternate": { "href": "https://www.zotero.org/jssgdejong", "type": "text/html" } } }, "creatorSummary": "Tranum-Jensen et al.", "parsedDate": "1991-08", "numChildren": 0 }, "data": { "key": "GENKG3T8", "version": 1, "itemType": "journalArticle", "title": "Morphology of electrophysiologically identified junctions between Purkinje fibers and ventricular muscle in rabbit and pig hearts", "creators": [ { "creatorType": "author", "firstName": "J", "lastName": "Tranum-Jensen" }, { "creatorType": "author", "firstName": "A A", "lastName": "Wilde" }, { "creatorType": "author", "firstName": "J T", "lastName": "Vermeulen" }, { "creatorType": "author", "firstName": "M J", "lastName": "Janse" } ], "abstractNote": "Purkinje fiber-ventricular muscle (PV) junctions were identified by extracellular recording in isolated, superfused preparations from rabbit and pig hearts. Microelectrode recordings from different cell types at the PV junctions were obtained, and the cells recorded from were retrieved microscopically. To this end 26 tissue blocks were serially sectioned at 4 microns. Microscopic identification of the very cell recorded from was obtained in five of seven Purkinje, five of 16 transitional, and two of two ventricular muscle cell recordings. In addition, some tissue blocks from both junctional and nonjunctional sites identified only by extracellular recording were examined in serial sections. Transitional cells in the rabbit heart are thin, broad bandlike cells (30-35 by 3-5 microns) arranged in one or two sheets in the subendocardium between the Purkinje layer and ventricular mass. Transitional cells are coupled via short, thin strands to both Purkinje and ventricular muscle cells. A second type of PV coupling was observed frequently in the pig, but in only one of 21 cases in the rabbit. Here, a short, linear segment of small transitional cells connected large-diameter Purkinje cells to ventricular muscle cells. Distances found between Purkinje-transitional cell coupling sites and transitional cell-ventricular muscle coupling sites varied from 100 to 1,000 microns in the rabbit heart and from 50 to several hundred micrometers in the pig heart. Action potentials from transitional cells typically showed multiple components in their upstroke. Both our morphological and electrophysiological findings are compatible with the existence of a relatively high-resistance barrier between Purkinje and transitional cells and between transitional and ventricular muscle cells.", "publicationTitle": "Circulation Research", "publisher": "", "place": "", "date": "Aug 1991", "volume": "69", "issue": "2", "section": "", "partNumber": "", "partTitle": "", "pages": "429-437", "series": "", "seriesTitle": "", "seriesText": "", "journalAbbreviation": "Circ. Res", "DOI": "", "citationKey": "", "url": "http://www.ncbi.nlm.nih.gov/pubmed/1860183", "accessDate": "2009-11-12T22:50:24Z", "PMID": "", "PMCID": "", "ISSN": "0009-7330", "archive": "", "archiveLocation": "", "shortTitle": "", "language": "", "libraryCatalog": "NCBI PubMed", "callNumber": "", "rights": "", "extra": "PMID: 1860183", "tags": [], "collections": [], "relations": {}, "dateAdded": "2009-11-12T22:50:24Z", "dateModified": "2009-11-12T22:50:24Z" } }, { "key": "PFTCRU72", "version": 1, "library": { "type": "group", "id": 7574, "name": "AMC Heart Center", "links": { "alternate": { "href": "https://www.zotero.org/groups/amc_heart_center", "type": "text/html" } } }, "links": { "self": { "href": "https://api.zotero.org/groups/7574/items/PFTCRU72", "type": "application/json" }, "alternate": { "href": "https://www.zotero.org/groups/amc_heart_center/items/PFTCRU72", "type": "text/html" } }, "meta": { "createdByUser": { "id": 