ST elevation myocardial infarction pathophysiology of reperfusion: Difference between revisions

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==[[TIMI Frame Count (TFC)|The TIMI Frame Count]]: A More Precise Angiographic Index of Coronary Blood Flow==
==[[TIMI Frame Count (TFC)|The TIMI Frame Count]]: A More Precise Angiographic Index of Coronary Blood Flow==


There are several limitations to the TFG classification scheme <ref name="Gibson 1"> Gibson CM, Cannon CP, Daley WL, et al. The TIMI frame count: a quantitative method of assessing coronary artery flow. Circulation. 1996; 93: 879–888.</ref>. To overcome these limitations, Gibson developed a more objective and precise index of coronary blood flow called the corrected TIMI frame count (CTFC). In this method, the number of cineframes required for dye to reach standardized distal landmarks are counted. Each frame is 1/30th of a second, and the angiogram is therefore essentially a measure of the time for dye to go down the artery <ref name="Gibson 1"> Gibson CM, Cannon CP, Daley WL, et al. The TIMI frame count: a quantitative method of assessing coronary artery flow. Circulation. 1996; 93: 879–888.</ref> <ref name="Gibson2">Gibson CM, Murphy SA, Rizzo MJ, et al. The relationship between the TIMI frame count and clinical outcomes after thrombolytic administration. Circulation. 1999; 99: 1945–1950. </ref> <ref name="Gibson3"> Gibson CM, Cannon CP, Murphy SA, et al. Relationship of the TIMI myocardial perfusion grades, flow grades, frame count, and percutaneous coronary intervention to long-term outcomes after thrombolytic administration in acute myocardial infarction. Circulation. 2002; 105: 1909–1913. </ref>. In the first frame used for TIMI frame counting, a column of dye touches both borders of the coronary artery and moves forward <ref name="Gibson 1"> Gibson CM, Cannon CP, Daley WL, et al. The TIMI frame count: a quantitative method of assessing coronary artery flow. Circulation. 1996; 93: 879–888.</ref>. In the last frame, dye begins to enter (but does not necessarily fill) a standard distal landmark in the artery. These standard distal landmarks are as follows: in the RCA, the first branch of the posterolateral artery; in the circumflex system, the most distal branch of the obtuse marginal branch, which includes the culprit lesion in the dye path; and in the LAD, the distal bifurcation, which is also known as the "moustache," "pitchfork" or "whale’s tail". These frame counts are corrected for the longer length of the LAD by dividing by 1.7 to arrive at the CTFC <ref name="Gibson 1"> Gibson CM, Cannon CP, Daley WL, et al. The TIMI frame count: a quantitative method of assessing coronary artery flow. Circulation. 1996; 93: 879–888.</ref>. Knowing the time for dye to go down the artery from the CTFC (CTFC/30=seconds), and length of the artery (either from an angioplasty guide wire or by planimetry), dye velocity (cm/s) can also be calculated in a more refined fashion.<ref name="Gibson7"> Gibson CM, Dodge JT, Goel M, et al. The PTCA guidewire velocity. A new simple method to measure absolute coronary velocity and blood flow. Am J Cardiol. 1997; 80: 1536–1539.</ref>. This refined measure allows calculation of the velocity proximal and distal to the lesion <ref name="Gibson7"> Gibson CM, Dodge JT, Goel M, et al. The PTCA guidewire velocity. A new simple method to measure absolute coronary velocity and blood flow. Am J Cardiol. 1997; 80: 1536–1539.</ref>.  
There are several limitations to the TFG classification scheme <ref name="pmid8598078">{{cite journal |author=Gibson CM, Cannon CP, Daley WL, ''et al'' |title=TIMI frame count: a quantitative method of assessing coronary artery flow |journal=Circulation |volume=93 |issue=5 |pages=879–88 |year=1996 |month=March |pmid=8598078 |doi= |url=http://circ.ahajournals.org/cgi/pmidlookup?view=long&pmid=8598078}}</ref>. To overcome these limitations, Gibson developed a more objective and precise index of coronary blood flow called the corrected TIMI frame count (CTFC). In this method, the number of cineframes required for dye to reach standardized distal landmarks are counted. Each frame is 1/30th of a second, and the angiogram is therefore essentially a measure of the time for dye to go down the artery <ref name="pmid8598078">{{cite journal |author=Gibson CM, Cannon CP, Daley WL, ''et al'' |title=TIMI frame count: a quantitative method of assessing coronary artery flow |journal=Circulation |volume=93 |issue=5 |pages=879–88 |year=1996 |month=March |pmid=8598078 |doi= |url=http://circ.ahajournals.org/cgi/pmidlookup?view=long&pmid=8598078}}</ref><ref name="pmid10208996">{{cite journal |author=Gibson CM, Murphy SA, Rizzo MJ, ''et al'' |title=Relationship between TIMI frame count and clinical outcomes after thrombolytic administration. Thrombolysis In Myocardial Infarction (TIMI) Study Group |journal=Circulation |volume=99 |issue=15 |pages=1945–50 |year=1999 |month=April |pmid=10208996 |doi= |url=http://circ.ahajournals.org/cgi/pmidlookup?view=long&pmid=10208996}}</ref><ref name="pmid11997276">{{cite journal |author=Gibson CM, Cannon CP, Murphy SA, Marble SJ, Barron HV, Braunwald E |title=Relationship of the TIMI myocardial perfusion grades, flow grades, frame count, and percutaneous coronary intervention to long-term outcomes after thrombolytic administration in acute myocardial infarction |journal=Circulation |volume=105 |issue=16 |pages=1909–13 |year=2002 |month=April |pmid=11997276 |doi= |url=http://circ.ahajournals.org/cgi/pmidlookup?view=long&pmid=11997276}}</ref>. In the first frame used for TIMI frame counting, a column of dye touches both borders of the coronary artery and moves forward <ref name="pmid8598078">{{cite journal |author=Gibson CM, Cannon CP, Daley WL, ''et al'' |title=TIMI frame count: a quantitative method of assessing coronary artery flow |journal=Circulation |volume=93 |issue=5 |pages=879–88 |year=1996 |month=March |pmid=8598078 |doi= |url=http://circ.ahajournals.org/cgi/pmidlookup?view=long&pmid=8598078}}</ref>. In the last frame, dye begins to enter (but does not necessarily fill) a standard distal landmark in the artery. These standard distal landmarks are as follows: in the RCA, the first branch of the posterolateral artery; in the circumflex system, the most distal branch of the obtuse marginal branch, which includes the culprit lesion in the dye path; and in the LAD, the distal bifurcation, which is also known as the "moustache," "pitchfork" or "whale’s tail". These frame counts are corrected for the longer length of the LAD by dividing by 1.7 to arrive at the CTFC <ref name="pmid8598078">{{cite journal |author=Gibson CM, Cannon CP, Daley WL, ''et al'' |title=TIMI frame count: a quantitative method of assessing coronary artery flow |journal=Circulation |volume=93 |issue=5 |pages=879–88 |year=1996 |month=March |pmid=8598078 |doi= |url=http://circ.ahajournals.org/cgi/pmidlookup?view=long&pmid=8598078}}</ref>. Knowing the time for dye to go down the artery from the CTFC (CTFC/30=seconds), and length of the artery (either from an angioplasty guide wire or by planimetry), dye velocity (cm/s) can also be calculated in a more refined fashion.<ref name="pmid9416931">{{cite journal |author=Gibson CM, Dodge JT, Goel M, ''et al'' |title=Angioplasty guidewire velocity: a new simple method to calculate absolute coronary blood velocity and flow |journal=Am. J. Cardiol. |volume=80 |issue=12 |pages=1536–9 |year=1997 |month=December |pmid=9416931 |doi= |url=http://linkinghub.elsevier.com/retrieve/pii/S0002914997007479}}</ref>. This refined measure allows calculation of the velocity proximal and distal to the lesion<ref name="pmid9416931">{{cite journal |author=Gibson CM, Dodge JT, Goel M, ''et al'' |title=Angioplasty guidewire velocity: a new simple method to calculate absolute coronary blood velocity and flow |journal=Am. J. Cardiol. |volume=80 |issue=12 |pages=1536–9 |year=1997 |month=December |pmid=9416931 |doi= |url=http://linkinghub.elsevier.com/retrieve/pii/S0002914997007479}}</ref>.  


