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Page 1: Prevalence of Early Left Ventricular Thrombus after Primary Coronary Intervention for Acute Myocardial Infarction

Journal of Thrombosis and Thrombolysis 10,133±136,2000.

# Kluwer Academic Publishers. Printed in The Netherlands.

Prevalence of Early Left Ventricular Thrombus after PrimaryCoronary Intervention for Acute Myocardial Infarction

Aman Kalra and Ik-Kyung Jang

Massachusetts General Hospital and Harvard Medical School,

Boston, Massachusetts, USA

Abstract. The prevalence of left ventricular (LV) throm-bus after acute myocardial infarction (AMI) has beenreported high at 20±60%. Current reperfusion therapiessuch as thrombolysis have shown a trend toward redu-cing the incidence of LV thrombosis. However, theprevalence of LV thrombus after primary percutaneouscoronary intervention (PCI) for AMI has not beensystematically studied. At Massachusetts GeneralHospital 71 consecutive patients who underwentprimary PCI for acute ST elevation MI were reviewedfor the prevalence of LV thrombus evaluated by echo-cardiography. Echocardiography was performedwithin 5 days of infarction. PCI was successful in allpatients. The time delay from symptom onset to inter-vention was 191 minutes. Thrombolysis in MyocardiolInfarction (TIMI) grade 3 ¯ow was achieved in morethan 80% of cases. Only 3 patients (4%) had echocardio-graphic evidence of LV thrombus. All 3 patients hadanterior infarctions. The incidence among patientswith anterior MI was 10% (3 of 30 patients). The preva-lence of LV thrombus in patients treated with primaryPCI for AMI is low (4%).

Key Words. left ventricular thrombus; acutemyocardial infarction; primary percutaneous coronaryintervention; stenting

LV thrombus is a well-recognized complication ofAMI. Traditionally, the incidence of LV thrombusdetected by echocardiography has been reportedbetween 20 and 60% [1±8]. LV thrombi usuallydevelop in the ®rst few days after AMI in mostpatients [1,5,6,9]. LV regional wall akinesia anddyskinesia with resultant blood stasis, endocar-dial tissue injury, and a hypercoagulable statehave been thought to be important contributorsto thrombus formation [3,5,8,10±12].

In the modern era, there is widespread use ofreperfusion therapies such as thrombolysis andprimary PCI for the management of AMI. Throm-bolytic therapy may be expected to prevent muralthrombi after AMI by reduction of myocardialdamage and preservation of LV function throughearly reperfusion and by maintaining a persis-tent lytic state. The incidence of LV thrombusafter thrombolysis for AMI varies in differentreports. Some studies reported a positive trend

toward reducing the prevalence of LV thrombus[11,13±19]; in others, the reduction did notachieve statistical signi®cance [20,21]. Bhatna-gar and al-Yusuf reported a threefold reduction inthe incidence of LV thrombosis in patients receiv-ing early intravenous recombinant tissue plasmi-nogenfactor (rt-PA) [11]. In a subsequent meta-analysis by Vaitkus and Barnathan [19], 390patients from six studies were analyzed. Five ofthe six studies reported a trend in favor ofthrombolysis [19]. On the contrary, Vecchio etal. [20] in their substudy of Gruppo Italiano perlo Studio della Sopravvivenza nell'Infarto Miocar-dico (GISSI-2) failed to demonstrate a signi®cantreduction in the incidence of LV thrombus in 180patients with AMI treated with thrombolytictherapy and anticoagulation for 12 hours [20].The results of recent studies are summarized inTable 1.

In recent years, primary PCI with stenting hasbecome the reperfusion therapy of choice for AMIin institutions with emergency cardiac catheter-ization facilities [22,23]. Primary PCI achievesfull and sustained reperfusion, which promotesearly recovery of the infarcted myocardium andmay therefore theoretically decrease the inci-dence of LV thrombosis. However, with limitedduration of anticoagulation after PCI and in theabsence of a lytic state, the prevalence of LVthrombus may be higher than that after throm-bolytic therapy. No study, so far, has systemati-cally evaluated the incidence of LV thrombus inpatients treated with primary stenting for AMI.In this study, we evaluated the prevalence ofechocardiographic LV thrombus in patients withAMI treated with primary PCI.

