Outcome of urgent percutaneous transluminal coronary angioplasty in acute myocardial infarction: Comparison of single-vessel versus multivessel coronary artery disease Despite recent clinical trials of percutaneous transluminal coronary angioplasty (PTCA) in acute myocardial infarction, specific groups of patients that may benefit from adjunctive or alternative therapy have yet to be adequately characterized. The in-hospital outcome of 151 consecutive patients treated for acute myocardial infarction with urgent PTCA of the infarct-related artery was studied to identify a subgroup of patients at high risk. Patients were divided into two groups based on the angiographic presence of either single-vessel (n = 88) or multivessel (n = 85) coronary artery disease. Despite PTCA of only the infarct-related artery and similar baseline clinical characteristics such as age, peak serum creatine kinase concentration, left ventricular ejection fraction, and time from the onset of chest pain to arrival at the hospital, the group with multivessel disease had a lower rate of successful angioplasty (75% vs 92%, p < 0.005), with higher incidences of persistent total occlusion of the infarct-related artery (14% vs 3%, p < 0.02) and procedural complications during PTCA (28% vs 13%, p 5 0.02), and were more likely to have multiple complications (12% vs l%, p < 0.004). In addition, the group with multivessel disease had a higher rate of urgent (~24 hours) coronary artery bypass graft surgery (13% vs 2%, p < 0.05) and a trend toward a higher in-hospital mortality rate (8% vs l%, p I 0.17). By stepwise logistic regression, only the presence of single-vessel versus multivessel disease was predictive of PTCA success (p < 0.005). The location of the infarct-related artery was not associated with any differences in outcome. We conclude from these data that urgent PTCA of the infarct-related artery only as treatment for acute myocardial infarction has a lower success rate and higher associated risk in patients with multivessel disease. This may be due to their greater ischemic burden and/or a fundamental biochemical or pathologic difference in the involved lesions. Thus in patients with multivessel coronary artery disease, alternative revasculariration, improved mechanical hemodynamic support, or both may be warranted to achieve a better success rate and reduce complications and mortality. (AM HEART J 1992;124:1427.)

Brian E. Jaski, MD, Joshua D. Cohen, Josefina Trausch, MD, David G. Marsh, MD, Gregory R. Bail, BA, Paul A. Overlie, MD, Evan W. Skowronski, BS, and Sidney C. Smith, Jr., MD San Diego, Calif.

Percutaneous transluminal coronary angioplasty (PTCA) has been used in numerous clinical trials for treatment of acute myocardial infarction (AMI), both with and without prior pharmacologic thrombolysis. Recent studies have focused on the efficacy and the optimal use and timing of PTCA in AMI,le5 From

the San Diego

Cardiac

Center.

Supported in part by the Rose Azus Cardiology Education Research Fund and the Samuel H. Lasry Cardiology Grant, Sharp Foundation, San Diego, Calif., and the General Clinical Research Center, University of California, San Diego, grant MOlRR00827. Received

for publication

Reprint address: Frost St., Suite 4/l/41311

May

4, 1992;

accepted

Sidney C. Smith, Jr., MD, 200, San Diego, CA 92123.

June

San Diego

15, 1992. Cardiac

Center,

8010

but specific risk factors indicative of an adverse clinical outcome remain uncertain. Despite advances in thrombolytic therapy, PTCA may still be indicated as adjunctive therapy,6, 7 particularly after unsuccessful thrombolysis, 8,g which occurs 20 % to 25 % of the time,lO or as primary therapy,‘l-l4 especially when contraindications to thrombolysis exist.15, l6 Prethrombolytic studies have shown that multivessel disease is an important predictor of long-term AM1 surviva1,17-20 but few studies have focused on the number of diseased vessels as a determining factor for an acute treatment protoco1.21-24 Specific treatment strategies for patients with varying degrees of coronary artery disease remain to be adequately characterized. The following patient review was 1427

December

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Jaski et al.

