Scandinavian cardiovascular journal. Supplement最新文献

{"title":"Clinical consequences of the autonomic imbalance in hypertension and congestive heart failure.","authors":"S Julius,&nbsp;S Nesbitt","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The reduction of coronary mortality is not as large as one would expect from the observed blood pressure lowering in trials of antihypertensive medications. This is not surprising; hypertension is a complex disease where the high blood pressure is only one of numerous coronary risk factors. Sympathetic overactivity in hypertension, independent of the blood pressure, may be conducive to premature atherosclerosis by inducing insulin resistance and dyslipidemia. Through its trophic effect on blood vessels, sympathetic overactivity potentiates vasoconstriction. This, in turn, accelerates hypertension and the metabolic syndrome. The hypertrophy of small coronary arterioles decreases the coronary reserve and enhances coronary spasms. Tachycardia, which is due to increased sympathetic tone and a decreased parasympathetic tone, favors arrhythmias and sudden death in congestive heart failure and hypertension. Increased hematocrit is frequently found in male patients with hypertension, and high hematocrit is a predictor of coronary heart disease/thrombosis. The increase of hematocrit is in part due to an alpha adrenergic postcapillary venoconstriction. Enhanced sympathetic drive, insulin resistance and dyslipidemia have been demonstrated also in congestive heart failure, but the clinical importance of these findings is not fully understood.</p>","PeriodicalId":79533,"journal":{"name":"Scandinavian cardiovascular journal. Supplement","volume":"47 ","pages":"23-30"},"PeriodicalIF":0.0,"publicationDate":"1998-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20463964","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":"From Hypertension to Heart Failure. Symposium proceedings. Stockholm, Sweden, January 1997.","authors":"","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":79533,"journal":{"name":"Scandinavian cardiovascular journal. Supplement","volume":"47 ","pages":"1-80"},"PeriodicalIF":0.0,"publicationDate":"1998-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20519631","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":"Early and late sympathetic activation in hypertension.","authors":"G Mancia,&nbsp;M Di Rienzo,&nbsp;C Giannattasio,&nbsp;G Parati,&nbsp;G Grassi","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>In several experimental animal models of hypertension, sympathetic factors have been shown to be involved in the development and/or maintenance of high blood pressure. Although the information available on this issue in man is more scarce, recent evidence clearly indicates the participation of adrenergic mechanisms in the early and late phases of the hypertensive process. In addition, several cardiovascular risk factors frequently associated with hypertension, such as obesity, insulin-resistance, cigarette smoking, and the atherogenic process, are also characterized by alterations in sympathetic cardiovascular drive. This contributes to a further activation of the sympathetic nervous system thus favoring the development of the end organ damage (e.g. cardiac and vascular hypertrophy) associated with the hypertensive state.</p>","PeriodicalId":79533,"journal":{"name":"Scandinavian cardiovascular journal. Supplement","volume":"47 ","pages":"9-14"},"PeriodicalIF":0.0,"publicationDate":"1998-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20463962","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":"Treating hypertension--effect of treatment and cost-effectiveness in respect to later cardiovascular diseases.","authors":"T Hedner","doi":"10.1080/140174398428027","DOIUrl":"https://doi.org/10.1080/140174398428027","url":null,"abstract":"<p><p>A large number of prospective intervention trials have clearly demonstrated that drug treatment of hypertension lower cardiovascular morbidity and mortality. In the elderly, where treatment results in higher absolute decreases in morbidity and mortality, drug treatment is clearly cost-effective or even cost-saving in some groups of patients. Although the concept of treating hypertension is generally well accepted, a significant portion of patients remain insufficiently treated. In spite of major advances in the management of hypertension during the last decades, there is an excess morbidity and mortality in the hypertensive population. Thus, treatment is still imperfect, and a number of measures need to be taken in order to bring down cardiovascular risk in hypertensive patients to that of the normotensive population.</p>","PeriodicalId":79533,"journal":{"name":"Scandinavian cardiovascular journal. Supplement","volume":"47 ","pages":"31-5"},"PeriodicalIF":0.0,"publicationDate":"1998-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/140174398428027","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20463965","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":"Early and late sympathetic activation in hypertension.","authors":"G. Mancia, M. Di Rienzo, C. Giannattasio, G. Parati, G. Grassi","doi":"10.1080/140174398427992","DOIUrl":"https://doi.org/10.1080/140174398427992","url":null,"abstract":"In several experimental animal models of hypertension, sympathetic factors have been shown to be involved in the development and/or maintenance of high blood pressure. Although the information available on this issue in man is more scarce, recent evidence clearly indicates the participation of adrenergic mechanisms in the early and late phases of the hypertensive process. In addition, several cardiovascular risk factors frequently associated with hypertension, such as obesity, insulin-resistance, cigarette smoking, and the atherogenic process, are also characterized by alterations in sympathetic cardiovascular drive. This contributes to a further activation of the sympathetic nervous system thus favoring the development of the end organ damage (e.g. cardiac and vascular hypertrophy) associated with the hypertensive state.","PeriodicalId":79533,"journal":{"name":"Scandinavian cardiovascular journal. Supplement","volume":"35 1","pages":"9-14"},"PeriodicalIF":0.0,"publicationDate":"1998-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"77549837","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":"Hypertension-induced congestive heart failure.","authors":"L Hansson","doi":"10.1080/140174398427974","DOIUrl":"https://doi.org/10.1080/140174398427974","url":null,"abstract":"<p><p>Arterial hypertension used to be the most common cause of congestive left ventricular failure. With the availability and common use of antihypertensive treatment the incidence and prevalence of hypertension-induced left ventricular failure has gradually declined. Today congestive heart failure due to underlying coronary heart disease is by far more common than the hypertension-induced variety. The effect of treatment of left ventricular failure in recent years, in particular with angiotensin converting enzyme inhibitors and carvedilol, has been impressive.