Some of the advantages of the TIMI frame count method are as follows. In contrast to the TFG classification scheme, the CTFC is quantitative rather than qualitative, it is objective rather than subjective, it is a continuous rather than a categorical variable, and it is reproducible <ref name="Gibson 1"> Gibson CM, Cannon CP, Daley WL, et al. The TIMI frame count: a quantitative method of assessing coronary artery flow. Circulation. 1996; 93: 879–888.</ref>. The CTFC demonstrates that flow is not divided into arbitrary slow and fast categories, but rather coronary blood flow is unimodally distributed as a continuous variable <ref name="Gibson 1"> Gibson CM, Cannon CP, Daley WL, et al. The TIMI frame count: a quantitative method of assessing coronary artery flow. Circulation. 1996; 93: 879–888.</ref>. The CTFC has been shown to be quite reproducible with a 1- to 2-frame difference between observers <ref name="Abaci1">Abaci A, Oguzhan A, Eryol NK, et al. Effects of potential confounding factors on the Thrombolysis In Myocardial Infarction (TIMI) trial frame count and its reproducibility. Circulation. 1999; 100: 2219–2223. </ref> <ref>Manginas A, Gatzov P, Chasikidis C, et al. Estimation of coronary flow reserve using the Thrombolysis In Myocardial Infarction (TIMI) frame count method. Am J Cardiol. 1999; 83: 1562–1565.  
Some of the advantages of the TIMI frame count method are as follows. In contrast to the TFG classification scheme, the CTFC is quantitative rather than qualitative, it is objective rather than subjective, it is a continuous rather than a categorical variable, and it is reproducible <ref name="pmid8598078">{{cite journal |author=Gibson CM, Cannon CP, Daley WL, ''et al'' |title=TIMI frame count: a quantitative method of assessing coronary artery flow |journal=Circulation |volume=93 |issue=5 |pages=879–88 |year=1996 |month=March |pmid=8598078 |doi= |url=http://circ.ahajournals.org/cgi/pmidlookup?view=long&pmid=8598078}}</ref>. The CTFC demonstrates that flow is not divided into arbitrary slow and fast categories, but rather coronary blood flow is unimodally distributed as a continuous variable <ref name="pmid8598078">{{cite journal |author=Gibson CM, Cannon CP, Daley WL, ''et al'' |title=TIMI frame count: a quantitative method of assessing coronary artery flow |journal=Circulation |volume=93 |issue=5 |pages=879–88 |year=1996 |month=March |pmid=8598078 |doi= |url=http://circ.ahajournals.org/cgi/pmidlookup?view=long&pmid=8598078}}</ref>. The CTFC has been shown to be quite reproducible with a 1- to 2-frame difference between observers <ref name="pmid10577994">{{cite journal |author=Abaci A, Oguzhan A, Eryol NK, Ergin A |title=Effect of potential confounding factors on the thrombolysis in myocardial infarction (TIMI) trial frame count and its reproducibility |journal=Circulation |volume=100 |issue=22 |pages=2219–23 |year=1999 |month=November |pmid=10577994 |doi= |url=http://circ.ahajournals.org/cgi/pmidlookup?view=long&pmid=10577994}}</ref><ref name="pmid10363873">{{cite journal |author=Manginas A, Gatzov P, Chasikidis C, Voudris V, Pavlides G, Cokkinos DV |title=Estimation of coronary flow reserve using the Thrombolysis In Myocardial Infarction (TIMI) frame count method |journal=Am. J. Cardiol. |volume=83 |issue=11 |pages=1562–5, A7 |year=1999 |month=June |pmid=10363873 |doi= |url=http://linkinghub.elsevier.com/retrieve/pii/S0002-9149(99)00149-6}}</ref><ref name="pmid10704161">{{cite journal |author=Stankovic G, Manginas A, Voudris V, ''et al'' |title=Prediction of restenosis after coronary angioplasty by use of a new index: TIMI frame count/minimal luminal diameter ratio |journal=Circulation |volume=101 |issue=9 |pages=962–8 |year=2000 |month=March |pmid=10704161 |doi= |url=http://circ.ahajournals.org/cgi/pmidlookup?view=long&pmid=10704161}}</ref><ref name="pmid12586269">{{cite journal |author=Barcin C, Denktas AE, Garratt KN, Higano ST, Holmes DR, Lerman A |title=Relation of Thrombolysis in Myocardial Infarction (TIMI) frame count to coronary flow parameters |journal=Am. J. Cardiol. |volume=91 |issue=4 |pages=466–9 |year=2003 |month=February |pmid=12586269 |doi= |url=http://linkinghub.elsevier.com/retrieve/pii/S0002914902032502}}</ref><ref name="pmid11870267">{{cite journal |author=Umman B, Nisanci Y, Sezer M, ''et al'' |title=The relationship between corrected TIMI frame count and myocardial fractional flow reserve |journal=J Invasive Cardiol |volume=14 |issue=3 |pages=125–8 |year=2002 |month=March |pmid=11870267 |doi= |url=}}</ref><ref>French JK, Hyde TA, Amos DJ, et al. Corrected TIMI frame count at 3 weeks influences survival at 5 years but not 10 years after myocardial infarction. Eur Heart J. 1998; 19: 630.</ref><ref>Straznicky IT, French JK, Webber BJ, et al. Corrected TIMI frame count at 90 minutes predicts left ventricular function at 48 hours following myocardial infarction treated with streptokinase and heparin or hirulog. Eur Heart J. 1998; 19: 285. </ref><ref name="pmid9527071">{{cite journal |author=French JK, Ellis CJ, Webber BJ, ''et al'' |title=Abnormal coronary flow in infarct arteries 1 year after myocardial infarction is predicted at 4 weeks by corrected Thrombolysis in Myocardial Infarction (TIMI) frame count and stenosis severity |journal=Am. J. Cardiol. |volume=81 |issue=6 |pages=665–71 |year=1998 |month=March |pmid=9527071 |doi= |url=http://linkinghub.elsevier.com/retrieve/pii/S0002914997010047}}</ref><ref name="pmid9922346">{{cite journal |author=French JK, Straznicky IT, Webber BJ, ''et al'' |title=Angiographic frame counts 90 minutes after streptokinase predict left ventricular function at 48 hours following myocardial infarction |journal=Heart |volume=81 |issue=2 |pages=128–33 |year=1999 |month=February |pmid=9922346 |pmc=1728934 |doi= |url=http://heart.bmj.com/cgi/pmidlookup?view=long&pmid=9922346}}</ref><ref name="pmid10807455">{{cite journal |author=French JK, Hyde TA, Straznicky IT, ''et al'' |title=Relationship between corrected TIMI frame counts at three weeks and late survival after myocardial infarction |journal=J. Am. Coll. Cardiol. |volume=35 |issue=6 |pages=1516–24 |year=2000 |month=May |pmid=10807455 |doi= |url=http://linkinghub.elsevier.com/retrieve/pii/S0735-1097(00)00577-5}}</ref><ref name="pmid11275924">{{cite journal |author=Amos DJ, French JK, Andrews J, ''et al'' |title=Corrected TIMI frame counts correlate with stenosis severity and infarct zone wall motion after thrombolytic therapy |journal=Am. Heart J. |volume=141 |issue=4 |pages=586–91 |year=2001 |month=April |pmid=11275924 |doi=10.1067/mhj.2001.113393 |url=}}</ref><ref name="pmid12464786">{{cite journal |author=Sahin M, Basoglu T, Canbaz F, Elcik M, Kosus A |title=The value of the TIMI frame count method in the diagnosis of coronary no-reflow: a comparison with myocardial perfusion SPECT in patients with acute myocardial infarction |journal=Nucl Med Commun |volume=23 |issue=12 |pages=1205–10 |year=2002 |month=December |pmid=12464786 |doi=10.1097/01.mnm.0000046213.83338.9e |url=}}</ref><ref>Moliterno D, Antman EM, Ohman M, et al. Concordance between core labs in trial results using TIMI flow grades and frame counts. Circulation. 2000; 102 (suppl II): II–590. </ref>. The CTFC is also highly correlated with other measures of flow such as Doppler velocity wire measures of coronary flow reserve, distal velocity, average peak velocity, and volumetric flow, <ref name="pmid10363873">{{cite journal |author=Manginas A, Gatzov P, Chasikidis C, Voudris V, Pavlides G, Cokkinos DV |title=Estimation of coronary flow reserve using the Thrombolysis In Myocardial Infarction (TIMI) frame count method |journal=Am. J. Cardiol. |volume=83 |issue=11 |pages=1562–5, A7 |year=1999 |month=June |pmid=10363873 |doi= |url=http://linkinghub.elsevier.com/retrieve/pii/S0002-9149(99)00149-6}}</ref><ref name="pmid10704161">{{cite journal |author=Stankovic G, Manginas A, Voudris V, ''et al'' |title=Prediction of restenosis after coronary angioplasty by use of a new index: TIMI frame count/minimal luminal diameter ratio |journal=Circulation |volume=101 |issue=9 |pages=962–8 |year=2000 |month=March |pmid=10704161 |doi= |url=http://circ.ahajournals.org/cgi/pmidlookup?view=long&pmid=10704161}}</ref><ref name="pmid12586269">{{cite journal |author=Barcin C, Denktas AE, Garratt KN, Higano ST, Holmes DR, Lerman A |title=Relation of Thrombolysis in Myocardial Infarction (TIMI) frame count to coronary flow parameters |journal=Am. J. Cardiol. |volume=91 |issue=4 |pages=466–9 |year=2003 |month=February |pmid=12586269 |doi= |url=http://linkinghub.elsevier.com/retrieve/pii/S0002914902032502}}</ref> as well as fractional flow reserve (r=0.85)<ref name="pmid11870267">{{cite journal |author=Umman B, Nisanci Y, Sezer M, ''et al'' |title=The relationship between corrected TIMI frame count and myocardial fractional flow reserve |journal=J Invasive Cardiol |volume=14 |issue=3 |pages=125–8 |year=2002 |month=March |pmid=11870267 |doi= |url=}}</ref>  
</ref> <ref>Stankovic G, Manginas A, Voudris V, et al. Prediction of restenosis after coronary angioplasty by use of a new index: TIMI frame count/minimal luminal diameter ratio. Circulation. 2000; 101: 962–968.</ref> <ref>Barcin C, Denktas AE, Garratt KN, et al. Relation of Thrombolysis In Myocardial Infarction (TIMI) frame count to coronary flow parameters. Am J Cardiol. 2003; 91: 466–469.</ref> <ref>Umman B, Nisanci Y, Sezer M, et al. The relationship between corrected TIMI frame count and myocardial fractional flow reserve. J Invasive Cardiol. 2002; 14: 125–128. </ref> <ref>French JK, Hyde TA, Amos DJ, et al. Corrected TIMI frame count at 3 weeks influences survival at 5 years but not 10 years after myocardial infarction. Eur Heart J. 1998; 19: 630.</ref> <ref>Straznicky IT, French JK, Webber BJ, et al. Corrected TIMI frame count at 90 minutes predicts left ventricular function at 48 hours following myocardial infarction treated with streptokinase and heparin or hirulog. Eur Heart J. 1998; 19: 285. </ref> <ref>French JK, Ellis CJ, Webber BJ, et al. Abnormal coronary flow in infarct arteries 1 year after myocardial infarction is predicted at 4 weeks by corrected Thrombolysis In Myocardial Infarction (TIMI) frame count and stenosis severity. Am J Cardiol. 1998; 81: 665–671.</ref> <ref>French JK, Straznicky IT, Webber BJ, et al. Angiographic frame counts 90 minutes after streptokinase predict left ventricular function at 48 hours following myocardial infarction. Heart. 1999; 81: 128–133. </ref> <ref>French JK, Hyde TA, Straznicky IT, et al. Relationship between corrected TIMI frame counts at three weeks and late survival after myocardial infarction. J Am Coll Cardiol. 2000; 35: 1516–1524.</ref> <ref> Amos DJ, French JK, Andrews J, et al. Corrected TIMI frame counts correlate with stenosis severity and infarct zone wall motion after thrombolytic therapy. Am Heart J. 2001; 141: 586–591. </ref> <ref>Bahin M, Basoglu T, Canbaz F, et al. The value of the TIMI frame count method in the diagnosis of coronary no-reflow: a comparison with myocardial perfusion SPECT in patients with acute myocardial infarction. Nucl Med Commun. 2002; 23: 1205–1210. </ref> <ref>Moliterno D, Antman EM, Ohman M, et al. Concordance between core labs in trial results using TIMI flow grades and frame counts. Circulation. 2000; 102 (suppl II): II–590. </ref>. The CTFC is also highly correlated with other measures of flow such as Doppler velocity wire measures of coronary flow reserve, distal velocity, average peak velocity, and volumetric flow, <ref>Manginas A, Gatzov P, Chasikidis C, et al. Estimation of coronary flow reserve using the Thrombolysis In Myocardial Infarction (TIMI) frame count method. Am J Cardiol. 1999; 83: 1562–1565.</ref> <ref>Stankovic G, Manginas A, Voudris V, et al. Prediction of restenosis after coronary angioplasty by use of a new index: TIMI frame count/minimal luminal diameter ratio. Circulation. 2000; 101: 962–968.</ref> <ref>Barcin C, Denktas AE, Garratt KN, et al. Relation of Thrombolysis In Myocardial Infarction (TIMI) frame count to coronary flow parameters. Am J Cardiol. 2003; 91: 466–469.</ref> as well as fractional flow reserve (r=0.85)<ref>Umman B, Nisanci Y, Sezer M, et al. The relationship between corrected TIMI frame count and myocardial fractional flow reserve. J Invasive Cardiol. 2002; 14: 125–128. </ref>  


