Myocardial infarction, lactate diagnosis

Assay of plasma enzymes aids diagnosis and prognosis. For example, a myocardial infarction elevates serum levels of lactate dehydrogenase isozyme I,. 

At present the determination of lactate does not belong to the most frequently performed analyses in clinical chemistry yet its popularity in the diagnosis of shock and myocardial infarction and in neonatology and sports medicine is increasing. Strong efforts are therefore being made to develop sensor-based lactate analyzers which may be readily used at the bedside. 

Interruption of the heart s blood supply leads to the death of cardiac muscle cells. The symptoms of myocardial infarction include pain in the left side of the chest that may radiate to the neck, left shoulder, and arm, and irregular breathing. The initial diagnosis is based on these and other symptoms. Therapy is instituted immediately. Physicians then use several enzyme assays to confirm the diagnosis and to monitor the course of treatment. The enzymes most commonly assayed are creatine kinase (CK) and lactate dehydrogenase (LDH). Each enzyme s activity shows a characteristic time profile in terms of its release from damaged cardiac muscle cells and rate of clearance from blood (Figure 6A). 

The determination of lactate is becoming increasingly popular in the diagnosis of shock and myocardial infarction and in neonatology and sports medicine. Therefore, great efforts are being made to develop sensor-based lactate analyzers which may readily be used at the bedside. The first enzyme electrode-based lactate analyzer was developed in 1976 by La Roche (Switzerland) (see Thble 14-8). It contains cytochrome in a small reaction chamber in front of a platinum electrode polarized at +0.25-0.40 V. The lactate values measured with the analyzer correlate fairly well with those obtained with the spectrophotometric reference method using deproteinized blood ... 

Serum enzyme estimations can be of assistance in the diagnosis of myocardial infarction. Creatine kinase levels reach a peak value 24-30 hours after the infarction while, aspartate aminotransferase reaches a peak value around 36 hours after the event. Lactate dehydrogenase (or hydroxybutyrate dehydrogenase) reaches peak levels 2-3 days after the infarction. 

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