- Email: [email protected]
Late angiographic follow-up after successful coronary arterial thrombolysis and angioplasty during acute myocardial infarction
late AngiographicFollow-UpAfter Successful Coronary Arterial Thrombolysisand Angioplasty During Acute Myocardial Infarction LOWELL F. SATLER, MD, CURTIS E. GREEN, MD, NANCY M. McNAMARA, MD, JAMES P. LAVELLE, MD, RANDOLPH S. PALLAS, MD, DAVID L. PEARLE, MD, KENNETH M. KENT, MD, PhD, and CHARLES E. RACKLEY, MD
terization at an average of 22 months after AMI and 6 underwent repeat catheterization because of recurrent chest pain. Restenosis of the PTCA site was found in 10 of the 31 patients (32%) restudied. Also, 14 (45%) of these 31 patients showed progression of narrowing in the non-infarct-related coronary arteries. In summary, patients in whom AMI is treated by PTCA are at risk for restenosis and for progressive narrowing of the non-infarct artery. (Am J Cardiol 1967;60:21 O-21 3)
Emergency percutaneous transluminal coronary angioplasty (PTCA) is accepted as an important reperfusion intervention for acute myocardial infarction (AMI). Although its primary success rate is well documented, the frequency of restenosis after this procedure is unclear. The frequency of restenosis was determined in patients undergoing emergency PTCA at least 6 months after PTCA was performed during AMI. of 66 consecutive patlents undergoing emergency PTCA, 25 had a second, elective cathe-
E
mergency revascularization in acute myocardial infarction (AMI] has been shown to limit infarct sizelJ and reduce mortality risk.3 In many centers, percutaneous transluminal coronary angioplasty (PTCA) is accepted as the primary reperfusion intervention,4 or is used in association with a thrombolytic agents-9 to maximally improve blood flow in the infarct-related artery. Many investigators have documented that both the early reocclusion and restenosi&lo rates after successful emergency PTCA for AM1 may be higher than those after elective PTCA. Information regarding the long-term results of PTCA after AM1 is limited. This investigation evaluates the late angiographic changes after emergency PTCA for AMI.
Methods One hundred ninety-two patients were treated with streptokinase for AM1 over a 3.5-year period; 69 also underwent PTCA within 7 days of receiving the lytic From the Department of Medicine, Division of Cardiology Georgetown University Hospital, Washington, DC. Manuscript received January 30,1987; revised manuscript received and accepted March 26,1987. Address for reprints: Lowell F. Satler, MD, Georgetown University Hospital, Division of Cardiology, 3800 Reservoir Road, NW, Washington, D.C. 20007. 210
agent due to recurrent ischemia or the presence of coronary stenosis of at least 70% but less than 10 mm long, unassociated with left main disease or side branch involvement. Two other patients underwent emergency revascularization by PTCA alone during the same period. All 71 patients were subsequently treated with heparin for 24 to 72 hours in addition to aspirin, dipyridamole and a calcium blocking drug through the time of discharge. Three patients subsequently showed reocclusion (Z of whom underwent coronary bypass) and 2 patients died (due to cardiogenie shock] during hospitalization. The remaining 66 patients who initially underwent PTCA for AM1 were considered eligible for reevaluation by repeat cardiac catheterization at least 6 months after emergency PTCA. Of these 66 patients, 26 refused repeat cardiac catheterization, 9 could not be contacted, 6 had already undergone repeat catheterization and coronary bypass surgery and 25 consented and completed elective repeat cardiac catheterization. The patients were informed of the investigative nature of the study as approved by the Institutional Review Board. Of the 25 patients who underwent repeat elective cardiac catheterization, 23 received a thrombolytic agent before PTCA: intracoronary streptokinase in 13, intravenous streptokinase in 9 and combined intracoronary and intravenous streptokinase in 1 patient. In 2
August
TABLE I Progression
Comparison of Coronary
of Clinical Characteristics Artery Disease
1, 1987
of
WE
atients
Mean Median Range Men Months of follow-up Smoking before AMI Smoking after AMI Cholesterol (mg/dl)
239
(p
IO)
48 f II” 45 35-69 IO/IO 19 f 9 9110 2/10 f 32 (n = 6)f
IRV = infarct-related
patients, PTCA was the sole reperfusion intervention. The average interval between the emergency PTCA and follow-up catheterization was 22 f 11 months. Symptoms were graded according to the Canadian Cardiovascular Society criteria.1’ Sixteen patients were in class I, 6 were in class II and 3 were in class III. Of the 26 patients who refused repeat catheterization, 25 were in class I and 1 was in class II. No patient had a history of congestive heart failure. Medications included aspirin in 19 of 25 [76%], dipyridamole in 7 (23%), calcium blocking drugs in 9 (36%) and P-blocking drugs in 6 (24%). The serum total cholesterol level [measured by using enzymatic-calorimetric procedures on Beckman Instruments’ Astra System) was determined in most patients undergoing repeat catheterization, Evaluation of the severity of residual stenosis was performed by 3 experienced angiographers. The coronary angiograms were projected and magnified and calipers used to measure the stenoses. Side-by-side simultaneous projections of the initial and follow-up catheterizations were made to identify the precise sites of change. The stenoses recorded by each angiographer were averaged and then rounded upward to the nearest tenth percentile. Axial angiography was performed, and the views in the 2 studies were nearly identical. Before angiography for both the initial and follow-up catheterizations, intracoronary nitroglycerin was administered. A difference between the initial and follow-up catheterization was considered significant if the degree of stenosis changed by 20 percentage points or more. In addition to evaluation of the infarct vessel, the non-infarct vessels were similarly analyzed. Statistical analysis was performed by using analysis of variance to determine the differences between the means of groups, and by chi-square analysis to determine the differences of proportions between groups.
