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(Circulation. 2008;118:2783-2789.)
© 2008 American Heart Association, Inc.
Coronary Heart Disease |
From the Unitat Coronària, Servei de Cardiologia, Hospital Universitari Vall d'Hebron, Barcelona, Spain.
Correspondence to Jaume Figueras, MD, Unitat Coronària, Servei de Cardiologia, Hospital General Universitari Vall d'Hebron, Universitat Autònoma de Barcelona, P. Vall d'Hebron 119–129, 08035 Barcelona, Spain. E-mail 5751jfb{at}comb.es
Received March 5, 2008; accepted October 14, 2008.
| Abstract |
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Methods and Results— The incidence of cardiac rupture in ST-elevation myocardial infarction patients and its mortality rate were investigated during a 30-year period divided into 5 intervals (1977 to 1982, 1983 to 1988, 1989 to 1994, 1995 to 2000, and 2001 to 2006). Of a total of 6678 consecutive patients, 425 experienced a free wall rupture (280 with cardiac tamponade: 227 with electromechanical dissociation and 53 with hypotension) or a septal rupture (145). After the exclusion of referrals from other centers (n=44), the incidence of definite cardiac rupture (septal rupture, anatomic evidence of free wall rupture, or electromechanical dissociation) declined progressively (6.2% in 1977 to 1982 to 3.2% in 2001 to 2006; P<0.001) in parallel with a progressive use of reperfusion therapy (0% to 75.1%; P<0.001). In addition, among patients with cardiac rupture, there was a progressive fall in the rate of death (94% to 75%; P<0.001) despite a trend toward increasing age (66±8 to 75±8 years; P<0.054) in conjunction with better control of systolic blood pressure at 24 hours (130±24 versus 110±18 mm Hg; P<0.001); an increased use of reperfusion therapy (0% to 59%; P<0.001), β-blockers (0% to 45%; P<0.001), angiotensin-converting enzyme inhibitors (0% to 38%; P<0.001), and aspirin (0% to 96%; P<0.001); and a lower use of heparin (99% to 67%; P<0.001).
Conclusion— The decline in the incidence in cardiac rupture and its rate of death over the last 30 years appears to be associated with the increasing use of reperfusion strategies and adjunct medical therapy.
Key Words: heart rupture mortality myocardial infarction reperfusion
| Introduction |
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Clinical Perspective p 2789
Therefore, the aim of our study was 2-fold: to investigate the incidence of CR in consecutive STEMI patients during a 30-year span and to analyze possible changes in in-hospital death rates and clinical features of patients with CR over this period and in patient management.
| Methods |
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1 mm in 2 inferior or lateral leads or
2 mm in
2 precordial leads. Elevated myocardial enzymes (creatine kinase-MB) were found in most patients admitted within 72 hours from STEMI onset, but peak levels often were not available because of late arrival or early death. There were 280 patients with FWR, 29 with associated SR, and 145 with SR alone. Of the 280 with FWR, 227 presented with electromechanical dissociation (EMD) and 53 with arterial hypotension. Other patients with cardiac tamponade but with a strong suspicion of right ventricular perforation by a pacing catheter or an acute aortic dissection were excluded.
Diagnosis of FWR was confirmed in 142 patients, 97 at autopsy and 45 at surgery. In 90 other patients, diagnosis of FWR was based on the development of cardiac arrest caused by EMD in the absence of preceding heart failure, and each of the 73 in whom a 2-dimensional echocardiogram was performed showed evidence of cardiac tamponade. In the remaining 48 patients, FWR was suspected by the development of hypotension with echocardiographic evidence of cardiac tamponade (pericardial effusion
10 mm with right atrial compression). Clinical diagnosis of tamponade was entertained in the presence of hypotension, jugular venous distention, and a paradoxical pulse (
20 mm Hg). In addition, a raised right atrial pressure (
10 mm Hg) was documented by a central venous or a Swan Ganz catheter in 215 patients. From January 1990 to December 1991, a 2-dimensional echocardiogram was performed only in STEMI patients who became hypotensive or died; from January 1992 on, it was performed in all STEMI patients within the first 12 hours after admission and was repeated in those who developed arterial hypotension and in those who died before or during resuscitative maneuvers. Diagnosis of SR was made by at least one of the following methods: right-sided heart catheterization (n=95), 2-dimensional Doppler echocardiography (n=103), contrast left ventriculogram (n=69), or necropsy study (n=28).