aimed at investigating differences in acute outcome after urgent PTCA for AM1 in patients with singlevessel versus multivessel coronary artery disease. METHODS Study patients. Patients with a typical history and ECG evidence of AM1 with ongoing chest pain were candidates for aggressive PTCA therapy. Informed consent was obtained from all patients. Urgent catheterization and angioplasty were at the discretion of the physician and were not determined by a prospective protocol. Results of 151 consecutive procedures of urgent PTCA as treatment for AM1 performed between March 1983 and February 1990 were retrospectively reviewed. Assessments were made of each patient’s in-hospital clinical course during and after the PTCA procedure. All patients entered into this study had angioplasty within 24 hours of the onset of chest pain (75 Y 56 hours) and were divided into two groups based on the angiographic presence of single-vessel or multivessel coronary artery disease. In 111 patients (74%) PTCA was performed as primary therapy for AM1 (direct). Of these, 55 received intracoronary streptokinase, six received urokinase, and two received intravenous streptokinase, all as adjunctive therapy at the time of direct angioplasty, usually after PTCA; the remaining 48 did not receive adjunctive thrombolytic therapy. In 40 patients (26%) PTCA was preceded by pharmacologic thrombolysis. In 26 of them PTCA was performed immediately after successful thrombolytic therapy (immediate), and in 14 PTCA was performed after unsuccessful thrombolysis with persistent total occlusion of the infarct-related artery (rescue). Primary thrombolytic therapy, administered to the 40 immediate and rescue angioplasty patients, was intravenous streptokinase in 13 patients, intracoronary streptokinase in 14, tissue-type plasminogen activator in eight, and anisoylated plasminogen-streptokinase activator complex in five. All patients were given aspirin by mouth and heparin intravenously for at least 24 hours after angioplasty. In all instances angioplasty was performed only on the infarct-related artery, regardless of the number of vessels with significant stenosis. Clinical data. In addition to the baseline clinical and demographic characteristics, acute clinical outcome data were also obtained for comparison and analysis. Angiographic findings, including the number of diseased vessels, the location of the infarct-related artery, the presence or absence of collateral vessels, and the percentage of stenosis before and after PTCA, were obtained. Acute outcome in each patient was characterized by success or failure of the angioplasty procedure (successful angioplasty was defined as residual stenosis ~40%), length of hospital stay, necessity of urgent (within 24 hours) or elective (during hospital admission for myocardial infarction) coronary artery bypass graft surgery (CABG), and in-hospital mortality. Procedural arrhythmias requiring acute therapy, hypotension requiring treatment, acute reocclusion, cardiac arrest, cardiac tamponade, cardiogenic shock, inability to

American

Heart

1992 Journal

cross a lesion with either a guide wire or balloon catheter, and procedural death were recorded as complications. Statistics. All data are expressed as mean rt standard deviation where applicable. In comparing single-vessel with multivessel disease, a Fisher’s exact test or a Pearson’s chi-square analysis was performed for categoric data, and a two-tailed Student’s t test was used for continuous variables. A p value of , with a lower incidence of post-PTCA persistent total occlusion of

Voltme

124

Number

6

Table

PTCA

I. Baseline clinical characteristics Characteristics

N Age

Single

(yr)

Peak CK (W/L) EF (“; ) Chest pain to hospital Hospital stay (days) Anterior/Lateral Inferior/Posterior Smoker Diabetes Hypertension Previous angina Previous MI Previous CABG

(min)

56 2,217 56 112 7.5

uessel 86 + + + + t

12 1,887 11 115 3.6

43 (52%) 40 (48%) 59 (77%) 6 (8%) 23 (30%) 20 (23%) 8 (9%) l(lPF)

Table Multivessel

57 2,288 54 130 8.2

65 2 10 + 1,916 + 13 z!T 154 * 3.7

22 (35%)* 41 (65%)* 46 (78%) 7 (117) 14 (24%) 24 (37%) 10 (15%) 7 (llS)*

Anterior,‘Lateral, ECG changes consistent with anterior/lateral infarction; CABG, coronary artery bypass graft surgery; Chest pain to hospiLa2, elapsed time from onset of chest pain to arrival at the hospital; EF, left ventricular ejection fraction; Inferior/Posterior, ECG changes consistent with inferior/ posterior infarction; MI, myocardial infarction; Peak CK, peak total serum creatine kinase level. ‘p < 0.05.