Results Coronary angiograms were reviewed in each of the 25 patients undergoing elective repeat cardiac catheterization. The infarct-related artery was the left anterior descending in 10 patients, left circumflex in 2 and
with
(n = 6)
303
JOURNAL
Progression
Progression in IRV
No Progression (n =
AMERICAN
64 f 5” 62 58-73 4/6 15 f 117 5/6 O/6 i 62 (n = 5)$
OF CARDIOLOGY
Volume
60
a12
Versus
Progression in Non-IRV (n = 9)
53 f 7 56 40-65 9/9 29 zk 11t a/9 219 244 f 51 (n = 6)
vessel.
right coronary artery in 13. Six of the 25 PTCA sites showed restenosis, with the average residual stenosis increasing from 33 f 10% to 70 f 11%. Among patients in whom restenosis was present, 4 were in functional class I, 1 patient was in class II and 1 was in class III. One patient subsequently underwent coronary bypass surgery because of recurrent chest pain and multivesse1 coronary artery disease, 2 patients underwent repeat PTCA because stress test results were abnormal and 3 continued medical therapy because of normal stress test results and absence of symptoms. Both patients who underwent successful repeat PTCA had pain during balloon occlusion, implying persistent myocardial viability.12 Angiographic changes in the non-infarct-related vessels of the 25 patients were also evaluated. Twelve of the patients had angiographic evidence of disease progression. Of these 12 patients, 3 were in class I, 2 were in class II and 2 were in class III. Disease progression was documented in these 12 patients in 23 sites, with an increase in stenosis from 14 f 19% to 46 f 23%. Both class III patients were treated medically due to inoperable multivessel disease: 2 patients in class I and 1 patient in class II had repeat successful PTCA. In the 25 patients who underwent elective recatheterization, determination of any differences among patients with no disease progression, patients with restenosis of the infarct vessel and patients with disease progression was made by analysis of 5 variables: sex, age, months of follow-up, smoking history and cholesterol level [Table I). The only significant differences were that patients with disease progression were older and the average duration of follow-up was longer in patients with disease progression in the non-infarctvessel group. Six patients had recurrent chest pain and were reevaluated by repeat catheterization within the first year after emergency PTCA for AMI. Coronary angiograms were reviewed in a manner similar to that used for elective procedures. Infarct vessel restenosis was noted in 4 of the 6 patients. Non-infarct vessel disease progression was noted in 2 other patients in 4 additional sites. All patients had multivessel coronary disease and underwent coronary bypass surgery.
