Small artery remodelling in hypertension: causes, consequences and therapeutic implications
Essential hypertension is treated primarily with a view to reducing blood pressure, and not with regard to normalizing the main pathological changes: the peripheral resistance and the cardiovascular structure. The aim of this review is to discuss whether normalization of the latter parameters, in pa...
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Veröffentlicht in: | Medical & biological engineering & computing 2008-05, Vol.46 (5), p.461-467 |
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Format: | Artikel |
Sprache: | eng |
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Zusammenfassung: | Essential hypertension is treated primarily with a view to reducing blood pressure, and not with regard to normalizing the main pathological changes: the peripheral resistance and the cardiovascular structure. The aim of this review is to discuss whether normalization of the latter parameters, in particular resistance vessel structure, may also be a target for therapy. The review presents first the evidence for altered structure of the resistance vasculature, an increase in the media:lumen ratio of the vessels due to inward eutrophic remodelling. Secondly the degree to which it may be possible to rectify the abnormal structure is discussed, where it is shown that there is strong evidence that this requires a therapy which causes vasodilatation in the patient concerned. Thirdly evidence is presented that altered small artery structure appears to have prognostic consequences. Fourthly, the cellular mechanisms which may be involved are discussed, where there is evidence that vasoconstriction in itself can cause inward remodelling, and that this can be prevented by vasodilators. Finally, the consequences of these findings are considered as regards clues for strategies that may be able to improve the outcome of antihypertensive therapy. The review concludes that there is reasonably strong evidence that a treatment which reduces peripheral resistance in the individual patient will, apart from reducing blood pressure, also improve the abnormal structure. |
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ISSN: | 0140-0118 1741-0444 |
DOI: | 10.1007/s11517-008-0305-3 |