the infarct-related artery (3 % vs 15%) p I 0.03). Also the incidence of urgent bypass surgery was less frequent (3% vs 13 %, p < 0.05) than in the group with multivessel disease. The administration of adjunctive thrombolysis, generally given to patients in whom residual thrombus was present after direct angioplasty, did not have a significant impact on clinical outcome including procedural success,urgent CABG, complications, and mortality. Individually there tended to be more complications after PTCA in the group with multivessel disease, but these differences for any particular complication did not achieve statistical significance. However, the overall PTCA procedural complication rate was higher in the group with multivessel disease (28% vs 13%, p I 0.02). Moreover, the group with multivessel disease had a higher incidence of multiple complications (12 % vs 1% , p < 0.004). A trend toward a higher in-hospital mortality rate was also observed for the group with multivessel disease (6 % vs 1% ) p 5 0.17) (Table III). When analyzed separately, the direct PTCA patients with multivessel diseasehad a higher incidence of overall complications (32% vs 13%) p < 0.02)) as well as higher rates of individual complications. Incidences of arrhythmia (17% vs 5%) p < 0.05), hypotension (11% vs 2%) p < 0.05), and multiple complications (15 OLvs 2 % , p < 0.05) were all higher in the group with multivessel disease. Direct PTCA patients with multivessel disease also showed a trend

for AMI

in

single versus multi-CAD

1429

II. Angiographic data Angiographic

data

Single

vessel

Multivessel

No. of diseased coronary arteries 1 86 (100 ‘7 ) 2 0 3 0 4 (3 + graft) 0 Infarct-related artery LAD 43 (50%) LCX 11 (13%) RCA 32 (37%) Graft 0 Pre-PTCA occluded 57 (66%) Post-PTCA occluded 3 (3%) Collaterals to IRA 31 (44%) PTCA procedural success 79 (920; )

20 7 36 2 47 9 23 49

Pre-PTCA Post-PTCA

99 + 4 42 2 27*

stenosis (% ) stenosis (% )

99 * 2 29 + 18

0 40 (62%) 24 (37%) 1 (1%) (31%) (11%) (55%)* (328) (72%) (14%)* (44 70 ) (75% )t

Graft, Bypass surgery saphenous vein grafts; LAD, left anterior descending coronary artery; LCz, left circumflex coronary artery; RCA, right coronary artery; IRA, infarct-related artery; Post-PTCA occluded, persistent total occlusion of IRA after attempted angioplasty; Post-PTCA stenosis, IRA stenosis after attempted angioplasty; Pre-PTCA occluded, total occlusion of IRA before attempted angioplasty; Pre-PTCA stenosis, IRA stenosis before angioplasty; PTCA, percutaneous transluminal coronary angioplasty; PTC’A procedural success, post-PTCA stenosis 540%. *p < 0.05. tp < 0.005.

toward a higher in-hospital mortality 2%,p

rate (6% vs

50.31).

DISCUSSION

This study represents a retrospective analysis of the in-hospital outcome of 151 consecutive procedures of urgent PTCA for AM1 at our institution. Patients were divided into two groups based on the angiographic presence of either single-vessel or multivessel coronary artery disease. The group with multivessel disease had a lower rate of successful angioplasty, with a higher incidence of persistent total occlusion of the infarct-related artery, and underwent urgent CABG more often than the group with single-vessel disease. Patients with multivessel disease also had more residual stenosis of the infarctrelatated artery after PTCA and showed a trend toward higher rates for almost all complications including death, than did the group with single-vessel disease. The overall mortality and success rates of PTCA in this study are comparable to those in other series with similar patient compositions.22*25 Although the group with multivessel disease did show a higher frequency of previous CABG, only two patients (3 % ) underwent angioplasty of bypass graft occlusions. For this reason it is likely that although the incidence of previous bypass surgery is associated

December

1430

Jaski et al.