212
LATE
ANGlOGRAPHIC
FOLLOW-UP
AFTER
ANGIOPLASTY
Discussion Reperfusion in AM1 lowers in-hospital3 and late mortality13 risk as well as limiting infarct size.2,3J14 Emergency PTCA in this setting is now believed to be an important intervention because it can be used after thrombolytic therapy to mechanically disrupt the underlying atherosclerotic plaque to prevent reocclusion6 and allow for maximal early coronary reperfusion in an attempt to stimulate maximal improvement in left ventricular performance.1°J5 The major potential limitation of PTCA, apart from the initial complications associated with the procedure, is the incidence of restenosis. During elective PTCA, restenosis occurs in 23 to 38% of patients .16J7 Few investigators, however, have evaluated the overall restenosis rate after PTCA in AMI. Hartzler et al8 reported a restenosis rate of 17% within 6 months after PTCA in AMI, but only restudied patients who were symptomatic. Gold et al9 documented a restenosis or reocclusion rate of 45% at an average of 5.5 months after PTCA, but evaluated only 11 patients. Meyer6 described reocclusion or restenosis in 4 of 19 patients, but the follow-up period of time was unclear, as was the indication for reevaluation. The purpose of this study was to eliminate these shortcomings by evaluating the late [at least 6 months) angiographic changes after successful PTCA in AM1 in a large series of consecutive patients undergoing this intervention. Of the 66 consecutive patients who underwent emergency PTCA in the setting of infarction, repeat cardiac catheterization was performed on an elective basis in 25 and due to clinical symptoms requiring urgent hospitalization in 6. Elective reevaluation documented restenosis in 6 of the 25 patients (24%). Restenosis was also noted in 4 of the 6 patients undergoing repeat cardiac catheterization due to clinical instability, resulting in overall angiographic evidence of disease progression in the infarct-related vessels in 10 of the 31 patients (32%). Most surprising was the information obtained in the evaluation of non-infarct-related coronary arteries. Over a 22-month period, 14 patients showed progression of narrowing in the non-infarct-related vessel in a total of 23 sites. Although in most patients the progression of narrowing still resulted in a diameter stenosis of less than 5070, it nonetheless indicates presence of unfavorable factors allowing for the rapid progression of atherosclerosis. There appeared to be no single factor responsible for disease progression. Patients with disease progression of the infarct vessel tended to be older, while those with progression of the non-infarct vessels had a longer follow-up. Serum total cholesterol levels were not statistically different in patients with no progression vs those with progressive narrowing, although a statistical difference was approached between the no progression group and the infarct-vessel restenosis group (p = 0.06). There are some limitations in interpretation of our results. We performed repeat cardiac catheterizations in only 31 of the 66 patients (47%) undergoing PTCA for AMI. It is possible that the restenosis rate reported represents a “worst-case” scenario, because symptom-
atic patients are more likely to undergo repeat catheterization. If the 35 patients who did not have a repeat catheterization had no restenosis, the restenosis rate for the entire group of 66 patients would be as low as 15% (10 of 661. It is important to recognize that of the 26 patients who were contacted but refused repeat catheterization, 25 were either asymptomatic or mildly symptomatic. Of the 25 patients consenting to elective repeat catheterization, most were also either asymptomatic or mildly symptomatic, suggesting a clinical condition similar to that of the patients refusing restudy. Finally, since 5 of the 6 patients (84%) found to have restenosis were also either asymptomatic or mildly symptomatic, it is likely that a similar restenosis rate would be found among asymptomatic or mildly symptomatic patients who refused restudy. It is also anticipated that the progressive narrowing in non-infarct-related vessels would be similar in both groups. The only other potential criticism is the demonstration of changes in angiographic stenoses by hand-held calipers, rather than by quantitative computer-based automatic edge detection for measuring cross-sectional area or by cinevideodensimetry.lsJg Although these quantitative techniques are more precise in measuring small changes, they are not widely available to the clinician for making therapeutic decisions. In addition, a Task Force of the World Health Organization and the International Society and Federation of Cardiology indicated that for purposes of clinical research, quantitation of arterial narrowing based on multiple views still referred to a reduction of luminal diameter, and could be described in incremental steps of percentages as small as 5 to 10% .20Although other investigators have accepted a 10% change in the degree of obstruction as significant,21 we accepted a minimal change in the stenosis of 20% in an attempt to clearly demonstrate changes in angiographic progression.