Several technical and physiological variables may impact the CTFC <ref name="Abaci1">Abaci A, Oguzhan A, Eryol NK, et al. Effects of potential confounding factors on the Thrombolysis In Myocardial Infarction (TIMI) trial frame count and its reproducibility. Circulation. 1999; 100: 2219–2223. </ref> <ref name="Dodge"> Dodge JT, Rizzo M, Nykiel M, et al. Impact of injection rate on the TIMI frame count. Am J Cardiol. 1998; 81: 1268–1270.</ref> <ref>Gibson CM, Anshelevich M, Murphy S, et al. Impact of injections during diagnostic coronary angiography on coronary patency in the setting of acute myocardial infarction from the TIMI trials. Am J Cardiol. 2000; 86: 1378–1379.</ref> <ref>Gibson CM, Kirtane AJ, Murphy SA, et al. Impact of contrast agent type (ionic versus non-ionic) used for coronary angiography on angiographic, electrocardiographic and clinical outcomes following thrombolytic administration in acute MI. Catheter Cardiovasc Interv. 2001; 53: 6–11. </ref> <ref>Faile BA, Guzzo JA, Tate DA, et al. Effect of sex, hemodynamics, body size, and other clinical variables on the corrected thrombolysis in myocardial infarction frame count used as an assessment of coronary blood flow. Am Heart J. 2000; 140: 308–314. </ref>:  
Several technical and physiological variables may impact the CTFC <ref name="pmid10577994">{{cite journal |author=Abaci A, Oguzhan A, Eryol NK, Ergin A |title=Effect of potential confounding factors on the thrombolysis in myocardial infarction (TIMI) trial frame count and its reproducibility |journal=Circulation |volume=100 |issue=22 |pages=2219–23 |year=1999 |month=November |pmid=10577994 |doi= |url=http://circ.ahajournals.org/cgi/pmidlookup?view=long&pmid=10577994}}</ref><ref name="pmid9604968">{{cite journal |author=Dodge JT, Rizzo M, Nykiel M, ''et al'' |title=Impact of injection rate on the Thrombolysis in Myocardial Infarction (TIMI) trial frame count |journal=Am. J. Cardiol. |volume=81 |issue=10 |pages=1268–70 |year=1998 |month=May |pmid=9604968 |doi= |url=http://linkinghub.elsevier.com/retrieve/pii/S0002-9149(98)00138-6}}</ref><ref name="pmid11113418">{{cite journal |author=Gibson CM, Anshelevich M, Murphy S, ''et al'' |title=Impact of injections during diagnostic coronary arteriography on coronary patency in the setting of acute myocardial infarction from the TIMI trials. Thrombolysis In Myocardial Infarction |journal=Am. J. Cardiol. |volume=86 |issue=12 |pages=1378–9, A5 |year=2000 |month=December |pmid=11113418 |doi= |url=http://linkinghub.elsevier.com/retrieve/pii/S0002914900012480}}</ref><ref name="pmid11329210">{{cite journal |author=Gibson CM, Kirtane AJ, Murphy SA, ''et al'' |title=Impact of contrast agent type (ionic versus nonionic) used for coronary angiography on angiographic, electrocardiographic, and clinical outcomes following thrombolytic administration in acute myocardial infarction |journal=Catheter Cardiovasc Interv |volume=53 |issue=1 |pages=6–11 |year=2001 |month=May |pmid=11329210 |doi=10.1002/ccd.1121 |url=}}</ref><ref name="pmid10925348">{{cite journal |author=Faile BA, Guzzo JA, Tate DA, Nichols TC, Smith SC, Dehmer GJ |title=Effect of sex, hemodynamics, body size, and other clinical variables on the corrected thrombolysis in myocardial infarction frame count used as an assessment of coronary blood flow |journal=Am. Heart J. |volume=140 |issue=2 |pages=308–14 |year=2000 |month=August |pmid=10925348 |doi=10.1067/mhj.2000.108003 |url=}}</ref>:  


1. Injection force: A power injector to change the force of injection (cc/sec) from the 10th to the 90th percentile of human injection rates lowers the CTFC by only 2 frames <ref name="Dodge"> Dodge JT, Rizzo M, Nykiel M, et al. Impact of injection rate on the TIMI frame count. Am J Cardiol. 1998; 81: 1268–1270.</ref>.  
1. Injection force: A power injector to change the force of injection (cc/sec) from the 10th to the 90th percentile of human injection rates lowers the CTFC by only 2 frames <ref name="pmid9604968">{{cite journal |author=Dodge JT, Rizzo M, Nykiel M, ''et al'' |title=Impact of injection rate on the Thrombolysis in Myocardial Infarction (TIMI) trial frame count |journal=Am. J. Cardiol. |volume=81 |issue=10 |pages=1268–70 |year=1998 |month=May |pmid=9604968 |doi= |url=http://linkinghub.elsevier.com/retrieve/pii/S0002-9149(98)00138-6}}</ref>.  


