CLINICAL STUDIES
Impaired coronary blood flow in nonculprit arteries in the setting of acute myocardial infarction
C. Michael Gibson, MD, MS, FACCa,
Kathryn A. Ryan, BSa,
Sabina A. Murphy, MPHa,
Rebecca Mesley, BSa,
Susan J. Marble, RN, MSa,
Robert P. Giugliano, MD, SM ,
Christopher P. Cannon, MD, FACC,
Elliott M. Antman, MD, FACC,
Eugene Braunwald, MD, FACC for the TIMI Study Group
a Cardiovascular Divisions of the Departments of Medicine, the University of California at San Francisco, San Francisco, California, USA
Brigham & Women’s Hospital, Boston, Massachusetts, USA
Manuscript received December 30, 1998;
revised manuscript received March 29, 1999,
accepted June 25, 1999.
Reprint requests and correspondence: Dr. C. Michael Gibson, Associate Chief of Cardiology, Cardiovascular Division, UCSF Medical Center, 505 Parnassus Avenue, Box 0124, San Francisco, California 94143-0124, USA
OBJECTIVES AND BACKGROUND
While attention has focused on coronary blood flow in the culprit artery in acute myocardial infarction (MI), flow in the nonculprit artery has not been studied widely, in part because it has been assumed to be normal. We hypothesized that slower flow in culprit arteries, larger territories infarcted and hemodynamic perturbations may be associated with slow flow in nonculprit arteries.
METHODS
The number of frames for dye to first reach distal landmarks (corrected TIMI [Thrombolysis in Acute Myocardial Infarction] frame count [CTFC]) were counted in 1,817 nonculprit arteries from the TIMI 4, 10A, 10B and 14 thrombolytic trials.
RESULTS
Nonculprit artery flow was slowed to 30.9 ± 15.0 frames at 90 min after thrombolytic administration, which is 45% slower than normal flow in the absence of acute MI (21 ± 3.1, p < 0.0001). Patients with TIMI grade 3 flow in the culprit artery had faster nonculprit artery CTFCs than those patients with TIMI grades 0, 1 or 2 flow (29.1 ± 13.7, n = 1,050 vs. 33.3 ± 16.1, n = 752, p < 0.0001). The nonculprit artery CTFC improved between 60 and 90 min (3.3 ± 17.9 frames, n = 432, p = 0.0001), and improvements were related to improved culprit artery flow (p = 0.0005). Correlates of slower nonculprit artery flow included a pulsatile flow pattern (i.e., systolic flow reversal) in the nonculprit artery (p < 0.0001) and in the culprit artery (p = 0.01), a left anterior descending artery culprit artery location (p < 0.0001), a decreased systolic blood pressure (p = 0.01), a decreased ventriculographic cardiac output (p = 0.02), a decreased double product (p = 0.0002), a greater percent diameter stenosis of the nonculprit artery (p = 0.01) and a greater percent of the culprit artery bed lying distal to the stenosis (p = 0.04). Adjunctive percutaneous transluminal coronary angioplasty (PTCA) of the culprit artery restored a culprit artery CTFC (30.4 ± 22.2) that was similar to that in the nonculprit artery at 90 min (30.2 ± 13.5), but both were slower than normal CTFCs (21 ± 3.1, p < 0.0005 for both). If flow in the nonculprit artery was abnormal (CTFC  28 frames) then the CTFC after PTCA in the culprit artery was 17% slower (p = 0.01). Patients who died had slower global CTFCs (mean CTFC for the three arteries) than patients who survived (46.8 ± 21.3, n = 47 vs. 39.4 ± 16.7, n = 1,055, p = 0.02).
CONCLUSIONS
Acute MI slows flow globally, and slower global flow is associated with adverse outcomes. Relief of the culprit artery stenosis by PTCA restored culprit artery flow to that in the nonculprit artery, but both were 45% slower than normal flow.
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Abbreviations and Acronyms
| | ANOVA | = analysis of variance | | CHF | = congestive heart failure | | CTFC | = corrected TIMI frame count | | EF | = ejection fraction | | LAD | = left anterior descending artery | | LCx | = left circumflex artery | | MI | = myocardial infarction | | MRI | = magnetic resonance imaging | | PTCA | = percutaneous transluminal coronary angioplasty | | RCA | = right coronary artery | | rt-PA | = recombinant tissue plasminogen activator | | TIMI | = Thrombolysis in Acute Myocardial Infarction | | tPA | = tissue plasminogen activator |
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