Methods

Among 1150 consecutive patients who wereadmitted to the Massachusetts General Hospitalbetween January 1997 and January 1999 with

133

Address for correspondence: Ik-Kyung Jang, MD, CardiologyDivision, Bul®nch 105, Massachusetts General Hospital, 55Fruit Street, Boston, MA, 02114, USA E-mail: [email protected]

Page 2: Prevalence of Early Left Ventricular Thrombus after Primary Coronary Intervention for Acute Myocardial Infarction

a diagnosis of acute coronary syndrome, 71patients who underwent primary PCI for acuteST elevation MI were identi®ed. After obtainingapproval from the human studies committee atthe Massachusetts General Hospital, data wereobtained for baseline demographic characteris-tics, preintervention and postintervention TIMI¯ows, and echocardiographic evidence of LVthrombus. Two-dimensional echocardiographywas performed within 5 days of AMI in allpatients. LV thrombus was de®ned as a distinctmass of echoes in the LV cavity that was seenclearly throughout the cardiac cycle in at leasttwo different echocardiographic views. In addi-tion, the mass had to be adjacent to the endocar-dium in an area of asynergic myocardium [1,4,7].All patients received aspirin and full-dose anti-coagulation with intravenous heparin for at least

48 hours. None of the patients received thrombo-lytic therapy.

Results

Baseline demographic characteristics are shownin Table 2. Among the 71 patients, 30 (43%) hadanterior MI and 37 (54%) had inferior or posteriorwall MI. Sixty-eight (95.8%) patients receivedcoronary stent. LV thrombus was detected echo-cardiographically in 3 of the 71 patients (4%). Allthree patients had anterior infarctions. The inci-dence of LV thrombus among patients with ante-rior wall AMI was 10% (3 of 30 patients). The LVthrombus group had a higher peak phosphoki-nase creatinine phosphokinase (CPK) (4299 U=Lversus 2282 U=L), although the mean ejectionfraction (EF) was comparable at 54% and 51%.

Table 1. Summary of Published Studies

Study Incidence of LV thrombus p ValueInclusion No. ofcriteria patients Control SK rt-PA

Bhatnagar and al-Yusef [11] Anterior Q wave MI 98 18% (8=44) 5.5%(3=54) <0.05Pizzetti et al. [12] AMI 418 45% (109=243) 26% (45=175)* 0.04Eigler et al. [13] Anterior Q wave MI 22 70% (7=10) 8.3% (1=12)Held et al. [14] Q wave MI 96 23% (7=31) 5% (1=22) 19% (8=43) NSMotro et al. [15] Q wave MI 144 6.25% (9=144)Lupi et al. [17] Anterior Q wave MI 63 52% (23=44) 21% (4=19) 0.02Vecchio et al. [20] Anterior Q wave MI 180 28% (51=180)*Greaves et al. [24] Q wave MI 309 3.7% (11=309)*Chiarella et al. [25] Q wave MI 8326 5.1% (427=8326)*

NS, not signi®cant; SK, streptokinase.* Both streptokinase and rt-PA were used.

Table 2. Clinical Characteristics

Total LV thrombus No LV thrombus

Number of patients (%) 71 3 (4.2%) 68 (95.7%)Men 54 (76%) 3 (100%) 51 (75%)Mean age (y) 61.6 57 61Systematic hypertension 29 (40.8%) 1 (33%) 28 (41%)Diabetes mellitus 11 (15.4%) 1 (33%) 10 (14.7%)CHF 4 (5.6%) 1 (33%) 3 (4.4%)CVA 2 (2.8%) 1 (33%) 1 (1.4%)Prior MI 8 (11.2%) 1 (33%) 7 (10%)Prior revascularization 8 (11.2%) 1 (33%) 7 (10%)Location:

