Systolic Left Ventricular Function After Reperfusion Therapy for Acute Myocardial Infarction An Analysis of Determinants of Improvement

BackgroundContrast ventriculograms of 542 patients treated with intravenous thrombolytic agents for acute myocardial infarction were examined to define changes in left ventricular ejection fraction and regional wall motion that occur during the first week after reperfusion therapy for acute myocardial infarction and define clinical, acute angiographic and treatment variables related to improvement in global and regional left ventricular function. Methods and ResultsIntravenous tissue-type plasminogen activator and/or urokinase was administered to 805 patients during acute myocardial infarction. Mean time from symptom onset to thrombolytic therapy was 3 hours (22 patients received therapy within the first hour). Acute and 7-day catheterizations were performed. Paired left ventricular ejection fraction and centerline regional wall motion were available in 542 patients (67%). Stepwise, multivariable analysis of clinical, acute angiographic and treatment variables was used to develop two models: One related to improvement in left ventricular ejection fraction, and the second related to improvement in infarct zone regional function. Left ventricular ejection fraction did not change (51.2±11.1% for acute versus 51.9±11.0% for 1 week, p=0.19). Improvement in infarct zone regional function was modest (14%) at 1 week (-2.54±+1.07 standard deviation per chord for acute versus -2.17+ 1.24 at 1 week, p<0.001). Subgroup analysis demonstrated modest improvement in ejection fraction (1.4±9.5%) and greater improvement in infarct zone function (19%) in patients with successful sustained reperfusion at 1 week. Depressed left ventricular ejection fraction and infarct zone regional wall motion at the acute study were strongly associated with improvement of these parameters at 1 week. Resolution of chest pain before acute catheterization, infarct-related artery flow at acute catheterization, and depressed regional wall motion in the noninfarct zone were associated with improvement in both ejection fraction and regional infarct zone function at 1 week. Notably, the time from the onset of symptoms to initiation of thrombolytic treatment was not related to subsequent improvement in ventricular function. ConclusionsDramatic improvement in left ventricular systolic function is not common after thrombolytic therapy for acute myocardial infarction. Improvement in global and regional systolic function is most closely related to acutely depressed ventricular function and successful acute coronary recanalization. Thus, patients with the most myocardium in jeopardy and successful coronary reperfusion demonstrate the greatest improvement in global and infarct zone ventricular function. Overall, the magnitude of this improvement is modest, suggesting that the benefits of coronary reperfusion are not solely related to improvement in systolic left ventricular function.

[1]  R. Califf,et al.  Coronary bypass surgery improves global and regional left ventricular function following thrombolytic therapy for acute myocardial infarction , 1991 .

[2]  W. Rogers,et al.  Long-term effect of thrombolytic therapy on left ventricular ejection fraction after acute myocardial infarction. , 1991, The American journal of cardiology.

[3]  P. Armstrong,et al.  Coronary patency, infarct size and left ventricular function after thrombolytic therapy for acute myocardial infarction: results from the tissue plasminogen activator: Toronto (TPAT) placebo-controlled trial. TPAT Study Group. , 1991, Journal of the American College of Cardiology.

[4]  F. Sheehan,et al.  Early beneficial effect of streptokinase on left ventricular function in acute myocardial infarction. , 1991, The American journal of cardiology.

[5]  J. K. Dunn,et al.  Factors determining improvement in left ventricular function after reperfusion therapy for acute myocardial infarction: primacy of baseline ejection fraction. , 1991, Journal of the American College of Cardiology.

[6]  I. Belenkie,et al.  Relation between flow grade after thrombolytic therapy and the effect of angioplasty on left ventricular function: a prospective randomized trial. , 1991, American heart journal.

[7]  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.

[8]  M. Reznikoff,et al.  Bootstrapping: a tool for clinical research. , 1990, Journal of clinical psychology.

[9]  E J Topol,et al.  Left ventricular ejection fraction may not be useful as an end point of thrombolytic therapy comparative trials. , 1990, Circulation.

[10]  F. Harrell,et al.  Cardiac rupture, mortality and the timing of thrombolytic therapy: a meta-analysis. , 1990, Journal of the American College of Cardiology.

[11]  R. Stack,et al.  Results of high dose intravenous urokinase for acute myocardial infarction. , 1990, The American journal of cardiology.

[12]  N. Knight Quantitative radionuclide assessment of regional ventricular function after thrombolytic therapy for acute myocardial infarction; results of phase I thrombolysis in myocardial infarction (TIMI) trial , 1990 .

[13]  M Gent,et al.  Tissue plasminogen activator: Toronto (TPAT) placebo-controlled randomized trial in acute myocardial infarction. , 1989, Journal of the American College of Cardiology.

