Clinical utility of Myoglobin and LDH

Myoglobin:

It is known for its excellent clinical sensitivity early after MI (even before troponin and CK) but has lack of tissue specificity. Serum level rises 1 hr after MI, with peak at 2-12 hours. An attempt to improve clinical specificity of Mb is the measurement of carbonic anhydrase III (CA III). After an AMI, serum CA III remain unchanged, while both CK-2 and Mb increased. In patients with skeletal muscle trauma, Mb CK-2, CA III (skeletal muscle specific) were all elevated.

Lactate Dehydrogenase:

Due to its wide distribution, elevations occur in various clinical conditions like MI, hemolysis, liver, kidney, lung, muscle disorders. Hemolysis if severe produces the LD isoenzyme pattern similar to MI and also during megaloblastic anaemia where LD1 increases.

These are no longer measured. For historical perspective, for patients with AMI, serum LD values become elevated at 12-18 hr after the onset of symptoms, peaking at 48-72 hrs and normalizing after 6-10 days. LD-1 rises within 10-12 hours, peaks at 72-144 hours and normalizes in 10 days after AMI, paralleling total LD. Due to prolonged half-life LD-1 is a clinically sensitive marker for infarction when used more than 24 hours after occurrence. In the serum LD2 is more than LD1 but the appearance of more LD1 than LD2 is called flipped pattern typical of cardiac muscle damage but is non specific as it is seen during hemolysis, megaloblastic anaemia, chronic exercise, etc. This flipped ratio persists for 3 to 4 days after heart attack.