transluminal coronary angioplasty - NCBI

I Clinical and Community Studies

Efficacy of delayed percutaneous transluminal coronary angioplasty after intravenous use of streptokinase in myocardial infarction Roger-Marie Gagnon, MD Martin Morissette, MD Pierre Laramee, MD Guy Dumont, MD Francois Sestier, MD Guy Leclerc, MD Evelyne Goudreau, MD

Between June 1984 and December 1986, 35 patients with acute myocardial infarction received streptokinase intravenously within 3 hours after the beginning of chest pain and underwent percutaneous transluminal coronary angioplasty (PTCA) either immediately (in 2 cases) or 1 to 19 (mean 4.4) days later (in 33). The rate of successful PTCA was 89%. Reocclusion occurred in one patient. The mean percentage of stenosis decreased from 86% to 11%. The mean trans-stenotic gradient was reduced from 41 to 11 mm Hg. The results suggest that in patients whose condition is stable, PTCA performed a few days after thrombolysis is a valuable alternative to more aggressive treatment with immediate PTCA. Entre juin 1984 et decembre 1986 nous avons pratique, dans 35 cas d'infarctus aigu du myocarde, la perfusion endoveineuse de streptokinase dans les 3 heures suivant le debut de la douleur thoracique et l'angioplastie coronarienne percutanee transluminale (ACPT) soit immediatement (2 fois), soit dans un delai variant de 1 a 19 (moyenne 4,4) jours (33 fois). Cette ACPT reussit dans 89% des cas; un malade montrera une occlusion iterative. Le pourcentage moyen de stenose passe de 86% a 11% et le gradient

trans-stenotique moyen de 41 a 11 mm Hg. Nos resultats laissent penser que chez le malade dont l'etat est stable, l'ACPT pratiquee quelques jours apres la thrombolyse est aussi valable que si on lentreprend immediatement. R5 ecent studies have shown that early thrombolysis with intravenously given streptokinase can reduce infarct size and preserve ventricular function and may improve survival after myocardial infarction.1-5 Very early intravenous administration, in the emergency department or even at home,4 eliminates the need for urgent coronary arteriography, which is necessary for intracoronary administration of the agent. After thrombolysis, there is frequently significant residual coronary stenosis at the site of the occlusion, which may cause rethrombosis.67 Percutaneous transluminal coronary angioplasty (PTCA) or coronary artery bypass surgery may be necessary to prevent postinfarction ischemia or reinfarction.7-10 In some studies angioplasty was done early after thrombolysis,8-10'11 but this is not always feasible. We carried out a study to determine the efficacy of PTCA performed a few days after intravenous administration of streptokinase and to evaluate the risk of reocclusion in the interval between thrombolysis and PTCA.

From the Cardiology Division, Department of Medicine, University of Montreal, Notre-Dame Hospital, Montreal

Methods

Reprint requests to: Dr. Roger-Marie Gagnon, Cardiology Division, Notre-Dame Hospital, 1560 Sherbrooke St. E, Montreal,

In June 1984 a protocol for intravenous administration of streptokinase followed by PTCA in acute myocardial infarction was instituted at our

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CMAJ, VOL. 139, SEPTEMBER 1, 1988