American

SINGLE

MULTI

-l

SINGLE

MULTI

SINGLE

MULTI

lo1

SINGLE

* PC.05

1992 Journal

28*

307

15

Heart

MULTI

** p< .005

Fig. 1. Acute clinical outcome of patients with single-vesselversus multivessel coronary artery disease.

CABG, Coronary artery bypassgraft surgery; Multi, multivessel coronary artery disease;PTCA, percutaneoustransluminal coronary angioplasty; PTCA success,post-PTCA stenosis~40%; Single, single-vessel coronary artery disease;Urgent, 524 hours.

Table

III. Complications Complications

PTCA procedural complications Multiple complications In-hospital mortality Arrhythmias Hypotension Reocclusion Cardiac arrest Tamponade Cardiogenic shock Wire Balloon Balloon, Inability

Single vessel

11(13%) l(l%) 1(1X) 4 (5%,)

1 (1 “i )

Multivessel

18 (28% )* 8 (12%)? 4 (6%) 9 (14%)

3 (4%)

5 (8%) 4 (6”;)

l(l%) l(lS)

1 (2°C) 0

2 (2%)

1 (2°C)

l(l%TF) 0

3 (5%) 2 (3%)

to cross infarct-related artery lesion with ter; PTCA, percutaneous transluminal coronary angioplasty; ity to cross infarct-related artery lesion with guide wire. *p < 0.05.

balloon Wire,

catheinabil-

tp < 0.005.

with advanced multivessel disease, it is not a contraindication for urgent PTCA, especially since with the use of multivariate analysis it was not an independent predictor of angioplasty failure. Inclusion of rescue and immediate PTCA patients (presumably high-risk groups) did not prejudice the data, inas-

much as analysis of the direct PTCA group alone showed similar differences between patients with single-vessel and multivessel disease. Angioplasty may be useful as an adjunct to thrombolytic therapy,6, 7 in the setting of unsuccessful pharmacologic thrombolysis,8t g or as primary therapy for AMI,11-14 especially when there are contraindications to thrombolytic therapy.15q l6 PTCA results in less residual stenosis of infarct-related arteries than thrombolysis alone. Improved left ventricular ejection fraction and better regional wall motion have been reported with the increased vessel diameter after PTCA therapy compared with intracoronary streptokinase.2 However, several studies have found no difference in short- or long-term outcome after PTCA and have noted increased complications, at least when PTCA is performed after administration of tissue-type plasminogen activat0r.l. 3, 4 Results of the present study suggest that different subgroups of patients may benefit from different treatment strategies Although triple-vessel disease has been identified as a predictor of late mortality after AMI in prethrombolytic studies, 17-20few studies have addressed

Volume

124

Number

6

the issue of multivessel disease as it relates to acute clinical management. Several investigators have reported data similar to ours with regard to the direct PTCA success rates for single-, double-, and triplevessel coronary artery disease,13,22,23although these rates were not directly compared or drawn upon in their conclusions. Ellis et a1.21included triple-vessel disease as an independent predictor of PTCA failure after thrombolysis, and Muller et a1.24recently reported a higher in-hospital mortality rate for patients with multivessel disease. The present study, however, specifically compares the angioplasty procedural success rates for patients with single-vessel versus multivessel coronary artery disease in the setting of myocardial infarction. Although not confirmed by this study or earlier ones I4321 Gacioch and Top0126 found, in a series of patients composed of rescue and direct PTCA cases, that the incidence of residual stenosis and lifethreatening complications during and after PTCA was significantly higher in patients in whom the infarct-related artery was the right coronary artery. It is interesting t,o note that in their study, the patients in whom the involved artery was the right coronary artery also tended to have multivessel disease more often (p < 0.19). Because of the smaller size of their study (iv = 83) and the lack of multivariate statistical analysis, it is possible that the less successful clinical outcome of pat.ients in whom the infarct-related artery was the right coronary artery might have been partially due to a higher frequency of multivesse1disease in this group. Logistic regression analysis of our data did not identify any differences in outcome associated with the location of the involved artery. There are several explanations that could account for the differences observed between the groups with single-vessel and multivessel disease. Patients with single-vessel disease have more functional reserve and a lower overall ischemic burden than those with multivessel disease. This could explain the higher incidence of some of t.he procedural complications such as hypotension, arrhythmias, and mortality in the group with multivessel disease. Also the inability of PTCA to achieve complete revascularization in patients with multivessel diseasecould have contributed to the decision to perform CABG more often than in those with single-vessel disease. However, this does not explain why the PTCA procedural successrate was higher for the group with single-vessel disease despite the fact that only the infarct-related artery was dilated. Alternatively the actual biochemical nature and/or composition of the stenosis in the two groups may be