[14]  E. Braunwald,et al.  Quantitative radionuclide assessment of regional ventricular function after thrombolytic therapy for acute myocardial infarction: results of phase I Thrombolysis in Myocardial Infarction (TIMI) trial. , 1989, Journal of the American College of Cardiology.

[15]  E. Braunwald,et al.  Myocardial reperfusion, limitation of infarct size, reduction of left ventricular dysfunction, and improved survival. Should the paradigm be expanded? , 1989, Circulation.

[16]  K. Lee,et al.  A randomized controlled trial of intravenous tissue plasminogen activator and early intravenous heparin in acute myocardial infarction. , 1989, Circulation.

[17]  R. Kloner,et al.  Altered myocardial states. The stunned and hibernating myocardium. , 1989, The American journal of medicine.

[18]  F. Van de Werf Discrepancies between the effects of coronary reperfusion on survival and left ventricular function. , 1989, Lancet.

[19]  F. Van de Werf,et al.  Intravenous tissue plasminogen activator and size of infarct, left ventricular function, and survival in acute myocardial infarction. , 1988, BMJ.

[20]  T. Meinertz,et al.  The German multicenter trial of anisoylated plasminogen streptokinase activator complex versus heparin for acute myocardial infarction. , 1988, The American journal of cardiology.

[21]  F. Sheehan,et al.  Intravenous streptokinase for acute myocardial infarction. Effects on global and regional systolic function. , 1988, Circulation.

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

[23]  R. Califf,et al.  Coronary arterial thrombolysis with combined infusion of recombinant tissue-type plasminogen activator and urokinase in patients with acute myocardial infarction. , 1988, Circulation.

[24]  Aims Trial Study Group EFFECT OF INTRAVENOUS APSAC ON MORTALITY AFTER ACUTE MYOCARDIAL INFARCTION: PRELIMINARY REPORT OF A PLACEBO-CONTROLLED CLINICAL TRIAL , 1988, The Lancet.

[25]  E. Topol,et al.  A randomized trial of intravenous tissue plasminogen activator for acute myocardial infarction with subsequent randomization to elective coronary angioplasty. , 1987, The New England journal of medicine.

[26]  H. White,et al.  Effect of intravenous streptokinase on left ventricular function and early survival after acute myocardial infarction. , 1987, The New England journal of medicine.

[27]  K. Lee,et al.  A randomized trial of immediate versus delayed elective angioplasty after intravenous tissue plasminogen activator in acute myocardial infarction. , 1987, The New England journal of medicine.

[28]  R Roberts,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. , 1987, Circulation.

[29]  F H Sheehan,et al.  The effect of intravenous thrombolytic therapy on left ventricular function: a report on tissue-type plasminogen activator and streptokinase from the Thrombolysis in Myocardial Infarction (TIMI Phase I) trial. , 1987, Circulation.

[30]  A. Nyhuis,et al.  Effect of thrombolysis (streptokinase) on left ventricular function during acute myocardial infarction. , 1986, The American journal of cardiology.

[31]  H W Woo,et al.  Advantages and applications of the centerline method for characterizing regional ventricular function. , 1986, Circulation.

[32]  M. Krucoff,et al.  Noninvasive detection of coronary artery patency using continuous ST-segment monitoring. , 1986, The American journal of cardiology.

[33]  P. Serruys,et al.  Preservation of global and regional left ventricular function after early thrombolysis in acute myocardial infarction. , 1986, Journal of the American College of Cardiology.

[34]  G. Timmis,et al.  The influence of infarction site and size on the ventricular response to coronary thrombolysis. , 1985, Archives of internal medicine.

[35]  D. Ferguson,et al.  Influence of baseline ejection fraction and success of thrombolysis on mortality and ventricular function after acute myocardial infarction. , 1984, The American journal of cardiology.

[36]  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.

[37]  S. Vatner,et al.  Salvage of Myocardial Function by Coronary Artery Reperfusion 1, 2, and 3 Hours after Occlusion in Conscious Dogs , 1983, Circulation research.

[38]  J. Greenfield,et al.  Functional improvement of jeopardized myocardium following intracoronary streptokinase infusion in acute myocardial infarction. , 1983, The Journal of clinical investigation.

[39]  E. Braunwald,et al.  Time course of functional and biochemical recovery of myocardium salvaged by reperfusion. , 1983, Journal of the American College of Cardiology.

[40]  J. Lowe,et al.  The Wavefront Phenomenon of Ischemic Cell Death: 1. Myocardial Infarct Size vs Duration of Coronary Occlusion in Dogs , 1977, Circulation.

[41]  H Sandler,et al.  The use of single plane angiocardiograms for the calculation of left ventricular volume in man. , 1968, American heart journal.