8053, "username": "jssgdejong", "name": "", "links": { "alternate": { "href": "https://www.zotero.org/jssgdejong", "type": "text/html" } } }, "creatorSummary": "de Jong et al.", "parsedDate": "1992-08", "numChildren": 0 }, "data": { "key": "PFTCRU72", "version": 1, "itemType": "journalArticle", "title": "Persisting zones of slow impulse conduction in developing chicken hearts", "creators": [ { "creatorType": "author", "firstName": "F", "lastName": "de Jong" }, { "creatorType": "author", "firstName": "T", "lastName": "Opthof" }, { "creatorType": "author", "firstName": "A A", "lastName": "Wilde" }, { "creatorType": "author", "firstName": "M J", "lastName": "Janse" }, { "creatorType": "author", "firstName": "R", "lastName": "Charles" }, { "creatorType": "author", "firstName": "W H", "lastName": "Lamers" }, { "creatorType": "author", "firstName": "A F", "lastName": "Moorman" } ], "abstractNote": "We performed a correlative electrophysiological and immunohistochemical study of embryonic chicken hearts during the septational period (Hamburger and Hamilton stages 13-31 [2-7 days of incubation]). The analyses yield conclusive evidence for slow conduction, up to 7 days of development, in the outflow tract, in the atrioventricular canal, and in the sinoatrial junction. The conduction velocity remains approximately 1 cm/sec in the outflow tract and increases in the ventricle 20-fold to approximately 20 cm/sec between 2 and 7 days of development. Transmembrane potentials of myocytes in the outflow tract and atrioventricular canal slowly rise (less than 5 V/sec), whereas in the atrium and ventricle, the upstroke velocity is eightfold to 13-fold higher. In the outflow tract, repolarization is completed only after the start of the next cycle. Because of the persistence of slow conduction, the myocardium flanking the developing atria and ventricle is thought to represent segments of persisting \"primary\" myocardium, whereas the more rapidly conducting \"working\" myocardium of the ventricle and atria is thought to represent more advanced stages of myocardial differentiation. The persisting primary myocardium was characterized by a continued coexpression of both the atrial and ventricular isoforms of myosin heavy chain. The developing atria and ventricle could be demarcated morphologically from the primary myocardium because the free walls of these segments only express their respective isoforms of myosin heavy chain. The slowly conducting myocardial zones appear to be essential for the function of the embryonic heart because 1) they provide the septating heart with alternating segments of slow and relatively fast conduction necessary for consecutive contraction of the atrial and ventricular segments and 2) their sphincterlike prolonged peristaltic contraction pattern can substitute for the adult type of one-way valves that start to develop at the end of septation.", "publicationTitle": "Circulation Research", "publisher": "", "place": "", "date": "Aug 1992", "volume": "71", "issue": "2", "section": "", "partNumber": "", "partTitle": "", "pages": "240-250", "series": "", "seriesTitle": "", "seriesText": "", "journalAbbreviation": "Circ. Res", "DOI": "", "citationKey": "", "url": "http://www.ncbi.nlm.nih.gov/pubmed/1628384", "accessDate": "2009-11-12T22:50:21Z", "PMID": "", "PMCID": "", "ISSN": "0009-7330", "archive": "", "archiveLocation": "", "shortTitle": "", "language": "", "libraryCatalog": "NCBI PubMed", "callNumber": "", "rights": "", "extra": "PMID: 1628384", "tags": [], "collections": [], "relations": {}, "dateAdded": "2009-11-12T22:50:21Z", "dateModified": "2009-11-12T22:50:21Z" } }, { "key": "ATN72TR2", "version": 1, "library": { "type": "group", "id": 7574, "name": "AMC Heart