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J Am Coll Cardiol, 2004; 43:1170-1176, doi:10.1016/j.jacc.2003.11.035
© 2004 by the American College of Cardiology Foundation
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CLINICAL RESEARCH: ACUTE MYOCARDIAL INFARCTION

Association of a pulsatile blood flow pattern on coronary arteriography and short-term clinical outcomes in acute myocardial infarction

C. Michael Gibson, MS, MD*,*, Juhana Karha, MD*, Sabina A. Murphy, MPH*, James A. de Lemos, MD{dagger}, David A. Morrow, MD*, Robert P. Giugliano, MD, SM*, Mathew T. Roe, MD, MHS{ddagger}, Robert A. Harrington, MD{ddagger}, Christopher P. Cannon, MD*, Elliott M. Antman, MD*, Robert M. Califf, MD{ddagger}, Eugene Braunwald, MD* TIMI Study Group

* TIMI Study Group, Cardiovascular Division, Department of Medicine, Brigham & Women's Hospital, Boston, Massachusetts, USA
{dagger} Department of Medicine, University of Texas Southwestern Medical Center, Dallas, Texas, USA
{ddagger} Duke Clinical Research Institute, Durham, North Carolina, USA

Manuscript received August 13, 2003; revised manuscript received October 8, 2003, accepted November 13, 2003.

* Reprint requests and correspondence: Dr. C. Michael Gibson, Director TIMI Data Coordinating Center, 350 Longwood Avenue, 1st Floor, Boston, Massachusetts 02115, USA.
mgibson{at}perfuse.org


   Abstract
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 Abstract
Methods
 Results
 Discussion
 References
 
OBJECTIVES: We hypothesized that recognition of systolic flow reversal (pulsatile flow) after thrombolytic administration on coronary angiography is associated with angiographic and electrocardiogram findings reflecting impaired myocardial perfusion, as well as poorer clinical outcomes.

BACKGROUND: Reversal of systolic flow on Doppler velocity wire recordings has been associated with impaired tissue perfusion on myocardial contrast echocardiography in the setting of myocardial infarction (MI).

METHODS: Patients (n = 1,062) with a patent infarct-related artery were drawn from the Thrombolysis In Myocardial Infarction (TIMI) 10, TIMI 14, and Integrillin and Tenecteplase acute MI trials.

RESULTS: Pulsatile flow (systolic flow reversal with cessation of antegrade contrast-dye motion or frank reversal of contrast-dye motion during systole) at 60 min after fibrinolytic administration was present in 11.0% of patients. Pulsatile flow was associated with higher corrected TIMI frame counts (slower epicardial flow) (median 40.1 frames, IQ 30 of 63 vs. 30 frames, interquartile 22 of 42, p < 0.0001), a closed microvasculature (TIMI myocardial perfusion grades 0 of 1, 57.1% vs. 37.8%, p = 0.03) and less complete (≥70%) ST-segment resolution (23.5% vs. 58.9%, p = 0.008). Patients with pulsatile flow had a higher risk of death or reinfarction at 30 days (10.3% vs. 5.0%, p = 0.019). After controlling for age, pulse, blood pressure, anterior MI location, epicardial flow, and creatine kinase, pulsatile flow remained associated with an increased risk of death/MI (odds ratio 3.1, p = 0.006).

CONCLUSIONS: A pulsatile pattern of flow is associated with impaired myocardial perfusion and poorer clinical outcomes independent of the velocity of antegrade flow in the epicardial artery. This simple and easily identifiable angiographic flow pattern may be useful in clinical risk stratification.