PTCA for AMI

in single versus multi-CAD

1431

fundamentally different. The type or quantity of atheroma present may account for the different rates of successful angioplasty. For example, the group with multivessel diseasemay represent a subgroup of patients in whom the infarct-related lesion is composed of a higher proportion of plaque rather than thrombus. By contrast, the group with single-vessel diseasemay in general have had a plaque rupture of a more recent lesion, suggested in part by their lower frequency of previous angina. Thus single-vessel disease might be more amenable to angioplasty than multivessel diseasein which older more advanced lesions might be expected to occur. Diagnostic advances such as intravascular ultrasound imaging may help to further define primary differences in the lesions of patients with single-vessel and multivessel disease. These two explanations are not mutually exclusive and may be jointly responsible for the disparity observed between the two groups. Nevertheless, the less successful clinical outcome of the group with multivessel disease suggests that alternative revascularization and management strategies may be indicated for patients with multivessel disease. Recent studies utilizing alternative interventional technologies, such as the transluminal extraction catheter27 and excimer laser coronary angioplasty,28 have demonstrated more favorable acute outcome and superior shortterm patency in the management of lesions associated with acute coronary thrombus. These new devices may be appropriate for improving clinical outcome in patients with multivessel disease. Immediate CABG has also been suggested and applied to patients with multivessel disease,24 although the risk-benefit ratio of this approach as a general strategy remains unknown. Conversely, thrombolytic therapy alone may be all that is justified for immediate revascularization of patients with multivessel disease to avoid the complications associated with PTCA. When clinically indicated, support devices such the intraaortic balloon pump, which has been shown to improve noninfarct zone function and reduce hemodynamic deterioration in AMI,2g could be a desirable adjunct for improving overall acute outcome in this group. Recently asynergy of the noninfarct region has been found to be a significant predictor of multivessel disease24,30,31; therefore a noninvasive technique such as two-dimensional echocardiography may aid in early identification of patients with multivessel disease without angiography. This study demonstrates the need to define treatment strategies for AM1 based on the extent of coronary artery disease. Future prospective studies will

December

1432

Jaski et al.

American

be necessary to determine which strategies are most appropriate for identifying and treating patients with multivessel coronary artery disease and other high-risk subgroups. Study limitations. The present study is limited because it is a retrospective analysis of a data base without randomized treatment protocols or specific controls for concomitant therapy. However, this data base is an accurate representation of the clinical care given to aggressively treat AM1 during the time period specified. Future prospective multicenter trials will have the statistical power to determine more clearly the risk factors predictive of PTCA success. Long-term follow-up studies will also help to shed light on the optimal acute treatment strategies for specific subsets of patients by examining late survival and reinfarction rates. We thank Nancy Kaczmerek and Ray Jacobson on the patient data base and John Gordon, MD, contributions.

