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European Heart Journal Advance Access originally published online on July 17, 2006
European Heart Journal 2006 27(17):2040-2045; doi:10.1093/eurheartj/ehl149
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© The European Society of Cardiology 2006. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org

Angiographically evident thrombus following fibrinolytic therapy is associated with impaired myocardial perfusion in STEMI: a CLARITY-TIMI 28 substudy

Ajay J. Kirtane1, Jonathan J. Vafai1, Sabina A. Murphy2, Julian M. Aroesty1, Marc S. Sabatine2, Christopher P. Cannon2, C. Michael Gibson1,* for the TIMI Study Group

1 Cardiovascular Division, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215, USA
2 Cardiovascular Division, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02215, USA

Received 16 May 2006; revised 14 June 2006; accepted 22 June 2006; online publish-ahead-of-print 17 July 2006.

* Corresponding author: 350 Longwood Avenue, First Floor, Boston, MA 02115, USA. Tel: +1 617 278 0145; fax: +1 888 249 5261. E-mail address: mgibson{at}timi.org


   Abstract
Top
 Abstract
Introduction
 Methods
 Results
 Discussion
 Limitations
 Conclusions
 Acknowledgement
 References
 
Aims The presence of residual thrombus following fibrinolytic therapy for ST-segment elevation myocardial infarction (STEMI) may predispose to greater embolization and microvascular dysfunction.

Methods and results We hypothesized that even in the presence of a patent epicardial artery, residual thrombus would be associated with worsened TIMI myocardial perfusion grades (TMPG), independent of epicardial flow. Data were analysed from the angiograms of 2684 patients enrolled in the CLARITY-TIMI 28 trial, with angiographically patent arteries (TIMI 2/3 flow) at a median of 88 h following fibrinolytic therapy. Thrombus in a patent epicardial artery was observed more frequently among patients with shorter times from randomization to angiography, among patients with non-left anterior descending infarctions, and among patients treated with placebo (vs. clopidogrel). Thrombus was associated with more frequent TIMI 2 flow (35.1 vs. 22.1%, P<0.001), higher corrected TIMI frame counts (CTFC) (42 vs. 33 frames, P<0.001), and a lower incidence of normal TMPG 3 (48.7 vs. 63.9%, P<0.001), irrespective of treatment with clopidogrel or placebo. In multivariable analyses, thrombus remained associated with higher CTFC (P<0.001) and worse TMPG (OR 1.6 for TMPG 0/1/2, P<0.001) after adjustment for baseline covariates as well as known correlates of TMPG. The association between thrombus and impaired TMPG remained even after further adjustment for CTFC or TIMI flow grade.

Conclusion Residual angiographic thrombus following fibrinolytic therapy in STEMI patients is associated with impaired myocardial perfusion, independent of epicardial flow. This finding emphasizes the roles of platelet aggregation and distal embolization in the pathogenesis of microvascular dysfunction in STEMI.

Key Words: Thrombus • TIMI myocardial perfusion grade • Corrected TIMI frame count • TIMI flow grade • ST-elevation myocardial infarction


   Introduction
Top
 Abstract
 Introduction
Methods
 Results
 Discussion
 Limitations
 Conclusions
 Acknowledgement
 References
 
The goal of reperfusion therapy for ST-segment elevation myocardial infarction (STEMI) is to achieve early, full, and sustained perfusion of the myocardium in the distribution of the infarct-related artery. Despite the restoration of epicardial artery patency and normal epicardial flow following reperfusion therapy, patients frequently have abnormalities of myocardial perfusion. Abnormal myocardial perfusion in STEMI has been associated with larger infarct sizes,1 worsened myocardial salvage,2 and increased mortality following treatment with fibrinolytic therapy3 or with primary percutaneous coronary intervention (PCI).4,5

Angiographically evident residual thrombus within the culprit coronary artery has been independently linked to impaired myocardial perfusion following fibrinolytic therapy for STEMI at 60 and 90 min angiography.6,7 Similarly, among patients with non-ST segment elevation acute coronary syndromes, angiographic thrombus has been associated with both greater troponin release and impaired myocardial perfusion.8,9 However, whether angiographic thrombus is associated with impaired myocardial perfusion on late angiography following reperfusion therapy for STEMI and in the context of modern anti-platelet therapies, including clopidogrel, is unknown. We sought to examine the association of angiographically evident thrombus and myocardial perfusion among a large cohort of patients treated with fibrinolytic therapy and either aspirin plus placebo or aspirin plus clopidogrel. We hypothesized that residual thrombus following fibrinolytic therapy would be associated with worsened TIMI myocardial perfusion grades (TMPG) and slower epicardial flow, independent of treatment with adjunctive clopidogrel.