Anterior 30 (42.2%) 3 (100%) 27 (39%)Inferior=posterior 37 (52.1%) 0 37 (54%)Peak CPK (U=L) 2395 4299 2282Mean EF (%) 54% 51%GP IIb=IIIa inhibitors 40 (56.3%) 2 (66%) 38 (55%)TIMI 3 ¯ow 57 (80.2%) 2 (66%) 55 (80.8%)

CHF, congestive heart failure; CVA cerebrovascular accident; GP, glycoprotein.

134 Kalra and Jang

Page 3: Prevalence of Early Left Ventricular Thrombus after Primary Coronary Intervention for Acute Myocardial Infarction

Postintervention TIMI 3 ¯ow was achieved in 2 ofthe 3 patients (66%) in the LV thrombus groupand in 80% in the rest of the group. The averagetime delay from symptom onset to intervention inthe thrombus group was 150 minutes, comparedwith 191 minutes in the nonthrombus group.Glycoprotein IIb=IIIa inhibitors were used in 2patients (66%) in the LV thrombus group ascompared with 52% in the nonthrombus group.None of the patients had clinical evidence ofarterial embolism during the hospital course.

Discussion

The incidence of LV thrombus in our study wasonly 4% (3 of 71 patients). This is very low incomparison to earlier studies that reported LVthrombus in 20±60% of patients with AMI. Tworecent studies have also reported a low incidenceof LV thrombosis [24,25]. Greaves et al. [24]reported in a cohort of 309 patients an incidenceof 3.7% at 14 days and 6.4% at 90 days. Thepossible explanation for the low incidence wasattributed to the frequent use of early reperfu-sion. The GISSI-3 study showed that in 8326patients at low to medium risk for LV thrombus,the predischarge echocardiogram (9� 5 days)demonstrated LV thrombus in 5.1% of patients[25]. Patients with severe heart failure, severerespiratory insuf®ciency, and other life-threaten-ing diseases were excluded from the study.

The current lower prevalence of LV thrombusin AMI in recent studies compared with previousreports is probably due to changes in AMImanagement. Modern reperfusion strategies,which promote early recovery of LV function,may be responsible for the low incidence.

The genesis of a thrombus is probably relatedto a combination of factors such as relative stasisof blood in areas of akinetic or dyskinetic wallmotion, and a hypercoagulable state during theperi-infarction period [1,3,5,8,11]. Frequent useof early reperfusion theraphy for AMI may repre-sent a protective factor against thrombus forma-tion by salvaging the myocardium, reducing theinfarct area, and restoring LV function. Indeed,in a study by Pizzetti et al. [12], a signi®cantreduction in the prevalence of LV thrombus wasobserved in a subgroup of patients who demon-strated angiographic evidence of reperfusionafter thrombolytic therapy as compared withthose with failed reperfusion (14% versus 54%).Other studies have also reported a relationshipbetween the absence of thrombus and the patencyof the infarct-related artery [10,14,16].

Primary PCI with stenting has become thereperfusion therapy of choice in recent years.Numerous randomized trials comparing primaryangioplasty with intravenous thrombolysis have

shown advantages of primary angioplasty [22,23,26±32]. The improved clinical outcome is prob-ably related to better recovery of LV function.Although our study is too small to show thedifference in the incidence of LV thrombus, it ispossible that early primary stenting furtherdecreases the incidence of LV thrombus ascompared with thrombolysis.

Study Limitations

This study is a retrospective analysis without anyrandomization in a relatively small number ofpatients. LV thrombus is a dynamic phenomenon,and it is possible that some patients developed athrombus after the initial echocardiographicstudy. Serial echocardiographic studies at differ-ent time intervals could have identi®ed addi-tional patients with LV thrombus. Contrast andharmonic echo were not used which could haveincreased the sensitivity of the study. Finally, therole of glycoproteins IIb=IIIa inhibitors or dura-tion of anticoagulation in reducing LV thrombuscould not be evaluated because of the smallnumber.

