Latency from the onset of myocardial ischemia to the rise of serum creatine kinase activity is correlated inversely with infarct size in dogs.

Sixteen dogs were subjected to acute, permanent coronary occlusion to assess the relationship between latency for the rise of serum creatine kinase (CK) activity and infarct size. Serum CK activity was measured every 30 min from 0 h to 6 h and serially afterwards until 72 h after coronary occlusion. The serum CK activity immediately before coronary occlusion (0 h) was 61 +/- 18 (SD, n = 16) (range 37-95) IU/l. It exceeded the normal threshold value (100 IU/l) at 3.7 +/- 1.4 (range 1.5-6) h, increased at a maximal rate at 7.0 +/- 1.2 h and reached a peak value of 1700 +/- 1308 (range 304-5109) IU/l at 11.0 +/- 1.8 h after coronary occlusion. The cumulative CK release (CKr) was 6556 +/- 5984 (range 454-21580) IU/l, indicating that various sizes of infarction were produced. In 7 dogs, the infarct size was determined anatomically with an enzyme staining technique. The latency of the CK rise was significantly (p less than 0.01, n = 16) and inversely correlated with the max dE/dt (r = -0.692), peak CK (r = -0.716) and CKr (r = -0.691). The CKr was correlated well (p less than 0.001, n = 16) with max dE/dt (r = 0.946), peak CK (r = 0.984) and the infarct size (r = 0.912, p less than 0.005, n = 7). Thus, the latency of the rise of serum CK activity was inversely correlated with myocardial infarct size.