Protocol
In all patients, a 12-lead ECG was performed on admission, daily thereafter, and during and after episodes of chest pain or hemodynamic deterioration. Myocardial enzymes (creatine kinase-MB) were measured every 4 to 6 hours during the first 48 hours and after episodes of angina >30 minutes. Patients with cardiac tamponade without EMD were initially managed with intravenous volume (colloid solution preferred), inotropic agents, and pericardiocentesis whenever feasible. Those presenting with EMD were treated with cardiac massage, intravenous volume, inotropic agents, mechanical ventilation if required, and pericardiocentesis. Since 1986 and in patients who recovered hemodynamic stability, a surgical thoracotomy with repair of the possible FWR was considered, weighing the risk associated with comorbidity conditions (chronic obstructive pulmonary disease, extensive myocardial damage, chronic renal failure, etc). Our center had a cardiac surgeon and cardiology staff in the cardiac care unit on call, and in patients in whom surgery was initially not considered, subsequent treatment included inotropic support as needed. This was followed by administration of oral propranolol starting at 5 to 10 mg every 6 hours and was gradually increased to keep systolic blood pressure between 100 and 120 mm Hg. Heparin was withdrawn but aspirin was not discontinued, whereas clopidogrel was discontinued. All patients were kept on strict bedrest for at least 5 days.
In patients with SR, surgical repair was generally attempted in those <80 years of age without cardiogenic shock with or without the assistance of intraaortic balloon counterpulsation.
Statistical Analysis
The analysis sought to discover possible differences in the incidence of CR and in the use of reperfusion therapy among the 5 STEMI groups. The clinical, ECG, and angiographic variables of CR patients corresponding to these groups and their in-hospital outcome also were compared, and differences in medical and surgical management were investigated. For comparison of
3 subsets over time, we used linear regression analysis for continuous variables with normal distribution and the Jonckheere-Tergstra test for nonnormally distributed variables. For categorical variables, the
2 or Fishers exact test for trend also was used. The analysis was performed with SPSS 13.0 (SPSS Inc, Chicago, Ill). Data are expressed as mean±SD or median, and differences were considered significant at P<0.05.
The authors had full access to and take full responsibility for the integrity of the data. All authors have read and agree to the manuscript as written.
| Results |
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The decline in the incidence of CR was associated with a progressive increase in the use of reperfusion therapy (0% versus 75.1%; P<0.001). It was particularly striking in the last period (2001 to 2006) when the use of primary coronary intervention was highest (Figure 1).
Clinical and ECG Data Among Patients With CR
Age tended to increase progressively over time, but the 5 groups showed a similar incidence of risk factors and peripheral vascular disease (Table 1). The frequency of previous angina and old myocardial infarction was low and similar in the 6 groups, whereas admission Killip class I to II was high and also comparable. ST segment remained similarly elevated at 24 and 48 hours in the 5 groups; admission arterial systolic blood pressure and heart rate also were similar (Table 1). At 24 hours, however, they were progressively lower, which was coincidental with the introduction of early β-blocker treatment (Table 2). Complete atrioventricular block occurred more frequently in the first period than in the remaining 4 periods, which could be explained in part by the inclusion of a greater proportion of patients with inferior infarction and perhaps by more extensive and transmural necrosis infarcts caused by the absence of reperfusion therapy, which tends to reduce infarct size and transmurality. Furthermore, among the 216 of 280 patients (77%) with FWR/cardiac tamponade in whom onset EMD could be determined precisely, it occurred between 6 PM and 7 AM in 125 (58%), indicating that an important proportion of these events occurred outside the regular office schedule.
