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- W2301441605 abstract "Background Tachycardia in ischemic acute heart failure (AHF) is believed to be a compensatory response to sustain cardiac output and perfusion pressure. Little is known about early diastole in this setting. Methods In a pig model (n=8, mean±SD) we simultaneously measured myocardial strain (sonometric crystals), mitral-inflow (conductance-catheter) and mitral-pressure difference MITRP (LV-LA micromanometer). Pacing-induced tachycardia was induced in the control state and in ischemic AHF (following coronary microembolization). Results Tachycardia (160 bpm) shortened the long axis é-delay (see Figure) from 43±30 to 20±21 ms (p=0.0066), compared to E wave in control, but not in AHF (22±13 to 25±17 ms). Interestingly, by reducing preload to similar levels as control, the é-delay became evident also in the AHF condition (22±13 vs 48±23 ms p=0.0067). Additionally, tachycardia increased peak MITRP from 4±1 to 9±4 (p=0.007) mmHg in control, but not in AHF (6±2 to 7±2 mmHg). The enhanced relaxation following tachycardia caused a maintained potential energy across the mitral valve in early filling phase (MITRPINTG) in control (0.4±0.2 to 0.4±0.2 mmHg*s), which was reduced following tachycardia in AHF (0.6±0.2 to 0.4±0.2 mmHg*s p=0.0246). Conclusion Tachycardia during AHF fails to hasten é and thereby amplifying the pressure driving force across the mitral valve." @default.
- W2301441605 created "2016-06-24" @default.
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- W2301441605 date "2013-04-01" @default.
- W2301441605 modified "2023-09-23" @default.
- W2301441605 title "Elevated preload is critical for synchronization of myocardial lengthening (é) and mitral inflow (E) in acute ischemic acute heart failure" @default.
- W2301441605 doi "https://doi.org/10.1096/fasebj.27.1_supplement.lb663" @default.
- W2301441605 hasPublicationYear "2013" @default.
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