2. Nitrate administration significantly increases the CTFC by 6 frames (P<0.001)<ref name="Abaci1">Abaci A, Oguzhan A, Eryol NK, et al. Effects of potential confounding factors on the Thrombolysis In Myocardial Infarction (TIMI) trial frame count and its reproducibility. Circulation. 1999; 100: 2219–2223. </ref>  
2. Nitrate administration significantly increases the CTFC by 6 frames (P<0.001)<ref name="pmid10577994">{{cite journal |author=Abaci A, Oguzhan A, Eryol NK, Ergin A |title=Effect of potential confounding factors on the thrombolysis in myocardial infarction (TIMI) trial frame count and its reproducibility |journal=Circulation |volume=100 |issue=22 |pages=2219–23 |year=1999 |month=November |pmid=10577994 |doi= |url=http://circ.ahajournals.org/cgi/pmidlookup?view=long&pmid=10577994}}</ref>  


3. Dye injection at the beginning of diastole decreases the CTFC by 3 to 6 frames <ref name="Abaci1">Abaci A, Oguzhan A, Eryol NK, et al. Effects of potential confounding factors on the Thrombolysis In Myocardial Infarction (TIMI) trial frame count and its reproducibility. Circulation. 1999; 100: 2219–2223. </ref>
3. Dye injection at the beginning of diastole decreases the CTFC by 3 to 6 frames <ref name="pmid10577994">{{cite journal |author=Abaci A, Oguzhan A, Eryol NK, Ergin A |title=Effect of potential confounding factors on the thrombolysis in myocardial infarction (TIMI) trial frame count and its reproducibility |journal=Circulation |volume=100 |issue=22 |pages=2219–23 |year=1999 |month=November |pmid=10577994 |doi= |url=http://circ.ahajournals.org/cgi/pmidlookup?view=long&pmid=10577994}}</ref>


4. Increasing the heart rate by 20 beats per minute significantly decreases the CTFC by 5 frames (P<0.001)<ref name="Abaci1">Abaci A, Oguzhan A, Eryol NK, et al. Effects of potential confounding factors on the Thrombolysis In Myocardial Infarction (TIMI) trial frame count and its reproducibility. Circulation. 1999; 100: 2219–2223. </ref>  
4. Increasing the heart rate by 20 beats per minute significantly decreases the CTFC by 5 frames (P<0.001)<ref name="pmid10577994">{{cite journal |author=Abaci A, Oguzhan A, Eryol NK, Ergin A |title=Effect of potential confounding factors on the thrombolysis in myocardial infarction (TIMI) trial frame count and its reproducibility |journal=Circulation |volume=100 |issue=22 |pages=2219–23 |year=1999 |month=November |pmid=10577994 |doi= |url=http://circ.ahajournals.org/cgi/pmidlookup?view=long&pmid=10577994}}</ref>  


===Association of the CTFC with Clinical Outcomes===
===Association of the CTFC with Clinical Outcomes===

Revision as of 15:24, 11 February 2009

Myocardial infarction
ICD-10 I21-I22
ICD-9 410
DiseasesDB 8664
MedlinePlus 000195
eMedicine med/1567  emerg/327 ped/2520

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

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Pathophysiology of Reperfusion

The Importance of Restoring and Sustaining Complete Epicardial and Myocardial Perfusion

Recently, it has become recognized that it is necessary but not sufficient to restore epicardial flow in ST elevation MI. Not all TIMI grade 3 flow is created equally. [1] In addition to epicardial flow, myocardial perfusion must be restored as well. This has been demonstrated in both myocardial contrast echo studies as well as angiographic studies[1] [2][3][4][5][6][7][8][9][10][11][12][13] As a result of this new understanding, the goal of reperfusion therapies has shifted to include reperfusion downstream at the level of capillary bed, and it might be more appropriate that the current reperfusion hypothesis now be termed "the time dependent open muscle hypothesis." This wiki article reviews the angiographic methods used to evaluate myocardial ischemia and infarction and discusses the insights into the pathophysiology of acute coronary syndromes provided by these angiographic indexes of coronary artery blood flow and myocardial perfusion.

TIMI Flow Grades (TFGs)

The Thrombolysis In Myocardial Infarction (TIMI) flow grade classification scheme has been widely used to assess coronary blood flow in acute coronary syndromes.[1] TFG 0 means the artery is closed; TFG 1 means that dye penetrates the stenosis but does not reach the downstream bed; TFG 2 means that flow is slow down the artery and TFG 3 means that normal flow has been restored. The association of the TFGs with clinical outcomes (including mortality) has been well documented [2][3][4][5][6][7][8]

The association of the TFGs with mortality must be interpreted with caution as there are several confounders:

1. The majority of TIMI grade 2 flow is observed in the left anterior descending artery (LAD) territory, whereas the majority of TIMI grade 3 flow is observed in the right coronary artery (RCA)[7]. Thus, the improved mortality observed among patients with TIMI grade 3 flow may be explained at least in part by the fact that inferior myocardial infarction (MI) location is associated with a lower mortality rate [7]

2. The clinical improvement associated with TIMI grade 3 flow may have be nonlinear. For example, greater clinical benefits may be observed if a closed artery (TFG 0/1) is opened (TFG 2) compared with the improvement that might occur if an artery with TFG 2 is converted to TFG 3 flow.

3. As more arteries with TFG 2 flow are treated with adjunctive percutaneous coronary intervention (PCI), the prognosis associated with this flow grade may improve. The fact that patients who were treated with an inferior fibrinolytic monotherapy strategy faired so well in GUSTO V may be explained in part by the fact that these patients underwent PCI more often [14][15]. Two-year follow-up in more recent studies indicates that the survival advantage of TFG 3 flow over TFG 2 flow at 2 years may not be as great as it once was in the era before aggressive utilization of rescue and adjunctive (PCI) [10]

Reocclusion

While PCI may obviously improve epicardial flow, another often unrecognized benefit is the fact that rescue PCI (dilating a closed artery) and adjunctive PCI (dilating an open artery) following fibrinolytic administration may reduce the risk of reocclusion. Reinfarction doubles early mortality by 30 days [15] [16]. Controversy has surrounded the use of PCI immediately following PCI, and for many years, immediate PCI was classified as a class III contraindication. These early trials preceded the use of stents, thienopyridines, platelet GP IIb/IIIa inhibitors, and the monitoring of activated clotting times. Among 20 101 patients enrolled in recent TIMI trials, Gibson et al have reported that the performance of PCI during the index hospitalization was associated with a lower rate of in-hospital recurrent MI (1.6% versus 4.5%, P<0.001) and a lower 2-year mortality (5.6% versus 11.6%, P<0.001)[16][17]. In addition to flow other nonangiographic findings and processes may also underlie the pathophysiology of reocclusion as well as other clinical outcomes[18].

The TIMI Frame Count: A More Precise Angiographic Index of Coronary Blood Flow

There are several limitations to the TFG classification scheme [7]. To overcome these limitations, Gibson developed a more objective and precise index of coronary blood flow called the corrected TIMI frame count (CTFC). In this method, the number of cineframes required for dye to reach standardized distal landmarks are counted. Each frame is 1/30th of a second, and the angiogram is therefore essentially a measure of the time for dye to go down the artery [7][8][10]. In the first frame used for TIMI frame counting, a column of dye touches both borders of the coronary artery and moves forward [7]. In the last frame, dye begins to enter (but does not necessarily fill) a standard distal landmark in the artery. These standard distal landmarks are as follows: in the RCA, the first branch of the posterolateral artery; in the circumflex system, the most distal branch of the obtuse marginal branch, which includes the culprit lesion in the dye path; and in the LAD, the distal bifurcation, which is also known as the "moustache," "pitchfork" or "whale’s tail". These frame counts are corrected for the longer length of the LAD by dividing by 1.7 to arrive at the CTFC [7]. Knowing the time for dye to go down the artery from the CTFC (CTFC/30=seconds), and length of the artery (either from an angioplasty guide wire or by planimetry), dye velocity (cm/s) can also be calculated in a more refined fashion.[19]. This refined measure allows calculation of the velocity proximal and distal to the lesion[19].