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Management and Outcome
As expected, medical treatment before CR in patients who presented the event while in the hospital (n=307) varied significantly in the different time intervals, with an increasing use of β-blockers, ACE inhibitors, aspirin, and reperfusion therapy since the late 1980s (Table 2). Implementation of reperfusion therapy, however, continued to be somewhat limited because a sizable proportion of CR patients were late in seeking medical attention. In fact, mean admission delay, defined as the interval from pain onset to emergency room arrival, was >24 hours in 4 of the 5 groups, with virtually no change in the last 18 years, and the proportion of patients who already presented CR on admission (prehospital CR) was comparable in the 5 groups (Table 1). In contrast, average admission delay for our STEMI patients without CR has been progressively shortened to <10 hours in the last 12 years. Procedures performed during CR in the 425 patients are listed in Table 3. Use of pericardiocentesis increased progressively over the years except for the 1989 to 1994 period, in part because of the lower proportion of FWR during this interval. Only a few patients were operated on during the first period, which is largely ascribable to the unavailability of a medical and surgical strategy for the management of CR. The rest of the time periods showed a similar incidence of surgical treatment except for the 1989 to 1994 period, when surgical interventions almost doubled, mainly because of the increased number of SR cases (Table 3). Most surgical interventions were performed within the first 5 days after hospital admission (SR, 51 of 74 [69%]; FWR, 23 of 33 [70%]); only a few were performed beyond the ninth day (SR, 15 [20%]; FWR, 5 [15%]).
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In-hospital death declined over the years (Figure 2) despite a strong trend toward a progressive increase in age (Table 1) and was due mostly to a cardiac cause, EMD (71.8%, 76.7%, 50.8%, 62.9%, and 47.2% in each time period, respectively), or cardiogenic shock (25.6%, 18.6%, 33.3%, 25.8%, and 49%). Among patients who were operated on, the rate of death was higher in those operated on early (
5 days) than in those operated on late (>9 days; SR, 37 of 51 [73%] versus 4 of 15 [27%], P=0.004; FWR, 18 of 23 [78%] versus 1 of 5 [20%], P
0.046). Improvement in survival appeared to relate principally to changes in medical management (Table 2) and to an earlier recognition of CR, particularly in patients presenting with subacute FWR.
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| Discussion |
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Incidence of CR
The incidence of CR in our study was higher than reported in other series, possibly because of the exclusion of patients with non-STEMI, our keen interest in documenting the mode of death in our MI patients, and the inclusion as FWR patients those who died of EMD without antecedent heart failure, an association previously validated.28 Moreover, most series did not combine FWR and SR.1,2,16,19,20,22,23 We believe that the progressive reduction in the frequency of CR was, in all likelihood, multifactorial. Indeed, the increasing awareness of the need to seek early medical attention on the development of anginal symptoms has resulted in earlier hospital admission and earlier pain and blood pressure control. This is pertinent to the development of CR, for the mean admission delay in these patients was long and comparable delays were seen throughout the 30 years, whereas admission delay in our non-CR STEMI patients had been progressively shortened. Prolonged admission delay enhances the risk of CR,8,27 possibly by facilitating transmurality of STEMI and increasing wall tension.
Effects of Medical Treatment
The reduction in the incidence of CR was coincidental with the widespread use of reperfusion therapy, particularly in the last 6 years when the use of percutaneous coronary intervention was highest, and is in keeping with previous studies.3,15–17,19,21 Moreover, reperfusion therapy also seemed to be associated with a reduction in death caused by CR despite the progressive ageing of our population. Thus, it might be speculated that effective reperfusion could have reduced the incidence of CR, and perhaps its death rate, by sparing the outer zone of jeopardized myocardium, thereby reducing the extent and transmurality of STEMI.22,29,30
Most of our CR patients were treated with nitrates, an agent claimed to reduce the incidence of this event,23 but we had no comparison group without nitrates to assess this protective effect. Moreover, since the late 1980s, β-blockers have been added to treatment, although, as in other series,3,5,31 they were given to <50% of STEMI patients in the early stage, partly because of arterial hypotension, chronic lung disease, incipient heart failure, or conduction abnormalities.31,32 In addition, only a few cases were treated intravenously. Thus, according to the First International Study of Infarct Survival (ISIS-1), in which β-blockers lowered the incidence of and death associated with CR during the first 24 to 48 hours in >200 patients,11 we could ascribe these agents in part to the progressive reduction mortality rates seen in our CR patients. In this respect, the significantly lower blood pressure attained 24 hours after admission during the last three 6-year intervals in which β-blockers were used might be an argument in favor of their protective effect.11,33 In contrast, 2 other investigations have disputed such a preventive role,12,13 although they included only 2512 and 14 cases13 of CR. To further compound the issue, observations from a recent large clinical trial of STEMI patients have even called into question the overall survival benefit of β-blockers in the acute phase.14 ACE inhibitors also have been administered to a small proportion of our patients since the early 1990s, and even though no randomized trials have investigated their effects on preventing CR, their contribution to lower CR-related incidence and mortality rates, perhaps by reducing infarct expansion, cannot be ruled out.34 Aspirin, introduced in the late 1980s, might also have participated in reducing the incidence of or rate of death from CR by improving myocardial perfusion,25 but this hypothetical beneficial effect has not been investigated. However, other unmeasured factors such as differences in blood pressure control and anticoagulant therapy that were not available in STEMI patients without CR for comparison might also have contributed to the decline in the incidence of CR.