Abbreviations and Acronyms
  CTFC = corrected TIMI frame count
  INTEGRITI = Integrillin and Tenecteplase in Acute Myocardial Infarction trial
  LAD = left anterior descending artery
  PCI = percutaneous coronary intervention
  STEMI = ST-elevation myocardial infarction
  TFG = TIMI flow grade
  TIMI = Thrombolysis In Myocardial Infarction
  TMPG = TIMI myocardial perfusion grade
  TNK = tenecteplase

The open artery hypothesis calls for early, complete, and sustained restoration of blood flow in the culprit epicardial artery in ST-elevation myocardial infarction (STEMI). However, despite the presence of normal epicardial Thrombolysis In Myocardial Infarction (TIMI) grade 3 flow (TFG), impaired myocardial perfusion on coronary arteriography has also been independently associated with increased mortality (1). Other tools to interrogate the microvasculature have, likewise, underscored the importance of restoring microvascular perfusion. For instance, Doppler velocity studies have demonstrated an association between systolic flow reversal in the epicardial coronary artery with dysfunction in the myocardial microvasculature on myocardial contrast echocardiography (2). Furthermore, systolic flow reversal on Doppler velocity studies that persists after primary percutaneous coronary intervention (PCI) has also been associated with increased in-hospital mortality (3).

While these observations have relied upon the technology of Doppler velocity wires, pulsatile flow (flow reversal with cessation of antegrade contrast-dye motion or frank reversal of contrast-dye motion during systole) can also be evaluated visually on the coronary arteriogram. We have previously demonstrated that the simple pattern of pulsatile flow on the coronary angiogram is associated with higher culprit artery corrected TIMI frame counts (CTFC) (i.e., slower blood flow) (4). We also observed that pulsatile flow in the culprit artery was associated with slower flow in the distribution of the nonculprit artery and that pulsatile flow in the nonculprit artery is also associated with slower flow in the nonculprit artery (5).

The association of pulsatile flow in the epicardial artery and tissue perfusion on the angiogram has not been evaluated. We hypothesized that pulsatile flow after thrombolytic administration would be associated with impaired myocardial tissue-level perfusion on coronary arteriography, poorer electrocardiographic ST-segment resolution, and its detection could be used as an adjunct in clinical risk stratification.


   Methods
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 Abstract
 Methods
Results
 Discussion
 References
 
Patients with suitable coronary angiograms and a patent epicardial culprit artery (TFG 2 of 3) (n = 1,062) were drawn from a total of 2,600 patients enrolled in the trials. Patients included were from TIMI 10A (n = 23), TIMI 10B (n = 361), TIMI 14 (n = 369), and Integrillin and Tenecteplase (INTEGRITI) (n = 309) acute MI trials. The TIMI 10A trial was a nonrandomized, open-label, dose escalation study of eight ascending doses of tenecteplase (TNK) (6). Thrombolysis in Myocardial Infarction 10B was a randomized trial comparing various doses of TNK with front-loaded rt-PA (7). The TIMI 14 trial compared abciximab plus reduced-dose thrombolytic agent versus full-dose thrombolytic agent (8,9). The INTEGRITI trial randomized acute ST-elevation MI patients prospectively to a combination of eptifibatide and reduced dose tenecteplase (TNK) versus full dose TNK (10).

The presence of a pulsatile flow pattern on the angiogram at 60 min (range, 55 to 75 min) after study drug administration was assessed visually by a single experienced observer (C.M.G.) blinded to treatment assignment and clinical outcomes. A pulsatile flow pattern was defined as cessation of antegrade contrast-dye motion or frank reversal of contrast-dye motion during systole. The presence or absence of a pulsatile flow pattern was also assessed on the angiogram after PCI. The TFG, CTFC, and TIMI myocardial perfusion grade (TMPG) were assessed (1,11,12).

The magnitude of ST-segment resolution and the frequency of complete (≥70%) ST-segment resolution on the 12-lead electrocardiogram (ECG) at 60 min compared with the baseline ECG were determined by the TIMI Electrocardiographic Core Laboratory (Boston, Massachusetts), blinded to treatment assignment and clinical and angiographic findings, using previously established techniques (13). Recurrent MI was diagnosed by local investigators, except in TIMI 14 where it was adjudicated by a clinical events committee. Recurrent MI was defined as previously described (6–10). Cardiac biomarker determination was performed at each site's local laboratory, and the data are reported as multiples of the upper reference limit of the particular laboratory that analyzed the sample. All studies were approved by each participating center's institutional review board, and the trials were conducted according to the principles of the Declaration of Helsinki.