References 1. Fine DG, Weiss AT, Sapoznikov D, Welber S, Applcbaum D, Lotan C, Hasin Y, Ben-David Y, Karen G, Gotsman M. Importance of early initiation of intravenous streptokinase therapy for acute myocardiai infarction. Am J Cardiol 1686;58:411-417. 2. I.S.A.M. Study Group. A prospective trial of intravenous sfrepfokinase in acute myocardial infarction (I.S.A.M.]. Mortality, morbidity, and infarct size at 21 days. N Engl J Med 1986;314:1465-1471. 3. GISSI. Effectiveness of intravenous fhromboiytic treatment in acute myocardial infarction. Lancet 1986;1:397-402. 4. Harfzler GO, Rutheriord BD, McConahey DR, Johnson WL Jr, McCallister BD, Gura GM Jr, Conn RC, Crockett JE. Percutaneous transluminal coronary angioplasfy with and without fhrombolyfic therapy for treatment of acute myocardial infarction. Am Heart 1 1983;106:965-973. 5. Fung AY, Lai P, Top01 EJ, Bates ER, Bourdillon PDV, Walton JA, Mancini GBJ, Kryski T, Pitt B, O’Neill WW. Value of percutaneous transluminal coronary angioplasfy after unsuccessful intravenous strepfokinase therapy in acute myocardial infarction. Am J Cardiol 1986;58:686-691. 9. Meyer J. Merx W, Schmitz H, Erbel R, Kiesslich T, Dorr R, Lambertz H, Bethge C, Krebs W, Bardos P, MinaIe C, Messmer BJ, Effert S. Percutaneous transluminal coronary angioplasfy immediately after introcoronary sfreptoIySiS of franshtminai myocardial infarction. Circulation 1982;66:905-913. 7. Papapietro SE, MacLean WAH, Stanley AWN, Hess RG, Corley N, Arciniegas JG, Cooper TB. Percutaneous fransluminal coronary angioplasfy after intracoronary sfrepfokinase in evolving acute myocardial infarction. Am J Cardiol 1~&i;55:5!8-53. 6. Hartzler GO, Rutherford BD, McConahay DR. Percutaneous fronsluminal coronary angioplasty: application for acute myocardial infarction. Am 1 Cardial 1984:53:117C-321C. 9. Gold HK, Cowley MJ, Palacios IF, Vetrovec GW, Akins CW, Block PC, Leinbach RC. Combined infracoronary sfrepfokinase infusion and coronary angioplasty during acute myocardial infarction. Am 1 Cardiol 1984;53:122C-
JWJSt
125c.
10. Erbel R, Pop T, Henrichs
KJ, von Olshausen K, Schuster C]. Rupprecht HG, Steuernagel C, Meyer J. Percutaneous transluminaf coronary angioplasty after thrombolytic therapy: a prospective controifed randomized trial. jACC 1986;8:485-495. Il. Campeau L. Grading of angina pecforis (letter]. Circulation 1976;54: 5&?. 12. Satler LF, Rackley GE, Green CE, Pallas RS, Pearle DL, Del Negro AA, Kent KM. Ischemia during angioplasty after streptokinase: a marker of myocardiaf s&age. Am J Cdrdiol 1985;56:749-752. 13. Kennedv 1W. Ritchie 1L. Davis KB. Stadius ML. Mavnard C. Fritz 1K. The Western W>Hhington randomized trial of intracoronary streptokinase in acute myocardial infarction. A la-month follow-up report. N EngJ J Med 1985;312:1073-2078.
14. SimoonsML,SerruysPW,vandenBrandM,Res],VerheugtFWA,Krauss XH, Remme WJ, Bar F, de Zwann C, van der Laarse A, Vermeer F, Lubsen J and Collaborators. Early thrombolysis in acute myocardiai infarction: Iimitation of infarct size and imoroved survival. TACC 1986:7:717-728. 15. U’Nei?l W, Timmis GC,‘Bourdillon PD, Lii P, Ganghadarhan V, Walton J, Ramos R, Laufer N, Gordon S, Schork A, Pitt B. A prospective randomized clinical trial of intracoronary streptokinase versus coronary angioplasty for
f, 1987
WE
AxRICAN
JOURNAL
OF CARDIOLOGY
Volume 60
293
acute myocardial infarction. N Engi J Med 1986;314:822-818. 16. Levine S. Ewels Cl, Rosinn DR, Kent KM. Coronarv annionlastv: clinical and angiographic fohv-up. Am J Cardiol 1985;55:673-676. ’ ’ 17. Holmes DR Jr, Vliestra RE, Smith HC, Vetrovec GW, Kent KM, Cowley Ml, Faxon DP. Gruentzig AR. Kelsev SF. Detre KM. Van Raden MI. Mock Mb. Restenosis followingpercutanedus transluminai coronary angioplasty: a report from the NHLBI registry. Am I CardioJ 1984;53:77G8ZC. la. Nichols AB, Gabrieli CFO,.Fenogiio JJ Jr, Esser PD. Quantification of relative coronary arterial stenosisby cinevideodensitometric anaiysis ofcoronary orteriograms. Circulation 1984:69:512-522. 19. Serruvs PW, Reiber JHC, Wiins W, van den Brand M, Kooiiman CJ, ten Katen HJ.‘HugenholtzPd. Assessment of percutaneous transfuminal cordnary angioplasty by quantitative coronary ongiography: diameter versus densitometric area measurements. Am J CardioI 1984:54:482-488. 20. lames TN. Bruschke AVG. Bothig S. Dodu SRA, Gil IF, Kawamura K, Pa&n SJ, Piessens J. Report of WHO%‘FC Task Force on’Nomenclature of Coronary Arteriograms. Circulation 198G;74:451A-455A. 21. Rosinn DR, Cannon RO III, Watson RM, Bonow RO, Mincemover R, Ewels C, Leon MB, Lakatos E, Epstein SE, Kent KM. Three year anatomic, functional and clinical follow-up after successful percutaneous transluminal coronary angioplasty. [ACC 1987;9:1-7.