Some of the advantages of the TIMI frame count method are as follows. In contrast to the TFG classification scheme, the CTFC is quantitative rather than qualitative, it is objective rather than subjective, it is a continuous rather than a categorical variable, and it is reproducible [7]. The CTFC demonstrates that flow is not divided into arbitrary slow and fast categories, but rather coronary blood flow is unimodally distributed as a continuous variable [7]. The CTFC has been shown to be quite reproducible with a 1- to 2-frame difference between observers [20][21][22][23][24][25][26][27][28][29][30][31][32]. The CTFC is also highly correlated with other measures of flow such as Doppler velocity wire measures of coronary flow reserve, distal velocity, average peak velocity, and volumetric flow, [21][22][23] as well as fractional flow reserve (r=0.85)[24]

Several technical and physiological variables may impact the CTFC [20][33][34][35][36]:

1. Injection force: A power injector to change the force of injection (cc/sec) from the 10th to the 90th percentile of human injection rates lowers the CTFC by only 2 frames [33].

2. Nitrate administration significantly increases the CTFC by 6 frames (P<0.001)[20]

3. Dye injection at the beginning of diastole decreases the CTFC by 3 to 6 frames [20]

4. Increasing the heart rate by 20 beats per minute significantly decreases the CTFC by 5 frames (P<0.001)[20]

Association of the CTFC with Clinical Outcomes

Following fibrinolytic administration as well as PCI, the CTFC is related to a variety of clinical outcomes [37] [38] [39] [40] [41] [42] [43] [44] [45] Flow in the infarct-related artery in survivors is significantly faster than in patients who die (49.5 versus 69.6 frames; P=0.0003)[38]. In NSTEMI and STEMI, the post-PCI culprit flow among survivors is significantly faster than among those patients who died (CTFCs 20.4 versus 33.4 frames, P=0.017)[46]. Among patients undergoing PCI, the CTFC has demonstrated greater sensitivity in detecting improvements in epicardial flow compared with the use of TIMI grade 3 flow among patients treated with new device interventions and in the detection of transplant rejection.[47] [48] [49] [50] [51] [52]

The Pathophysiology of STEMI and UA/NSTEMI Based on measures of epicardial flow

One of the more interesting observations learned with the use of the CTFC is the fact that flow in nonculprit arteries in the setting of acute coronary syndromes is "abnormal." For instance, the CTFC in uninvolved arteries in acute STEMI (30.5 frames) is in fact 40% slower than normal (21 frames, P<0.001)[37] [53] [54] [55] Adjunctive and rescue PCI following fibrinolysis restores flow in culprit vessels that is nearly identical to that of nonculprit arteries in the STEMI setting (30.5 versus 30.5 frames, p=NS)[53], but this flow remains slower than normal (21 frames). It is notable that PCI of the culprit lesion is also associated with improvements in the nonculprit artery after the intervention in both the STEMI and UA/NSTEMI settings [53] [54]. Slower flow throughout all 3 arteries in STEMI is associated with a higher risk of adverse outcomes [53], poorer wall motion in remote territories[53], poorer tissue perfusion on digital subtraction angiography (DSA)[54], and a greater magnitude of ST depression in remote territories such as the anterior precordium in inferior MI [56]. The basis of slowed flow in non-culprit arteries is not clear. It has been speculated that the delayed flow in the non-culprit artery may be the result of spasm in shared territories of microvasculature, or a result of global vasoconstriction mediated through either a local neurohumoral or paracrine mechanism. Gregorini et al[57] have highlighted the importance of sympathetic storm. Consistent with this hypothesis, they have demonstrated that the CTFC and fractional wall shortening is improved in both the culprit and nonculprit arteries after administration of alpha-blockers. Willerson and others [58] [59] [60] [61] [62] [63] [64] have also demonstrated that a wide range of vasoconstrictors including thromboxane A2, serotonin, endothelin, oxygen-derived free radicals, and thrombin are all released in the setting of vessel injury, thrombosis and reperfusion. While a residual stenosis following PCI in the setting of STEMI may be responsible for the delay in flow, it is important to note that despite a minimal 13% residual stenosis and the relief of intraluminal obstruction with stent placement, flow remains persistently abnormal in 34% of stented vessels.[65]

Assessment of Myocardial Perfusion on the Angiogram: The TIMI Myocardial Perfusion Grade (TMPG)

Studies of myocardial constrast echocardiography (MCE) and angiography have demonstrated that restoration of epicardial flow does not necessarily lead to restoration of tissue level or microvascular perfusion[66] [67] [68]. Perfusion of the myocardium can also be assessed using the angiogram. In the TMPG system, TMPG 0 represents minimal or no myocardial blush; in TMPG 1, dye stains the myocardium, and this stain persists on the next injection; in TMPG 2, dye enters the myocardium but washes out slowly so that dye is strongly persistent at the end of the injection; and in TMPG 3, there is normal entrance and exit of dye in the myocardium. Another method of assessing myocardial perfusion on the angiogram is the myocardial blush grade (MBG) developed by van’t Hof et al.[69] A grade of 0 (no blush) and a grade of 3 (normal blush) are the same in the TMPG and MBG systems. An MBG grade 1 or 2 represents diminished intensity in the myocardium and corresponds to a value of 0.5 in the expanded TMPG grading system. A TMPG of 1 or a stain in the TIMI system is subsumed within the value of a 0 in the MBG system. Thus, normal perfusion in the myocardium carries a score of 3 in both the TMPG and MBG systems, and a closed muscle carries a score of 0 in both systems. Lepper et al.[70] have demonstrated that angiographic and echocardiographic myocardial perfusion are closely related, and among patients undergoing primary PCI for acute MI, impaired MBG was the best multivariate predictor of nonreperfusion on myocardial contrast echocardiography.

Independent of flow in the epicardial artery and other covariates such as age, blood pressure, and pulse, the TMPG has been shown to be multivariate predictors of mortality in acute STEMI at 2 years.[39] The TMPG permits risk stratification even within epicardial TIMI grade 3 flow. Despite achieving epicardial patency with normal TIMI grade 3 flow, those patients whose microvasculature fails to open (TMPG 0/1) have a 7-fold increase in mortality compared with those patients with both TIMI grade 3 flow in the epicardial artery. Achievement of both TIMI grade 3 flow in both the artery and the myocardium is associated with a mortality under 1%10. Likewise, in the setting of primary PCI, both van’t Hof et al.[71] and Haager et al.[70] have demonstrated an association between impaired myocardial perfusion and early and late mortality. These improvements in early and late mortality may be mediated by improvements in myocardial salvage.[72] As Dibra et al.[72] have demonstrated, restoration of TMPG 2/3 is associated with a higher salvage index (0.49±0.42 versus 0.34±0.49, P=0.01) and a smaller final infarct size (15.4±15.5% versus 22.1±16.2% of the left ventricle, P=0.001). Indeed, second only to stent placement, restoration of TMPG 2/3 was the next most powerful independent determinant of the myocardial salvage index, and was more closely associated with higher salvage indexes than the TFGs.[72] [73] [74] [75] [76] [77] [78] [79] [80] [81] [82] [83] [84] [85] [86] [87] [88] [89] [90] [91] [92] [93] [94] [95] [96] [97]