   Methods
Top
 Abstract
 Introduction
 Methods
Results
 Discussion
 Limitations
 Conclusions
 Acknowledgement
 References
 
CLARITY-TIMI 28 was a multicentre, international, randomized, double-blind, placebo-controlled trial of aspirin vs. aspirin plus clopidogrel in 3491 patients treated with fibrinolytic therapy for STEMI. The study design and overall results have been described previously.10,11 Enrolled patients were 18–75 years of age, presented within 12 h of the onset of STEMI, and had undergone coronary angiography 2–8 days after randomization.

Angiographic analysis
In CLARITY-TIMI 28, all angiograms were analysed offline and blinded to treatment assignment at the TIMI Angiographic Core Laboratory (Boston, MA). For this study, analyses were restricted to the 2684 patients who underwent angiography during the index hospitalization, who demonstrated a patent culprit artery (TIMI grade 2 or 3 flow), and in whom the TMPG and presence or absence of thrombus could be ascertained by the core laboratory. Quantitative coronary angiography and assessments of TIMI flow grade,12 corrected TIMI frame count (CTFC),13 and TMPG3 were measured as previously described by Gibson.

Thrombus was categorized and defined as the presence of an angiographically apparent luminal filling defect, as described previously by Gibson.6 For this analysis, a patient was considered to have thrombus if grades 2–4 were present (grades 5 and 6 were not applicable to this analysis, restricted to patent arteries): grade 0: no cineangiographic characteristics of thrombus present; grade 1: hazy, possible thrombus present with angiography demonstrating characteristics such as reduced contrast density, haziness, irregular lesion contour, or a smooth convex ‘meniscus’ at the site of total occlusion suggestive but not diagnostic of thrombus; grade 2: thrombus present—small size: definite thrombus with greatest dimensions less than or equal to half the vessel diameter; grade 3: thrombus present—moderate size: definite thrombus but with the greatest linear dimension greater than half but less than two vessel diameters; grade 4: thrombus present—large size: as in Grade 3 but with the largest dimension greater than or equal to two vessel diameters.

Statistical analysis
Patients were categorized according to the presence or absence of angiographically apparent thrombus. {chi}2 test was used for the analysis of categorical variables. Continuous variables are reported as the mean±standard deviation unless otherwise specified, and given the large sample size of the study population, Student's t-test was used for comparisons between the two groups. All tests were two-sided, with a P-value <0.05 used for significance.

Bivariate stratified analyses were performed to assess the relationship between thrombus and TMPG among placebo- and clopidogrel-treated patients. Multivariable linear and logistic regression models were constructed using CTFC and TMPG, respectively, as outcome variables and incorporating thrombus, treatment assignment, potential confounders, and known correlates of CTFC and TMPG. Covariates assessed in the models were thrombus, treatment assignment (clopidogrel or placebo), age, gender, infarct location, history of hyperlipidaemia, time from randomization to symptoms, time from randomization to angiography, predominant heparin, TIMI risk index,14 blood glucose, white blood cell count, and haemoglobin. Stepwise selection algorithms were used with P<0.10 for entry and P<0.20 for retention in the models. Models were then refitted over the remaining covariates to minimize the effect of missing data. All statistical analyses were performed using Stata v8.2 and 9.1 (College Station, TX).