terization at an average of 22 months after AMI and 6 underwent repeat catheterization because of recurrent chest pain. Restenosis of the PTCA site was found in 10 of the 31 patients (32%) restudied. Also, 14 (45%) of these 31 patients showed progression of narrowing in the non-infarct-related coronary arteries. In summary, patients in whom AMI is treated by PTCA are at risk for restenosis and for progressive narrowing of the non-infarct artery. (Am J Cardiol 1967;60:21 O-21 3)
Emergency percutaneous transluminal coronary angioplasty (PTCA) is accepted as an important reperfusion intervention for acute myocardial infarction (AMI). Although its primary success rate is well documented, the frequency of restenosis after this procedure is unclear. The frequency of restenosis was determined in patients undergoing emergency PTCA at least 6 months after PTCA was performed during AMI. of 66 consecutive patlents undergoing emergency PTCA, 25 had a second, elective cathe-
E
mergency revascularization in acute myocardial infarction (AMI] has been shown to limit infarct sizelJ and reduce mortality risk.3 In many centers, percutaneous transluminal coronary angioplasty (PTCA) is accepted as the primary reperfusion intervention,4 or is used in association with a thrombolytic agents-9 to maximally improve blood flow in the infarct-related artery. Many investigators have documented that both the early reocclusion and restenosi&lo rates after successful emergency PTCA for AM1 may be higher than those after elective PTCA. Information regarding the long-term results of PTCA after AM1 is limited. This investigation evaluates the late angiographic changes after emergency PTCA for AMI.
Methods One hundred ninety-two patients were treated with streptokinase for AM1 over a 3.5-year period; 69 also underwent PTCA within 7 days of receiving the lytic From the Department of Medicine, Division of Cardiology Georgetown University Hospital, Washington, DC. Manuscript received January 30,1987; revised manuscript received and accepted March 26,1987. Address for reprints: Lowell F. Satler, MD, Georgetown University Hospital, Division of Cardiology, 3800 Reservoir Road, NW, Washington, D.C. 20007. 210
agent due to recurrent ischemia or the presence of coronary stenosis of at least 70% but less than 10 mm long, unassociated with left main disease or side branch involvement. Two other patients underwent emergency revascularization by PTCA alone during the same period. All 71 patients were subsequently treated with heparin for 24 to 72 hours in addition to aspirin, dipyridamole and a calcium blocking drug through the time of discharge. Three patients subsequently showed reocclusion (Z of whom underwent coronary bypass) and 2 patients died (due to cardiogenie shock] during hospitalization. The remaining 66 patients who initially underwent PTCA for AM1 were considered eligible for reevaluation by repeat cardiac catheterization at least 6 months after emergency PTCA. Of these 66 patients, 26 refused repeat cardiac catheterization, 9 could not be contacted, 6 had already undergone repeat catheterization and coronary bypass surgery and 25 consented and completed elective repeat cardiac catheterization. The patients were informed of the investigative nature of the study as approved by the Institutional Review Board. Of the 25 patients who underwent repeat elective cardiac catheterization, 23 received a thrombolytic agent before PTCA: intracoronary streptokinase in 13, intravenous streptokinase in 9 and combined intracoronary and intravenous streptokinase in 1 patient. In 2
August
TABLE I Progression
Comparison of Coronary
of Clinical Characteristics Artery Disease
1, 1987
of
WE
atients
Mean Median Range Men Months of follow-up Smoking before AMI Smoking after AMI Cholesterol (mg/dl)
239
(p
IO)
48 f II” 45 35-69 IO/IO 19 f 9 9110 2/10 f 32 (n = 6)f
IRV = infarct-related
patients, PTCA was the sole reperfusion intervention. The average interval between the emergency PTCA and follow-up catheterization was 22 f 11 months. Symptoms were graded according to the Canadian Cardiovascular Society criteria.1’ Sixteen patients were in class I, 6 were in class II and 3 were in class III. Of the 26 patients who refused repeat catheterization, 25 were in class I and 1 was in class II. No patient had a history of congestive heart failure. Medications included aspirin in 19 of 25 [76%], dipyridamole in 7 (23%), calcium blocking drugs in 9 (36%) and P-blocking drugs in 6 (24%). The serum total cholesterol level [measured by using enzymatic-calorimetric procedures on Beckman Instruments’ Astra System) was determined in most patients undergoing repeat catheterization, Evaluation of the severity of residual stenosis was performed by 3 experienced angiographers. The coronary angiograms were projected and magnified and calipers used to measure the stenoses. Side-by-side simultaneous projections of the initial and follow-up catheterizations were made to identify the precise sites of change. The stenoses recorded by each angiographer were averaged and then rounded upward to the nearest tenth percentile. Axial angiography was performed, and the views in the 2 studies were nearly identical. Before angiography for both the initial and follow-up catheterizations, intracoronary nitroglycerin was administered. A difference between the initial and follow-up catheterization was considered significant if the degree of stenosis changed by 20 percentage points or more. In addition to evaluation of the infarct vessel, the non-infarct vessels were similarly analyzed. Statistical analysis was performed by using analysis of variance to determine the differences between the means of groups, and by chi-square analysis to determine the differences of proportions between groups.