References

  1. ↑ 1.0 1.1 1.2 "The Thrombolysis in Myocardial Infarction (TIMI) trial. Phase I findings. TIMI Study Group". N. Engl. J. Med. 312 (14): 932–6. 1985. PMID 4038784. Unknown parameter |month= ignored (help)
  2. ↑ 2.0 2.1 Simes RJ, Topol EJ, Holmes DR; et al. (1995). "Link between the angiographic substudy and mortality outcomes in a large randomized trial of myocardial reperfusion. Importance of early and complete infarct artery reperfusion. GUSTO-I Investigators". Circulation. 91 (7): 1923–8. PMID 7895348. Unknown parameter |month= ignored (help)
  3. ↑ 3.0 3.1 "The effects of tissue plasminogen activator, streptokinase, or both on coronary-artery patency, ventricular function, and survival after acute myocardial infarction. The GUSTO Angiographic Investigators". N. Engl. J. Med. 329 (22): 1615–22. 1993. PMID 8232430. Unknown parameter |month= ignored (help)
  4. ↑ 4.0 4.1 Vogt A, von Essen R, Tebbe U, Feuerer W, Appel KF, Neuhaus KL (1993). "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". J. Am. Coll. Cardiol. 21 (6): 1391–5. PMID 8473646. Unknown parameter |month= ignored (help)
  5. ↑ 5.0 5.1 Karagounis L, Sorensen SG, Menlove RL, Moreno F, Anderson JL (1992). "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". J. Am. Coll. Cardiol. 19 (1): 1–10. PMID 1729317. Unknown parameter |month= ignored (help)
  6. ↑ 6.0 6.1 Anderson JL, Karagounis LA, Becker LC, Sorensen SG, Menlove RL (1993). "TIMI perfusion grade 3 but not grade 2 results in improved outcome after thrombolysis for myocardial infarction. Ventriculographic, enzymatic, and electrocardiographic evidence from the TEAM-3 Study". Circulation. 87 (6): 1829–39. PMID 8504495. Unknown parameter |month= ignored (help)
  7. ↑ 7.0 7.1 7.2 7.3 7.4 7.5 7.6 7.7 7.8 7.9 Gibson CM, Cannon CP, Daley WL; et al. (1996). "TIMI frame count: a quantitative method of assessing coronary artery flow". Circulation. 93 (5): 879–88. PMID 8598078. Unknown parameter |month= ignored (help)
  8. ↑ 8.0 8.1 8.2 Gibson CM, Murphy SA, Rizzo MJ; et al. (1999). "Relationship between TIMI frame count and clinical outcomes after thrombolytic administration. Thrombolysis In Myocardial Infarction (TIMI) Study Group". Circulation. 99 (15): 1945–50. PMID 10208996. Unknown parameter |month= ignored (help)
  9. ↑ Gibson CM, Cannon CP, Murphy SA; et al. (2000). "Relationship of TIMI myocardial perfusion grade to mortality after administration of thrombolytic drugs". Circulation. 101 (2): 125–30. PMID 10637197. Unknown parameter |month= ignored (help)
  10. ↑ 10.0 10.1 10.2 Gibson CM, Cannon CP, Murphy SA, Marble SJ, Barron HV, Braunwald E (2002). "Relationship of the TIMI myocardial perfusion grades, flow grades, frame count, and percutaneous coronary intervention to long-term outcomes after thrombolytic administration in acute myocardial infarction". Circulation. 105 (16): 1909–13. PMID 11997276. Unknown parameter |month= ignored (help)
  11. ↑ Angeja BG, Gunda M, Murphy SA; et al. (2002). "TIMI myocardial perfusion grade and ST segment resolution: association with infarct size as assessed by single photon emission computed tomography imaging". Circulation. 105 (3): 282–5. PMID 11804979. Unknown parameter |month= ignored (help)
  12. ↑ Ito H, Tomooka T, Sakai N; et al. (1992). "Lack of myocardial perfusion immediately after successful thrombolysis. A predictor of poor recovery of left ventricular function in anterior myocardial infarction". Circulation. 85 (5): 1699–705. PMID 1572028. Unknown parameter |month= ignored (help)
  13. ↑ Ito H, Maruyama A, Iwakura K; et al. (1996). "Clinical implications of the 'no reflow' phenomenon. A predictor of complications and left ventricular remodeling in reperfused anterior wall myocardial infarction". Circulation. 93 (2): 223–8. PMID 8548892. Unknown parameter |month= ignored (help)
  14. ↑ Topol EJ (2001). "Reperfusion therapy for acute myocardial infarction with fibrinolytic therapy or combination reduced fibrinolytic therapy and platelet glycoprotein IIb/IIIa inhibition: the GUSTO V randomised trial". Lancet. 357 (9272): 1905–14. PMID 11425410. Unknown parameter |month= ignored (help)
  15. ↑ 15.0 15.1 Hudson MP, Granger CB, Topol EJ; et al. (2001). "Early reinfarction after fibrinolysis: experience from the global utilization of streptokinase and tissue plasminogen activator (alteplase) for occluded coronary arteries (GUSTO I) and global use of strategies to open occluded coronary arteries (GUSTO III) trials". Circulation. 104 (11): 1229–35. PMID 11551872. Unknown parameter |month= ignored (help)
  16. ↑ 16.0 16.1 Gibson CM, Karha J, Murphy SA; et al. (2003). "Early and long-term clinical outcomes associated with reinfarction following fibrinolytic administration in the Thrombolysis in Myocardial Infarction trials". J. Am. Coll. Cardiol. 42 (1): 7–16. PMID 12849652. Unknown parameter |month= ignored (help)
  17. ↑ Gibson CM (2000). "A union in reperfusion: the concept of facilitated percutaneous coronary intervention". J. Am. Coll. Cardiol. 36 (5): 1497–9. PMID 11079648. Unknown parameter |month= ignored (help)
  18. ↑ Gibson CM, Cannon CP, Piana RN; et al. (1995). "Angiographic predictors of reocclusion after thrombolysis: results from the Thrombolysis in Myocardial Infarction (TIMI) 4 trial". J. Am. Coll. Cardiol. 25 (3): 582–9. PMID 7860900. Unknown parameter |month= ignored (help)
  19. ↑ 19.0 19.1 Gibson CM, Dodge JT, Goel M; et al. (1997). "Angioplasty guidewire velocity: a new simple method to calculate absolute coronary blood velocity and flow". Am. J. Cardiol. 80 (12): 1536–9. PMID 9416931. Unknown parameter |month= ignored (help)
  20. ↑ 20.0 20.1 20.2 20.3 20.4 Abaci A, Oguzhan A, Eryol NK, Ergin A (1999). "Effect of potential confounding factors on the thrombolysis in myocardial infarction (TIMI) trial frame count and its reproducibility". Circulation. 100 (22): 2219–23. PMID 10577994. Unknown parameter |month= ignored (help)
  21. ↑ 21.0 21.1 Manginas A, Gatzov P, Chasikidis C, Voudris V, Pavlides G, Cokkinos DV (1999). "Estimation of coronary flow reserve using the Thrombolysis In Myocardial Infarction (TIMI) frame count method". Am. J. Cardiol. 83 (11): 1562–5, A7. PMID 10363873. Unknown parameter |month= ignored (help)
  22. ↑ 22.0 22.1 Stankovic G, Manginas A, Voudris V; et al. (2000). "Prediction of restenosis after coronary angioplasty by use of a new index: TIMI frame count/minimal luminal diameter ratio". Circulation. 101 (9): 962–8. PMID 10704161. Unknown parameter |month= ignored (help)
  23. ↑ 23.0 23.1 Barcin C, Denktas AE, Garratt KN, Higano ST, Holmes DR, Lerman A (2003). "Relation of Thrombolysis in Myocardial Infarction (TIMI) frame count to coronary flow parameters". Am. J. Cardiol. 91 (4): 466–9. PMID 12586269. Unknown parameter |month= ignored (help)
  24. ↑ 24.0 24.1 Umman B, Nisanci Y, Sezer M; et al. (2002). "The relationship between corrected TIMI frame count and myocardial fractional flow reserve". J Invasive Cardiol. 14 (3): 125–8. PMID 11870267. Unknown parameter |month= ignored (help)
  25. ↑ French JK, Hyde TA, Amos DJ, et al. Corrected TIMI frame count at 3 weeks influences survival at 5 years but not 10 years after myocardial infarction. Eur Heart J. 1998; 19: 630.
  26. ↑ Straznicky IT, French JK, Webber BJ, et al. Corrected TIMI frame count at 90 minutes predicts left ventricular function at 48 hours following myocardial infarction treated with streptokinase and heparin or hirulog. Eur Heart J. 1998; 19: 285.
  27. ↑ French JK, Ellis CJ, Webber BJ; et al. (1998). "Abnormal coronary flow in infarct arteries 1 year after myocardial infarction is predicted at 4 weeks by corrected Thrombolysis in Myocardial Infarction (TIMI) frame count and stenosis severity". Am. J. Cardiol. 81 (6): 665–71. PMID 9527071. Unknown parameter |month= ignored (help)
  28. ↑ French JK, Straznicky IT, Webber BJ; et al. (1999). "Angiographic frame counts 90 minutes after streptokinase predict left ventricular function at 48 hours following myocardial infarction". Heart. 81 (2): 128–33. PMC 1728934. PMID 9922346. Unknown parameter |month= ignored (help)
