Corrected TIMI frame counts correlate with stenosis severity and infarct zone wall motion after thrombolytic therapy.
BACKGROUND
The majority of patients with patent infarct-related arteries after thrombolytic therapy have slower than normal flow, which relates to myocardial perfusion.


METHODS
To evaluate the relationships between blood levels of creatine kinase (CK) and the corrected Thrombolysis in Myocardial Infarction (TIMI) frame count (CTFC), infarct artery stenosis, and left ventricular function, we studied 397 patients with a first myocardial infarction who underwent angiography at 3 weeks. TIMI flow grades, the CTFC, infarct artery stenosis, and infarct zone wall motion (by contrast ventriculography using the centerline method) were assessed, and CK levels (in units per liter) were measured hourly for the first 4 hours after streptokinase (1.5 x 10(6) U over 30-60 minutes) and then every 4 hours over the next 20 hours, all blinded to treatment and outcome.


RESULTS
Infarct artery stenosis and the CTFC, assessed as continuous variables, correlated in patients with patent infarct arteries (r = 0.33, P <.001). Also, there was a significant correlation between the CTFC and the sum of hypokinetic chords in the infarct zone (r = 0.15, P =.01). Patients with total occlusion or markedly slowed infarct artery flow (CTFC >100) had a higher fraction of chords with wall motion >2 SDs below normal (0.65 [0.41, 0.80] vs 0.37 [0.0, 0.67]) compared with patients with normal flow (CTFC < or =27) (P <.001). The rates of increase of median CK levels with respect to TIMI flow grades were 342 U/L/h for TIMI 3 versus 212 U/L/h for TIMI 2 versus 140 U/L/h for TIMI 0-1 (P <.0001).


CONCLUSIONS
Prolonged corrected TIMI frame counts correlate with stenosis severity in the infarct artery after infarction, infarct zone regional wall motion, and CK levels.
Cardiology Department, Green Lane Hospital, Auckland 1030, New Zealand.
D J
DJ
Amos
J K
JK
French
J
J
Andrews
N G
NG
Ashton
B F
BF
Williams
R M
RM
Whitlock
S O
SO
Manda
H D
HD
White
D003251:Constriction, Pathologic; D017023:Coronary Angiography; D003331:Coronary Vessels / Q000473:pathology / Q000503:physiopathology*; D003402:Creatine Kinase / Q000097:blood*; D005343:Fibrinolytic Agents / Q000627:therapeutic use*; D006801:Humans; D009203:Myocardial Infarction / Q000188:drug therapy* / Q000473:pathology / Q000503:physiopathology*; D012039:Regional Blood Flow; D013300:Streptokinase / Q000627:therapeutic use*; D015912:Thrombolytic Therapy
D005343:Fibrinolytic Agents; D003402:Creatine Kinase; D013300:Streptokinase