Association of a pulsatile blood flow pattern on coronary arteriography and short-term clinical outcomes in acute myocardial infarction.
OBJECTIVE
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 (> or =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.
Gibson
C Michael
CM
Cardiovascular Division, Department of Medicine, Brigham & Women's Hospital, Boston, Massachusetts 02115, USA. mgibson@perfuse.org
Karha
Juhana
J
Murphy
Sabina A
SA
de Lemos
James A
JA
Morrow
David A
DA
Giugliano
Robert P
RP
Roe
Mathew T
MT
Harrington
Robert A
RA
Cannon
Christopher P
CP
Antman
Elliott M
EM
Califf
Robert M
RM
Braunwald
Eugene
E
D000077284:Abciximab; D000328:Adult; D000368:Aged; D015906:Angioplasty, Balloon, Coronary; D000911:Antibodies, Monoclonal / Q000627:therapeutic use; D017023:Coronary Angiography; D003326:Coronary Circulation / Q000187:drug effects / Q000502:physiology*; D004359:Drug Therapy, Combination; D004562:Electrocardiography; D000077542:Eptifibatide; D005260:Female; D005343:Fibrinolytic Agents / Q000627:therapeutic use; D006339:Heart Rate / Q000187:drug effects / Q000502:physiology; D006801:Humans; D007140:Immunoglobulin Fab Fragments / Q000627:therapeutic use; D015994:Incidence; D008297:Male; D008875:Middle Aged; D015999:Multivariate Analysis; D009203:Myocardial Infarction / Q000175:diagnosis* / Q000503:physiopathology* / Q000628:therapy; D010455:Peptides / Q000627:therapeutic use; D010960:Plasminogen Activators / Q000627:therapeutic use; D010975:Platelet Aggregation Inhibitors / Q000627:therapeutic use; D019039:Platelet Glycoprotein GPIIb-IIIa Complex / Q000627:therapeutic use; D011673:Pulsatile Flow / Q000187:drug effects / Q000502:physiology*; D013223:Statistics as Topic; D000077785:Tenecteplase; D013997:Time Factors; D010959:Tissue Plasminogen Activator / Q000627:therapeutic use; D016896:Treatment Outcome
D000911:Antibodies, Monoclonal; D005343:Fibrinolytic Agents; D007140:Immunoglobulin Fab Fragments; D010455:Peptides; D010975:Platelet Aggregation Inhibitors; D019039:Platelet Glycoprotein GPIIb-IIIa Complex; D010960:Plasminogen Activators; D010959:Tissue Plasminogen Activator; D000077542:Eptifibatide; D000077785:Tenecteplase; D000077284:Abciximab