BRIEF REPORTS

Outcome of Attempted Rescue Coronary An@oplasty After Failed Thrombolysis for Acute Myocardial Infarction The CORAMI Study Group

I n 20% to 50% of cases, depending on the agent, in- travenous thrombolysis during acute myocardial in-

farction (AMI) fails to achieve early reperfusion of the infarct-related artery. These “thrombolysis failures” carry a substantially increased risk of early and late death, compared with patients who have a patent infarct- related vessel within 90 minutes of thrombolysis. 1-3 Suc- cessful emergent “rescue” angioplasty of the infarct ves- sel may improve prognosis in these patients.4-6 Its indications remain controversial because of an imperfect success rate, the very high mortality of patients with failed angioplasty5 which may outweigh the clinical ben- efit, the high incidence of bleeding complications at the access site, the high incidence of reocclusion of the in- farct vessel,4 and the logistic constraints associated with its use. We hypothesized that improvements in angio- plasty equipment as well as improved medical adjunc- tive therapy may have changed the outcome of rescue angioplasty. This study evaluates, in a recent consecu- tive and multicenter cohort, the short- and midterm re- sults of rescue angioplasty performed within 8 hours of symptom onset.

Between April 1989 and October 1993,299 consec- utive patients with AMI were treated by intravenous thrombolysis ~6 hours after the onset of symptoms and underwent emergency angiography 90 minutes after the start of thrombolysis. AMI was diagnosed when chest pain was present for >30 minutes, resistant to nitrates, and with ST-segment elevation of >l mm in standard or 2 mm in contiguous chest electrocardiographic leads. The diagnosis of AMI was eventually confirmed in all patients by enzymes and angiography. Of these patients, 29% (87 of 299) had a “thrombolysis failure,” defined as flow grade 0 or 1 in the infarct-related artery, ac- cording to the Thrombolysis in Myocardial Infarction (TIMI) trial score? persisting after 24 injections and in- tracoronary injection of nitrates. Of these 87 patients with failures, 72 underwent an attempt at emergent “res- cue” angioplasty within 8 hours of symptom onset; the remaining patients were excluded because the occlusion was judged too distal or unsuitable for angioplasty by clinical judgment of the operator (n = IO), or because of randomization to the medical arm of a randomized protocol (n = 5). Success was defined as TIMI grade 3 flow in the infarct-related artery, with a residual steno- sis of <40% on visual assessment. All patients received 2160 mg of aspirin and p blockade unless contraindi- cated. Angioplasty of a non-infarct-related artery was never attempted in the acute phase. Intravenous heparin

From the Service de Cardiologie, HBpital Bichat, 46 rue Henri Huchard, 75018 Paris, France. Manuscript received November 1, 1993; revised manuscript received and accepted December 20, 1993.

was maintained 248 hours in all patients except 1, and was titrated to achieve an activated partial thrombo- plastin time of twice the control. Patients underwentpre- discharge repeat coronary angiography. Follow-up data were collected during regular visits and by mailed ques- tionnaires.

Baseline characteristics and angiographic ftndings in the 72 patients are shown in Table I. The mean age of the patients was 57 _+ 10 years (range 35 to 76); 67 of 72 (93%) were men. Nine had a previous AMI (ante- rior in 6, inferior in 3), and 10 had a history of angina without infarction. Ten percent of the patients (n = 7) were in cardiogenic shock (defined as a combination of systolic blood pressure <80 mm Hg unresponsive to in- otropic agents, mental andlor cutaneous signs of acute low cardiac output, and signs of congestive heart fail- ure) at the time of angiography. In 34% (25 of 72 pa- tients), thrombolysis was begun before admission. The average delay between the onset of pain and admission was 168 f 96 minutes (range 0 to 390), and the delay between pain and thrombolysis was 169 f 93 minutes (range 30 to 360). Sixty-nine percent of the patients were admitted outside of “ofice hours” (between 8:00 P.M. and 8:00 A.M. or during weekends). The delay between thrombolysis and angiography was 96 + 43 minutes (range 30 to 300). The TIMI grade flow in the infarct vessel before angioplasty was 0 in 88% and I in 12% of patients. Adjunctive intraaortic balloon pumping was performed in 7 patients.

