Residual Flow to the Infarct Zone as a Determinant of Infarct Size After Direct Angioplast

BackgroundIn acute myocardial infarction, residual flow to the infarct zone either through antegrade flow in the infarct-related coronary artery or collateral flow from the non-infarct-related arteries is often present before reperfusion therapy. The purpose of this study was to assess the influence of antegrade flow in the infarct-related artery and/or collateral flow to the infarct zone before successful direct angioplasty on infarct size and myocardial salvage in patients with acute evolving myocardial infarction. Methods and ResultsSixty patients with acute evolving myocardial infarction underwent direct successful angioplasty without prior thrombolytic therapy. The myocardium at risk of infarction, the final infarct size, and myocardial salvage were measured by tomographic perfusion imaging with “Tc sestamibi. Antegrade flow in the infarct-related artery before intervention was graded according to the Thrombolysis in Myocardial Infarction (TIMI) study group classification. Collateral flow to the infarct zone before angioplasty was also graded (0 through 3, 0 being no collateral flow). The presence of even minimal antegrade flow before angioplasty (TIMI grade 1) in the infarct-related artery compared with absent flow was associated with a significant reduction in final infarct size (9±17% versus 23±19% of left ventricle, P=.02) and a significant increase in myocardial salvage (23±16% versus 14±13% of left ventricle, P=.05) after angioplasty. When antegrade flow in the infarct-related artery was absent before angioplasty, the presence of collateral flow before angioplasty resulted in a significantly smaller final infarct size (P=.01) and more myocardial salvage (P=.05) after angioplasty. Both antegrade infarctrelated artery flow and collateral flow to the infarct zone had significant independent ability to predict infarct size after angioplasty. When collateral grade and TIM grade were added to provide an estimate of residual flow, a model including residual flow, myocardium at risk, and the interaction of residual flow and infarct site explained 83% of the variability in infarct size after angioplasty. ConclusionsThe presence of antegrade flow in the infarct-related artery and/or collateral flow to the infarct zone before direct angioplasty in acute evolving infarction results in a smaller infarct size after direct successful angioplasty.

[1]  K. Bailey,et al.  Immediate angioplasty compared with the administration of a thrombolytic agent followed by conservative treatment for myocardial infarction. The Mayo Coronary Care Unit and Catheterization Laboratory Groups. , 1993, The New England journal of medicine.

[2]  R. Gibbons,et al.  Determinants of Infarct Size in Reperfusion Therapy for Acute Myocardial Infarction , 1992, Circulation.

[3]  R. Gibbons,et al.  Measurement of myocardium at risk by technetium-99m sestamibi: correlation with coronary angiography. , 1992, Journal of the American College of Cardiology.

[4]  B. Gersh,et al.  Relation of left ventricular volume and function over one year after acute myocardial infarction to infarct size determined by technetium-99m sestamibi. , 1991, The American journal of cardiology.

[5]  R. Gibbons,et al.  Noninvasive Identification of Myocardium at Risk in Patients With Acute Myocardial Infarction and Nondiagnostic Electrocardiograms With Technetium‐99im‐Sestaimibi , 1991, Circulation.

[6]  R. Gibbons,et al.  Mismatch of left ventricular function and infarct size demonstrated by technetium-99m isonitrile imaging after reperfusion therapy for acute myocardial infarction: identification of myocardial stunning and hyperkinesia. , 1990, Journal of the American College of Cardiology.

[7]  D D Watson,et al.  Quantification of area at risk during coronary occlusion and degree of myocardial salvage after reperfusion with technetium-99m methoxyisobutyl isonitrile. , 1990, Circulation.

[8]  E. Leidholdt,et al.  Technetium-99m hexakis 2-methoxy-2-isobutyl isonitrile and thallium-201 extraction, washout, and retention at varying coronary flow rates in rabbit heart. , 1990, Circulation.

[9]  L. Becker,et al.  Myocardial redistribution of technetium-99m-methoxyisobutyl isonitrile (SESTAMIBI). , 1990, Journal of nuclear medicine : official publication, Society of Nuclear Medicine.

[10]  A. Sinusas,et al.  Effect of ischemia and postischemic dysfunction on myocardial uptake of technetium-99m-labeled methoxyisobutyl isonitrile and thallium-201. , 1989, Journal of the American College of Cardiology.

[11]  M. Cohen,et al.  Late thrombolytic therapy preserves left ventricular function in patients with collateralized total coronary occlusion: primary end point findings of the Second Mount Sinai-New York University Reperfusion Trial. , 1989, Journal of the American College of Cardiology.

[12]  M. Verani,et al.  Quantification of myocardial infarction during coronary occlusion and myocardial salvage after reperfusion using cardiac imaging with technetium-99m hexakis 2-methoxyisobutyl isonitrile. , 1988, Journal of the American College of Cardiology.

[13]  L. Bolognese,et al.  RANDOMISED TRIAL OF INTRAVENOUS STREPTOKINASE, ORAL ASPIRIN, BOTH, OR NEITHER AMONG 17 187 CASES OF SUSPECTED ACUTE MYOCARDIAL INFARCTION: ISIS-2 , 1988, The Lancet.

[14]  Dwight E. Peake,et al.  Thrombolysis in myocardial infarction (TIMI) trial: Phase I. A comparison between intravenous tissue plasminogen activator and intravenous streptokinase , 1988 .

[15]  A. Jaffe,et al.  Recent changes in management of acute myocardial infarction: implications for emergency care physicians. , 1988, Journal of the American College of Cardiology.

[16]  R. Okada,et al.  Myocardial kinetics of technetium-99m-hexakis-2-methoxy-2-methylpropyl-isonitrile. , 1988, Circulation.

[17]  S. Chierchia,et al.  Intermittent coronary occlusion in acute myocardial infarction. Value of combined thrombolytic and vasodilator therapy. , 1987, The New England journal of medicine.

[18]  C. White,et al.  The importance of the determination of the myocardial area at risk in the evaluation of the outcome of acute myocardial infarction in patients. , 1987, Circulation.

[19]  Gruppo Italiano per lo Studio della Soprawivenza nell'Inf Miocardico..  EFFECTIVENESS OF INTRAVENOUS THROMBOLYTIC TREATMENT IN ACUTE MYOCARDIAL INFARCTION , 1986, The Lancet.

[20]  K. Bailey,et al.  Animal Models for Protecting Ischemic Myocardium: Results of the NHLBI Cooperative Study Comparison of Unconscious and Conscious Dog Models , 1985, Circulation research.

[21]  M. Cohen,et al.  Changes in collateral channel filling immediately after controlled coronary artery occlusion by an angioplasty balloon in human subjects. , 1985, Journal of the American College of Cardiology.

[22]  S. M. Collins,et al.  Rethrombosis after reperfusion with streptokinase: importance of geometry of residual lesions. , 1984, Circulation.

[23]  A. Ross,et al.  A randomized, angiographically controlled trial of intracoronary streptokinase in acute myocardial infarction. , 1984, The American journal of cardiology.

[24]  W. Rogers,et al.  Return of left ventricular function after reperfusion in patients with myocardial infarction: importance of subtotal stenoses or intact collaterals. , 1984, Circulation.

[25]  M S Golden,et al.  Prevalence of total coronary occlusion during the early hours of transmural myocardial infarction. , 1980, The New England journal of medicine.