  29. ↑ French JK, Hyde TA, Straznicky IT; et al. (2000). "Relationship between corrected TIMI frame counts at three weeks and late survival after myocardial infarction". J. Am. Coll. Cardiol. 35 (6): 1516–24. PMID 10807455. Unknown parameter |month= ignored (help)
  30. ↑ Amos DJ, French JK, Andrews J; et al. (2001). "Corrected TIMI frame counts correlate with stenosis severity and infarct zone wall motion after thrombolytic therapy". Am. Heart J. 141 (4): 586–91. doi:10.1067/mhj.2001.113393. PMID 11275924. Unknown parameter |month= ignored (help)
  31. ↑ Sahin M, Basoglu T, Canbaz F, Elcik M, Kosus A (2002). "The value of the TIMI frame count method in the diagnosis of coronary no-reflow: a comparison with myocardial perfusion SPECT in patients with acute myocardial infarction". Nucl Med Commun. 23 (12): 1205–10. doi:10.1097/01.mnm.0000046213.83338.9e. PMID 12464786. Unknown parameter |month= ignored (help)
  32. ↑ Moliterno D, Antman EM, Ohman M, et al. Concordance between core labs in trial results using TIMI flow grades and frame counts. Circulation. 2000; 102 (suppl II): II–590.
  33. ↑ 33.0 33.1 Dodge JT, Rizzo M, Nykiel M; et al. (1998). "Impact of injection rate on the Thrombolysis in Myocardial Infarction (TIMI) trial frame count". Am. J. Cardiol. 81 (10): 1268–70. PMID 9604968. Unknown parameter |month= ignored (help)
  34. ↑ Gibson CM, Anshelevich M, Murphy S; et al. (2000). "Impact of injections during diagnostic coronary arteriography on coronary patency in the setting of acute myocardial infarction from the TIMI trials. Thrombolysis In Myocardial Infarction". Am. J. Cardiol. 86 (12): 1378–9, A5. PMID 11113418. Unknown parameter |month= ignored (help)
  35. ↑ Gibson CM, Kirtane AJ, Murphy SA; et al. (2001). "Impact of contrast agent type (ionic versus nonionic) used for coronary angiography on angiographic, electrocardiographic, and clinical outcomes following thrombolytic administration in acute myocardial infarction". Catheter Cardiovasc Interv. 53 (1): 6–11. doi:10.1002/ccd.1121. PMID 11329210. Unknown parameter |month= ignored (help)
  36. ↑ Faile BA, Guzzo JA, Tate DA, Nichols TC, Smith SC, Dehmer GJ (2000). "Effect of sex, hemodynamics, body size, and other clinical variables on the corrected thrombolysis in myocardial infarction frame count used as an assessment of coronary blood flow". Am. Heart J. 140 (2): 308–14. doi:10.1067/mhj.2000.108003. PMID 10925348. Unknown parameter |month= ignored (help)
  37. ↑ 37.0 37.1 Gibson CM, Cannon CP, Daley WL, et al. The TIMI frame count: a quantitative method of assessing coronary artery flow. Circulation. 1996; 93: 879–888.
  38. ↑ 38.0 38.1 Gibson CM, Murphy SA, Rizzo MJ, et al. The relationship between the TIMI frame count and clinical outcomes after thrombolytic administration. Circulation. 1999; 99: 1945–1950.
  39. ↑ 39.0 39.1 Gibson CM, Cannon CP, Murphy SA, et al. Relationship of the TIMI myocardial perfusion grades, flow grades, frame count, and percutaneous coronary intervention to long-term outcomes after thrombolytic administration in acute myocardial infarction. Circulation. 2002; 105: 1909–1913.
  40. ↑ French JK, Hyde TA, Amos DJ, et al. Corrected TIMI frame count at 3 weeks influences survival at 5 years but not 10 years after myocardial infarction. Eur Heart J. 1998; 19: 630.
  41. ↑ Straznicky IT, French JK, Webber BJ, et al. Corrected TIMI frame count at 90 minutes predicts left ventricular function at 48 hours following myocardial infarction treated with streptokinase and heparin or hirulog. Eur Heart J. 1998; 19: 285.
  42. ↑ French JK, Ellis CJ, Webber BJ, et al. Abnormal coronary flow in infarct arteries 1 year after myocardial infarction is predicted at 4 weeks by corrected Thrombolysis In Myocardial Infarction (TIMI) frame count and stenosis severity. Am J Cardiol. 1998; 81: 665–671.
  43. ↑ French JK, Straznicky IT, Webber BJ, et al. Angiographic frame counts 90 minutes after streptokinase predict left ventricular function at 48 hours following myocardial infarction. Heart. 1999; 81: 128–133.
  44. ↑ French JK, Hyde TA, Straznicky IT, et al. Relationship between corrected TIMI frame counts at three weeks and late survival after myocardial infarction. J Am Coll Cardiol. 2000; 35: 1516–1524.
  45. ↑ Amos DJ, French JK, Andrews J, et al. Corrected TIMI frame counts correlate with stenosis severity and infarct zone wall motion after thrombolytic therapy. Am Heart J. 2001; 141: 586–591.
  46. ↑ Gibson CM, Dotani MI, Murphy SA, et al. Correlates of coronary blood flow before and after percutaneous coronary intervention and their relationship to angiographic and clinical outcomes in the RESTORE trial. Am Heart J. 2002; 144: 130–135.
  47. ↑ Edep ME, Guarneri EM, Teirstein PS, et al. Differences in TIMI frame count following successful reperfusion with stenting or percutaneous transluminal coronary angioplasty for acute myocardial infarction. Am J Cardiol. 1999; 83: 1326–1329.
  48. ↑ Vrachatis AD, Alpert MA, Georgulas VP, et al. Comparative efficacy of primary angioplasty with stent implantation and thrombolysis in restoring basal coronary artery flow in acute ST segment elevation myocardial infarction: quantitative assessment using the corrected TIMI frame count. Angiology. 2001; 52: 161–166.
  49. ↑ Hamada S, Nishiue T, Nakamura S, et al. TIMI frame count immediately after primary coronary angioplasty as a predictor of functional recovery in patients with TIMI 3 reperfused acute myocardial infarction. J Am Coll Cardiol. 2001; 38: 666–671.
  50. ↑ Capozzolo C, Piscione F, De Luca G, et al. Direct coronary stenting: effect on coronary blood flow, immediate and late clinical results. Catheter Cardiovasc Interv. 2001; 53: 464–473.
  51. ↑ Bickel C, Rupprecht HJ, Maimaitiming A, et al. The superiority of TIMI frame count in detecting coronary flow changes after coronary stenting compared to TIMI flow classification. J Invasive Cardiol. 2002; 14: 590–596.
  52. ↑ Fang JC, Kinlay S, Wexberg P, et al. Use of the TIMI frame count for the quantitative assessment of transplant associated arteriosclerosis. Am J Cardiol. 2000; 86: 890–892.
  53. ↑ 53.0 53.1 53.2 53.3 53.4 Gibson CM, Ryan KA, Murphy SA, et al. Impaired coronary blood flow in non-culprit arteries in the setting of acute myocardial infarction. J Am Coll Cardiol. 1999; 34: 974–982.
  54. ↑ 54.0 54.1 54.2 Gibson CM, Goel M, Murphy SA, et al. Global impairment of coronary blood flow in the setting of acute coronary syndromes: a RESTORE substudy. Am J Cardiol. 2000; 86: 1375–1377.
  55. ↑ Goldstein JA, Demetriou D, Grines CL, et al. Multiple complex coronary plaques in patients with acute myocardial infarction. N Engl J Med. 2000; 343: 915–922.
  56. ↑ Gibson CM, Chen M, Goel M, et al. Precordial ST-segment depression in inferior myocardial infarction is associated with slow flow in the non-culprit left anterior descending artery. J Thromb Thrombolysis. 2002; 13: 9–12.
  57. ↑ Gregorini L, Marco J, Kozakova M, et al. -Adrenergic blockade improves recovery of myocardial perfusion and function after coronary stenting in patients with acute myocardial infarction. Circulation. 1999; 99: 482–490.
  58. ↑ Hirsh PD, Hillis LD, Campbell WB, et al. Release of prostaglandins and thromboxane into the coronary circulation in patients with ischemic heart disease. N Engl J Med. 1981; 304: 685–691.
  59. ↑ Bush LR, Campbell WB, Kern K, et al. The effects of 2-adrenergic and serotonergic receptor antagonists on cyclic blood flow alterations in stenosed canine coronary arteries. Circ Res. 1984; 55: 642–652.
  60. ↑ Willerson JT, Campbell WB, Winniford MD, et al. Conversion from chronic to acute coronary artery disease: speculation regarding mechanisms. Am J Cardiol. 1984; 54: 1349–1354.
  61. ↑ Apprill P, Schmitz JM, Campbell WB, et al. Cyclic blood flow variations induced by platelet-activating factor in stenosed canine coronary arteries despite inhibition of thromboxane synthetase, serotonin receptors, and -adrenergic receptors. Circulation. 1985; 72: 397–405.
