Pub Date : 2009-04-01DOI: 10.1080/14017430902853457
Background Blood pressure research is an extensive, expensive and profitable activity. During a five year period more than 21 000 articles were published on the subject blood pressure and almost 21 000 articles on the subject hypertension. There are physiological, anatomical and pathological differences between men and women and it is therefore of importance to see how gender is reported in the scientific abstracts.
{"title":"Abstracts from the XI Swedish Heart Association, April 22-24, 2009, Uppsala, Sweden.","authors":"","doi":"10.1080/14017430902853457","DOIUrl":"https://doi.org/10.1080/14017430902853457","url":null,"abstract":"Background Blood pressure research is an extensive, expensive and profitable activity. During a five year period more than 21 000 articles were published on the subject blood pressure and almost 21 000 articles on the subject hypertension. There are physiological, anatomical and pathological differences between men and women and it is therefore of importance to see how gender is reported in the scientific abstracts.","PeriodicalId":79533,"journal":{"name":"Scandinavian cardiovascular journal. Supplement","volume":"57 ","pages":"3-38"},"PeriodicalIF":0.0,"publicationDate":"2009-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/14017430902853457","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"28055913","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Abstracts from the Xth Swedish Heart Association Meeting, April 23-25, 2008, Malmo, Sweden.","authors":"","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":79533,"journal":{"name":"Scandinavian cardiovascular journal. Supplement","volume":"56 ","pages":"1-60"},"PeriodicalIF":0.0,"publicationDate":"2008-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"27558972","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Abstracts from the IX Swedish Cardiovascular Meeting, Goteborg, April 25-27, 2007.","authors":"","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":79533,"journal":{"name":"Scandinavian cardiovascular journal. Supplement","volume":"55 ","pages":"1-39"},"PeriodicalIF":0.0,"publicationDate":"2007-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"26859822","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2006-04-01DOI: 10.1080/14017430600664511
Oral presentations / Doctors
{"title":"Abstracts from VIII Swedish Heart Association meeting, Linköping, Sweden, April 26-28, 2006.","authors":"","doi":"10.1080/14017430600664511","DOIUrl":"https://doi.org/10.1080/14017430600664511","url":null,"abstract":"Oral presentations / Doctors","PeriodicalId":79533,"journal":{"name":"Scandinavian cardiovascular journal. Supplement","volume":"54 ","pages":"2-42"},"PeriodicalIF":0.0,"publicationDate":"2006-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/14017430600664511","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25995127","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2005-04-01DOI: 10.1080/14017430510009195
{"title":"Abstracts from VII Swedish Heart Association Meeting and the XX Nordic Congress of Cardiology. Malmo, Sweden, April 27-29, 2005.","authors":"","doi":"10.1080/14017430510009195","DOIUrl":"https://doi.org/10.1080/14017430510009195","url":null,"abstract":"","PeriodicalId":79533,"journal":{"name":"Scandinavian cardiovascular journal. Supplement","volume":"53 ","pages":"2-48"},"PeriodicalIF":0.0,"publicationDate":"2005-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/14017430510009195","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25036019","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2003-12-01DOI: 10.1080/14017430310024053
s from XIX Nordic Congress of Cardiology, Odense, Denmark, June 4–6 2003 The abstracts are placed in chronological order related to the sessions in which they are presented. The number of the abstract refers to the number in the final programme.
