Please use this identifier to cite or link to this item: https://hdl.handle.net/10216/67155
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dc.creatorLeite-Moreira, AF
dc.creatorLourenço, AP
dc.creatorRoncon-Albuquerque R, Jr.
dc.creatorHenriques-Coelho, T
dc.creatorAmorim, MJ
dc.creatorAlmeida, J
dc.creatorPinho, P
dc.creatorGillbert, TC
dc.date.accessioned2022-09-09T03:39:57Z-
dc.date.available2022-09-09T03:39:57Z-
dc.date.issued2012
dc.identifier.issn0300-8428
dc.identifier.othersigarra:81019
dc.identifier.urihttps://hdl.handle.net/10216/67155-
dc.description.abstractIn animal experiments, elevating systolic pressures induces diastolic dysfunction and may contribute to congestion, a finding not yet translated to humans. Coronary surgery patients (63 +/- 8 years) were studied with left ventricular (LV) pressure (n = 17) or pressure volume (n = 3) catheters, immediately before cardiopulmonary bypass. Single-beat graded pressure elevations were induced by clamping the ascending aorta. Protocol was repeated after volume loading (n = 7). Consecutive patients with a wide range of systolic function were included. Peak isovolumetric LV pressure (LVPiso) ranged from 113 to 261 mmHg. With preserved systolic function, LVP elevations neither delayed relaxation nor increased filling pressures. With decreasing systolic function, diastolic tolerance to afterload progressively disappeared: relaxation slowed and filling pressures increased (diastolic dysfunction). In severely depressed systolic function, filling pressures increased even with minor LVP elevations, suggesting baseline load-dependent elevation of diastolic pressures. The magnitude of filling pressure elevation induced in isovolumetric heartbeats was closely and inversely related to systolic performance, evaluated by LVPiso (r = -0.96), and directly related to changes in the time constant of relaxation tau (r = 0.95). The maximum tolerated systolic LVP (without diastolic dysfunction) was similarly correlated with LVPiso (r = 0.99). Volume loading itself accelerated relaxation, but augmented afterload-induced upward shift of filling pressures (7.9 +/- 3.7 vs. 3.0 +/- 1.5; P < 0.01). The normal human response to even markedly increased systolic pressures is no slowing of relaxation and preservation of normal filling pressures. When cardiac function deteriorates, the LV becomes less tolerant, responding with slowed relaxation and increased filling pressures. This increase is exacerbated by volume loading.
dc.language.isoeng
dc.rightsopenAccess
dc.rights.urihttps://creativecommons.org/licenses/by-nc/4.0/
dc.subjectCiências médicas e da saúde
dc.subjectMedical and Health sciences
dc.titleDiastolic tolerance to systolic pressures closely reflects systolic performance in patients with coronary heart disease
dc.typeArtigo em Revista Científica Internacional
dc.contributor.uportoFaculdade de Medicina
dc.identifier.doi10.1007/s00395-012-0251-y
dc.identifier.authenticusP-002-CDQ
dc.subject.fosCiências médicas e da saúde
dc.subject.fosMedical and Health sciences
Appears in Collections:FMUP - Artigo em Revista Científica Internacional

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