ADVERTISEMENT
Coronary Angioplasty Reduces Free Wall Rupture and Improves Mortality and Morbidity of Acute Myocardial Infarction
October 2004
Free wall rupture (FWR) is one of the major causes of mortality of acute myocardial infarction (AMI).1–3 Acute free wall rupture leads to cardiac tamponade, rapid hemodynamic deterioration and almost instantaneous death. Previous studies demonstrated some clinical predictors of FWR, such as anterior or lateral location, female gender, ST-elevation, protracted or recurrent chest pain, history of hypertension and advanced age.1,3–10
Because emergent coronary angiography and durable reperfusion strategy with coronary angioplasty was demonstrated to reduce rates of death or nonfatal reinfarction,11–15 the indication of angiography for patients with AMI is becoming more frequent than ever. But it is not clear whether FWR can be predicted with coronary angiography.
The effect of thrombolytic therapy on the incidence of FWR is still controversial. While a meta-analysis of 33 randomized trials of thrombolysis for patients with AMI16 failed to show a decrease in the cardiac rupture incidence from that of control groups, a lower incidence of FWR with thrombolysis has been reported.4 Whether emergent coronary angiography and durable coronary angioplasty for AMI would affect the natural history of FWR has not been definitively established, though some studies have suggested that successful early reperfusion with coronary angioplasty reduces or might even prevent FWR.5
Methods
Study population. In our prospective database of 3,138 consecutive AMI patients seen between May 1985 and May 2002, 3,096 patients (98.7%) who underwent emergent coronary angiography were analyzed retrospectively. Forty-two patients (1.3%) did not undergo emergent coronary angiography due to a lack of patient consent. All patients underwent transthoracic echocardiography on arrival; FWR had occurred already in 3 of these patients when they were first seen and they were thus excluded from the study; 40 patients developed FWR after admission to the hospital.
The clinical profiles of the patients are summarized in Table 1. The criteria for referring patients for coronary angioplasty and the type of coronary angioplasty, thrombolysis and CABG have varied over the years throughout the world, depending on the time period — and our institution is no exception. Stents were implanted and abciximab was administrated when considered appropriate individually, or when the patient was assigned to a particular clinical trial. The incidence of FWR was first determined in relation to the type of reperfusion strategy by univariate and multivariate analyses.
Definitions. The diagnosis of FWR was made when there was: 1) rapid cardiac tamponade and hemodynamic deterioration, or sudden death from electromechanical dissociation associated with large pericardial effusion on the echocardiogram; or 2) confirmation post-mortem or in surgery. FWR was defined as acute when abrupt transmural “blow-out” rupture caused hemopericardium and/or death. Subacute FWR was defined as a gradual or incomplete “woozing” rupture with slow or repetitive bleeding into the pericardial sac, causing progressive or recurrent cardiac tamponade.6
Two coronary risk factors were coded: diabetes and hypertension if previously diagnosed by another physician or if they were being treated with either insulin or oral antidiabetic drugs or antihypertensive drugs, respectively. Patients were considered to have an old MI if previously diagnosed by ECG or coronary angiography.
Time (hours) was defined as the time from the onset of symptoms to the establishment of durable reperfusion. Successful reperfusion was considered to be achieved when coronary angiography showed a final TIMI grade flow of 3.17 Significant stenosis was defined as > 75% stenosis according to the AHA classification by visual estimation and patients were considered to have single-vessel disease when there was significant stenosis in one vessel only.
In-hospital outcome and clinical follow-up. Medical records and procedural reports were reviewed. Patients were followed as out-patients or by telephone directly, or with their physicians. All major adverse c1inical events were confirmed on the hospital records and through review of the coronary cine angiograms. Myocardial infarction was defined by at least a two-fold increase of creatine kinase over the upper limit of normal, or by the development of new Q-waves on the 12-lead electrocardiogram. In some cases, patients who died soon after arrival due to an acute type of FWR, were defined as having suffered from acute myocardial infarction when angiographic coronary occlusion was demonatrated, along with severe angina or ST-elevation on the 12-lead electrocardiogram.
Study endpoints. The primary endpoint was FWR. The secondary endpoints were in-hospital death with or without FWR.
Statistical analysis. Statistical tests were performed using Stat-view version 5.0 (SAS institute Inc., North Carolina). Continuous variables are displayed as mean ± SD and were compared with t-tests. Categorical data are presented as frequencies and were compared with the chi-square test. All statistical tests were 2-tailed; a p value of Baseline characteristics. In our prospective database of AMI, 3,096 consecutive patients who underwent emergent coronary angiography were analyzed retrospectively. Coronary angioplasty was the mode of therapy in 2,536 patients (82.0%), thrombolysis in 666 patients (21.5%) and emergent CABG in 62 patients (2.0%). Coronary angiography reperfusion could not be achieved in 294 patients (9.5%), and 199 patients (6.4%) died in the hospital (Table 1).