   Results
Top
 Abstract
 Introduction
 Methods
 Results
Discussion
 Limitations
 Conclusions
 Acknowledgement
 References
 
Baseline characteristics
A total of 382 of the 2684 patients (14.2%) with patent epicardial arteries following fibrinolytic therapy had angiographic evidence of residual thrombus. Overall, baseline demographics among patients with and without thrombus were largely similar (Table 1). Patients with thrombus were less likely to have a history of hyperlipidaemia (P=0.003), less likely to have an anterior infarction (P<0.001), had shorter times from randomization to angiography (P<0.001), and had slightly shorter times from symptom onset to randomization. There were no significant differences in age, creatinine clearance, complete blood count parameters, or TIMI risk index between the two groups. Randomization to treatment with clopidogrel was associated with a lower incidence of thrombus (12.6 vs. 16.0%, P=0.014, Figure 1). There was also a strong trend for thrombus to be observed more frequently among patients with a recurrent MI prior to angiography [23.7% incidence of thrombus among patients with recurrent MI (n=59) vs. 14.1% among patients without recurrent MI (n=2625), P=0.06].


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  		Table 1 Baseline characteristics

 

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  		Figure 1 Association of clopidogrel with angiographic thrombus among patent arteries.

 
The associations of thrombus with other angiographic lesions and flow characteristics are shown in Table 2. In stratified analyses, irrespective of treatment with clopidogrel or placebo, the presence of thrombus was associated with less frequent TIMI grade 3 flow (overall rates 64.9 vs. 77.9%, P<0.001, Figure 2) and higher (slower) TIMI frame counts (Figure 3). Thrombus was also associated with a lower frequency of normal TMPG (48.7 vs. 63.9%, P<0.001), irrespective of treatment assignment (Figure 4). Thrombus was additionally associated with smaller minimum lumen diameters (0.84 vs. 0.95 mm, P<0.001) and a greater percent diameter stenosis (69 vs. 63%, P<0.001). A greater overall thrombus burden also was associated with a stepwise reduction in normal TMPG (Figure 5).


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  		Table 2 Angiographic characteristics of flow and perfusion

 

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  		Figure 2 Association of angiographic thrombus with TIMI flow grades among patent arteries.

 

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  		Figure 3 Association of angiographic thrombus with TIMI frame count among patent arteries.

 

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  		Figure 4 Association of angiographic thrombus with TIMI myocardial perfusion among patent arteries.

 

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  		Figure 5 Association of thrombus burden with TMPG.

 
In multivariable analyses, thrombus remained associated with higher TFC (additional seven frames with thrombus, P<0.001) and worse TMPG (OR 1.6 for TMPG 0/1/2, P<0.001; Table 3). The independent association between thrombus and worse TMPG remained after further adjustment for CTFC (for thrombus: OR 1.4 for TMPG 0/1/2, P=0.010) and TIMI grade 3 flow (for thrombus: OR 1.4 for TMPG 0/1/2, P=0.009). Thrombus was also associated with a greater incidence of revascularization following the protocol angiogram (53.4 vs. 42.6%, P<0.001).


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  		Table 3 Independent correlates of abnormal TMPG in patent epicardial arteries

 

   Discussion
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
Limitations
 Conclusions
 Acknowledgement
 References
 
This study demonstrates that among patients in whom epicardial patency is successfully restored with fibrinolytic therapy, residual thrombus observed on late angiography is associated with impaired myocardial perfusion, independent of epicardial flow and luminal geometry. These observations validate prior findings7 in a much larger cohort of 2684 patients and extend these findings to patients who are additionally treated with adjunctive clopidogrel, an agent associated with a lower frequency of residual thrombus following fibrinolytic therapy.

The pathophysiological basis for impaired myocardial perfusion in STEMI is multifactorial and may involve a combination of factors including distal embolization, myocardial oedema and cell swelling, inflammation, reperfusion injury, and vasoconstriction. Initial thrombus formation and ongoing thrombosis appear to be central in many of these processes by serving as a nidus for distal embolization, as well as a mediator of vasoconstrictor release. In patients with STEMI, thrombus can result in distal embolization of microthrombi and platelet-fibrin aggregates into the coronary microcirculation.15,16 The authors and others have demonstrated that the administration of potent antiplatelet agents such as glycoprotein IIb/IIIa inhibitors is associated with improvements in both angiographic thrombus as well as myocardial perfusion.6,17,18 Distal microembolization of thrombus is also, however, increasingly being implicated as a cause of ongoing inflammation and microvascular dysfunction.19 Microembolization has been linked to the release of vasoactive mediators such as adenosine and inflammatory cytokines.20

A major difference between this study and our prior report of pooled 60 min angiographic data from four prior fibrinolytic trials7 is that in CLARITY TIMI-28, angiographic analyses were performed later, or at a median of 88 h following fibrinolytic administration. The continued association between thrombus in the culprit artery and impaired myocardial perfusion, even after acute changes in microvascular vasomotor function have to a large extent resolved,21 is notable and re-emphasizes that thrombosis and embolization may be ongoing processes that continue in the short-term period after successful fibrinolysis.