The rates of hospital death were disturbingly high in all CR subsets. Unfortunately, however, our numbers are in agreement with findings in the "real world." In fact, previous studies have reported mortalities of FWR ranging from 75% to 90%,2,3,5,18–20,22,23,31 with survival generally linked to subacute forms,2,4,35,36 whereas in SR cases, mortality rates vary between 40% and 75%.22,37–39
Study Limitations and Strengths
This is a clinical report of a large number of consecutive cases of CR subjected to a variety of management protocols and gathered prospectively in a single center over 30 years. Indeed, the largest clinical series of consecutive STEMI patients available thus far (n=1457) included 7 SRs and 62 FWRs.2 One potential limitation of our study, however, is the lack of certainty in the diagnosis of FWR in some patients like the 17 with EMD in whom an echocardiogram was not performed and the 48 with tamponade without EMD in whom other causes of hemopericardia could not be entirely ruled out. In the setting of STEMI patients, however, FWR, with or without EMD, continues to be the principal cause of cardiac tamponade.2,4,8,28,35 Another drawback is the fact that an operation could be offered to only a fraction of our CR patients, particularly those with FWR, mostly because of the lack of initial hemodynamic recovery. Nevertheless, and as indicated, our low numbers are concordant with those reported by others.13,16,18–20 In fact, FWR most often presents as sudden death resulting from EMD3,6,19; is often unresponsive to resuscitative maneuvers, including pericardiocentesis4; and in our series frequently occurred in the evening or at night. Moreover, CR patients were elderly—40% were >75 years of age—and often presented extensive STEMI13 conditions that hamper recovery from a cardiac arrest.
Implications
Although CR continues to be a frequent cause of death in elderly STEMI patients even in the reperfusion era,3,5,16–20,23 our findings show that its incidence and rate of death have declined over the last 30 years. Although we recognize that the cause of this improvement is multifactorial, it is likely that it was associated in part with the progressive inclusion of reperfusion therapy, particularly with the increased use of mechanical reperfusion, and β-blockers, ACE inhibitors, and aspirin in our medical armamentarium. These beneficial effects were observed despite the increasing age of our patients, given that advanced age is one of the main risk factors for CR.1,6,7 Thus, our results would further emphasize the need for early implementation of medical measures that may potentially prevent CR such as early myocardial reperfusion and the use of β-blockers and ACE inhibitors11,23 in patients with high risk of CR, namely those with a first STEMI, >60 years of age, without overt heart failure, and without ST segment resolution. They also call for the ready availability of the medical-surgical team at almost any time of the day and highlight the urgency to shorten the time to hospital admission in STEMI patients, for the admission delay in CR patients was >29 hours even in the last 6-year period.
| Acknowledgments |
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This study was supported in part by a grant from Redes Temáticas de Investigación Cooperativa (RECAVA, C03/01) and by a grant from the Fundació Recerca Biomèdica i Docència Hospital Vall d'Hebron (CRHG-02–093–58), Barcelona, Spain.
