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Novel, single-beat approach for determining both end-systolic pressure–dimension relationship and preload recruitable stroke work
OBJECTIVE: The end-systolic pressure–dimension relationship (ESPDR) and the preload recruitable stroke work (PRSW) relationship are load-insensitive measures of contractility, but their clinical application has been limited by the need to record multiple beats over a wide volume range. In this study...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BMJ Publishing Group
2016
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4916631/ https://www.ncbi.nlm.nih.gov/pubmed/27347424 http://dx.doi.org/10.1136/openhrt-2016-000451 |
Sumario: | OBJECTIVE: The end-systolic pressure–dimension relationship (ESPDR) and the preload recruitable stroke work (PRSW) relationship are load-insensitive measures of contractility, but their clinical application has been limited by the need to record multiple beats over a wide volume range. In this study, we therefore sought to validate a new method to concomitantly determine the ESPDR and the PRSW relationship from a single beat. METHODS: Pressure–dimension loops were recorded in 14 conscious dogs under various haemodynamic and pathological conditions. Multiple-beat PRSW relationship was determined for its slope (M(w)) and for a dimension-axis intercept (D(w)). The ESPDR represented by the formula [Image: see text], was estimated from a steady-state, single-beat late-systolic pressure–dimension relationship. The single-beat M(w) was determined as an end-systolic pressure when the end-systolic dimension was equal to D(w). RESULTS: A strong correlation was observed between multiple-beat and single-beat ESPDRs (zero-stress dimension; r=0.98, p<0.0001). The single-beat estimation of M(w) calculated using the wall thickness was strongly correlated with the actual M(w) (r=0.93, p<0.0001) and was sensitive enough to detect the change in contractility by dobutamine infusion (p<0.001) and by tachycardia-induced heart failure (p<0.001). Similar results were obtained for M(w) estimated without information on wall thickness. CONCLUSIONS: M(w) can be interpreted as an end-systolic pressure when the end-systolic dimension is equal to D(w). By using the non-linear ESPDR, accurate single-beat estimation of the ESPDR and M(w) is possible even without information on wall thickness. These results should enhance the applicability of pressure–volume framework to clinical medicine. |
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