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Optimizing CRT to Minimize ATP Consumption Heterogeneity Throughout the Left Ventricle: A Simulation Analysis Using a Canine Heart Failure Model
Filetype[PDF - 1.28 MB]


Details:
  • Pubmed ID:
    24657430
  • Pubmed Central ID:
    PMC4049272
  • Description:
    Background

    Cardiac resynchronization therapy (CRT) has been demonstrated to lead to the restoration of oxygen consumption homogeneity throughout the left ventricle (LV), which is important for long-term reverse remodeling of the ventricles. However, research has focused exclusively on identifying the LV pacing sites that led to acute hemodynamic improvements. It remains unclear whether there exist LV pacing sites that could both improve the hemodynamics and result in ATP consumption homogeneity throughout the LV, thus maximizing both CRT short-term and long-term benefits.

    Objective

    We aimed to demonstrate the feasibility of optimizing CRT pacing locations to achieve maximal improvement in both ATPCTHI (an ATP consumption heterogeneity index) and stroke work.

    Methods

    We employed an MRI-based electromechanical model of the dyssynchronous failing (DHF) canine ventricles. ATPCTHI and stroke work improvement were determined for each of 34 CRT pacing sites evenly spaced over the LV epicardium.

    Results

    Results demonstrated the feasibility of determining the optimal LV pacing site that achieves simultaneous maximum improvements in ATPCTHI and stroke work. The optimal LV CRT pacing sites in the DHF canine ventricles were located midway between apex and base. The improvement in ATPCTHI decreased more rapidly with the distance from the optimal sites as compared to stroke work improvement. CRT from the optimal sites homogenized ATP consumption by increasing septal ATP consumption and decreasing that of the lateral wall.

    Conclusion

    Simulation results using a canine heart failure model demonstrated that CRT can be optimized to achieve improvements in both ATPCTHI and stroke work.

  • Document Type:
  • Collection(s):
  • Funding:
    DP1 HL123271/HL/NHLBI NIH HHS/United States
    DP1-HL123271/DP/NCCDPHP CDC HHS/United States
    F31-HL103090/HL/NHLBI NIH HHS/United States
    R01 HL103428/HL/NHLBI NIH HHS/United States
    R01-HL103428/HL/NHLBI NIH HHS/United States
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