</p>","PeriodicalId":79533,"journal":{"name":"Scandinavian cardiovascular journal. Supplement","volume":"47 ","pages":"5-7"},"PeriodicalIF":0.0,"publicationDate":"1998-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/140174398427974","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20463961","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":"New hormonal blockade strategies in cardiovascular disease.","authors":"C I Johnston,&nbsp;M Naitoh,&nbsp;J Risvanis,&nbsp;N Farina,&nbsp;L M Burrell","doi":"10.1080/140174398428063","DOIUrl":"https://doi.org/10.1080/140174398428063","url":null,"abstract":"The circulation is controlled by overlapping haemodynamic, structural and neurohumoral mechanisms. Many hormonal vasoactive substances, mostly derived from endothelial cells, are also growth regulators. Although neurohormonal systems are involved in normal physiological compensatory responses they often become maladaptive in conditions such as congestive heart failure. The success of blocking the renin angiotensin system by angiotensin converting enzyme (ACE) inhibitors has led to efforts to block other hormonal systems. Neutral endopeptidase (NEP), the major enzymatic pathway for degradation of natriuretic peptides, has a similar catalytic site to ACE. This has led to compounds that simultaneously inhibit both enzymes. Such dual ACE/NEP inhibitors show promise in experimental hypertension and heart failure. Similar dual NEP/ECE (endothelin converting enzyme) inhibitors are becoming available. The hormone vasopressin has dual actions on the vasculature and the kidney via specific membrane receptors. Specific orally active vasopressin receptor antagonists have been developed and their therapeutic potential in hypertension, heart failure and oedematous states are being explored.","PeriodicalId":79533,"journal":{"name":"Scandinavian cardiovascular journal. Supplement","volume":"47 ","pages":"61-6"},"PeriodicalIF":0.0,"publicationDate":"1998-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/140174398428063","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20463969","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":"Assessment of left ventricular dysfunction and remodeling by determination of atrioventricular plane displacement and simplified echocardiography.","authors":"R Willenheimer","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Heart failure is a common disease characterised by poor prognosis and frequent hospitalisations, constituting a major economic burden to society. Mortality and morbidity can be reduced by optimal treatment, requiring objective evaluation of cardiac function and anatomy. The development of symptomatic HF can be prevented by initiating adequate treatment in early stages when LVD is still asymptomatic. Asymptomatic patients can be identified only by screening for LVD among patients at risk of developing HF, such as those with IHD, HT, and diabetes. However, there is a severe lack of resources to assess cardiac function and anatomy in all patients at risk. Consequently, many patients with latent HF will remain undetected, and in patients with symptomatic HF treatment will not be optimal. Simplified echocardiography, a 5-minute echocardiogram based on visual estimation of cardiac function and anatomy, is an inexpensive and accurate method for diagnosis and screening for latent and symptomatic HF. The long axis shortening of the LV is related to LV function and can be measured by AVPD. Determination of left AVPD is a reliable, reproducible, readily mastered, quickly performed and, therefore, inexpensive method that can be used in almost all patients for evaluation of LV function, as well as for prognostication in HF. Left AVPD reflects both systolic and diastolic LV function. Simplified echocardiography is useful for screening of asymptomatic patients at risk of developing HF, and for routine diagnostic purposes in patients with symptoms suggestive of HF. In patients with LVSD, simplified echocardiography may be combined with a determination of left AVPD for prognostication and for optimal detection of changes in LV function over time.</p>","PeriodicalId":79533,"journal":{"name":"Scandinavian cardiovascular journal. Supplement","volume":"48 ","pages":"1-31"},"PeriodicalIF":0.0,"publicationDate":"1998-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20555529","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":"Molecular genetics of congestive heart failure.","authors":"H Schunkert","doi":"10.1080/140174398428036","DOIUrl":"https://doi.org/10.1080/140174398428036","url":null,"abstract":"<p><p>The manifestation of congestive heart failure occurs secondary to a great variety of cardiac or systemic disorders that share a temporal or permanent loss of cardiac function. In order to enhance our knowledge about the genetics of heart failure it is mandatory to analyse the aetiologic factors of these underlying disorders separately. Monogenic forms of congestive heart failure have initially been described by observant physicians in consecutive generations of affected families. Molecular genetic analyses of these families subsequently allowed us to localise and identify some of the genes that cause hypertrophic, dilative, or restrictive cardiomyopathies, congenital heart disease, as well as a number of inborn errors of metabolism. However, the great majority of patients develops heart failure as a final consequence of multifactorial conditions such as hypertension, cardiac hypertrophy, or coronary artery disease. Each of these conditions may be the product of a complex equation that includes environmental and genetic factors. Indeed, some of these factors may be harmful, others protective and for most it takes decades before a phenotype will be clinically detectable. Given this complex scenario it was not unexpected that early studies on candidate genes came up with partially controversial information. This review aims to summarize and to comment on the principal findings of this work.</p>","PeriodicalId":79533,"journal":{"name":"Scandinavian cardiovascular journal. Supplement","volume":"47 ","pages":"37-43"},"PeriodicalIF":0.0,"publicationDate":"1998-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/140174398428036","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20463966","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":"Release and effects of calcitonin gene-related peptide in myocardial ischaemia.","authors":"G Källner","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>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.</p>","PeriodicalId":79533,"journal":{"name":"Scandinavian cardiovascular journal. Supplement","volume":"49 ","pages":"1-35"},"PeriodicalIF":0.0,"publicationDate":"1998-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20677877","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}