Via practica 9/2006

METABOLISM OF THE MYOCARDIUM IN THE CONDITION OF CHRONIC HEART FAILURE

There are older theories suggesting, that failing myocardium has different metabolism than intact myocardium. The most notorious is the evidence about the defective production of energy. The evidence was mostly experimental, or it was hardly reproducible. With positron emission tomography (PET) was the experimental evidence verified also in clinical conditions. With the help of PET it was observed, that some drugs with hemodynamic effect also have metabolic effect – utilisation of glucose is prior to utilisation of the fatty acids. There is a drug, which has the basic effect in direct inhibition of the enzyme 3-ketoacyl koenzyme-A tiolase, which is a part of beta oxidation (it is a direct compound)of fatty acids. By that glucose will be indirectly preferred as an energy source, which needs less oxygen for oxidation. This effect is used for the treatment of stable angina pectoris. The evidence of presence of fetal isoforms of myosine, which are able to utilize glycolysis better in failing myocardium, supports the correct choice of this treatment. The altered metabolism of myocardium and change of metabolic treatment resulting from that is not reflected in last guidelines of ESC for treatment of CHF (congestive heart failure). We bring the evidence for improvement of contractility of myocardium without influencing the hemodynamics, or under conditions, when use of hemodynamically active drugs is doubtfull or contraindicated because of hypotension or bradycardia

Keywords: Metabolism of failing myocardium, fetal isoforms of myosine, ß-oxidation of fatty acids, utilisation of glucose, trimetazidine MR.