Statistical analysis.   All analyses were performed using Stata version 7.0 (Stata Corp., College Station, Texas). All continuous variable values are reported as the mean ± SD or median where appropriate. Student t test was used for the analysis of continuous variables. The nonparametric Wilcoxon rank sum test was used for the CTFC analysis because a value of 100 was imputed to an occluded vessel. The chi-square test was used for the analysis of categorical variables when sample size was ≥5 for all cells in a table. When the sample size was <5 in a given cell of a table, Fisher exact test was used. A multivariate logistic regression model was used for the analysis of death or MI by 30 days. A Kaplan-Meier curve was generated for recurrent MI through 30-day follow-up by pulsatile flow pattern. The log-rank test was used to test the equality of the survivor function by pulsatile flow pattern.


   Results
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 Abstract
 Methods
 Results
Discussion
 References
 
A total of 1,062 patients with an open epicardial culprit artery (TFG 2 or 3) on the angiogram 60 min after study drug administration were included in the analysis. Pulsatile flow was present in 117 patients (11.0%), and the remainder (945, 89.0%) had normal antegrade culprit coronary artery flow during the entire cardiac cycle. Patients with pulsatile flow were younger and had a higher heart rate on presentation (Table 1). Pulsatile flow was more frequent if the culprit artery was the left anterior descending (LAD) artery and if angiographically apparent thrombus was present. Patients treated with combination therapy of platelet glycoprotein IIb/IIIa inhibitor plus reduced dose fibrinolytic agent tended to less frequently have pulsatile flow compared with patients treated with fibrinolytic monotherapy (9.5%, 47 of 494 vs. 12.4%, 70 of 567, p = 0.14). Patients with pulsatile flow tended to have higher median peak creatine kinase values compared with patients with nonpulsatile flow (Table 1).


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  		Table 1 Baseline Clinical and Angiographic Characteristics

 
The incidence of TIMI grade 2 flow was increased among patients with pulsatile flow on the 60-min angiogram (Fig. 1). Likewise, the median CTFC among patients with pulsatile flow pattern was higher (slower flow) compared with patients with nonpulsatile flow pattern (Fig. 2). Furthermore, the presence of pulsatile flow was associated with a higher incidence of closed microvasculature compared with nonpulsatile flow (TMPG 0 of 1, 57.1%, 20 of 35 vs. 37.8%, 113 of 299, p = 0.03, Fig. 3). All angiographic analyses (TFG, CTFC, TMPG) were similar for both LAD and non-LAD culprit arteries. Pulsatile flow resolved in 66.7% (24 of 36) patients after the performance of PCI. On the other hand, 4.1% (12 of 296) of the patients who had nonpulsatile flow before PCI developed new pulsatile flow after PCI.



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  		Figure 1 (A) Incidence of 60-min Thrombolysis In Myocardial Infarction (TIMI) grade 2 flow among patients with pulsatile versus nonpulsatile flow pattern. (B) Incidence of pulsatile flow among patients with TIMI flow grade (TFG) 2 and grade 3 at 60 min. PCI = percutaneous coronary intervention.

 


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  		Figure 2 (A) Median 60-min corrected Thrombolysis In Myocardial Infarction (TIMI) frame count (CTFC) with interquartile range for patients with pulsatile versus nonpulsatile flow pattern. p value from Wilcoxon rank-sum test. (B) Incidence of pulsatile flow among patients with above versus below median (30.6 frames) (CTFC) at 60 min.

 


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  		Figure 3 (A) Incidence of TIMI myocardial perfusion grade (TMPG) 0 to 1 at 60 min among patients with pulsatile versus nonpulsatile flow pattern. (B) Incidence of pulsatile flow among patients with TMPG 0 to 1 versus TMPG 2 to 3 at 60 min.

 
The incidence of complete (≥70%) ST-segment resolution on a static 12-lead ECG 60 min after study drug administration was reduced among patients with pulsatile flow (23.5%, 4 of 17 vs. 58.9%, 86 of 146, p = 0.008 by Fisher exact test, Fig. 4). Likewise, the median extent of ST-segment resolution at 60 min was lower among patients with pulsatile flow (median 55.7%, IQ range 40/68%, n = 17 vs. median 79.1%, IQ 56/93%, n = 146, p = 0.011, Fig. 4).