Center", "links": { "alternate": { "href": "https://www.zotero.org/groups/amc_heart_center", "type": "text/html" } } }, "links": { "self": { "href": "https://api.zotero.org/groups/7574/items/ATN72TR2", "type": "application/json" }, "alternate": { "href": "https://www.zotero.org/groups/amc_heart_center/items/ATN72TR2", "type": "text/html" } }, "meta": { "createdByUser": { "id": 8053, "username": "jssgdejong", "name": "", "links": { "alternate": { "href": "https://www.zotero.org/jssgdejong", "type": "text/html" } } }, "creatorSummary": "Wilde", "parsedDate": "1992-11", "numChildren": 0 }, "data": { "key": "ATN72TR2", "version": 1, "itemType": "journalArticle", "title": "KATP channel opening and cardioprotection", "creators": [ { "creatorType": "author", "firstName": "A A", "lastName": "Wilde" } ], "abstractNote": "", "publicationTitle": "Cardiovascular Research", "publisher": "", "place": "", "date": "Nov 1992", "volume": "26", "issue": "11", "section": "", "partNumber": "", "partTitle": "", "pages": "1156-1157", "series": "", "seriesTitle": "", "seriesText": "", "journalAbbreviation": "Cardiovasc. Res", "DOI": "", "citationKey": "", "url": "http://www.ncbi.nlm.nih.gov/pubmed/1291096", "accessDate": "2009-11-12T22:50:17Z", "PMID": "", "PMCID": "", "ISSN": "0008-6363", "archive": "", "archiveLocation": "", "shortTitle": "", "language": "", "libraryCatalog": "NCBI PubMed", "callNumber": "", "rights": "", "extra": "PMID: 1291096", "tags": [], "collections": [], "relations": {}, "dateAdded": "2009-11-12T22:50:17Z", "dateModified": "2009-11-12T22:50:17Z" } }, { "key": "UCZ2VMCF", "version": 1, "library": { "type": "group", "id": 7574, "name": "AMC Heart Center", "links": { "alternate": { "href": "https://www.zotero.org/groups/amc_heart_center", "type": "text/html" } } }, "links": { "self": { "href": "https://api.zotero.org/groups/7574/items/UCZ2VMCF", "type": "application/json" }, "alternate": { "href": "https://www.zotero.org/groups/amc_heart_center/items/UCZ2VMCF", "type": "text/html" } }, "meta": { "createdByUser": { "id": 8053, "username": "jssgdejong", "name": "", "links": { "alternate": { "href": "https://www.zotero.org/jssgdejong", "type": "text/html" } } }, "creatorSummary": "von Kaenel et al.", "parsedDate": "1993-04", "numChildren": 0 }, "data": { "key": "UCZ2VMCF", "version": 1, "itemType": "journalArticle", "title": "Vancomycin does not enhance hypotension under anesthesia", "creators": [ { "creatorType": "author", "firstName": "W E", "lastName": "von Kaenel" }, { "creatorType": "author", "firstName": "E L", "lastName": "Bloomfield" }, { "creatorType": "author", "firstName": "L", "lastName": "Amaranath" }, { "creatorType": "author", "firstName": "A A", "lastName": "Wilde" } ], "abstractNote": "The rapid administration of vancomycin is associated with flushing and hypotension, a consequence of histamine release. The manufacturer discourages administering vancomycin to anesthetized patients, stating that vancomycin aggravates the hypotensive effects of anesthetics. To test this, we randomly assigned 36 adults (ASA classes I through III) to one of two groups: preinduction (Preind, n = 19) and postinduction (Postind, n = 17). Both groups received two different infusions: vancomycin (1 g/250 mL normal saline) and saline (250 mL normal saline) over 30-60 min. The Preind group received vancomycin before anesthesia was induced and saline was administered immediately after anesthesia was induced; for the Postind group, this order was reversed. This was done in a double-blind fashion. The anesthetic induction was standardized by the intravenous administration of thiopental and vecuronium and anesthetic maintenance by inhalation of nitrous oxide and enflurane. End-tidal enflurane, heart rate (HR), and blood pressure (BP) were measured every 3 min. Independent (unpaired) t-test was