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hospital, and enrolled patients were prospectively studied. Acute myocardial infarction was defined as typical chest pain lasting more than 30 minutes and ST-segment elevation of more than 1 mm in at least two electrocardiograph leads. Patients were excluded from the study if they had recently undergone surgery, had hemorrhagic diathesis, had recently had a cerebrovascular accident, were older than 75 years, were pregnant or had uncontrolled hypertension (blood pressure more than 200/120 mm Hg), suspected active peptic ulcer or a significant other illness considered to increase the risk of bleeding (e.g., liver disease or cancer). Between June 1984 and December 1986, 65 patients with suspected acute myocardial infarction each received 750 000 to 1.5 million IU of streptokinase intravenously within 3 hours after the beginning of chest pain, according to the protocol described by Ganz and colleagues.' Of the 65, 57 underwent coronary angiography 1 to 19 days after thrombolysis, and 8 refused the procedure. Of the 57, 15 were referred for coronary artery bypass surgery because of multiple coronary artery lesions, and 7 were treated medically because of persistent complete occlusion or nonsignificant coronary artery obstruction. PTCA was performed in the remaining 35 patients (28 men and 7 women with a mean age of 53 years). Of the 35, 2 underwent angiography immediately and underwent PTCA at the same time. The remaining 33 patients underwent angiography 1 to 19 days after thrombolysis; PTCA was done at the time of angiography in 16 and 1 to 15 days after angiography in 17. The mean interval between administration of streptokinase and PTCA was 4.4 days. The timing of the angiography was determined by the availability of cardiac catheterization and the clinical judgement of the attending cardiologist. The indication for PTCA was significant localized and proximal obstruction of the coronary artery (reduction in diameter of more than 70%). The procedure was not done if there were diffuse or distal lesions or if there was significant obstruction of more than two coronary arteries. PTCA was performed by means of the Gruntzig technique12 with a steerable guidewire and balloon catheter system (C-R Bard Inc., Billerica, Massachusetts). The procedure was considered successful if the coronary gradient was decreased by 50% and the residual coronary lesion was reduced to 50% or less of the diameter of the artery. The coronary gradient was measured as the difference between the mean aortic pressure and the mean distal coronary artery pressure. Coronary stenosis was defined as the percentage reduction in the diameter of the artery compared with the diameter of a normal proximal segment of the artery. The angiographic view with the most severe narrowing was chosen. The artery was said to be patent if there was anterograde flow through the obstruction. PTCA was performed at the time of angiography if the lesions were very proximal or tight, if there were filling defects suggestive of residual 406


thrombi, or if the patient had recurrent angina. It was delayed if the patient's condition was stable and the coronary lesions appeared less "critical". Delaying the procedure was also felt to be reasonable for logistic and psychologic reasons (e.g., describing the lesions to the patient, giving details of the procedure and obtaining better informed consent). In patients in whom PTCA was delayed, therapy with antiplatelet drugs was begun the day before the procedure. All patients received continuous intravenous perfusion of heparin following thrombolysis. Before PTCA was done an additional bolus of 5000 to 10 000 IU of heparin was injected intravenously. After the procedure the patient received either acetylsalicylic acid (ASA) (325 mg/d) or ASA (325 mg three times a day) and dipyridamole (75 mg three times a day). Heparin therapy was continued until the next morning in patients whose angiogram suggested that residual thrombi may have been present at the site of the coronary lesions. Of the 35 patients who underwent PTCA 26 had disease in one vessel, 5 had disease in two vessels and 4 had disease in three vessels. The vessel involved was the left anterior descending branch in 17 patients, the right coronary artery in 16, the circumflex branch in 4 and the first diagonal branch in 1. One of the patients with subtotal occlusion of the circumflex branch had patent grafts of the right coronary and anterior descending arteries. PTCA was done in one vessel in 32 patients and in two vessels in 3 patients. Results Intravenous administration of streptokinase resulted in patency of 91% of the infarct-related arteries among the 57 patients who underwent angiography. PTCA was successful in 31 (89%) of the 35 patients who underwent it. The mean percentage of stenosis decreased from 86% (standard deviation [SD] 7%) before PTCA to 11% (SD 12%) after the procedure (p < 0.0001), and the mean coronary gradient decreased from 41 (SD 15) to 11 (SD 4) mm Hg (p < 0.0001). Two patients had acute occlusion of the infarct-related artery after angiography; in both cases the reocclusion may have been due to inadequate heparin treatment. In one patient a right femoral hematoma developed after angiography, necessitating blood transfusion. In two of the four cases in which PTCA was unsuccessful the dilatation catheter could not be advanced through the lesion, although the guidewire had crossed the obstruction; both patients underwent coronary artery surgery, without incident. In one case, with complete occlusion, a similar problem occurred. In the remaining case, with subtotal obstruction of the proximal left anterior descending branch, sudden electromechanical dissociation occurred while a smaller dilatation catheter was being inserted. Cardiopulmonary

