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Treatments targeting inotropy.

Christoph Maack1, Thomas Eschenhagen2,3, Nazha Hamdani4

  • 1Comprehensive Heart Failure Center, University Clinic Würzburg, Am Schwarzenberg 15, Würzburg, Germany.

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|October 9, 2018
PubMed
Summary
This summary is machine-generated.

Newer heart failure drugs targeting sarcomeres may improve systolic function without increasing mortality. Research reviews mechanisms and mitochondrial impacts, seeking safer, long-term treatments for heart failure.

Keywords:
Acute decompensated heart failureAdrenergic receptorsCalciumCardiogenic shockContractilityEnergeticsExcitation–contraction couplingHeart failureInotropesLevosimendanMitochondriaNitroxylOmecamtiv mecarbilSarcomeres

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Area of Science:

  • Cardiology and Pharmacology
  • Mitochondrial Bioenergetics and Redox Regulation

Background:

  • Acute heart failure (HF), especially cardiogenic shock, presents high mortality risks.
  • Conventional positive inotropic agents (catecholamines, phosphodiesterase-inhibitors) are linked to increased mortality.
  • Novel agents like levosimendan and omecamtiv mecarbil target sarcomeres, aiming to improve systolic function without raising intracellular Ca2+.

Purpose of the Study:

  • To review the pathophysiological basis of systolic dysfunction in heart failure.
  • To examine the mechanisms of action for various inotropic agents.
  • To explore the impact of these agents on mitochondrial bioenergetics and redox regulation.

Main Methods:

  • Review of existing literature on heart failure pathophysiology and inotropic agents.
  • Analysis of clinical trial data for levosimendan and omecamtiv mecarbil.
  • Discussion of the link between mitochondrial function, excitation-contraction coupling, and inotropic drug effects.

Main Results:

  • Meta-analyses of smaller trials suggested levosimendan improved outcomes compared to dobutamine, but larger trials did not confirm this.
  • Omecamtiv mecarbil shows a favorable hemodynamic profile in Phase II trials for acute and chronic HF.
  • A Phase III trial for omecamtiv mecarbil in chronic HF is underway.

Conclusions:

  • Identifying novel therapeutic targets is crucial for safely improving acute systolic and diastolic function in HF.
  • Further research may lead to treatments that also enhance long-term myocardial structure and function.
  • Understanding the impact on mitochondrial bioenergetics is key to developing safer inotropic strategies.