Incidence of FWR. FWR after admission occurred in 40 (1.3%) patients. Acute FWR occurred in 28/40 patients (70.0%) and subacute FWR occurred in 12/40 patients (30.0%). Of the 199 (6.4%) AMI patients who died in the hospital, 25 (13.3%) died from FWR, yielding a 62.5% (25/40) mortality rate. In-hospital mortality was higher in acute-type FWR (21/28 patients, 75.0%), compared with subacute-type FWR (4/12 patients, 33.3%), but the difference was not significant. Surgical repair was performed in 17/40 patients (42.5%), 8 of whom died after surgery.
Incidence of free wall rupture independent of therapy. Coronary angioplasty alone (n = 2,236; 72.3%) resulted in a higher reperfusion success rate, a lower incidence of FWR and a mortality rate due to FWR significantly lower than with thrombolysis alone (n = 366; 11.8%), coronary angioplasty with thrombolysis (n = 300; 9.7%), and without either treatment (n = 191, 6.2%) (Figure 1, Table 2).
Predictors of FWR. FWR involved a LMT-related infarct more frequently (Table 3). Univariate analysis revealed that patients who did not undergo coronary angioplasty, failed reperfusion, were female or who were given thrombolytic agents experienced a significantly higher rate of FWR (Table 3). Coronary angioplasty significantly protected patients from FWR, while failed reperfusion, LMT-related infarct, female gender and age were significant predictors of FWR by multivariate logistic regression analysis (Figure 2).
Discussion
FWR is one of the major causes of mortality in AMI. Reddy et al. found the FWR frequency rose to as high as 15% of necropsy cases from 1970 to 1987.3 Our 1.5% incidence of FWR was lower than that of previous studies of AMI patients treated conservatively or with thrombolysis.4,7,16 Univariate and multivariate analyses showed that coronary angioplasty offers significant protection from FWR. Failed reperfusion was the most significant predictor of FWR by both univariate and multivariate analyses. Early and effective coronary revascularization could reduce FWR by preventing transmural completion and expansion of the myocardial infarction, thus relieving protracted or recurrent chest pain caused by residual ischemia.
Revascularization with coronary angioplasty versus thrombolysis. While many controlled studies have failed to demonstrate a significant difference in the incidence of FWR between coronary angioplasty and thrombolysis,11–15 others have suggested coronary angioplasty may reduce the incidence of FWR.10,18,19 Contraindications for thrombolysis compounds the selection process, making it difficult to directly compare FWR with coronary angioplasty. To overcome such bias, we performed not only univariate, but also multivariate analysis, of whether coronary angioplasty protects patients from FWR.
The incidence of FWR after thrombolytic therapy in combination with coronary angioplasty was significantly higher than with either thrombolysis or coronary angioplasty alone. The most likely explanation is that coronary angioplasty was performed in patients with thrombolysis only if there was inadequate reperfusion. The time delay until mechanical reperfusion could be established is the likely cause for this increase in event rates.
Conclusions and practical implications. Angiographic reperfusion success was the most significant protective factor from FWR. Prompt coronary revascularization could reduce the risk of FWR complicating AMI. Coronary angioplasty provides more effective and early coronary revascularization than does thrombolysis, even in those patients contraindicated for thrombolysis. Coronary angioplasty effectively reduced FWR complicating AMI and its concomitant fatality.
Study limitations. This is a retrospective, non-randomized, single-center study. However, in this study, we were able to obtain angiographic assessment of nearly consecutive patients with AMI due to the fact that our institution advocates the importance of emergent coronary angiography with durable reperfusion strategy for AMI. Thus, nearly all of our AMI patients receive emergent coronary angiography.
Despite the high sensitivity echocardiographic criteria studied for the diagnosis of FWR (97–100%), the specificity was reported to be low (61–27%).20 The lack of specificity is most likely related to the misdiagnosis of pericardial fat as thrombus or other conditions such as fibrinous pericarditis which may mimic pericardial thrombus. However, Purcaro et al. demonstrated signs of cardiac tamponade and intrapericardial echocardiography suggested that clots coexisted in most patients with subacute FWR (sensitivity 85%; specificity 100%).6
Because long-term survival of selected patients with prompt hemodynamic recovery after subacute-type FWR without surgical repair has been reported as possible,21,22 some patients with subacute-type FWR might have been overlooked despite the immediate transthoracic echocardiographic study of all patients on arrival. Echocardiography was not routinely repeated if the patients were hemodynamically stable. Although this study population may not be large enough to be definitively conclusive, it was nevertheless large enough to yield a statistically significant lower incidence of FWR in patients treated with coronary angioplasty by univariate and multivariate analyses.
1. Lewis AJ, Burchell HB, Titus JL. Clinical and pathologic features of postinfarction cardiac rupture. Am J Cardiol 1969;23:43–53.