One pathophysiological explanation for our findings is that residual thrombus may reflect a larger overall thrombotic burden, which may predispose to greater microembolization and microvascular dysfunction. However, it is also possible that residual thrombus may be a marker of thromboresistance, or may even be a surrogate of a more intense prothrombotic and inflammatory process with associated microcirculatory dysfunction. In addition, activation of the coagulation system may also be involved in the persistence and/or recurrence of intracoronary thrombus following the administration of fibrinolytic therapy. Thus, causality or the directionality of the association between thrombus and impaired myocardial perfusion cannot be proved by this analysis, and thus these findings should be considered to be hypothesis-generating.

It is notable that although the association between thrombus and impaired myocardial perfusion was independent of treatment with adjunctive clopidogrel, the co-administration of clopidogrel with fibrinolytic therapy was associated with a lower incidence of observed thrombus even among the patients with patent infarct-related arteries. Despite a reduction in the incidence of thrombus in this subset of patients with patent arteries from CLARITY-TIMI, 28 clopidogrel was not independently associated with improved TMPG. Nonetheless, in the primary trial analysis (including all patients enrolled, irrespective of artery patency on initial angiography), clopidogrel was associated with significant improvements in epicardial patency, TIMI flow grade, and TMPG.22


   Limitations
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 Limitations
Conclusions
 Acknowledgement
 References
 
The true prevalence of intracoronary thrombus exceeds that observed by angiography,23 and it is possible that patients categorized as having no thrombus actually had a thrombus burden that was below the detection threshold of conventional coronary angiography, although this would have minimized the observed differences between groups. This is a non-randomized analysis of a clinical trial population, and despite efforts to control for confounding, unmeasured confounders may have affected or influenced our observed results.


   Conclusions
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 Limitations
 Conclusions
Acknowledgement
 References
 
The presence of residual angiographic thrombus following the administration of fibrinolytic therapy in patients with STEMI is associated with impaired indices of epicardial flow and myocardial perfusion, irrespective of treatment with clopidogrel.


   Acknowledgement
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 Limitations
 Conclusions
 Acknowledgement
References
 
CLARITY-TIMI 28 was supported in part by a grant from Bristol Myers Squibb (New York, NY) and Sanofi-Aventis (Paris, France).

Conflict of interest: J.J.V. owns a small amount of stock in Pfizer. S.A.M., J.M.A., M.S.S., C.P.C., and C.M.G. have received research grant support from Bristol-Myers Squibb and Sanofi-Aventis. M.S.S. and C.P.C. have received honoraria from and have served as consultants and/or on scientific advisory boards for Bristol-Myers Squibb and Sanofi-Aventis. C.P.C reports having received research grant support and/or honoraria from and/or served on scientific advisory boards for AstraZeneca, GlaxoSmithKline, Guilford Pharmaceuticals, Merck, Schering Plough, Accumetrics, and Pfizer.


   References
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 Limitations
 Conclusions
 Acknowledgement
 References
 