for their work for his clinical

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WJ, Bairn DS, Gore JM, Brown BG, Roberts R, Williams DO, Chesebro JH, Babb JD, Sheehan FH, Wackers FJ, Zaret BL, Robertson TL, Passamani ER, Ross R, Knatterud GL, Braunwald E, for the TIM1 II-A investigators. Comparison of immediate invasive, delayed invasive, and conservative strategies after tissue-type plasminogen activator: results of the Thrombolvsis in Mvocardial Infarction (TIMI) phase II-A trial. Circulation 199&81:1457-76. O’Neill W, Timmis GC, Bourdillon PD, Lai P, Ganghadarhan V. Walton J. Ramos R. Laufer N. Gordon S. Schork MA. Pitt B: A randomized clinical trial of’intracoronary streptokinase versus coronary angioplasty for acute myocardial infarction. N Engl J Med 1986;314:812-8. The TIM1 Research Group. Immediate vs delayed catheterization and angioplasty following thrombolytic therapy for acute myocardial infarction: TIM1 II A results. JAMA 1988; 260:2849-59. Passamani E, Hodges M, Herman M, Grose R, Chaitman B, Rogers W, Forman S, Terrin M, Knatterud G, Robertson T, Braunwald E, for the TIM1 investigators. The Thrombolysis in Myocardial Infarction (TIMI) phase II pilot study: tissue plasminogen activator followed by percutaneous transluminal coronary angioplasty. J Am Co11 Cardiol 1987;10351B-64B. Lavie CJ, Gersh BJ, Chesebro JH. Reperfusion in acute myocardial infarction. Mayo Clin Proc 1990;65:549-64. Stack RS, Califf RM, Hinohara T, Phillips HR, Pryor DB, Simonton CA, Carlson EB, Morris KG, Behar VS, Kong Y, Peter RH, Hlatky MA, O’Connor CM, Mark DB. Survival and cardiac event rates in the first year after emergency coronary angioplastv for acute mvocardial infarction. J Am Co11 Cardiol 1988;11:1i41-9. Guerci AD. Gerstenblith G. Brinker JA. Chandra NC. Gottlieb SO, Bahr RD, Weiss JL, Shapiro EP, Flaherty JT, Bush DE, Chew PH, Gottlieb SH, Halperin HR, Ouyang P, Walford GD, Bell WR, Fatterpaker AK, Llewellyn M, Top01 EJ, Healy B, Siu CO. Becker LC. Weisfeldt ML. A randomized trial of intravenous tissue plasminogen activator for acute myocardial infarction with subsequent-randomization to elective coronary angioplasty. N Engl J Med 1987;317:1613-8. Holmes DR, Gersh BJ, Bailey KR, Reeder GS, Bresnahan JF, Bresnahan DR. Vliestra RE. Emernencv “rescue” nercutaneous angioplasty after failed thrombolysis with streptokinase: early and late results. Circulation 1990;81(suppl IV):IV-51-6.