Disclosures
None.
| References |
|---|
|
|
|---|
2. Lopez-Sendon J, Gonzalez A, Lopez de Sa E, Coma-Canella I, Roldan I, Dominguez F, Maqued I, Jadraque LM. Diagnosis of subacute ventricular wall rupture after acute myocardial infarction: sensitivity and specificity of clinical, hemodynamic and echocardiographic criteria. J Am Coll Cardiol. 1992; 19: 1145–1153.[Abstract]
3. Becker RC, Gore JM, Lambrew C, Weaver WD, Rubison RM, French WJ, Tiffenbrunn AJ, Bowlby LJ, Rogers WJ. A composite view of cardiac rupture in the United States National Registry of Myocardial Infarction. J Am Coll Cardiol. 1996; 27: 1321–1326.[Abstract]
4. Figueras J, Cortadellas J, Evangelista A, Soler-Soler J. Medical management of selected patients with left ventricular free wall rupture during acute myocardial infarction. J Am Coll Cardiol. 1997; 29: 512–518.[Abstract]
5. Becker RC, Hochman JS, Cannon CP, Spencer FA, Ball SP, Rizzo MJ, Antman EM. Fatal cardiac rupture among patients treated with thrombolytic agents and adjunctive thrombin antagonists: observations from the Thrombolysis and Thrombin Inhibition in Myocardial Infarction study. J Am Coll Cardiol. 1999; 33: 479–487.
6. Bates R, Beutler S, Resnekov L, Anagnostopoulos C. Cardiac rupture: challenge in diagnosis and management. Am J Cardiol. 1977; 40: 429–437.[CrossRef][Medline] [Order article via Infotrieve]
7. Figueras J, Curos A, Cortadellas J, Sans M, Soler J. 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.[CrossRef][Medline] [Order article via Infotrieve]
8. Friedman HS, Kuhn LA, Katz AM. Clinical and electrocardiographic features of cardiac rupture following acute myocardial infarction. Am J Med. 1971; 50: 709–720.[CrossRef][Medline] [Order article via Infotrieve]
9. Mann JM, 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 infarctions without rupture. Am J Cardiol. 1988; 62: 847–859.[CrossRef][Medline] [Order article via Infotrieve]
10. Wessler S, Zoll PM, Schlesinger MJ. The pathogenesis of spontaneous cardiac rupture. Circulation. 1952; 6: 334–351.[Medline] [Order article via Infotrieve]
11. ISIS-1 (First International Study of Infarct Survival) Collaborative Group. Mechanisms for the early mortality reduction produced by beta-blockade started early in acute myocardial infarction: ISIS-1. Lancet. 1988; 1: 921–923.[CrossRef][Medline] [Order article via Infotrieve]
12. Herlitz J, Elmfeldt D, Holmberg S, Málek I, Nyberg G, Pennert K, Rydén L, Swedberg K, Vedin A, Waagstein F. Göteborg Metoprolol Trial: mortality and causes of death. Am J Cardiol. 1984; 53: 9D–14D.[CrossRef][Medline] [Order article via Infotrieve]
13. Pohjola-Sintonen S, Muller JE, Stone PH, Willich SN, Antman EM, Davis VG, Parker CB, Braunwald E. Ventricular septal and free wall rupture complicating acute myocardial infarction: experience in the Multicenter Investigation of Limitation of Infarct Size. Am Heart J. 1989; 117: 809–818.[CrossRef][Medline] [Order article via Infotrieve]
14. Chen ZM, Pan HC, Chen YP, Peto R, Collins R, Jiang LX, Xie JX, Liu LS, for the COMMIT (Clopidogrel and Metoprolol in Myocardial Infarction Trial) Collaborative Group. Early intravenous then oral metoprolol in 45,852 patients with acute myocardial infarction: randomised placebo-controlled trial. Lancet. 2005; 366: 1622–1632.[CrossRef][Medline] [Order article via Infotrieve]
15. Honan MB, Harrell FE, Reimer KA, Califf RM, Mark DB, Pryor DB, Hlatky MA. Cardiac rupture, mortality and the timing of thrombolytic therapy: a meta-analysis. J Am Coll Cardiol. 1990; 16: 359–367.[Abstract]
16. Nakamura F, Minamino T, Higashino Y, Ito H, Fujii K, Fujita T, Nagano M, Higaki J, Ogihara T. Cardiac free wall rupture in acute myocardial infarction: ameliorative effect of coronary reperfusion. Clin Cardiol. 1992; 15: 244–250.[Medline] [Order article via Infotrieve]
17. Cortadellas J, Figueras J. Does reperfusion therapy modify the risk of cardiac rupture? Effects of early reperfusion. Rev Esp Cardiol. 1992; 45 (suppl 2): 66–71.[Medline] [Order article via Infotrieve]
18. Solodky A, Behar S, Herz I, Assali A, Porter A, Bayko V, Batller A, Birnbaum Y. Comparison of incidence of cardiac rupture among patients with acute myocardial infarction treated by thrombolysis versus percutaneous transluminal coronary angioplasty. Am J Cardiol. 2001; 87: 1105–1108.[CrossRef][Medline] [Order article via Infotrieve]
19. Yip H, Wu C, Chang H, Wang C, Cheng C, Chua S, Chen M. Cardiac rupture complicating acute myocardial infarction in the direct percutaneous coronary intervention reperfusion era. Chest. 2003; 124: 561–571.
