Linked Life Data

12732279

Source:http://linkedlifedata.com/resource/pubmed/id/12732279

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pubmed-article:12732279pubmed:dateCreated2003-5-6lld:pubmed
pubmed-article:12732279pubmed:abstractTextHeart failure (HF) is a progressive degenerative and malignant syndrome with a large number of aetiologies including coronary artery disease, chronic hypertension, exposure to toxins, bacteria and viruses and in a significant percentage of HF patients, the causal mechanism is unclear. The HF trail of morbidity and mortality is well documented and is characterised by step-like periods of relative symptomatic stability, compensation, separated by decompensatory episodes. The homeostatic response to the decline in cardiac function is diverse and involves most organs. There is an increase in resting rate, intra-cardiac hormone production (catecholamines, aldosterone, etc.) and in particular structural changes occur with increased mass and dilatation (dilated cardiomyopathy, DCM). DCM is associated with decreased cardiac output, contractility and energy efficiency and an increase in pro-arrhythmia and conduction defects. Kass et al. (Circulation 91(9) (1995) 2314) first demonstrated in patients who had undergone a dynamic cardio-myoplasty procedure, that, preventing further dilatation in DCM was beneficial and that the improved cardiovascular status was largely independent of muscle stimulation. We hypothesised that this outcome could be achieved by implanting a fabric cardiac support device around both ventricles to the AV junction. Subsequently, it was shown by us and others (Kass et al., 1995) (Cardiovasc. Res. 44(3) (1999) 549); (Ann. Thorac. Surg. 70(4) (2000) 1275) (in different animal models of DCM) that passive ventricular constraint prevented further dilatation, initiated left ventricular volume reduction and reversed the decline in ejection fraction, mitral valve integrity and left ventricular contractility, when compared with untreated controls. Subsequent European and North American clinical trials in patients with DCM of varying aetiologies have shown equal promise and an absence of device related complications (Circulation 104(12 Suppl. 1) (2001) I270); (Ann. Thorac. Cardiovasc. Surg. 7(5) (2001) 278). The mechanisms behind this improvement have yet to be fully clarified however the support generated by the device upon the right and ventricular freewall would lower wall tension. Not only is passive ventricular constraint a very promising treatment modality for heart failure and DCM it should provide a useful research tool for the study of the role of ventricular dilatation in the progression of heart failure.lld:pubmed
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pubmed-article:12732279pubmed:authorpubmed-author:PowerJohn MJMlld:pubmed
pubmed-article:12732279pubmed:authorpubmed-author:RamanJaiJlld:pubmed
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pubmed-article:12732279pubmed:volume82lld:pubmed
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pubmed-article:12732279pubmed:pagination197-206lld:pubmed
pubmed-article:12732279pubmed:dateRevised2007-11-15lld:pubmed
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pubmed-article:12732279pubmed:articleTitlePassive ventricular constraint.lld:pubmed
pubmed-article:12732279pubmed:affiliationBaker Medical Research Institute, P.O. Box 6492, St Kilda Road Central, Victoria 8008, Melbourne, Australia. john.power@back.edu.aulld:pubmed
pubmed-article:12732279pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:12732279pubmed:publicationTypeReviewlld:pubmed