resuscitation measures were started immediately while PTCA was performed, but cardiogenic shock persisted, and the patient died despite repeated resuscitation efforts. Autopsy was not done. One patient had a small infarction secondary to occlusion of the diagonal branch during PTCA of the left anterior descending branch. One patient had reocclusion of the right coronary artery a few minutes after the procedure. PTCA was performed again without difficulty or complication, and there was no evidence of a new infarction. One patient, who had extensive anterior infarction, remained in shock despite thrombolysis. PTCA for a subtotal obstruction of the left anterior descending branch was technically successful, but the patient remained in shock. There were associated significant lesions of the right artery and the circumflex branch. Heart transplantation was successfully performed the same day. One patient died suddenly 10 days after PTCA of the left anterior descending branch. One patient had sudden hemiplegia 6 hours after PTCA of the left anterior descending branch; there was no evidence of reocclusion. An embolism from a left ventricular thrombus was suspected but not documented. All the other patients were free of angina. 7 to 10 days after PTCA.

Discussion The concept that early reperfusion by means of thrombolysis offers a "second chance"13 to the patient with acute myocardial infarction has been increasingly accepted recently.2'5'7 To maximize this second chance, appropriate aggressive therapy must follow thrombolysis. Until recently the ideal approach was to perform coronary angiography and PTCA simultaneously as soon as possible after thrombolysis in order to restore coronary blood flow and preserve myocardial function. There have been reports of less residual stenosis and more improved ventricular function with PTCA than with streptokinase therapy alone.8'9'14'15 In addition, angina9 and reocclusion14 are less frequent after PTCA than after thrombolysis. However, two recent studies of angioplasty after thrombolysis with intravenously given tissue plasminogen activator showed that delayed angioplasty has a higher success rate than immediate angioplasty.16'17 It is possible that these conclusions can be applied to thrombolysis with streptokinase. Immediate coronary angioplasty may not always be feasible for practical reasons, such as limited cardiac catheterization facilities and referral of patients from community hospitals. Intravenous administration of streptokinase followed by adequate anticoagulant therapy may safely permit delaying coronary angiography if the patient's condition is stable. Furthermore, continued improvement in coronary artery lesions in the days after thrombolysis has been reported.6'7'18'19 Although the purpose of our study was not to

determine the effects of PTCA and streptokinase therapy on ventricular function, it is noteworthy that recent studies have shown improvement in ventricular function following PTCA done late after thrombolysis.30'21 Our rate of successful PTCA, 89%, is comparable to those reported by other investigators, which range from 65%8 to 86%9 to 97%.10 However, our patients differed in some ways. Those in the other studies all had angioplasty in the acute phase of infarction, which may carry a higher risk because of possible residual thrombi and platelet aggregation. Furthermore, delayed angioplasty has been found to have a higher success rate than immediate angioplasty,16,17 and our patients may thus be considered to be a lower-risk group. Moreover, complete obstruction was more frequent in the patients in the other studies than in our patients. The rate of reocclusion in our patients (3%) is comparable to those reported in other studies (7% to 16%).8 1o011 However, in those studies reocclusion was evaluated by means of late angiography, whereas in our study it was assessed by means of electrocardiography and clinical findings. Although reocclusion may be clinically inapparent,8 in other reports it was symptomatic in almost all patients.11'22 In patients whose condition is stable, PTCA performed relatively late after thrombolysis for myocardial infarction appears to be a valuable alternative to more aggressive treatment with immediate PTCA. The former approach may be particularly useful in community hospitals without cardiac catheterization facilities: patients can benefit from early thrombolysis and then be scheduled for coronary angiography within the next few days at an appropriate centre. Immediate referral and transfer would be indicated only for patients whose condition was unstable. However, further study and longer follow-up are needed to evaluate the respective benefits of these strategies. Furthermore, appropriate strategies will have to be determined for the newer thrombolytic agents.23 References 1. Ganz W, Geft I, Shah PK et al: Intravenous streptokinase in evolving acute myocardial infarction. Am J Cardiol 1984; 53: 1209-1216 2. Koren G, Weiss AT, Hasin Y et al: Prevention of myocardial damage in acute myocardial ischemia by early treatment with intravenous streptokinase. N Engl J Med 1985; 313: 1384-1389 3. Gruppo Italiano per lo Studio della Streptochinasi nell'Infarto Miocardico (GISSI): Effectiveness of intravenous thrombolytic treatment in acute myocardial infarction. Lancet 1986; 1: 397-401 4. Simoons ML, Serruys PW, Brand M et al: Improved survival after early thrombolysis in acute myocardial infarction: a randomized trial by the Interuniversity Cardiology Institute in the Netherlands. Lancet 1985; 1: 578-582 5. ISAM Study Group: A prospective trial of intravenousstreptokinase in acute myocardial infarction. N Engi J Med 1986; 314: 1465-1471