Rescue angioplasty was successful in 90% (65 of 72), with a mean time between the onset of pain and reper- fusion of 300 f 101 minutes (range 13.5 to 465), and a mean delay between angiography and reperfusion of 31 f 25 minutes. There was 1 catheterization laboratory death (after angioplasty had been unsuccessful in a pa- tient in cardiogenic shock). Reperfision of the right coro- nary artery was simultaneous with 2 ventricularfibril- lations (successfully treated by immediate countershock) and 3 prolonged hypotensions (resolving after volume expansion). It resulted in immediate disappearance of atrioventricular block in 4 other patients. Peak serum creatine kinase elevation was reached 15 + 6 hours af- ter onset of symptoms, with a mean value of 2,530 _+ 2,020 IU (N <130). There was a 12% rate of access site hematomas (9 of 72 patients: 7 at the puncture site [I of which required surgical repair], and 2 asymptomatic retroperitoneal hematomas resolving spontaneously, but each requiring blood transfusion). Six percent of the pa- tients (n = 4) required transfusion, 3 for access site hematomas and 1 for gastrointestinal bleeding. There was no intracranial hemorrhage.

Predischarge angiography was performed in 88% of the survivors (61 of 69) at a mean interval of 8.3 f 3 days, and showed a patent TIMI 3 flow infarct-related

172 THE AMERICAN JOURNAL OF CARDIOLOGYa VOLUME 74 JULY 15,1994

TABLE I Baseline Characteristics and Angiographic Findings in 72 Patients

Number of Patients t%)

Infarct location Anterior Inferior

Thrombolytic agent t-PA Streptokinase APSAC t-PA + streptokinase

Infarct-related coronary artery Left antenor descending First diagonal Right Left circumflex

Extension of coronary artery disease Single vessel disease Multiple vessel disease

39 (54) 33 (46)

36 (50) 30 (4.2)

4 (5) 2 13)

38 (53) l(1)

30 (42) 3 (4)

38 (53) 34 (47)

APSAC = anisoylated plasminogen streptokmase activator complex; t-PA = bssue-type plasmlnogen activator.

artery with a residual stenosis <50% in 93% (57 of 61 patients), a persistent occlusion in 2% (I of 61), and an asymptomatic reocclusion in 5% (3 of 61). Two symp- tomatic reocclusions had required emergency repeat an- gioplasty without recurrent infarction. Thus, the overall rate of reocclusion was 7%. In patients who received only tissue-type plasminogen activator, the reocclusion rate was 10% (3 of 29), whereas in patients who received a nonfibrin specific thrombolytic agent (p = NS), it was 6% (2 of 31). Lef ventricular global ejection fraction was 49 f 11% (range 28 to 71).

The in-hospital death rate was 4% (3 of 72). Two pa- tients admitted in cardiogenic shock and with a previ- ous myocardial infarction died (1 during angioplasty, the other on day 3). A third patient died on day 5, de- spite an initially successful angioplasty. Of the 7patients with a failed rescue angioplasty, 1 died in the hospital. Thus, the death rate of failed rescue angioplasty was 14% (p = NS vs successful rescue). There was no rein- farction or emergency coronary artery bypass surgery during the hospital stay (Table II).

Long-term follow-up was available in 94% of pa- tients (65 of 69 hospital survivors), with a mean dura- tion of 16 f 12 months (range 2 to 44, median 21). There was 1 late death at 18 months, after heart transplanta- tion. The actuarial survival rate is 92% at 18 months. There was no additional myocardial infarction or by- pass surgery, and the rate of repeat angioplasty was 12% (8 of 65). Coronary angiography was performed in 46% ofpatients (30 of 65; the remaining patients were asymp- tomatic) and showed 7 reocclusions and 8 restenoses, yielding a combined incidence of reocclusion or resteno- sis of 50%. Seven of the 8 patients with restenosis un- derwent successful repeat angioplasty. Between the ini- tial predischarge angiogram and 6 months, the left ventricular angiographic ejection fraction had increased from 49.6 + 10% to 56 + 10% in patients without restenosis, while it only increased from 46.2 f 19% to 48.7 + 22% in patients with either restenosis or reoc- elusion (p = NS). At the last follow-up visit, 6 patients

TABLE II In-Hospital Outcome

Number of Patients (%)

Angioplasty success 65 (90) In-hospital survival 69 (96) Access site hematomas 9 (12) Transfusions 4 (4) Reocclusion 5 (7)* Reinfarction 0 (0) Emergency CABG 0 (0) Emergency PTCA 2 (3)

*Among 61 patients undergolng predischarge angiography. CABG = coronary artery bypass grafbng; PTCA = percutaneous translumlnal

coronary angioplasty.

had Canadian Cardiovascular Society class 2 angina, and none had class 3 or 4. In addition, only 15 patients had symptoms of heart failure (14 were in New York Heart Association class 2 and 1 was in class 3). Sev- enty-four percent (48 of 65) of patients were symptom- free, and 88% (57 of 65) were event--ee survivors (no infarction, no angioplasty, and no bypass surgery).