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9. Abbottsmith CW, Top01 EJ, George BS, Stack RS, Kereiakes DJ, Candela RJ, Anderson LC, Harrelson-Woodlief SL, Califf RM. Fate of patients with acute myocardial infarction with patency of the infarct-related vessel achieved with successful thrombolysis versus rescue angioplasty. J Am Co11 Cardiol 1990;16:770-8. 10. Ross AM. Role of angioplasty in myocardial infarction management strategies: a review. Heart Lung 1990;19:604-7. 11. Hartzler GO, Rutherford BD, McConahay DR, Johnson WL. McCallister BD, Gura GM, Conn RC, Crockett JE. Percutaneous transluminal coronary angioplasty with and without thrombolytic therapy for treatment of acute myocardial infarction. AM HEART J 1983;1983:965-73. 12. Rothbaum DA, Linnemeier TJ, Landin RJ, Steinmetz EF, Hillis JS. Hallam CC, Noble RJ, See MR. Emergency percutaneous coronary angioplasty in acute myocardial infarction: a 3 year experience. J Am Co11 Cardiol 1987;10:264-72. 13. O’Keefe JH, Rutherford BD, McConahay DR, Ligon RW. Johnson WL, Giorgi LV, Crockett JE, McCallister BD, Conn RD, Gura GM, Good TH, Steinhaus DM, Bateman TM, Shimshak TM, Hartzler GO. Early and late results of coronary angioplasty without antecedent thrombolytic therapy for acute myocardial infarction. Am J Cardiol 1989;64:1221-30. 14. Kahn JK, Rutherford BD, McConahay DR, Johnson WL, Giorgi LV, Shimshak TM, Ligon RW, Hartzler GO. Catheterization laboratory events and hospital outcome with direct angioplasty for acute myocardial infarction. Circulation 1990: 82:1910-15. 15. Brodie BR, Weintraub RA, Stuckey TD, LeBauer EJ, Katz JD, Kelly TA, Hansen CJ. Outcomes of direct coronary angioplasty for acute myocardial infarction in candidates and non-candidates for thrombolytic therapy. Am J Cardiol 1991; 67:7-12. 16. Ellis SG. Interventions in acute myocardial infarction. Circulation 1990;81(suppl IV):IV-43-50. 17. Sanz G, Castaner A, Betriu A, Magrina J, Roig E, Co11 S, Pare JC, Navarro-Lopez F. Determinants of nroenosis in survivors of myocardial infarction: a prospective clinical angiographic study. N Engl J Med 1982;306:1065-70. 18. De Feyter PJ, van Eenige MJ, Dighton DH, Visser FC, De Jong J, Roos JP. Prognostic value of exercise testing, coronary angiography and left ventriculography 6-8 weeks after myocardial infarction. Circulation 1982;66:527-36. 19. Roubin GS, Harris PJ, Bernstein L, Kelly DT. Coronary anatomy and prognosis after myocardial infarction in patients 60 years of age and younger. Circulation 1983;67:743-9. 20. Taylor GJ, Humphries JO, Mellits ED, Pitt B, Schulze RA, Griffith LSC, Achuff SC. Predictors of clinical course, coronary anatomy and left ventricular function after recovery from acute myocardial infarction. Circulation 1980:62:960-70. 21. Ellis SG, Top01 EJ, Gallison L, Grines CL, Langburd AB, Bates ER, Walton JA, O’Neill WW. Predictors of success of coronary angioplasty performed for acute myocardial infarction. J Am Co11 Cardiol 1988;12:1407-15. 22. Kahn JK, Rutherford BD, McConahay DR, Johnson WL, Giorgi LV, Shimshak TM, Ligon R, Hartzler GO. Results of primary angioplasty for acute myocardial infarction in patients with multivessel coronary artery disease. J Am Co11 Cardiol 1990;16:1089-96. 23. Stone GW, Rutherford BD, McConahay DR, Johnson WL, Giorgi LV, Ligon RW, Hartzler GO. Direct coronary angioplasty in acute myocardial infarction: outcome in patients with single vessel disease. J Am Co11 Cardiol 1990:15:534-43. 24. Muller DWM, Top01 EJ, Ellis SG, Sigmon KN, Lee K, Califf RM, and the TAM1 studv eroun. Multivessel coronarv arterv disease: a key predictor of shori-term prognosis after reperfu”sion therapy for acute myocardial infarction. AM HEART J 1991;121:1042-9. 25. Top01 EJ. Coronary angioplasty for acute myocardial infarction. Ann Intern Med 1988;109:970-80. 26. Gacioch GM, Top01 EJ. Sudden paradoxic clinical deterioration during angioplasty of the occluded right coronary artery

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in acute myocardial infarction. J Am Co11 Cardiol 1989; 14:1202-g. 27. Kramer B, Larkin T, Niemyski P, Parker M. Coronary atherectomy in acute ischemic syndromes: implications of thrombus on treatment outcome [Abstract]. J Am Co11 Cardiol 1991;17:385A. 28. Shefer A, Forrester JS, Litvack F. Recanalization of acute thrombus: comparison of acute success and short-term patency after excimer laser coronary angioplasty, balloon angioplasty and intracoronary thrombolysis in pigs [Abstract]. J Am Co11 Cardiol 1991;17:205A. 29. Ohman EM, Califf RM, George BS, Quigley PJ, Kereiakes DJ, Harrelson-Woodlief L, Candela RJ, Flanagan C, Stack RS,

30.

