Myosin light chains release in acute myocardial infarction: non-invasive estimation of infarct size

Cardiovasc Res. 1988 Jul;22(7):456-63. doi: 10.1093/cvr/22.7.456.

Abstract

After the loss of membrane integrity cardiospecific myosin light chains are released as a result of proteolytic degradation of the insoluble myosin pool. Thus, as with cytosolic enzymes, the measurement of the serum concentration changes of myosin light chains may allow a non-invasive estimation of infarct size. A two compartment model was used to describe the serum concentration changes of myosin light chains after a bolus injection into awake beagle dogs. The initial distribution volume was 7.4% of body weight, whereas the second compartment accounted for 4.7% of body weight. The fractional disappearance rate of 0.0092.min-1 resulted in a serum half life of myosin light chains of 75 min. In 30 patients with acute non-reperfused myocardial infarction a close correlation was found between the cumulative appearance of myosin light chains and their maximal serum concentration. In these patients the cumulative appearance of myosin light chains correlated with serum creatine kinase estimates of infarct size, with impairment of left ventricular ejection fraction, and with mortality during hospital admission. Thus the maximal serum concentration and the cumulative appearance of myosin light chains allow a non-invasive estimation of infarct size and may serve as a serological indicator of the patient's prognosis.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Aged
  • Animals
  • Creatine Kinase / blood
  • Dogs
  • Female
  • Humans
  • Male
  • Middle Aged
  • Myocardial Infarction / blood*
  • Myocardial Infarction / pathology
  • Myosins / blood*
  • Myosins / pharmacokinetics
  • Prognosis

Substances

  • Creatine Kinase
  • Myosins