used in data analysis. The groups did not differ significantly. We conclude that vancomycin infusion may be given under anesthesia without significant adverse hemodynamic consequences if administered over a 30-60 min period of time.", "publicationTitle": "Anesthesia and Analgesia", "publisher": "", "place": "", "date": "Apr 1993", "volume": "76", "issue": "4", "section": "", "partNumber": "", "partTitle": "", "pages": "809-811", "series": "", "seriesTitle": "", "seriesText": "", "journalAbbreviation": "Anesth. Analg", "DOI": "", "citationKey": "", "url": "http://www.ncbi.nlm.nih.gov/pubmed/8466022", "accessDate": "2009-11-12T22:50:16Z", "PMID": "", "PMCID": "", "ISSN": "0003-2999", "archive": "", "archiveLocation": "", "shortTitle": "", "language": "", "libraryCatalog": "NCBI PubMed", "callNumber": "", "rights": "", "extra": "PMID: 8466022", "tags": [], "collections": [], "relations": {}, "dateAdded": "2009-11-12T22:50:16Z", "dateModified": "2009-11-12T22:50:16Z" } }, { "key": "HM9TZZRD", "version": 1, "library": { "type": "group", "id": 7574, "name": "AMC Heart Center", "links": { "alternate": { "href": "https://www.zotero.org/groups/amc_heart_center", "type": "text/html" } } }, "links": { "self": { "href": "https://api.zotero.org/groups/7574/items/HM9TZZRD", "type": "application/json" }, "alternate": { "href": "https://www.zotero.org/groups/amc_heart_center/items/HM9TZZRD", "type": "text/html" } }, "meta": { "createdByUser": { "id": 8053, "username": "jssgdejong", "name": "", "links": { "alternate": { "href": "https://www.zotero.org/jssgdejong", "type": "text/html" } } }, "creatorSummary": "Wilde", "parsedDate": "1993-05-29", "numChildren": 0 }, "data": { "key": "HM9TZZRD", "version": 1, "itemType": "journalArticle", "title": "[The ATP-sensitive potassium channel: function and potential for pharmacological modification]", "creators": [ { "creatorType": "author", "firstName": "A A", "lastName": "Wilde" } ], "abstractNote": "", "publicationTitle": "Nederlands Tijdschrift Voor Geneeskunde", "publisher": "", "place": "", "date": "May 29, 1993", "volume": "137", "issue": "22", "section": "", "partNumber": "", "partTitle": "", "pages": "1086-1090", "series": "", "seriesTitle": "", "seriesText": "", "journalAbbreviation": "Ned Tijdschr Geneeskd", "DOI": "", "citationKey": "", "url": "http://www.ncbi.nlm.nih.gov/pubmed/8510783", "accessDate": "2009-11-12T22:50:12Z", "PMID": "", "PMCID": "", "ISSN": "0028-2162", "archive": "", "archiveLocation": "", "shortTitle": "[The ATP-sensitive potassium channel", "language": "", "libraryCatalog": "NCBI PubMed", "callNumber": "", "rights": "", "extra": "PMID: 8510783", "tags": [], "collections": [], "relations": {}, "dateAdded": "2009-11-12T22:50:12Z", "dateModified": "2009-11-12T22:50:12Z" } }, { "key": "SPR5VIM5", "version": 1, "library": { "type": "group", "id": 7574, "name": "AMC Heart Center", "links": { "alternate": { "href": "https://www.zotero.org/groups/amc_heart_center", "type": "text/html" } } }, "links": { "self": { "href": "https://api.zotero.org/groups/7574/items/SPR5VIM5", "type": "application/json" }, "alternate": { "href": "https://www.zotero.org/groups/amc_heart_center/items/SPR5VIM5", "type": "text/html" } }, "meta": { "createdByUser": { "id": 8053, "username": "jssgdejong", "name": "", "links": { "alternate": { "href": "https://www.zotero.org/jssgdejong", "type": "text/html" } } }, "creatorSummary": "Wilde", "parsedDate": "1993-08", "numChildren": 0 }, "data": { "key": "SPR5VIM5", "version": 1, "itemType": "journalArticle", "title": "Role of ATP-sensitive K+ channel current in ischemic arrhythmias", "creators": [ { "creatorType": "author", "firstName": "A A", "lastName": "Wilde" } ], "abstractNote": "In acute myocardial ischemia slow conduction and