{"title":"Abstracts from XIX Nordic Congress of Cardiology. Odense, Denmark, June 4-6, 2003.","authors":"","doi":"10.1080/14017430310024053","DOIUrl":"https://doi.org/10.1080/14017430310024053","url":null,"abstract":"s from XIX Nordic Congress of Cardiology, Odense, Denmark, June 4–6 2003 The abstracts are placed in chronological order related to the sessions in which they are presented. The number of the abstract refers to the number in the final programme.","PeriodicalId":79533,"journal":{"name":"Scandinavian cardiovascular journal. Supplement","volume":"52 ","pages":"4-42"},"PeriodicalIF":0.0,"publicationDate":"2003-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/14017430310024053","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"24130457","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
1. Low pH and lactic acid perfusion evoke a reproducible, and concentration-dependent outflow of CGRP from the isolated heart. 2. PGI2 causes outflow of CGRP from the isolated heart. Furthermore, low pH perfusion causes release of PGI2, and cyclo-oxygenase inhibition attenuates not only this release of PGI2, but also the outflow of CGRP that is evoked by low pH perfusion, indicating that a portion of the C-fibre activation exerted by low pH is mediated by PGI2. 3. The outflow of CGRP that is caused by low pH but not that evoked by capsaicin or PGI2 is dependent on the endothelium, whereas the vasodilating effect of CGRP is preserved after removal of the endothelium. 4. TTX attenuates release of CGRP caused by low concentrations of capsaicin, indicating that an axon reflex mechanism in the peripheral endings of C-fibre afferents can augment local outflow of CGRP. 5. Outflow of CGRP evoked by low pH and capsaicin have common features, such as sensitivity to RR and CPZ. N-type calcium channels are involved in release of CGRP by both stimuli. 6. In the coronary vasculature, exogenous CGRP augmented post-occlusive hyperaemia. 7. In the pig in vivo, CGRP causes marked dose-dependent reduction of systemic vascular resistance. This effect of CGRP was partly reduced by CGRP(8-37). 8. Capsaicin pretreatment resulted in lower myocardial levels of CGRP, and ischaemic myocardium had lower content of CGRP than non-ischaemic areas. Capsaicin-treated animals had larger myocardial infarctions, possibly due to depletion of CGRP. When endogenous stores of CGRP were intact, administration of additional CGRP to the ischaemic myocardium had no cardioprotective effect. 9. In patients undergoing CABG without CPB, 10-20 minutes of local ischaemia (as evidenced by a net production of lactate) was associated with increased levels of CGRP in coronary sinus blood. 10. Based on the present findings it may therefore be suggested that local cardiac CGRP-release from capsaicin-sensitive C-fibre afferents during myocardial ischaemia functions as an endogenous physiological protective response. The possibility thus exists that effects of CGRP observed in animal studies may play a role in human myocardial ischaemia.
{"title":"Release and effects of calcitonin gene-related peptide in myocardial ischaemia.","authors":"Göran Källner","doi":"10.1080/140174398427956","DOIUrl":"https://doi.org/10.1080/140174398427956","url":null,"abstract":"1. Low pH and lactic acid perfusion evoke a reproducible, and concentration-dependent outflow of CGRP from the isolated heart. 2. PGI2 causes outflow of CGRP from the isolated heart. Furthermore, low pH perfusion causes release of PGI2, and cyclo-oxygenase inhibition attenuates not only this release of PGI2, but also the outflow of CGRP that is evoked by low pH perfusion, indicating that a portion of the C-fibre activation exerted by low pH is mediated by PGI2. 3. The outflow of CGRP that is caused by low pH but not that evoked by capsaicin or PGI2 is dependent on the endothelium, whereas the vasodilating effect of CGRP is preserved after removal of the endothelium. 4. TTX attenuates release of CGRP caused by low concentrations of capsaicin, indicating that an axon reflex mechanism in the peripheral endings of C-fibre afferents can augment local outflow of CGRP. 5. Outflow of CGRP evoked by low pH and capsaicin have common features, such as sensitivity to RR and CPZ. N-type calcium channels are involved in release of CGRP by both stimuli. 6. In the coronary vasculature, exogenous CGRP augmented post-occlusive hyperaemia. 7. In the pig in vivo, CGRP causes marked dose-dependent reduction of systemic vascular resistance. This effect of CGRP was partly reduced by CGRP(8-37). 8. Capsaicin pretreatment resulted in lower myocardial levels of CGRP, and ischaemic myocardium had lower content of CGRP than non-ischaemic areas. Capsaicin-treated animals had larger myocardial infarctions, possibly due to depletion of CGRP. When endogenous stores of CGRP were intact, administration of additional CGRP to the ischaemic myocardium had no cardioprotective effect. 9. In patients undergoing CABG without CPB, 10-20 minutes of local ischaemia (as evidenced by a net production of lactate) was associated with increased levels of CGRP in coronary sinus blood. 