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6. Harrison DG, Ferguson DW, Collins SM et al: Rethrombosis after reperfusion with streptokinase: importance of geometry. Circulation 1984; 69: 991-999 7. Dodge HT, Sheehan FH, Mathey DG et al: Usefulness of coronary artery bypass graft surgery or percutaneous transluminal angioplasty after thrombolytic therapy. Circulation 1985; 72 (suppl V): V39-V45 8. Erbel R, Pop T, Henrichs KJ et al: Percutaneous transluminal coronary angioplasty after thrombolytic therapy: a prospective controlled randomized trial. J Am Coll Cardiol 1986; 8: 485-495 9. Fung AY, Lai P, Juni JE et al: Prevention of subsequent exercise-induced peri-infarct ischemia by emergency coronary angioplasty in acute myocardial infarction: comparison with intracoronary streptokinase. Ibid: 496-503 10. Fung AY, Lai P, Topol EJ et al: Value of percutaneous transluminal coronary angioplasty after unsuccessful intravenous streptokinase therapy in acute myocardial infarction. Am J Cardiol 1986; 58: 686-691 11. Prida XE, Holland JP, Feldman RL et al: Percutaneous transluminal coronary angioplasty in evolving acute myocardial infarction. Am J Cardiol 1986; 57: 1069-1074 12. Gruntzig AR, Senning A, Siegenthaler WE: Nonoperative dilatation of coronary-artery stenosis. N Engi J Med 1979; 301: 61-68 13. Vogel JHIK: Coronary thrombolysis: second chance therapy - maximizing the advantage. J Am Coll Cardiol 1986; 8: 1218-1219 14. O'Neil W, Timmis GC, Bourdillon PD et al: A prospective randomized clinical trial of intracoronary streptokinase versus coronary angioplasty for acute myocardial infarction. NEnglJ Med 1986; 314: 812-818 15. Verani MS, Raizner AE, Tadros S et al: Coronary reperfusion using intracoronary streptokinase alone or combined

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with angioplasty in acute myocardial infarction [abstr]. Circulation 1985; 72: III-309 Topol EJ, Califf RM, George BS et al: A randomized trial of immediate versus delayed elective angioplasty after intravenous tissue plasminogen activator in acute myocardial infarction. N Engi J Med 1987; 317: 581-588 Guerci AD, Gerstenblith G, Brinker JA et al: A randomized trial of intravenous tissue plasminogen activator for acute myocardial infarction with subsequent randomization to elective coronary angioplasty. Ibid: 1613-1618 Collins GJ, Califf RM, Phillips HR et al: Quantitative angiographic changes occurring within 24 hours and one week following treatment with tissue plasminogen activator in patients randomized to immediate and late angioplasty [abstr]. Circulation 1986; 74:11-275 Brown BG, Gallery CA, Badger RS et al: Incomplete lysis of thrombus in the moderate underlying atherosclerotic lesion during intracoronary infusion of streptokinase for acute myocardial infarction: quantitative angiographic observations. Circulation 1986; 73: 653-661 Guerci AD, Brinker J, Gottlieb S et al: "Late" post-MI percutaneous transluminal coronary angioplasty (PTCA) improves LV function during submaximal exercise [abstr]. Circulation 1986; 74: II-23 Rosenheck S, Hasin Y, Mosseri M et al: Improvement in LV function following PTCA performed several months post transluminal MI treated with IV streptokinase [abstr]. Ibid Williams DO, Borer J, Braunwald E et al: Intravenous recombinant tissue-type plasminogen activator in patients with acute myocardial infarction trial: a report from the NHLBI thrombolysis in myocardial infarction trial. Circulation 1986; 73: 338-346 Sobel BE: Coronary thrombolysis with tissue-type plasminogen activator (t-PA): emerging strategies. I Am Coll Cardiol 1986; 8: 1220-1225

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