short refractoriness both predispose to cardiac arrhythmias. Moreover, spatial dispersion in these parameters, in part determined by inhomogeneity in extracellular potassium concentration ([K+]0), which develops within minutes, is considered highly arrhythmogenic. The incidence and time distribution of ventricular arrhythmias is determined by these electrophysiological changes and by factors pertinent to the experimental model. In the initial phase of ischemia, glibenclamide, a potent blocker of ATP-sensitive K+ channels (K+ATP channels), reduces the rate of increase in [K+]0 and therefore, presumably, also the inhomogeneity in [K+]0. During this phase of ischemia glibenclamide has an antiarrhythmic effect, which may be based on a reduction in inhomogeneity in [K+]0. In addition, glibenclamide prolongs the action potential of ischemic myocardium. Although under ischemic conditions action potential duration is no longer a reliable parameter or refractoriness, glibenclamide-induced prolongation or refractoriness may play a role in the prevention of arrhythmias. In contrast, openers of K+ATP channels increase the incidence of ventricular arrhythmias or, in other models, the time course of onset is accelerated. They shorten the duration of the action potential in ischemic tissue. In the globally ischemic rabbit heart, initial changes in [K+]0 are not influenced by cromakalim. It is concluded that activation of the K+ATP channel current during early myocardial ischemia potentially contributes to the development of ventricular arrhythmias. Particularly, the direct electrophysiological effect of increased K+ current is considered arrhythmogenic.", "publicationTitle": "Cardiovascular Drugs and Therapy / Sponsored by the International Society of Cardiovascular Pharmacotherapy", "publisher": "", "place": "", "date": "Aug 1993", "volume": "7 Suppl 3", "issue": "", "section": "", "partNumber": "", "partTitle": "", "pages": "521-526", "series": "", "seriesTitle": "", "seriesText": "", "journalAbbreviation": "Cardiovasc Drugs Ther", "DOI": "", "citationKey": "", "url": "http://www.ncbi.nlm.nih.gov/pubmed/8251422", "accessDate": "2009-11-12T22:50:11Z", "PMID": "", "PMCID": "", "ISSN": "0920-3206", "archive": "", "archiveLocation": "", "shortTitle": "", "language": "", "libraryCatalog": "NCBI PubMed", "callNumber": "", "rights": "", "extra": "PMID: 8251422", "tags": [], "collections": [], "relations": {}, "dateAdded": "2009-11-12T22:50:11Z", "dateModified": "2009-11-12T22:50:11Z" } }, { "key": "CQUS2GXX", "version": 1, "library": { "type": "group", "id": 7574, "name": "AMC Heart Center", "links": { "alternate": { "href": "https://www.zotero.org/groups/amc_heart_center", "type": "text/html" } } }, "links": { "self": { "href": "https://api.zotero.org/groups/7574/items/CQUS2GXX", "type": "application/json" }, "alternate": { "href": "https://www.zotero.org/groups/amc_heart_center/items/CQUS2GXX", "type": "text/html" } }, "meta": { "createdByUser": { "id": 8053, "username": "jssgdejong", "name": "", "links": { "alternate": { "href": "https://www.zotero.org/jssgdejong", "type": "text/html" } } }, "creatorSummary": "Wilde", "parsedDate": "1994", "numChildren": 0 }, "data": { "key": "CQUS2GXX", "version": 1, "itemType": "journalArticle", "title": "K+ ATP-channel opening and arrhythmogenesis", "creators": [ { "creatorType": "author", "firstName": "A A", "lastName": "Wilde" } ], "abstractNote": "The role of adenosine triphosphate (ATP)-sensitive potassium channels (K+ ATP channels) under physiologic and pathophysiologic conditions has been debated in recent years. Moreover, because of the reported pro-arrhythmic effects of potassium-channel openers in the setting of acute myocardial ischemia, the potential benefit of K+ ATP-channel modulation in clinical practice has been questioned. Such pro-arrhythmic potential, based on the ability of potassium-channel openers to exacerbate the ischemia-induced shortening of the action potential, is also disputed. Both pro- and antiarrhythmic effects of K+ ATP-channel openers (and blockers) have been described. These apparently conflicting results can (to a great extent) be explained by taking into account the electrophysiologic mechanism of a particular arrhythmia. In addition, under ischemic conditions other factors of importance for the development of arrhythmias may, when they are not controlled, determine the outcome. It is concluded that both in normoxia and in ischemia, pharmacologic opening of K+ ATP channels might facilitate ventricular arrhythmias when it leads to serious electrophysiologic inhomogeneity. Because such favorable conditions are created only by relatively high doses, the problem of pro-arrhythmogeneity may be overestimated. On the other hand, before widescale application in the treatment of ischemic heart disease is established, well designed clinical and experimental studies should be performed to determine the risk for pro-arrhythmogeneity.", "publicationTitle": "Journal of Cardiovascular Pharmacology", "publisher": "", "place": "", "date": "1994", "volume": "24 Suppl 4", "issue": "", "section": "", "partNumber": "", "partTitle": "", "pages": "S35-40", "series": "", "seriesTitle": "", "seriesText": "", "journalAbbreviation": "J. Cardiovasc. Pharmacol", "DOI": "", "citationKey": "", "url": "http://www.ncbi.nlm.nih.gov/pubmed/7898106", "accessDate": "2009-11-12T22:50:10Z", "PMID": "", "PMCID": "", "ISSN": "0160-2446", "archive": "", "archiveLocation": "", "shortTitle": "", "language": "", "libraryCatalog": "NCBI PubMed", "callNumber": "", "rights": "", "extra": "PMID: 7898106", "tags": [], "collections": [], "relations": {}, "dateAdded": "2009-11-12T22:50:10Z", "dateModified": "2009-11-12T22:50:10Z" } }, { "key": "UVNDUPMZ", "version": 1, "library": { "type": "group", "id": 7574, "name": "AMC Heart Center", "links": { "alternate": { "href": "https://www.zotero.org/groups/amc_heart_center", "type": "text/html" } } }, "links": { "self": { "href": "https://api.zotero.org/groups/7574/items/UVNDUPMZ", "type": "application/json" }, "alternate": { "href": "https://www.zotero.org/groups/amc_heart_center/items/UVNDUPMZ", "type": "text/html" } }, "meta": { "createdByUser": { "id": 8053, "username": "jssgdejong", "name": "", "links": { "alternate": { "href": "https://www.zotero.org/jssgdejong", "type": "text/html" } } }, "creatorSummary": "Wilde and Janse", "parsedDate": "1994-01", "numChildren": 0 }, "data": { "key": "UVNDUPMZ", "version": 1, "itemType": "journalArticle", "title": "Electrophysiological effects of ATP sensitive potassium channel modulation: implications for arrhythmogenesis", "creators": [ { "creatorType": "author", "firstName": "A A", "lastName": "Wilde" }, { "creatorType": "author", "firstName": "M J", "lastName": "Janse" } ], "abstractNote": "", "publicationTitle": "Cardiovascular Research", "publisher": "", "place": "", "date": "Jan 1994", "volume": "28", "issue": "1", "section": "", "partNumber": "", "partTitle": "", "pages": "16-24", "series": "", "seriesTitle": "", "seriesText": "", "journalAbbreviation": "Cardiovasc. Res", "DOI": "", "citationKey": "", "url": "http://www.ncbi.nlm.nih.gov/pubmed/8111787", "accessDate": "2009-11-12T22:50:09Z", "PMID": "", "PMCID": "", "ISSN": "0008-6363", "archive": "", "archiveLocation": "", "shortTitle": "Electrophysiological effects of ATP sensitive potassium channel modulation", "language": "", "libraryCatalog": "NCBI PubMed", "callNumber": "", "rights": "", "extra": "PMID: 