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[Antagonistic function of the heart muscle : Part II: Clinical implications]

P P Lunkenheimer1, P Niederer2, J M Lunkenheimer3

  • 1Experimentelle Thorax‑, Herz- und Gefäßchirurgie, Universitätskliniken Münster, Münster, Deutschland. P.P.Lunkenheimer@web.de.

Herz
|July 29, 2018
PubMed

Insights

Myocardial hypertrophy is worsened by myostructural afterload and connective tissue changes. Targeted negative inotropic medication and optimized mechanical support may offer new therapeutic avenues for heart disease.

Area of Science:

  • Cardiovascular Physiology
  • Cardiac Pathophysiology

Background:

  • Hypertrophic heart disease is characterized by predominant myostructural afterload from endoepicardial networks, exacerbating myocardial hypertrophy.
  • The intrinsic antagonism within the heart muscle is disrupted, leading to increased connective tissue (stromatogenic afterload) and regional cardiac dysfunction.

Purpose of the Study:

  • To explore the mechanisms underlying myocardial hypertrophy and identify potential therapeutic targets.
  • To evaluate the efficacy of negative inotropic medication and mechanical circulatory support in managing hypertrophic heart conditions.
  • To propose novel diagnostic approaches for assessing myocardial stiffness and local motion patterns.

Main Methods:

  • Analysis of myostructural and stromatogenic afterload in hypertrophic hearts.
  • Assessment of the susceptibility of the myocardial network to negative inotropic agents.
  • Evaluation of volume reduction surgery and external mechanical circulatory support parameters.
  • Consideration of takotsubo cardiomyopathy as a model for intrinsic antagonism dysfunction.

Main Results:

  • The oblique transmural myocardial network shows selective susceptibility to low-dose negative inotropic medication, suggesting a potential to attenuate hypertrophy.
  • Volume reduction surgery is effective in reducing wall stress, provided the myocardium is not severely fibrotic.
  • External mechanical circulatory support is most effective when maintaining the heart in a resting state with minimal motion.

Conclusions:

  • Targeting the auxotonic, contracting myocardial network with negative inotropic medication may slow hypertrophic progression.
  • Optimizing mechanical circulatory support for resting heart function is crucial for efficacy.
  • Clinical diagnostics for heart disease require advancements focusing on local motion patterns and myocardial stiffness as markers of antagonistic intensity.

Keywords:
Circulatory supportDerailed antagonismMyocardial hypertrophyTakotsubo cardiomyopathyVolume reduction surgery

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