The high success rate (90%) achieved in this multi- center series is somewhat in the high range of those pre- viously reported for rescue angioplasty? and may be re- lated to the systematic use of adjunctive aspirin and intravenous heparin, as well as to improvement in an- gioplasty equipment. However, this rate is consistent with that observed in recent studies of primary angio- plasty in AM17*s The low mortality is unlikely to result from the selection of low-risk patients, since in this con- secutive cohort, all patients undergoing thrombolysis un- derwent emergency angiography, and all occluded in- farct-related vessels were considered for angioplasty. With the exception of 5 patients randomized into the Randomized Evaluation of Salvage angioplasty with a Combined Utilization of Endpoints (RESCUE) trial, all patients excluded from rescue angioplasty had an oc- clusion judged too distal or unsuitable for angioplasty, and none actually died. Thus, our experience is repre- sentative of the outcome of rescue angioplasty applied consecutively to suitable patients. The rate of in-hospi- tal reocclusions (7%) was lower than that reported pre- viously,5 which may be due to the systematic use of con- tinuous titrated intravenous heparin in addition to aspirin, as well as to the achievement of an angiographic result as optimal as possible during the procedure.

The logistic constraints associated with the mainte- nance of a permanent capability for emergency angiog- raphy9 and angioplasty, further underscored by the fact that the vast majority of patients were admitted outside of “office hours,” have restricted the use of rescue an- gioplasty. Prehospital triage of patients with high-risk AM1 to institutions with the capability for emergency angioplasty as well as improved noninvasive detection of early reperfusion may help solve this problem. In ad- dition, it is possible that patients with myocardial no-re- flow, or TIM1 2 flow in the infarct vessel could benefit from rescue angioplasty, lo but this has not yet been tested.

Pending the completion of the randomized RES- CUE trial, and while these results should be inter-

BRIEFREPORTS 173

preted with caution owing to the absence of a control group, it is suggested that attempted rescue angio- plasty results in excellent short- and midterm out- come and may be an adequate alternative to conven- tional medical therapy after failed thrombolysis.

APPENDIX The CORAMI (Cohort of Rescue Angioplasty in

Myocardial Infarction) Study Group: Coordination: P. Gabriel Steg, MD, and Gdtan J. Karrillon, MD; Hopi- tal Bichat (45 patients): Jean-Michel Juliard, MD, Do- minique Himbert, MD, and RenC Gourgon, MD; Hopi- tal Cochin (14 patients): Christian M. Spaulding, MD, and Antoine Py, MD; and Hopital Broussais (13 pa- tients): Antoine Sarkis, MD, Marie-Christine Iliou, MD, Serge Makowski, MD, Gilles Bayet, MD, Jean-Paul Ri- naldi, MD, Louis Guize, MD, and Jean-Leon Guer- monprez, MD.

1. Califf RM, Top01 EJ, George BS, Boswick J, Lee KL, Stamp D, Dillon J, Ab- bottsmith C, Candela RJ, Kereiakes DJ, O’Neill WW, Stack RS. Characteristics and outcome of patients in whom reperfasion with intravenous tissue-type plas- minogen activator fails: results of the Thrombolysis and Angioplasty in Myocar- dial Infarction (TAMI) I trial. Circulation 1988;77:109C-1099. 2. Chesebro JH, Knattemd G, Roberts R, Borer J, Cohen LS, Dale” I, Dodge HT, Francis CK, Hillis D, Ludbrook P, Markis JE, Mueller H, Passamani ER, Powers ER. Rao AK, Robertson T, Ross A, Ryan TJ, Sobel BE, Willerson J, Williams DO,