  62. ↑ Ashton JH, Golino P, McNatt JM, et al. Serotonin S2 and thromboxane A2-prostaglandin H2 receptor blockade provide protection against epinephrine-induced cyclic flow variations in severely narrowed canine coronary arteries. J Am Coll Cardiol. 1989; 13: 755–763.
  63. ↑ Eidt JF, Allison P, Noble S, et al. Thrombin is an important mediator of platelet aggregation in stenosed canine coronary arteries with endothelial injury. J Clin Invest. 1989; 84: 18–27.
  64. ↑ Willerson JT, Golino P, Eidt J, et al. Specific platelet mediators and unstable coronary artery lesions: experimental evidence and potential clinical implications. Circulation. 1989; 80: 198–205.
  65. ↑ Gibson CM, Murphy SA, Menown I, et al. Determinants of coronary blood flow following thrombolytic administration. J Am Coll Cardiol. 1999; 34: 1403–1412.
  66. ↑ Angeja BG, Gunda M, Murphy SA, et al. TIMI myocardial perfusion grade and ST segment resolution: association with infarct size as assessed by single photon emission computed tomography imaging. Circulation. 2002; 105: 282–285.
  67. ↑ Ito H, Tomooka T, Sakai N, et al. Lack of myocardial perfusion immediately after successful thrombolysis. A predictor of poor recovery of left ventricular function in anterior myocardial infarction. Circulation. 1992; 85: 1699–1705.
  68. ↑ Ito H, Maruyama A, Iwakura K, et al. Clinical implications of the no reflow phenomenon. A predictor of complications and left ventricular remodeling in reperfused anterior wall myocardial infarction. Circulation. 1996; 93: 223–228.
  69. ↑ van’t Hof AW, Liem A, Suryapranata H, et al. Angiographic assessment of myocardial reperfusion in patients treated with primary angioplasty for acute myocardial infarction. Circulation. 1998; 97: 2302–2306.
  70. ↑ 70.0 70.1 Lepper W, Sieswerda GT, Vanoverschelde JL, et al. Predictive value of markers of myocardial reperfusion in acute myocardial infarction for follow-up left ventricular function. Am J Cardiol. 2001; 88: 1358–1363.
  71. ↑ van’t Hof AW, Liem A, Suryapranata H, et al. Angiographic assessment of myocardial reperfusion in patients treated with primary angioplasty for acute myocardial infarction. Circulation. 1998; 97: 2302–2306.
  72. ↑ 72.0 72.1 72.2 Dibra A, Mehilli J, Dirschinger J, et al. Thrombolysis In Myocardial Infarction myocardial perfusion grade in angiography correlates with myocardial salvage in patients with acute myocardial infarction treated with stenting or thrombolysis. J Am Coll Cardiol. 2003; 41: 925–929.
  73. ↑ Gibson CM, Murphy SA, Kirtane AJ, et al. Association of duration of symptoms at presentation with angiographic and clinical outcomes following fibrinolytic therapy in patients with ST elevation myocardial infarction.J Am Coll Cardiol. 2004.
  74. ↑ De Luca G, Suryapranata H, Zijlstra F, et al. Symptom-onset–to-balloon time and mortality in patients with acute myocardial infarction treated by primary angioplasty. J Am Coll Cardiol. 2003; 42: 991–997.
  75. ↑ De Luca G, van’t Hof AW, de Boer MJ, et al. Time-to-treatment significantly affects the extent of ST segment resolution and myocardial blush in patients with acute myocardial infarction treated by primary angioplasty.European Heart Journal 2004 25(12):1009-1013; doi:10.1016/j.ehj.2004.03.021
  76. ↑ Kirtane AJ, Bui A, Murphy SA, et al. Association of epicardial and tissue-level reperfusion with left ventricular end-diastolic pressures in ST-elevation myocardial infarction.J Thromb Thrombolysis.
  77. ↑ De Luca G, van’t Hof AW, de Boer MJ, et al. Impaired myocardial perfusion is a major explanation of the poor outcome observed in patients undergoing primary angioplasty for ST-segment-elevation myocardial infarction and signs of heart failure. Circulation. 2004; 109: 958–961.
  78. ↑ Tarantini G, Ramondo A, Napodano M, et al. Myocardial perfusion grade and survival after percutaneous transluminal coronary angioplasty in patients with cardiogenic shock. Am J Cardiol. 2004; 93: 1081–1085.
  79. ↑ Hoffmann R, Haager P, Lepper W, et al. Relation of coronary flow pattern to myocardial blush grade in patients with first acute myocardial infarction. Heart. 2003; 89: 1147–1151.
  80. ↑ Gibson CM. Has my patient achieved adequate myocardial reperfusion? Circulation. 2003; 108: 504–507.
  81. ↑ Poli A, Fetiveau R, Vandoni P, et al. Integrated analysis of myocardial blush and ST-segment elevation recovery after successful primary angioplasty: real-time grading of microvascular reperfusion and prediction of early and late recovery of left ventricular function. Circulation. 2002; 106: 313–318.
  82. ↑ Gibson CM, Karha J, Giugliano RP, et al. Association of the timing of ST-segment resolution with TIMI Myocardial Perfusion Grade in acute myocardial infarction. Am Heart J. 2004; 147: 847–852.
  83. ↑ Wong GC, Morrow DA, Murphy SA, et al. Elevations in troponin T and I are associated with abnormal tissue level perfusion: a TACTICS-TIMI 18 substudy. Circulation. 2002; 106: 202–207.
  84. ↑ Gibson CM, Murphy SA, Hynes C, et al. Relationship of CK-MB release to TIMI myocardial perfusion grade following intracoronary stent placement: an ESPRIT substudy. Am Heart J. 2002; 143: 106–110.
  85. ↑ Gibson CM, de Lemos JA, Murphy SA, et al. Methodologic and clinical validation of the TIMI myocardial perfusion grade in acute MI. J Thromb Thrombolysis. 2002; 14: 233–237.
  86. ↑ Gibson CM, Cohen D, Cohen E, et al. Treatment with eptifibatide and coronary flow reserve (CFR) following elective stent placement: an ESPRIT substudy. Am J Cardiol. 2001; 87: 1293–1295.
  87. ↑ Murphy SA, Chen C, Gourlay S, et al. Impaired tissue level perfusion in the non-culprit artery territory in the setting of acute MI. Am J Cardiol. 2003; 91: 325–328.
  88. ↑ Wong GC, Frisch D, Murphy SA, et al. Time for dye to traverse the epicardial artery and the myocardium in acute ST segment elevation myocardial infarction versus unstable angina/non ST elevation MI. Am J Cardiol. 2003; 91: 1163–1167.
  89. ↑ Gibson CM, Murphy SA, Morrow DA, et al. Angiographic perfusion score: an angiographic variable that integrates both epicardial and tissue level perfusion before and after facilitated percutaneous coronary intervention in acute myocardial infarction.Am Heart J. 2004.
  90. ↑ Karha J, Murphy SA, Kirtane AJ, et al. Association of proximal culprit artery lesion location with clinical outcomes in acute myocardial infarction. Am J Cardiol. 2003; 92: 913–918.
  91. ↑ Gibson CM, Karha J, Murphy SA, et al. Association of pulsatile blood flow pattern on coronary arteriography and short-term clinical outcomes in acute myocardial infarction. J Am Coll Cardiol. 2004; 43: 1170–1176.
  92. ↑ Ryan TJ, Faxon DP, Gunnar RM, et al. Guidelines for percutaneous transluminal coronary angioplasty: a report of the American College of Cardiology/Am Heart Association Task Force on Assessment of Diagnostic and Therapeutic Cardiovascular Procedures (Subcommittee on Percutaneous Transluminal Coronary Angioplasty). J Am Coll Cardiol. 1988; 12: 529–545.
  93. ↑ Ellis SG, Vandormael MG, Cowley MJ, et al. Coronary morphologic and clinical determinants or procedural outcome with angioplasty for multivessel coronary disease: implications for patient selection. Circulation. 1990; 82: 1193–1202.
  94. ↑ Myler RK, Shaw C, Stertzer SH, et al. Lesion morphology and coronary angioplasty: current experience and analysis. J Am Coll Cardiol. 1992; 19: 1641–1652.
  95. ↑ Krone RJ, Laskey WK, Johnson C, et al. A simplified lesion classification system for predicting success and complications of coronary angioplasty. Am J Cardiol. 2000; 85: 1179–1184.
  96. ↑ Wilensky RL, Selzer F, Johnston J, et al. Relation of percutaneous coronary intervention of complex lesions to clinical outcomes (from the NHLBI Dynamic Registry). Am J Cardiol. 2002; 90: 216–221.
  97. ↑ Gibson CM, Bigelow B, James D, et al. Association of lesion complexity following fibrinolytic administration with mortality in ST-elevation myocardial infarction. Am J Cardiol. 2004 Jul 1;94(1):108-11. PMID 15219518

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