8111787", "tags": [], "collections": [], "relations": {}, "dateAdded": "2009-11-12T22:50:09Z", "dateModified": "2009-11-12T22:50:09Z" } }, { "key": "HRZF8XG6", "version": 1, "library": { "type": "group", "id": 7574, "name": "AMC Heart Center", "links": { "alternate": { "href": "https://www.zotero.org/groups/amc_heart_center", "type": "text/html" } } }, "links": { "self": { "href": "https://api.zotero.org/groups/7574/items/HRZF8XG6", "type": "application/json" }, "alternate": { "href": "https://www.zotero.org/groups/amc_heart_center/items/HRZF8XG6", "type": "text/html" } }, "meta": { "createdByUser": { "id": 8053, "username": "jssgdejong", "name": "", "links": { "alternate": { "href": "https://www.zotero.org/jssgdejong", "type": "text/html" } } }, "creatorSummary": "Wilde et al.", "parsedDate": "1994-06", "numChildren": 0 }, "data": { "key": "HRZF8XG6", "version": 1, "itemType": "journalArticle", "title": "Phentolamine blocks ATP sensitive potassium channels in cardiac ventricular cells", "creators": [ { "creatorType": "author", "firstName": "A A", "lastName": "Wilde" }, { "creatorType": "author", "firstName": "M W", "lastName": "Veldkamp" }, { "creatorType": "author", "firstName": "A C", "lastName": "van Ginneken" }, { "creatorType": "author", "firstName": "T", "lastName": "Opthof" } ], "abstractNote": "OBJECTIVE: The alpha adrenoceptor antagonist phentolamine prevents ischaemia related arrhythmias in rat, guinea pig, and cat heart. This effect has been related to the attenuation of ischaemia induced shortening of the action potential and has been ascribed to its alpha adrenoceptor antagonist properties. The aim of this study was to examine the effect of phentolamine on the ATP sensitive potassium channel (KATP), because this channel seems to be involved in action potential shortening during ischaemia. METHODS: Single channel experiments were performed on inside-out and outside-out patches of isolated rabbit ventricular cells at room temperature. Cells were isolated with conventional isolation techniques. Pipette and bath solution contained (in mmol.litre-1): K-gluconate 140, KCl 10, and HEPES-KOH 10 (pH 7.4). RESULTS: Excision of the patch always resulted in KATP channel activity [single channel conductance 60(SD 2.8) pS n = 4], which could be completely blocked by 5 mM ATP. In 22 of 26 patches the addition of 5 microM phentolamine to the intracellular side of the membrane reduced KATP channel activity. In 17 of these patches the effect was reversible. In four patches no effect was observed. Open probability decreased by 94% (n = 12). Addition of 50 microM phentolamine resulted in the disappearance of channel activity in six of eight patches which was reversible in four patches. In outside-out patches 5 microM phentolamine was only effective in 50% of the patches, reducing open probability by 98 to 100%. CONCLUSIONS: Phentolamine blocks ATP sensitive potassium channels in rabbit ventricular cells independently of the alpha adrenoceptor. This blocking effect probably occurs at the intracellular side of the membrane. The antiarrhythmic effect of phentolamine may at least partially be explained by blockade of KATP channels and may thus partly be independent of its effects on the alpha adrenoceptor.", "publicationTitle": "Cardiovascular Research", "publisher": "", "place": "", "date": "Jun 1994", "volume": "28", "issue": "6", "section": "", "partNumber": "", "partTitle": "", "pages": "847-850", "series": "", "seriesTitle": "", "seriesText": "", "journalAbbreviation": "Cardiovasc. Res", "DOI": "", "citationKey": "", "url": "http://www.ncbi.nlm.nih.gov/pubmed/7923290", "accessDate": "2009-11-12T22:50:08Z", "PMID": "", "PMCID": "", "ISSN": "0008-6363", "archive": "", "archiveLocation": "", "shortTitle": "", "language": "", "libraryCatalog": "NCBI