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  		Figure 4 (A) Incidence of complete (≥70%) ST-segment resolution (ST Res) at 60 min among patients with pulsatile versus nonpulsatile flow pattern. p value from Fisher exact test. (B) Incidence of pulsatile flow among patients with complete (≥70%) versus incomplete ST Res at 60 min. p value from Fisher exact test. (C) Median ST Res with interquartile range at 60 min among patients with pulsatile versus nonpulsatile flow pattern.

 
A pulsatile pattern of coronary blood flow on the 60-min angiogram was associated with a higher incidence of death or recurrent MI at 30 days compared with patients with nonpulsatile flow: 10.3% (12 to 117) versus 5.0% (47 of 942), p = 0.019 (Fig. 5). A nonsignificant trend for this association persisted even among patients who subsequently underwent a PCI (7.1%, 3 of 42 vs. 3.0%, 10 of 334, p = 0.17 by Fisher exact test). The presence of a pulsatile flow pattern on the 60-min angiogram remained independently associated with a higher incidence of 30-day death or recurrent MI (odds ratio, 3.1, p = 0.006) after adjusting for age, heart rate, systolic blood pressure, LAD culprit location, TFG 3 epicardial blood flow, and peak creatine kinase. This composite end point was driven largely by the risk of recurrent MI, which differed significantly by pulsatile pattern (pulsatile 7.8%, 9 of 116 vs. nonpulsatile 2.8%, 26 of 925, p = 0.005; Fig. 6) rather than by death (pulsatile 2.6%, 3 of 117 vs. nonpulsatile 2.4%, 23 of 941, p = 1.0 by Fisher exact). In a multivariate model adjusting for previously identified correlates of angiographic reocclusion (TFG, LAD, thrombus, percent diameter stenosis, eccentric lesion, ulcerated lesion, and collaterals) (14) and clinical reinfarction (age and performance of adjunctive PCI) (15), a pulsatile flow pattern remained associated with recurrent MI by 30 days (odds ratio, 5.2; p = 0.001). Similar results for pulsatile flow were observed when CTFC was included in the model instead of TFG 3 (odds ratio, 2.8; p = 0.017 for death/MI and odds ratio, 3.7; p = 0.015 for MI).



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  		Figure 5 (A) Incidence of death or recurrent myocardial infarction (MI) at 30 days among patients with pulsatile versus nonpulsatile flow pattern at 60 min. (B) Incidence of pulsatile flow at 60 min among patients who died or sustained a recurrent MI within 30 days of the index MI versus patients who survived 30 days without recurrent MI.

 


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  		Figure 6 Kaplan-Meier curve for recurrent myocardial infarction through 30 days among patients with pulsatile versus nonpulsatile flow pattern at 60 min.

 

   Discussion
Top
 Abstract
 Methods
 Results
 Discussion
References
 
This study demonstrates that a pulsatile pattern of coronary blood flow is associated with impaired myocardial perfusion and poorer clinical outcomes. Prior studies have demonstrated that impaired epicardial blood flow, LAD culprit artery location, and multivessel or left main disease are all angiographic variables that are associated with poorer clinical outcomes after fibrinolytic administration for acute STEMI (1,14–18). This study extends these observations to demonstrate that a pulsatile pattern of epicardial blood flow is also associated with adverse clinical outcomes. A pulsatile flow pattern was associated with higher incidence of death or recurrent MI at 30 days even after adjusting for other confounding variables. In a multivariate model adjusting for previously identified correlates of angiographic reocclusion (14) (TFG, LAD, thrombus, percent diameter stenosis, eccentric lesion, ulcerated lesion, or collaterals) and clinical reinfarction (15) (PCI and age), the presence of pulsatile flow was associated with a highly significant fivefold increase in the risk of reinfarction. This simple and easily identifiable angiographic flow pattern may be useful in clinical risk stratification.