  1. Angeja BG, Gunda M, Murphy SA, Sobel BE, Rundle AC, Syed M, Asfour A, Borzak S, Gourlay SG, Barron HV, Gibbons RJ, Gibson CM. (2002) TIMI myocardial perfusion grade and ST segment resolution: association with infarct size as assessed by single photon emission computed tomography imaging. Circulation 105:282–285.[Abstract/Free Full Text]
  2. Dibra A, Mehilli J, Dirschinger J, Pache J, Neverve J, Schwaiger M, Schomig A, Kastrati A. (2003) 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 41:925–929.[Abstract/Free Full Text]
  3. Michaels AD, Gibson CM, Barron HV. (2000) Microvascular dysfunction in acute myocardial infarction: focus on the roles of platelet and inflammatory mediators in the no-reflow phenomenon. Am J Cardiol 85:50B–60B.[CrossRef][ISI][Medline]
  4. Stone GW, Peterson MA, Lansky AJ, Dangas G, Mehran R, Leon MB. (2002) Impact of normalized myocardial perfusion after successful angioplasty in acute myocardial infarction. J Am Coll Cardiol 39:591–597.[Abstract/Free Full Text]
  5. Haager PK, Christott P, Heussen N, Lepper W, Hanrath P, Hoffmann R. (2003) Prediction of clinical outcome after mechanical revascularization in acute myocardial infarction by markers of myocardial reperfusion. J Am Coll Cardiol 41:532–538.[Abstract/Free Full Text]
  6. Gibson CM, de Lemos JA, Murphy SA, Marble SJ, McCabe CH, Cannon CP, Antman EM, Braunwald E. (2001) Combination therapy with abciximab reduces angiographically evident thrombus in acute myocardial infarction: a TIMI 14 substudy. Circulation 103:2550–2554.[Abstract/Free Full Text]
  7. Kirtane AJ, Weisbord A, Karmpaliotis D, Murphy SA, Giugliano RP, Cannon CP, Antman EM, Ohman EM, Roe MT, Braunwald E, Gibson CM. (2005) Relation of impaired thrombolysis in myocardial infarction myocardial perfusion grades to residual thrombus following the restoration of epicardial patency in ST-elevation myocardial infarction. Am J Cardiol 95:224–227.[CrossRef][ISI][Medline]
  8. Wong GC, Morrow DA, Murphy S, Kraimer N, Pai R, James D, Robertson DH, Demopoulos LA, DiBattiste P, Cannon CP, Gibson CM. (2002) Elevations in troponin T and I are associated with abnormal tissue level perfusion: a TACTICS-TIMI 18 substudy. Treat angina with aggrastat and determine cost of therapy with an invasive or conservative strategy—thrombolysis in myocardial infarction. Circulation 106:202–207.[Abstract/Free Full Text]
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  10. Sabatine MS, Cannon CP, Gibson CM, Lopez-Sendon JL, Montalescot G, Theroux P, Claeys MJ, Cools F, Hill KA, Skene AM, McCabe CH, Braunwald E. (2005) Addition of clopidogrel to aspirin and fibrinolytic therapy for myocardial infarction with ST-segment elevation. N Engl J Med 352:1179–1189.[Abstract/Free Full Text]
  11. Sabatine MS, McCabe CH, Gibson CM, Cannon CP. (2005) Design and rationale of Clopidogrel as Adjunctive Reperfusion Therapy-Thrombolysis in Myocardial Infarction (CLARITY-TIMI) 28 trial. Am Heart J 149:227–233.[CrossRef][ISI][Medline]
  12. TIMI Study Group. (1985) The thrombolysis in myocardial infarction (TIMI) trial. Phase I findings. N Engl J Med 932–936.
  13. Gibson CM, Cannon CP, Daley WL, Dodge JT Jr, Alexander B Jr, Marble SJ, McCabe CH, Raymond L, Fortin T, Poole WK, Braunwald E. (1996) TIMI frame count: a quantitative method of assessing coronary artery flow. Circulation 93:879–888.[Abstract/Free Full Text]
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  15. Saber RS, Edwards WD, Bailey KR, McGovern TW, Schwartz RS, Holmes DR Jr. (1993) Coronary embolization after balloon angioplasty or thrombolytic therapy: an autopsy study of 32 cases. J Am Coll Cardiol 22:1283–1288.[Abstract]
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  22. Sabatine MS, Cannon CP, Gibson CM, Lopez-Sendon JL, Montalescot G, Theroux P, Claeys MJ, Cools F, Hill KA, Skene AM, McCabe CH, Braunwald E. (2005) Addition of clopidogrel to aspirin and fibrinolytic therapy for myocardial infarction with ST-segment elevation. N Engl J Med 352:1179–1189.[Abstract/Free Full Text]
  23. Mizuno K, Satomura K, Miyamoto A, Arakawa K, Shibuya T, Arai T, Kurita A, Nakamura H, Ambrose JA. (1992) Angioscopic evaluation of coronary-artery thrombi in acute coronary syndromes. N Engl J Med 326:287–291.[Abstract]

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