Results Coronary angiograms were reviewed in each of the 25 patients undergoing elective repeat cardiac catheterization. The infarct-related artery was the left anterior descending in 10 patients, left circumflex in 2 and
with
(n = 6)
303
JOURNAL
Progression
Progression in IRV
No Progression (n =
AMERICAN
64 f 5” 62 58-73 4/6 15 f 117 5/6 O/6 i 62 (n = 5)$
OF CARDIOLOGY
Volume
60
a12
Versus
Progression in Non-IRV (n = 9)
53 f 7 56 40-65 9/9 29 zk 11t a/9 219 244 f 51 (n = 6)
vessel.
right coronary artery in 13. Six of the 25 PTCA sites showed restenosis, with the average residual stenosis increasing from 33 f 10% to 70 f 11%. Among patients in whom restenosis was present, 4 were in functional class I, 1 patient was in class II and 1 was in class III. One patient subsequently underwent coronary bypass surgery because of recurrent chest pain and multivesse1 coronary artery disease, 2 patients underwent repeat PTCA because stress test results were abnormal and 3 continued medical therapy because of normal stress test results and absence of symptoms. Both patients who underwent successful repeat PTCA had pain during balloon occlusion, implying persistent myocardial viability.12 Angiographic changes in the non-infarct-related vessels of the 25 patients were also evaluated. Twelve of the patients had angiographic evidence of disease progression. Of these 12 patients, 3 were in class I, 2 were in class II and 2 were in class III. Disease progression was documented in these 12 patients in 23 sites, with an increase in stenosis from 14 f 19% to 46 f 23%. Both class III patients were treated medically due to inoperable multivessel disease: 2 patients in class I and 1 patient in class II had repeat successful PTCA. In the 25 patients who underwent elective recatheterization, determination of any differences among patients with no disease progression, patients with restenosis of the infarct vessel and patients with disease progression was made by analysis of 5 variables: sex, age, months of follow-up, smoking history and cholesterol level [Table I). The only significant differences were that patients with disease progression were older and the average duration of follow-up was longer in patients with disease progression in the non-infarctvessel group. Six patients had recurrent chest pain and were reevaluated by repeat catheterization within the first year after emergency PTCA for AMI. Coronary angiograms were reviewed in a manner similar to that used for elective procedures. Infarct vessel restenosis was noted in 4 of the 6 patients. Non-infarct vessel disease progression was noted in 2 other patients in 4 additional sites. All patients had multivessel coronary disease and underwent coronary bypass surgery.
