TIMI frame count: a quantitative method of assessing coronary artery flow.

BACKGROUND Although the Thrombolysis in Myocardial Infarction (TIMI) flow grade is valuable and widely used qualitative measure in angiographic trials, it is limited by its subjective and categorical nature. METHODS AND RESULTS In normal patients and patients with acute myocardial infarction (MI) (TIMI 4), the number of cineframes needed for dye to reach standardized distal landmarks was counted to objectively assess an index of coronary blood flow as a continuous variable. The TIMI frame-counting method was reproducible (mean absolute difference between two injections, 4.7 +/- 3.9 frames, n=85). In 78 consecutive normal arteries, the left anterior descending coronary artery (LAD) TIMI frame count (36.2 +/- 2.6 frames) was 1.7 times longer than the mean of the right coronary artery (20.4 +/- 3.0) and circumflex counts (22.2 +/- 4.1, P < .001 for either versus LAD). Therefore, the longer LAD frame counts were corrected by dividing by 1.7 to derive the corrected TIMI frame count (CTFC). The mean CTFC in culprit arteries 90 minutes after thrombolytic administration followed a continuous unimodal distribution (there were not subpopulations of slow and fast flow) with a mean value of 39.2 +/- 20.0 frames, which improved to 31.7 +/- 12.9 frames by 18 to 36 hours (P < .001). No correlation existed between improvements in CTFCs and changes in minimum lumen diameter (r=-.05, P=.59). The mean 90-minute CTFC among nonculprit arteries (25.5 +/- 9.8) was significantly higher (flow was slower) compared with arteries with normal flow in the absence of acute MI (21.0 +/- 3.1, P < .001) but improved to that of normal arteries by 1 day after thrombolysis (21.7 +/- 7.1, P=NS). CONCLUSIONS The CTFC is a simple, reproducible, objective and quantitative index of coronary flow that allows standardization of TIMI flow grades and facilitates comparisons of angiographic end points between trials. Disordered resistance vessel function may account in part for reductions in flow in the early hours after thrombolysis.

[1]  T. Huehns,et al.  1022-105 TIMI Grade 2 Flow is not Equivalent to TIMI 3: Implications for the Use of Thrombolytic Therapy. A Meta-Analysis of the Trials , 1995 .

[2]  C. Cannon,et al.  Comparison of front-loaded recombinant tissue-type plasminogen activator, anistreplase and combination thrombolytic therapy for acute myocardial infarction: results of the Thrombolysis in Myocardial Infarction (TIMI) 4 trial. , 1994, Journal of the American College of Cardiology.

[3]  A. Maseri,et al.  Reduced coronary vasodilator function in infarcted and normal myocardium after myocardial infarction. , 1994, The New England journal of medicine.

[4]  E. Braunwald,et al.  GUSTO, TIMI and the case for rapid reperfusion. , 1994, Acta cardiologica.

[5]  Gusto Angiographic Investigators The effects of tissue plasminogen activator, streptokinase, or both on coronary-artery patency, ventricular function, and survival after acute myocardial infarction. , 1993, The New England journal of medicine.

[6]  U. Tebbe,et al.  Impact of early perfusion status of the infarct-related artery on short-term mortality after thrombolysis for acute myocardial infarction: retrospective analysis of four German multicenter studies. , 1993, Journal of the American College of Cardiology.

[7]  L. Becker,et al.  TIMI Perfusion Grade 3 but Not Grade 2 Results in Improved Outcome After Thrombolysis for Myocardial Infarction Ventriculographic, Enzymatic, Electrocardiographic Evidence From the TEAM‐3 Study , 1993, Circulation.

[8]  C. Seiler,et al.  Measurement from arteriograms of regional myocardial bed size distal to any point in the coronary vascular tree for assessing anatomic area at risk. , 1993, Journal of the American College of Cardiology.

[9]  Frans Van de Werf,et al.  An international randomized trial comparing four thrombolytic strategies for acute myocardial infarction. , 1993, The New England journal of medicine.

[10]  T Sandor,et al.  Quantitative angiographic and statistical methods to assess serial changes in coronary luminal diameter and implications for atherosclerosis regression trials. , 1992, The American journal of cardiology.

[11]  A. Kitabatake,et al.  Lack of Myocardial Perfusion Immediately After Successful Thrombolysis: A Predictor of Poor Recovery of Left Ventricular Function in Anterior Myocardial Infarction , 1992, Circulation.

[12]  J. Anderson,et al.  Does thrombolysis in myocardial infarction (TIMI) perfusion grade 2 represent a mostly patent artery or a mostly occluded artery? Enzymatic and electrocardiographic evidence from the TEAM-2 study. Second Multicenter Thrombolysis Trial of Eminase in Acute Myocardial Infarction. , 1992, Journal of the American College of Cardiology.

[13]  F. Werf DISCREPANCIES BETWEEN THE EFFECTS OF CORONARY REPERFUSION ON SURVIVAL AND LEFT VENTRICULAR FUNCTION , 1989, The Lancet.

[14]  E. Bolson,et al.  Intrathoracic spatial location of specified coronary segments on the normal human heart. Applications in quantitative arteriography, assessment of regional risk and contraction, and anatomic display. , 1988, Circulation.

[15]  W. Ganz,et al.  The thrombolysis in myocardial infarction (TIMI) trial. , 1985, The New England journal of medicine.

[16]  E R Bates,et al.  Validation in dogs of a rapid digital angiographic technique to measure relative coronary blood flow during routine cardiac catheterization. , 1985, The American journal of cardiology.

[17]  H. S. Mueller,et al.  The Thrombolysis in Myocardial Infarction (TIMI) trial. Phase I findings. , 1985, The New England journal of medicine.

[18]  R. Kloner,et al.  The effect of streptokinase on intramyocardial hemorrhage, infarct size, and the no-reflow phenomenon during coronary reperfusion. , 1984, Circulation.

[19]  W. O’Neill,et al.  Application of digital techniques to selective coronary arteriography: use of myocardial contrast appearance time to measure coronary flow reserve. , 1984, American heart journal.

[20]  R. Kloner,et al.  The "no-reflow" phenomenon after temporary coronary occlusion in the dog. , 1974, The Journal of clinical investigation.