Zaret BL, Braunwald E. Thrombolysis In acute Myocardial Infarction (TIMl) trial Phase I. A comparison between intravenous tissue plasminogen activator and in- travenous streptokinase. Circhtion 1987:76:142-154. 8. Stack RS, O’Connor CM, Mark DB, Hinohara T, Phillips HR. Lee MM, Ram& NM, O’Callaghan WG, Simonton CA, Carlson EB, Morris KG, Behar VS, Kong Y, Peter RH, Califf RM. Coronary perfusion during acute myocardial infarction us- ing a combined therapy of coronary angioplasty and high dose intravenous strep- tokinase. Circularion 1988;77: 151-161. 4. Abbottsmith CW, Top01 El, George BS, Stack RS, Kereiakes DJ, Candela RJ, Anderson LC, Harrelson-Wocdlief LS, Califf RM. Fate of patients with acute myo- cardial infarction with patency of the infarct-related vessel achieved with success- ful thrombolysis versus rescue angioplasty. J Am Co/l Car&l 1990,16:770-778. 5. Ellis SG, Van der Werf F, Ribeiro-Da-Silva E, Top01 EJ. Present status of res- cue coronary angioplasty: current polarization of opinion and randomized trials. J Am CON Cardiol 1992;19:681-686. 6. Califf RM, Top01 EJ, Stack RS, Ellis SG, George BS, Kereiakes DJ, Samaha JK, Worley SJ, Anderson IL, Hanelson-Woodlief L, Wall TC, Phillips HR III, Ab- bottsmith CW, Candela RJ, Flanagan WH, Sasahara AA, Mantel1 SJ, Lee KL, for the TAM1 Study Group. Evaluation of combination thmmbolytic therapy and tim- ing of cardiac catheterization in acute myocardial infarction. Results of Thrombol- ysis and Angioplasty in Myocardial Infarction phase 5 randomized trial. Circula- rim 1991;83:1543-1556. 7. Grines CL, Browne KF, Marco J, Rothbaum D, Stone GW, O’Keefe I, Overlie P, Donahue B, Chelliah N, Timmis GC, Vlietstra RE, Strzelecki M, Puchrowicz- Ochocki S, O’Neill WW, for the Primary Angioplasty in Myocardial Infarction Study Group. A comparison of immediate angioplasty with thrombolytic therapy for acute myocardial infarction. N Engl J Med 1993;328:6713-679. 8. Ziljstra F, De Boer MJ, Hoomtje JCA, Reiffers S, Reiber JHC, Suryapranata H. A comparison of immediate coronary angioplasty with intravenous streptokinase in acute myocardial infarction. N Engl J Med 1993;326:68@684. 9. Califf RM, O’Neill W, Stack RS for the TAM1 Study Group. Failure of simple clinical measurementS to predict perfusion status after intravenous thrombolysis. Ann Intern Med 1988;108:658-562. 10. Lincoff AM, Topol El. Illusion of reperfusion: does anyone achieve optimal reperfusion during acute myocardial infarction? Circulation 1993;87: 1792-1805.

Variability of Acute ST-Segment Predicted Myocardial Infarct Size in the Absence of Thrombolytic Therapy Michelle L. Wilkins, Stanley T. Anderson, FRACP, Aurora D. Pryor, BSE, W. Douglas Weaver, MD, and Galen S. Wagner, MD

T he decision to initiate pharmacologic or mechanical reperfusion therapies in a patient with acute myo-

cardial ischemia/infarction is dependent on timely clin- ical assessment of the potential benefits. The most im- portant predictor of treatment benefit is the amount of myocardium that could potentially be salvaged by reper- fusion. Through formulas based on the measurements of ST-segment elevation on the presenting standard 12-lead electrocardiogram (ECG), the method of Aldrich et al1 predicts the amount of myocardium likely to infarct in the absence of reperfusion therapy. These formulas were developed by comparing various measures of ST-seg- ment deviation to Selvester QRS score2 on single 12- lead ECGs at the time of hospital admission and dis- charge, respectively. It is important to determine the consistency of predictions using these formulas on se- rial ECGs. To date, no previous studies have addressed this question. Therefore, the present study was per- formed to assess the consistency of predictions when ap-

From the Department of Medicine, Duke University Medical Center, Durham, North Carolina, and the Department of Medicine, University of Washington, Seattle, Washington. This study was supported in part by the Duke University Clinical Cardiovasculax Study (DUCCS) group, Durham, North Carolina Manuscript received December 2, 1993, and accepted January 5, 1994.

plying the formulas of Aldrich et al1 to serial ECGs recorded during the time interval preceding the initiation of thrombolytic therapy.

Standard 12-lead ECGs were obtained at the time of prehospital evaluation by paramedics (ECGl) and in the hospital emergency room (ECG2) in 18.5 patients who participated in the Myocardial Infarction Triage and In- tervention phase I project? and in the control group of the Myocardial infarction Triage and Intervention ran- domized trial conducted by Weaver et al4 at the Uni- versity of Washington. The time interval between ECGl and ECG2 rangedfrom 9 to 113 minutes (mean 48). Pa- tients were initially selected for the study by the follow- ing criteria: (I) ST-segment elevation of 20.1 mV, mea- sured at the Jpoint in >Z2 anatomically contiguous leads on ECGl; (2) no confounding factors on either ECG (missing or malpositioned leads, ventricular paced rhythm, 60 Hz artifact, unstable baseline, complete left or right bundle branch block, left andlor right ventricu- lar hypertrophy, or heart rate >I10 beatslmin); (3) <2 hours between ECGI and ECG2; and (4) no throm- bolytic therapy between ECGl and ECGZ. Patients with maximal ST-segment elevation in leads II, III, or aVF on ECGI were considered to have inferior locations, whereas those with maximal elevation in leads V,, Vz, or V, on ECGI were considered to have anterior loca- tions.

174 THE AMERICAN JOURNAL OF CARDIOLOGY@ VOLUME 74 JULY 15,1994