212
LATE
ANGlOGRAPHIC
FOLLOW-UP
AFTER
ANGIOPLASTY
Discussion Reperfusion in AM1 lowers in-hospital3 and late mortality13 risk as well as limiting infarct size.2,3J14 Emergency PTCA in this setting is now believed to be an important intervention because it can be used after thrombolytic therapy to mechanically disrupt the underlying atherosclerotic plaque to prevent reocclusion6 and allow for maximal early coronary reperfusion in an attempt to stimulate maximal improvement in left ventricular performance.1°J5 The major potential limitation of PTCA, apart from the initial complications associated with the procedure, is the incidence of restenosis. During elective PTCA, restenosis occurs in 23 to 38% of patients .16J7 Few investigators, however, have evaluated the overall restenosis rate after PTCA in AMI. Hartzler et al8 reported a restenosis rate of 17% within 6 months after PTCA in AMI, but only restudied patients who were symptomatic. Gold et al9 documented a restenosis or reocclusion rate of 45% at an average of 5.5 months after PTCA, but evaluated only 11 patients. Meyer6 described reocclusion or restenosis in 4 of 19 patients, but the follow-up period of time was unclear, as was the indication for reevaluation. The purpose of this study was to eliminate these shortcomings by evaluating the late [at least 6 months) angiographic changes after successful PTCA in AM1 in a large series of consecutive patients undergoing this intervention. Of the 66 consecutive patients who underwent emergency PTCA in the setting of infarction, repeat cardiac catheterization was performed on an elective basis in 25 and due to clinical symptoms requiring urgent hospitalization in 6. Elective reevaluation documented restenosis in 6 of the 25 patients (24%). Restenosis was also noted in 4 of the 6 patients undergoing repeat cardiac catheterization due to clinical instability, resulting in overall angiographic evidence of disease progression in the infarct-related vessels in 10 of the 31 patients (32%). Most surprising was the information obtained in the evaluation of non-infarct-related coronary arteries. Over a 22-month period, 14 patients showed progression of narrowing in the non-infarct-related vessel in a total of 23 sites. Although in most patients the progression of narrowing still resulted in a diameter stenosis of less than 5070, it nonetheless indicates presence of unfavorable factors allowing for the rapid progression of atherosclerosis. There appeared to be no single factor responsible for disease progression. Patients with disease progression of the infarct vessel tended to be older, while those with progression of the non-infarct vessels had a longer follow-up. Serum total cholesterol levels were not statistically different in patients with no progression vs those with progressive narrowing, although a statistical difference was approached between the no progression group and the infarct-vessel restenosis group (p = 0.06). There are some limitations in interpretation of our results. We performed repeat cardiac catheterizations in only 31 of the 66 patients (47%) undergoing PTCA for AMI. It is possible that the restenosis rate reported represents a “worst-case” scenario, because symptom-
atic patients are more likely to undergo repeat catheterization. If the 35 patients who did not have a repeat catheterization had no restenosis, the restenosis rate for the entire group of 66 patients would be as low as 15% (10 of 661. It is important to recognize that of the 26 patients who were contacted but refused repeat catheterization, 25 were either asymptomatic or mildly symptomatic. Of the 25 patients consenting to elective repeat catheterization, most were also either asymptomatic or mildly symptomatic, suggesting a clinical condition similar to that of the patients refusing restudy. Finally, since 5 of the 6 patients (84%) found to have restenosis were also either asymptomatic or mildly symptomatic, it is likely that a similar restenosis rate would be found among asymptomatic or mildly symptomatic patients who refused restudy. It is also anticipated that the progressive narrowing in non-infarct-related vessels would be similar in both groups. The only other potential criticism is the demonstration of changes in angiographic stenoses by hand-held calipers, rather than by quantitative computer-based automatic edge detection for measuring cross-sectional area or by cinevideodensimetry.lsJg Although these quantitative techniques are more precise in measuring small changes, they are not widely available to the clinician for making therapeutic decisions. In addition, a Task Force of the World Health Organization and the International Society and Federation of Cardiology indicated that for purposes of clinical research, quantitation of arterial narrowing based on multiple views still referred to a reduction of luminal diameter, and could be described in incremental steps of percentages as small as 5 to 10% .20Although other investigators have accepted a 10% change in the degree of obstruction as significant,21 we accepted a minimal change in the stenosis of 20% in an attempt to clearly demonstrate changes in angiographic progression.
References 1. Fine DG, Weiss AT, Sapoznikov D, Welber S, Applcbaum D, Lotan C, Hasin Y, Ben-David Y, Karen G, Gotsman M. Importance of early initiation of intravenous streptokinase therapy for acute myocardiai infarction. Am J Cardiol 1686;58:411-417. 2. I.S.A.M. Study Group. A prospective trial of intravenous sfrepfokinase in acute myocardial infarction (I.S.A.M.]. Mortality, morbidity, and infarct size at 21 days. N Engl J Med 1986;314:1465-1471. 3. GISSI. Effectiveness of intravenous fhromboiytic treatment in acute myocardial infarction. Lancet 1986;1:397-402. 4. Harfzler GO, Rutheriord BD, McConahey DR, Johnson WL Jr, McCallister BD, Gura GM Jr, Conn RC, Crockett JE. Percutaneous transluminal coronary angioplasfy with and without fhrombolyfic therapy for treatment of acute myocardial infarction. Am Heart 1 1983;106:965-973. 5. Fung AY, Lai P, Top01 EJ, Bates ER, Bourdillon PDV, Walton JA, Mancini GBJ, Kryski T, Pitt B, O’Neill WW. Value of percutaneous transluminal coronary angioplasfy after unsuccessful intravenous strepfokinase therapy in acute myocardial infarction. Am J Cardiol 1986;58:686-691. 9. Meyer J. Merx W, Schmitz H, Erbel R, Kiesslich T, Dorr R, Lambertz H, Bethge C, Krebs W, Bardos P, MinaIe C, Messmer BJ, Effert S. Percutaneous transluminal coronary angioplasfy immediately after introcoronary sfreptoIySiS of franshtminai myocardial infarction. Circulation 1982;66:905-913. 7. Papapietro SE, MacLean WAH, Stanley AWN, Hess RG, Corley N, Arciniegas JG, Cooper TB. Percutaneous fransluminal coronary angioplasfy after intracoronary sfrepfokinase in evolving acute myocardial infarction. Am J Cardiol 1~&i;55:5!8-53. 6. Hartzler GO, Rutherford BD, McConahay DR. Percutaneous fronsluminal coronary angioplasty: application for acute myocardial infarction. Am 1 Cardial 1984:53:117C-321C. 9. Gold HK, Cowley MJ, Palacios IF, Vetrovec GW, Akins CW, Block PC, Leinbach RC. Combined infracoronary sfrepfokinase infusion and coronary angioplasty during acute myocardial infarction. Am 1 Cardiol 1984;53:122C-
JWJSt
125c.