2. Brodie BR, Stuckey TD, Hansen CJ, et al. Timing and mechanism of death determined clinically after primary angioplasty for acute myocardial infarction. Am J Cardiol 1997;79:1586–1591.
3. Reddy SG and William WC. Frequency of rupture of the left ventricular free wall or ventricular septum among necropsy cases of fatal acute myocardial infarction since introduction of coronary care units. Am J Cardiol 1989;63:906–911.
4. Pollak H, Nobis H, Mlczoch J. Frequency of left ventricular free wall rupture complicating acute myocardial infarction since the advent of thrombolysis. Am J Cardiol 1994;74:184–186.
5. Moreno R, Lopez-Sendon J, Garcia E, et al. Primary angioplasty reduces the risk of left ventricular free wall rupture compared with thrombolysis in patients with acute myocardial infarction. J Am Coll Cardiol 2002;39:598–603.
6. Purcaro A, Costantini C, Ciampani N, et al. Diagnostic criteria and management of subacute ventricular free wall rupture complicating acute myocardial infarction. Am J Cardiol 1997;80:397–405.
7. Becker RC, Hochman JS, Cannon CP, et al. Fatal cardiac rupture among patients treated with thrombolytic agents and thrombin antagonists. J Am Coll Cardiol 1999;33:479–87.
8. Mann JM and Roberts WC. Rupture of the left ventricular free wall during acute myocardial infarction: Analysis of 138 necropsy patients and comparison with 50 necropsy patients with acute myocardial infarction without rupture. Am J Cardiol 1988;62:847–859.
9. Figueras J, Curos A, Cortadellas J, et al. Relevance of electrocardiographic findings, heart failure and infarct site in assessing risk and timing of left ventricular free wall rupture during acute myocardial infarction. Am J Cardiol 1995;76:543–547.
10. Yamaguchi J, Kawaguchi M, Kawana M, et al. Risk factors and effect of reperfusion therapy on left ventricular free wall rupture following acute myocardial infarction. J Cardiol 2000;35:257–65.
11. Grines CL, Browne KF, Marco J, et al. A comparison of immediate angioplasty with thrombolytic therapy for acute myocardial infarction. The Primary Angioplasty in Myocardial Infarction Study Group. N Engl J Med 1993;328:673–679.
12. Zijlstra F, de Boer MJ, Hoorntje JC, et al. A comparison of immediate coronary angioplasty with intravenous streptokinase in acute myocardial infarction. N Engl J Med 1993;328:680–684.
13. A clinical trial comparing primary coronary angioplasty with tissue plasminogen activator for acute myocardial infarction. The Global Use of Strategies to Open Occluded Coronary Arteries in Acute Coronary Syndromes (GUSTO IIb) Angioplasty Substudy Investigators. N Engl J Med 1997;336:1621–1628.
14. Weaver WD, Simes RJ, Betriu A, et al. Comparison of primary coronary angioplasty and intravenous thrombolytic therapy for acute myocardial infarction: A quantitative review. J Am Med Assoc 1997;278:2093–2098.
15. Aversano T, Aversano LT, Passamani E, et al. Thrombolytic therapy versus primary percutaneous coronary intervention for myocardial infarction in patients presenting to hospitals without on-site cardiac surgery: A randomized controlled trial. J Am Med Assoc 2002;287:1943–1951.
16. Yusuf S, Collins R, Peto R, et al. Intravenous and intracoronary fibrinolytic therapy in acute myocardial infarction: Overview of results on mortality, reinfarction and side-effects from 33 randomized controlled trials. Eur Heart J 1985;6:556–585.
17. The Thrombolysis in Myocardial Infarction (TIMI) trial. Phase I findings. TIMI Study Group. N Engl J Med 1985;312:932–936.
18. Kahn JK, O'Keefe HJ Jr, Rutherford BD, et al. Timing and mechanism of in-hospital and late death after primary coronary angioplasty during acute myocardial infarction. Am J Cardiol 1990;66:1045–1048.
19. Tanaka K, Sato N, Yasutake M, et al. Clinical course, timing of rupture and relationship with coronary recanalization therapy in 77 patients with ventricular free wall rupture following acute myocardial infarction. J Nippon Med Sch 2002;69:481–488.
20. Raitt MH, Kraft CD, Gardner CJ, et al. Subacute ventricular free wall rupture complicating acute myocardial infarction. Am Heart J 1993;126:946–955.
21. Figueras J, Cortadellas J, Evangelista, et al. Medical management of selected patients with left ventricular free wall rupture during acute myocardial infarction. J Am Coll Cardiol 1997;29:512–518.
22. Figueras J, Cortadellas J, Domingo E, et al. Survival following self-limited left ventricular free wall rupture during myocardial infarction. Management differences between patients with or without pseudoaneurysm formation. Int J Cardiol 2001;79:103–111.
