Fundamental Validity and Clinical Usefulness of Myocardial Lactate Balance During Ischaemia A comparison with Other Biochemical Markers

The normally perfused myocardium receives its energy from aerobic pathways. Changes in the amount and distribution of coronary blood flow may lead to changes in oxygen (O2) and substrate delivery to the myocardium. With an impaired O2 supply, oxidative phosphorylation is inhibited, so that the energy requirement cannot be met. This leads to the breakdown of high-energy phosphates. Under these conditions the aerobic pathways shift to anaerobic pathways (Pasteur effect), and this shift is accompanied by increased myocardial pyruvate and lactate synthesis and release. The rise in coronary venous lactate concentrations leads to a decrease in the normally positive arteriocoronary venous (A-CV) lactate difference, which may even become negative. Such abnormalities in myocardial lactate balance have been used as an indicator of the presence of myocardial ischaemia in the experimental animal and in man. However, the conditions under which the A-CV lactate difference truly reflects myocardial metabolism must be sharply defined. When one is not aware of the potential pitfalls, the use of lactate levels in the diagnosis of coronary arterial disease may lead to considerable errors. This fact is now generally recognised and has led to the search for other markers of myocardial ischaemia, without the drawbacks of lactate. The purpose of this review is to reconsider the validity and usefulness of lactate measurements during myocardial ischaemia in the light of current knowledge.