PubMed", "callNumber": "", "rights": "", "extra": "PMID: 7923290", "tags": [], "collections": [], "relations": {}, "dateAdded": "2009-11-12T22:50:08Z", "dateModified": "2009-11-12T22:50:08Z" } }, { "key": "Q43MTBT2", "version": 1, "library": { "type": "group", "id": 7574, "name": "AMC Heart Center", "links": { "alternate": { "href": "https://www.zotero.org/groups/amc_heart_center", "type": "text/html" } } }, "links": { "self": { "href": "https://api.zotero.org/groups/7574/items/Q43MTBT2", "type": "application/json" }, "alternate": { "href": "https://www.zotero.org/groups/amc_heart_center/items/Q43MTBT2", "type": "text/html" } }, "meta": { "createdByUser": { "id": 8053, "username": "jssgdejong", "name": "", "links": { "alternate": { "href": "https://www.zotero.org/jssgdejong", "type": "text/html" } } }, "creatorSummary": "Wilde and Aksnes", "parsedDate": "1995-01", "numChildren": 0 }, "data": { "key": "Q43MTBT2", "version": 1, "itemType": "journalArticle", "title": "Myocardial potassium loss and cell depolarisation in ischaemia and hypoxia", "creators": [ { "creatorType": "author", "firstName": "A A", "lastName": "Wilde" }, { "creatorType": "author", "firstName": "G", "lastName": "Aksnes" } ], "abstractNote": "", "publicationTitle": "Cardiovascular Research", "publisher": "", "place": "", "date": "Jan 1995", "volume": "29", "issue": "1", "section": "", "partNumber": "", "partTitle": "", "pages": "1-15", "series": "", "seriesTitle": "", "seriesText": "", "journalAbbreviation": "Cardiovasc. Res", "DOI": "", "citationKey": "", "url": "http://www.ncbi.nlm.nih.gov/pubmed/7895226", "accessDate": "2009-11-12T22:50:07Z", "PMID": "", "PMCID": "", "ISSN": "0008-6363", "archive": "", "archiveLocation": "", "shortTitle": "", "language": "", "libraryCatalog": "NCBI PubMed", "callNumber": "", "rights": "", "extra": "PMID: 7895226", "tags": [], "collections": [], "relations": {}, "dateAdded": "2009-11-12T22:50:07Z", "dateModified": "2009-11-12T22:50:07Z" } }, { "key": "PST7VNRN", "version": 1, "library": { "type": "group", "id": 7574, "name": "AMC Heart Center", "links": { "alternate": { "href": "https://www.zotero.org/groups/amc_heart_center", "type": "text/html" } } }, "links": { "self": { "href": "https://api.zotero.org/groups/7574/items/PST7VNRN", "type": "application/json" }, "alternate": { "href": "https://www.zotero.org/groups/amc_heart_center/items/PST7VNRN", "type": "text/html" } }, "meta": { "createdByUser": { "id": 8053, "username": "jssgdejong", "name": "", "links": { "alternate": { "href": "https://www.zotero.org/jssgdejong", "type": "text/html" } } }, "creatorSummary": "Wilde", "parsedDate": "1996-05", "numChildren": 0 }, "data": { "key": "PST7VNRN", "version": 1, "itemType": "journalArticle", "title": "ATP-sensitive potassium channels, transmural ischemia and the ECG implications for the non-insulin dependent diabetic patient?", "creators": [ { "creatorType": "author", "firstName": "A A", "lastName": "Wilde" } ], "abstractNote": "", "publicationTitle": "Cardiovascular Research", "publisher": "", "place": "", "date": "May 1996", "volume": "31", "issue": "5", "section": "", "partNumber": "", "partTitle": "", "pages": "688-690", "series": "", "seriesTitle": "", "seriesText": "", "journalAbbreviation": "Cardiovasc. Res", "DOI": "10.1016/0008-6363(96)00037-5", "citationKey": "", "url": "http://www.ncbi.nlm.nih.gov/pubmed/8763397", "accessDate": "2009-11-12T22:50:05Z", "PMID": "", "PMCID": "", "ISSN": "0008-6363", "archive": "", "archiveLocation": "", "shortTitle": "", "language": "", "libraryCatalog": "NCBI PubMed", "callNumber": "", "rights": "", "extra": "PMID: 8763397", "tags": [], "collections": [], "relations": {}, "dateAdded": "2009-11-12T22:50:05Z", "dateModified": "2009-11-12T22:50:05Z" } } ]