References

1. Asinger RW, Mikell FL, Elsperger J, Hodges M. Inci-dence of left-ventricular thrombosis after acute trans-mural myocardial infarction. Serial evaluation bytwo-dimensional echocardiography. N Engl J Med1981;305:297±302.

2. Friedman MJ, Carlson K, Marcus FI, Woolfenden JM.Clinical correlations in patients with acute myocardialinfarction and left ventricular thrombus detected bytwo-dimensional echocardiography. Am J Med1982;72:894±898.

3. Stratton JR, Lighty GW Jr, Pearlman AS, Ritchie JL.Detection of left ventricular thrombus by two-dimen-sional echocardiography: Sensitivity, speci®city, andcauses of uncertainty. Circulation 1982;66:156±166.

4. Keating EC, Gross SA, Schlamowitz RA, et al. Muralthrombi in myocardial infarctions. Prospective evalua-tion by two-dimensional echocardiography. Am J Med1983;74:989±995.

5. Visser CA, Kan G, David GK, Lie KI, Durrer D. Twodimensional echocardiography in the diagnosis of leftventricular thrombus. A prospective study of 67patients with anatomic validation. Chest 1983;83:228±232.

6. Weinreich DJ, Burke JF, Pauletto FJ. Left ventricularmural thrombi complicating acute myocardial infarc-tion. Long-term follow-up with serial echocardiogra-phy. Ann Intern Med 1984;100:789±794.

7. Spirito P, Bellotti P, Chiarella F, Domenicucci S,Sementa A, Vecchio C. Prognostic signi®cance andnatural history of left ventricular thrombi in patientswith acute anterior myocardial infarction: A two-dimensional echocardiographic study. Circulation1985;72:774±780.

Prevalence of Early LV Thrombus 135

Page 4: Prevalence of Early Left Ventricular Thrombus after Primary Coronary Intervention for Acute Myocardial Infarction

8. Domenicucci S, Bellotti P, Chiarella F, Lupi G, VecchioC. Spontaneous morphologic changes in left ventricu-lar thrombi: a prospective two-dimensional echocar-diographic study. Circulation 1987;75:737±743.

9. Davis MJ, Ireland MA. Effect of early anticoagulationon the frequency of left ventricular thrombi afteranterior wall acute myocardial infarction. Am JCardiol 1986;57:1244±1247.

10. Lamas GA, Vaughan DE, Pfeffer MA. Left ventricularthrombus formation after ®rst anterior wall acutemyocardial infarction. Am J Cardiol 1988;62:31±35.

11. Bhatnagar SK, al-Yusuf AR. Effects of intravenousrecombinant tissue-type plasminogen activator ther-apy on the incidence and associations of left ventricu-lar thrombus in patients with a ®rst acute Q waveanterior myocardial infarction. Am Heart J1991;122:1251±1256.

12. Pizzetti G, Belotti G, Margonato A, et al. Thrombolytictherapy reduces the incidence of left ventricularthrombus after anterior myocardial infarction. Rela-tionship to vessel patency and infarct size. Eur HeartJ 1996;17:421±428.

13. Eigler N, Maurer G, Shah PK. Effects of earlysystemic thrombolytic therapy on left ventricularmural thrombus formation in acute anterior myocar-dial infarction. Am J Cardiol 1984;54:261±263.

14. Held AC, Gore JM, Paraskos J, et al. Impact ofthrombolytic therapy on left ventricular muralthrombi in acute myocardial infarction. Am J Cardiol1988;62:310±311.

15. Motro M, Barbash GI, Hod H, et al. Incidence of leftventricular thrombi formation after thrombolytictherapy with recombinant tissue plasminogen activa-tor, heparin, and aspirin in patients with acutemyocardial infarction. Am Heart J 1991;122:23±26.