10. Based on the present findings it may therefore be suggested that local cardiac CGRP-release from capsaicin-sensitive C-fibre afferents during myocardial ischaemia functions as an endogenous physiological protective response. The possibility thus exists that effects of CGRP observed in animal studies may play a role in human myocardial ischaemia.","PeriodicalId":79533,"journal":{"name":"Scandinavian cardiovascular journal. Supplement","volume":"89 1","pages":"1-35"},"PeriodicalIF":0.0,"publicationDate":"1998-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"79928396","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Carvedilol is a novel antihypertensive agent. It is a multiple-action neurohormonal antagonist with a beta-adrenoceptor blocking effect combined with a vasodilating action based on alpha1-adrenoceptor blockade. In addition, carvedilol exerts a number of well documented ancillary effects such as being a scavenger of free radicals. It also has an antiproliferative action on smooth muscle cells. This combination of effects opens up a number of interesting clinical perspectives. It is the purpose of this brief review to summarize some of the clinical studies that have been performed with carvedilol. Investigations in hypertensive patients will form the basis of this review, but special interest will also be devoted to other patient groups. In particular the therapeutic value of carvedilol will be discussed in patients with concomitant disorders such as atheromatosis, left ventricular hypertrophy, angina pectoris, myocardial infarction, congestive heart failure, arrhythmias, stroke, renal failure or diabetes. Finally, the usefulness of carvedilol in the treatment of elderly hypertensive patients will be reviewed. It is evident from the available scientific literature that carvedilol is an antihypertensive agent with a novel mode of action. It is effective in many of the subpopulations of patients alluded to above. It appears reasonable to assume that some of these therapeutic effects can be attributed to its ancillary properties.
{"title":"Carvedilol in the treatment of hypertension--a review of the clinical data base.","authors":"L Hansson, A Himmelmann","doi":"10.1080/140174398428072","DOIUrl":"https://doi.org/10.1080/140174398428072","url":null,"abstract":"<p><p>Carvedilol is a novel antihypertensive agent. It is a multiple-action neurohormonal antagonist with a beta-adrenoceptor blocking effect combined with a vasodilating action based on alpha1-adrenoceptor blockade. In addition, carvedilol exerts a number of well documented ancillary effects such as being a scavenger of free radicals. It also has an antiproliferative action on smooth muscle cells. This combination of effects opens up a number of interesting clinical perspectives. It is the purpose of this brief review to summarize some of the clinical studies that have been performed with carvedilol. Investigations in hypertensive patients will form the basis of this review, but special interest will also be devoted to other patient groups. In particular the therapeutic value of carvedilol will be discussed in patients with concomitant disorders such as atheromatosis, left ventricular hypertrophy, angina pectoris, myocardial infarction, congestive heart failure, arrhythmias, stroke, renal failure or diabetes. Finally, the usefulness of carvedilol in the treatment of elderly hypertensive patients will be reviewed. It is evident from the available scientific literature that carvedilol is an antihypertensive agent with a novel mode of action. It is effective in many of the subpopulations of patients alluded to above. It appears reasonable to assume that some of these therapeutic effects can be attributed to its ancillary properties.</p>","PeriodicalId":79533,"journal":{"name":"Scandinavian cardiovascular journal. Supplement","volume":"47 ","pages":"67-80"},"PeriodicalIF":0.0,"publicationDate":"1998-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/140174398428072","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20461912","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
In summary, beta-blockade is currently the most promising "new" treatment undergoing Phase III testing in chronic heart failure. Multiple studies on the effects of these agents on LV function and chamber characteristics as well as limited survival data strongly suggest that these agents produce a beneficial effect on the natural history of heart failure. If this promise is borne out in the currently active or planned large-scale clinical trials, this form of therapy will emerge as the most valuable treatment available for chronic heart failure.
{"title":"Beta-adrenergic blockade in chronic heart failure.","authors":"M Bristow, J D Port","doi":"10.1080/140174398428045","DOIUrl":"https://doi.org/10.1080/140174398428045","url":null,"abstract":"<p><p>In summary, beta-blockade is currently the most promising \"new\" treatment undergoing Phase III testing in chronic heart failure. Multiple studies on the effects of these agents on LV function and chamber characteristics as well as limited survival data strongly suggest that these agents produce a beneficial effect on the natural history of heart failure. If this promise is borne out in the currently active or planned large-scale clinical trials, this form of therapy will emerge as the most valuable treatment available for chronic heart failure.</p>","PeriodicalId":79533,"journal":{"name":"Scandinavian cardiovascular journal. Supplement","volume":"47 ","pages":"45-55"},"PeriodicalIF":0.0,"publicationDate":"1998-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/140174398428045","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20463967","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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