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Elevated preload is critical for synchronization of myocardial lengthening (é) and mitral inflow (E) in ischemic acute heart failure complicated with tachycardia (1150.2)
Author(s) -
How OleJakob,
Naesheim Torvind,
Bakkehaug JensPetter,
Kondratiev Timofey,
Remme Espen,
Myrmel Truls
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.1150.2
Subject(s) - cardiology , preload , medicine , tachycardia , heart failure , hemodynamics
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.