Pulsatile flow was associated with impaired myocardial perfusion as assessed by the TMPG on the angiogram and by reduced ST-segment resolution. Distal embolization and the release of vasoconstrictors may explain, at least in part, the impairment in myocardial perfusion. Indeed, visible intracoronary thrombus was more commonly present among arteries with a pulsatile flow pattern. Combination therapy with platelet glycoprotein IIb/IIIa inhibitors and reduced-dose thrombolytic agents have been associated with a reduction in thrombus burden (19), and it is notable that the administration of glycoprotein IIb/IIIa inhibitors tended to be associated with a reduced incidence of pulsatile flow on the 60-min angiogram.

Pulsatile flow was also observed more frequently among patients in whom the LAD was the culprit vessel. The infarcts in these patients are characterized by a greater volume of myocardium distal to the stenosis (4), a thicker myocardium compared with the right coronary artery, and higher left ventricular filling pressures compared with right ventricular filling pressures. As a result of this, it could be speculated that the greater myocardial edema and consequent extrinsic compression of the capillary network as well as the higher left ventricular filling pressures that develop among patients with anterior infarction may play a role in pulsatile flow. Indeed, systolic flow reversal occurs when the downstream microvascular pressure during systole exceeds the upstream epicardial artery pressure. While pulsatile flow is associated with larger infarct sizes (larger peak creatine kinase levels), the directionality of the causal relationship is unknown; it is not clear if larger myocardial infarctions cause pulsatile flow, or if pulsatile flow (a surrogate for heightened downstream microvascular resistance), in turn, causes larger myocardial infarctions.

Among patients with pulsatile flow before PCI, flow reversal was resolved in 66.7% of patients after the performance of PCI. Previously we have reported that flow in the nonculprit artery improves after PCI of the culprit artery. There may be shared abnormalities in the downstream microvasculature, some of which may be mediated by heightened neuroadrenergic tone to maintain perfusion pressure. This tone is relieved after dilation of the stenosis. Finally, if the pressure beyond the stenosis is low, heightened pressure during systole may cause flow to reverse in this low pressure system.

Study limitations.   This is a retrospective analysis, and unidentified confounders may have contributed to the findings. Strict enrollment criteria are used in clinical trials, and the results observed here might not be applicable to all patients in clinical practice.

Conclusions.   Independent of the velocity of antegrade flow in the epicardial artery, a pulsatile pattern of flow with retrograde or reversed flow during systole is associated with impaired myocardial perfusion and poorer clinical outcome. This simple and easily identifiable angiographic flow pattern may be useful in clinical risk stratification.


   Footnotes
 
Supported, in part, by grants from Genentech, Inc., South San Francisco, California (TIMI 10A and TIMI 10B); Millennium Pharmaceuticals, Cambridge, Massachusetts, and Schering-Plough Research Institute in Kenilworth, New Jersey (INTEGRITI); Centocor, Malvern, Pennsylvania, and Eli Lilly, Inc., Indianapolis, Indiana (TIMI 14).


   References
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 Abstract
 Methods
 Results
 Discussion
 References
 