16. Ileri M, Tandogan I, Kosar F, Yetkin E, Buyukasik Y,Kutuk E. In¯uence of thrombolytic therapy on theincidence of left ventricular thrombi after acute ante-rior myocardial infarction: Role of successful reperfu-sion. Clin Cardiol 1999;22:477±480.

17. Lupi G, Domenicucci S, Chiarella F, Bellotti P, VecchioC. In¯uence of thrombolytic treatment followed by fulldose anticoagulation on the frequency of left ventri-cular thrombi in acute myocardial infarction. Am JCardiol 1989;64:588±590.

18. Natarajan D, Hotchandani RK, Nigam PD. Reducedincidence of left ventricular thrombi with intravenousstreptokinase in acute anterior myocardial infarction:Prospective evaluation by cross-sectional echocardio-graphy. Int J Cardiol 1988;20:201±207.

19. Vaitkus PT, Barnathan ES. Embolic potential, preven-tion and management of mural thrombus complicat-ing anterior myocardial infarction: A meta-analysis.J Am Coll Cardiol 1993;22:1004±1009.

20. Vecchio C, Chiarella F, Lupi G, Bellotti P, DomenicucciS. Left ventricular thrombus in anterior acutemyocardial infarction after thrombolysis. A GISSI-2connected study. Circulation 1991;84:512±519.

21. Sharma B, Carvalho A, Wyeth R, Franciosa JA. Leftventricular thrombi diagnosed by echocardiography inpatients with acute myocardial infarction treated withintracoronary streptokinase followed by intravenousheparin. Am J Cardiol 1985;56:422±425.

22. Weaver WD, Simes RJ, Betriu A, et al. Comparison ofprimary coronary angioplasty and intravenous throm-bolytic therapy for acute myocardial infarction: aquantitative review: JAMA 1997;278:2093±2098.

23. Yusuf S, Pogue J. Primary angioplasty compared withthrombolytic therapy for acute myocardial infarction.JAMA 1997;278:2110±2111.

24. Greaves SC, Zhi G, Lee RT, et al. Incidence andnatural history of left ventricular thrombus followinganterior wall acute myocardial infarction. Am JCardiol 1997;80:442±448.

25. Chiarella F, Santoro E, Domenicucci S, Maggioni A,Vecchio C. Predischarge two-dimensional echocardio-graphic evaluation of left ventricular thrombosis afteracute myocardial infarction in the GISSI-3 study. AmJ Cardiol 1998;81:822±827.

26. Zahn R, Koch A, Rustige J, Schiele R, Wirtzfeld A.Primary angioplasty versus thrombolysis in the treat-ment of acute myocardial infarction. ALKK studygroup. Am J Cardiol 1997;79:264±269.

27. Zijlstra F, de Boer JM, Hoorntje JC. A comparison ofimmediate coronary angioplasty with intravenousstreptokinase in acute myocardial infarction. N EnglJ Med 1993;328:680±684.

28. Grines CL, Browne KF, Marco J. A comparison ofimmediate angioplasty with thrombolytic therapy foracute myocardial infarction. N Engl J Med1993;328:673±679.

29. Gibbons RJ, Holmes DR, Reeder GS. Immediateangioplasty compared with administration of a throm-bolytic agent followed by conservative treatment formyocardial infarction. N Engl J Med 1993;328:685±691.

30. Every N, Parsons L, Hlatky M. A comparison ofthrombolytic therapy with primary coronary angio-plasty for acute myocardial infarction. N Engl J Med1996;335:1253±1260.

31. Ribeiro EE, Silva LA, Carneiro R. Randomized trial ofdirect coronary angioplasty versus intravenous strep-tokinase in acute myocardial infarction. J Am CollCardiol 1993;22:376±380.

32. O'Neill W, Timmis GC, Bourdillon PD. A prospectiverandomized clinical trial for intracoronary streptoki-nase versus coronary angioplasty for acute myocardialinfarction. N Engl J Med 1986;314:812±818.

136 Kalra and Jang