10. Erbel R, Pop T, Henrichs
KJ, von Olshausen K, Schuster C]. Rupprecht HG, Steuernagel C, Meyer J. Percutaneous transluminaf coronary angioplasty after thrombolytic therapy: a prospective controifed randomized trial. jACC 1986;8:485-495. Il. Campeau L. Grading of angina pecforis (letter]. Circulation 1976;54: 5&?. 12. Satler LF, Rackley GE, Green CE, Pallas RS, Pearle DL, Del Negro AA, Kent KM. Ischemia during angioplasty after streptokinase: a marker of myocardiaf s&age. Am J Cdrdiol 1985;56:749-752. 13. Kennedv 1W. Ritchie 1L. Davis KB. Stadius ML. Mavnard C. Fritz 1K. The Western W>Hhington randomized trial of intracoronary streptokinase in acute myocardial infarction. A la-month follow-up report. N EngJ J Med 1985;312:1073-2078.
14. SimoonsML,SerruysPW,vandenBrandM,Res],VerheugtFWA,Krauss XH, Remme WJ, Bar F, de Zwann C, van der Laarse A, Vermeer F, Lubsen J and Collaborators. Early thrombolysis in acute myocardiai infarction: Iimitation of infarct size and imoroved survival. TACC 1986:7:717-728. 15. U’Nei?l W, Timmis GC,‘Bourdillon PD, Lii P, Ganghadarhan V, Walton J, Ramos R, Laufer N, Gordon S, Schork A, Pitt B. A prospective randomized clinical trial of intracoronary streptokinase versus coronary angioplasty for
f, 1987
WE
AxRICAN
JOURNAL
OF CARDIOLOGY
Volume 60
293
acute myocardial infarction. N Engi J Med 1986;314:822-818. 16. Levine S. Ewels Cl, Rosinn DR, Kent KM. Coronarv annionlastv: clinical and angiographic fohv-up. Am J Cardiol 1985;55:673-676. ’ ’ 17. Holmes DR Jr, Vliestra RE, Smith HC, Vetrovec GW, Kent KM, Cowley Ml, Faxon DP. Gruentzig AR. Kelsev SF. Detre KM. Van Raden MI. Mock Mb. Restenosis followingpercutanedus transluminai coronary angioplasty: a report from the NHLBI registry. Am I CardioJ 1984;53:77G8ZC. la. Nichols AB, Gabrieli CFO,.Fenogiio JJ Jr, Esser PD. Quantification of relative coronary arterial stenosisby cinevideodensitometric anaiysis ofcoronary orteriograms. Circulation 1984:69:512-522. 19. Serruvs PW, Reiber JHC, Wiins W, van den Brand M, Kooiiman CJ, ten Katen HJ.‘HugenholtzPd. Assessment of percutaneous transfuminal cordnary angioplasty by quantitative coronary ongiography: diameter versus densitometric area measurements. Am J CardioI 1984:54:482-488. 20. lames TN. Bruschke AVG. Bothig S. Dodu SRA, Gil IF, Kawamura K, Pa&n SJ, Piessens J. Report of WHO%‘FC Task Force on’Nomenclature of Coronary Arteriograms. Circulation 198G;74:451A-455A. 21. Rosinn DR, Cannon RO III, Watson RM, Bonow RO, Mincemover R, Ewels C, Leon MB, Lakatos E, Epstein SE, Kent KM. Three year anatomic, functional and clinical follow-up after successful percutaneous transluminal coronary angioplasty. [ACC 1987;9:1-7.