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Top01 EJ, and the TAM1 study group. The use of intraaortic balloon pumping as an adjunct to reperfusion therapy in acute myocardial infarction. AM HEART J 1991;121:895-901. Stamm RB, Gibson RS, Bishop HL, Carabello BA, Beller GA, Martin RP. Echocardioarauhic detection of infarct-localized - asynergy and remote asynergy during acute myocardial infarction: correlation with the extent of angiographic coronary disease. Circulation 1983;67:233-44. Jaarsma W, Visser CA, Eenige MJ, Res JCJ, Kupper AJF, Verheugt FWA, Roos JP. Prognostic implications of regional hyperkinesia and remote asynergy of noninfarcted myocardium. Am J Cardiol 1986;58:394-8.

Calcitonin gene-related peptide in patients with and without early reperfusion after acute myocardial infarction Plasma concentrations of calcitonin gene-related peptide (CGRP), a potent regulator of vascular tone, creatine kinase, myoglobin, and cardiac troponin T were assessed in 31 patients with acute myocardial infarction. In patients who had sustained acute myocardial infarctions, maximum CGRP concentrations (median, 3.2 pmol/L; interquartile range, 1.5 to 4.8 pmol/L) were markedly elevated as compared with healthy control subjects (n = 23; median, 1.02 pmol/L; p = 0.02). However, no marked differences in CGRP levels were observed between patients with early reperfusion (n = 19; median, 3.5 pmol/L) and patients without early reperfusion (n = 12; median, 2.6 pmol/L; p = 0.96), as well as between those with congestive heart failure (n = 8; median, 3.9 pmol/L) and those without congestive heart failure (n = 23; median, 3.2 pmol/L; p = 0.62). CGRP did not correlate closely with myocardial protein release or hemodynamic parameters (heart rate and blood pressure) or the occurrence of arrhythmias. Therefore we conclude that elevated peripheral venous CGRP concentrations in patients who have sustained an acute myocardial infarction are independent of successful reperfusion and hemodynamic state. Although the cause of CGRP increase is not yet identified, CGRP may play a role in the regulation of coronary vascular tone in patients after acute myocardial infarction. (AM HEART J 1992;124:1433.)

Peter Lechleitner, MD,a Norbert Genser, MD,a Johannes Mair, MD,b Anton Dienstl, MD,a Christian Haring, MD,C Christian J. Wiedermann, Bernd Puschendorf, MD,b Alois Saria, PhD,” and Franz Dienstl, MD

MD,”

Innsbruck, Austria

Calcitonin gene-related peptide (CGRP) is a 37-amino-acid peptide that is formed from the pre-pro-calcitonin in chromosome ll.l* 2 It is widely distributed in the peripheral33 4 and central nervous system.5-8 From the Tntensive Care Unit of Department of Internal Medicine, bthe Department of Medical Chemistry and Biochemistry, and cthe Neurochemical Unit of Department of Psychiatry, University of Innsbruck, Innsbruck, Austria. Received

for publication

Reprint requests: Medizin-Intensivabteilung,

4/1141302

Peter

Nov.

18, 1992;

accepted

July

12, 1992.

Lechleitner, MD, Universitltsklinik Anichstrasse 35, 6020 Innsbruck,

fiir Innere Austria.

Outside the central nervous system, CGRP plays an important role in the control of regional blood flow. CGRP is the most powerful vasodilator yet identifiedg and appears to have positive chronotropic and inotropic effects on the isolated rat heart auricle.lO Intracoronary CGRP infusions showed a dose-dependent increase in diameter of human epicardial coronary arteries, which suggests that CGRP plays an important role in the regulation of coronary vascular smooth muscle tone. l1 In the heart, the highest concentration of CGRP receptors was found in the main coronary arteries. I2 The number of CGRP 1433