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


*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).  
*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)<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>. 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 <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 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.  
*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.  
*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 (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).  
*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<ref name="pmid11551872">{{cite journal |author=Hudson MP, Granger CB, Topol EJ, ''et al'' |title=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 |journal=Circulation |volume=104 |issue=11 |pages=1229–35 |year=2001 |month=September |pmid=11551872 |doi= |url=http://circ.ahajournals.org/cgi/pmidlookup?view=long&pmid=11551872}}</ref>. 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)<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>.  


===Reocclusion===
===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).  
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<ref name="pmid11551872">{{cite journal |author=Hudson MP, Granger CB, Topol EJ, ''et al'' |title=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 |journal=Circulation |volume=104 |issue=11 |pages=1229–35 |year=2001 |month=September |pmid=11551872 |doi= |url=http://circ.ahajournals.org/cgi/pmidlookup?view=long&pmid=11551872}}</ref><ref name="pmid12849652">{{cite journal |author=Gibson CM, Karha J, Murphy SA, ''et al'' |title=Early and long-term clinical outcomes associated with reinfarction following fibrinolytic administration in the Thrombolysis in Myocardial Infarction trials |journal=J. Am. Coll. Cardiol. |volume=42 |issue=1 |pages=7–16 |year=2003 |month=July |pmid=12849652 |doi= |url=http://linkinghub.elsevier.com/retrieve/pii/S0735109703005060}}</ref>. 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)<ref name="pmid12849652">{{cite journal |author=Gibson CM, Karha J, Murphy SA, ''et al'' |title=Early and long-term clinical outcomes associated with reinfarction following fibrinolytic administration in the Thrombolysis in Myocardial Infarction trials |journal=J. Am. Coll. Cardiol. |volume=42 |issue=1 |pages=7–16 |year=2003 |month=July |pmid=12849652 |doi= |url=http://linkinghub.elsevier.com/retrieve/pii/S0735109703005060}}</ref><ref name="pmid11079648">{{cite journal |author=Gibson CM |title=A union in reperfusion: the concept of facilitated percutaneous coronary intervention |journal=J. Am. Coll. Cardiol. |volume=36 |issue=5 |pages=1497–9 |year=2000 |month=November |pmid=11079648 |doi= |url=http://linkinghub.elsevier.com/retrieve/pii/S0735-1097(00)00926-8}}</ref>. In addition to flow other nonangiographic findings and processes may also underlie the pathophysiology of reocclusion as well as other clinical outcomes <ref name="pmid7860900">{{cite journal |author=Gibson CM, Cannon CP, Piana RN, ''et al'' |title=Angiographic predictors of reocclusion after thrombolysis: results from the Thrombolysis in Myocardial Infarction (TIMI) 4 trial |journal=J. Am. Coll. Cardiol. |volume=25 |issue=3 |pages=582–9 |year=1995 |month=March |pmid=7860900 |doi= |url=http://linkinghub.elsevier.com/retrieve/pii/073510979400423N}}</ref>.  


===The TIMI Frame Count: A More Precise Angiographic Index of Coronary Blood Flow===
===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).  
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>. 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><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 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.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 (20–32). 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, (21–23) as well as fractional flow reserve (r=0.85)(24).  
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 (20–32). 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, (21–23) as well as fractional flow reserve (r=0.85)(24).  

Revision as of 17:27, 9 February 2009

Angiogram of the coronary arteries.
Myocardial infarction
Diagram of a myocardial infarction (2) of the tip of the anterior wall of the heart (an apical infarct) after occlusion (1) of a branch of the left coronary artery (LCA, right coronary artery = RCA).
ICD-10 I21-I22
ICD-9 410
DiseasesDB 8664
MedlinePlus 000195
eMedicine med/1567  emerg/327 ped/2520

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Angiography

Main article: Coronary catheterization

In difficult cases or in situations where intervention to restore blood flow is appropriate, coronary angiography can be performed. A catheter is inserted into an artery (usually the femoral artery) and pushed to the vessels supplying the heart. Obstructed or narrowed arteries can be identified, and angioplasty applied as a therapeutic measure (see below). Angioplasty requires extensive skill, especially in emergency settings, and may not always be available out of hours. It is commonly performed by interventional cardiologists.

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. 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:

  • 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].
  • 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.
  • 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]. 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[14][15]. 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)[15][16]. In addition to flow other nonangiographic findings and processes may also underlie the pathophysiology of reocclusion as well as other clinical outcomes [17].

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]. In the first frame used for TIMI frame counting, a column of dye touches both borders of the coronary artery and moves forward[7][10]. 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 (20–32). 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, (21–23) as well as fractional flow reserve (r=0.85)(24).

Several technical and physiological variables may impact the CTFC (20,33–36):

  • 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).
  • Nitrate administration significantly increases the CTFC by 6 frames (P<0.001)(20).
  • Dye injection at the beginning of diastole decreases the CTFC by 3 to 6 frames (20).
  • 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 (7,8,10,25–30). 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)(8). 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)(37). 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 (38–43).

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)(7,44–46). 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)(44), 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 (44,45). Slower flow throughout all 3 arteries in STEMI is associated with a higher risk of adverse outcomes (44), poorer wall motion in remote territories (44), poorer tissue perfusion on digital subtraction angiography (DSA)(45), and a greater magnitude of ST depression in remote territories such as the anterior precordium in inferior MI(47). 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 (48) 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 (49–55) 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 (56).

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 (12,13). 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 (Table). Another method of assessing myocardial perfusion on the angiogram is the myocardial blush grade (MBG) developed by van’t Hof et al.57 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 al58 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.10 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 (Figure 4). Likewise, in the setting of primary PCI, both van’t Hof et al57 and Haager et al59 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.60 As Dibra et al60 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.60

==References==

  1. ↑ 1.0 1.1 "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 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. ↑ 14.0 14.1 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)
  15. ↑ 15.0 15.1 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)
  16. ↑ 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)
  17. ↑ 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)

References

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2. Simes RJ, Topol EJ, Holmes DR, et al. Link between the angiographic substudy and mortality outcomes in a large randomized trial of myocardial reperfusion: importance of early and complete infarct artery reperfusion. Circulation. 1995; 91: 1923–1928.

3. The GUSTO Angiographic Investigators. The effects of tissue plasminogen activator, streptokinase, or both on coronary artery patency, ventricular function, and survival after acute myocardial infarction. N Engl J Med. 1993; 329: 1615–1622.

4. Vogt A, Von Essen R, Tebbe U, 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. J Am Coll Cardiol. 1993; 21: 1391–1395.

5. Karagounis L, Sorensen SG, Menlove RI, 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. J Am Coll Cardiol. 1992; 17: 1–10.

6. Anderson JL, Karagounis LA, Becker LC, et al. 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. 1993; 87: 1829–1839.

7. 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.

8. 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.

9. Gibson CM, Cannon CP, Murphy SA, et al. Relationship of TIMI myocardial perfusion grade to mortality following thrombolytic administration. Circulation. 2000; 101: 125–130.

10. 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.

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77. 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.

78. 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.

79. 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.

80. 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.

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