  1. Gibson CM, Cannon CP, Murphy SA, et al. Relationship of TIMI myocardial perfusion grade to mortality after administration of thrombolytic drugs. Circulation. 2000;101:125–130[Abstract/Free Full Text]
  2. Iwakura K, Ito H, Takiuchi S, et al. Alteration in the coronary blood flow velocity pattern in patients with no reflow and reperfused acute myocardial infarction. Circulation. 1996;94:1269–1275[Abstract/Free Full Text]
  3. Yamamoro A, Akasaka T, Tamita K, et al. Coronary flow velocity pattern immediately after percutaneous coronary intervention as a predictor of complications and in-hospital survival after acute myocardial infarction. Circulation. 2002;106:3051–3056[Abstract/Free Full Text]
  4. Gibson CM, Murphy S, Menown IB, et al. Determinants of coronary blood flow after thrombolytic administration. J Am Coll Cardiol. 1999;34:1403–1412[Abstract/Free Full Text]
  5. Gibson CM, Ryan KA, Murphy SA, et al. Impaired coronary blood flow in nonculprit arteries in the setting of acute myocardial infarction. J Am Coll Cardiol. 1999;34:974–982[Abstract/Free Full Text]
  6. Cannon CP, McCabe CH, Gibson CM, et al. TNK-tissue plasminogen activator in acute myocardial infarction: Results of the Thrombolysis in Myocardial Infarction (TIMI) 10A dose-ranging trial. Circulation. 1997;95:351–356[Abstract/Free Full Text]
  7. Cannon CP, Gibson CM, McCabe CH, et al. TNK-tissue plasminogen activator compared with front-loaded alteplase in acute myocardial infarction: Results of the TIMI 10B trial. Thrombolysis in Myocardial Infarction (TIMI) 10B investigators. Circulation. 1998;98:2805–2814[Abstract/Free Full Text]
  8. Antman EM, Giugliano RP, Gibson CM, et al. Abciximab facilitates the rate and extent of thrombolysis: Results of the Thrombolysis in Myocardial Infarction (TIMI) 14 trial. The TIMI 14 investigators. Circulation. 1999;99:2720–2732[Abstract/Free Full Text]
  9. Antman EM, Gibson CM, de Lemos JA, et al. Combination reperfusion therapy with abciximab and reduced dose reteplase: Results from TIMI 14. The Thrombolysis in Myocardial Infarction (TIMI) 14 investigators. Eur Heart J. 2000;21:1944–1953[Abstract/Free Full Text]
  10. INTEGRITI InvestigatorsGiugliano RP, Roe MT, Harrington RA, et al. Combination reperfusion therapy with eptifibatide and reduced-dose tenecteplase for ST-elevation myocardial infarction: Results of the Integrilin and Tenecteplase in Acute Myocardial Infarction (INTEGRITI) phase II angiographic trial. J Am Coll Cardiol. 2003;41: 1251–1260ii
  11. Chesebro JH, Knatterud G, Roberts R, et al. Thrombolysis in Myocardial Infarction (TIMI) trial, phase I: A comparison between intravenous tissue plasminogen activator and intravenous streptokinase: clinical findings through hospital discharge. Circulation. 1987;76:142–154[Abstract/Free Full Text]
  12. Gibson CM, Cannon CP, Daley WL, et al. TIMI frame count: A quantitative method of assessing coronary artery flow. Circulation. 1996;93:879–888[Abstract/Free Full Text]
  13. de Lemos JA, Antman EM, Giugliano RP, et al. ST-segment resolution and infarct-related artery patency and flow after thrombolytic therapy: Thrombolysis in Myocardial Infarction (TIMI) 14 investigators. Am J Cardiol. 2000;85:299–304[CrossRef][Medline]
  14. Gibson CM, Cannon CP, Piana RN, et al. Angiographic predictors of early reocclusion in the TIMI 4 trial. J Am Coll Cardiol. 1995;25:582–589[Abstract]
  15. Gibson CM, Karha J, Murphy SA, et al. Early and long term clinical outcomes associated with reinfarction following fibrinolytic administration in the TIMI trials. J Am Coll Cardiol. 2003;42:7–16[Abstract/Free Full Text]
  16. Gibson CM, Murphy SA, Rizzo MJ, et al. Relationship between TIMI frame count and clinical outcomes after thrombolytic administration: Thrombolysis in Myocardial Infarction (TIMI) study group. Circulation. 1999;99:1945–1950[Abstract/Free Full Text]
  17. Lundergan CF, Reiner JS, McCarthy WS, et al. Clinical predictors of early infarct-related artery patency following thrombolytic therapy: Importance of body weight, smoking history, infarct-related artery and choice of thrombolytic regimen: the GUSTO-I experience. J Am Coll Cardiol. 1998;32:641–647[Abstract/Free Full Text]
  18. Muller DWM, Topol EJ, Ellis SG, et al. Multivessel coronary artery disease: A key predictor of short-term prognosis after reperfusion therapy for acute myocardial infarction. Am Heart J. 1991;121:1042–1049[CrossRef][Medline]
  19. Gibson CM, de Lemos JA, Murphy SA, et al. Combination therapy with abciximab reduces angiographically evident thrombus in acute myocardial infarction: A TIMI 14 substudy. Circulation. 2001;103:2550–2554[Abstract/Free Full Text]



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