20. Sugiura T, Nagahama Y, Nakamura S, Kuda Y, Yamasaki F, Iwasaka T. Left ventricular free wall rupture after reperfusion therapy for acute myocardial infarction. Am J Cardiol. 2003; 92: 282–284.[CrossRef][Medline] [Order article via Infotrieve]
21. Nakatami D, Sato H, Kinjo K, Mizuno H, Hishida E, Hirayama A, Mishima M, Ito H, Matsumura Y, Hori M. Effect of successful late reperfusion by primary coronary angioplasty on mechanical complications of acute myocardial infarction. Am J Cardiol. 2003; 92: 785–788.[CrossRef][Medline] [Order article via Infotrieve]
22. Yip H, Fang C, Tsai K, Chang H, Yeh K, Fu M, Wu C. The potential impact of primary percutaneous coronary intervention on ventricular septal rupture complicating acute myocardial infarction. Chest. 2004; 125: 1622–1628.[CrossRef][Medline] [Order article via Infotrieve]
23. Pollack H, Miczoch J. Effect of nitrates on the frequency of left ventricular free wall rupture complicating acute myocardial infarction: a case-controlled study. Am Heart J. 1994; 128: 446–471.
24. Effectiveness of intravenous thrombolytic treatment in acute myocardial infarction: Gruppo Italiano per lo Studio della Streptochinasi nell'Infarto Miocardico. (GISSI). Lancet. 1986; 1: 397–403.[CrossRef][Medline] [Order article via Infotrieve]
25. Randomised trial of intravenous streptokinase, oral aspirin, both, or neither among 17,187 cases of suspected acute myocardial infarction: ISIS-2 (Second International Study of Infarct Survival) Collaborative Group. Lancet. 1988; 2: 349–360.[Medline] [Order article via Infotrieve]
26. Bueno H, Martinez-Selles M, Perez-David E, Lopez-Palop R. Effect of thrombolytic therapy on the risk of cardiac rupture and mortality in older patients with first acute myocardial infarction. Eur Heart J. 2005; 26: 1705–1711.
27. Figueras J, Cortadellas J, Calvo F, Soler-Soler J. Relevance of delayed hospital admission on development of cardiac rupture during acute myocardial infarction: study on 225 patients with free wall, septal or papillary muscle rupture. J Am Coll Cardiol. 1998; 32: 135–139.
28. Figueras J, Curós A, Cortadellas J, Soler-Soler J. Reliability of electromechanical dissociation in the diagnosis of left ventricular free wall rupture in patients with acute myocardial infarction. Am Heart J. 1996; 131: 861–864.[CrossRef][Medline] [Order article via Infotrieve]
29. Westaby S, Parry A, Ormerod O, Gooneratne P, Pillai R. Thrombolysis and postinfarction ventricular septal rupture. J Thorac Cardiovasc Surg. 1992; 104: 1506–1509.[Abstract]
30. Bogaert J, Maes A, Van de Werf F, Bosmans H, Herregods MC, Nuyts J, Desmet W, Mortelmans L, Marchal G, Rademakers FE. Functional recovery of subepicardial myocardial tissue in transmural myocardial infarction after successful reperfusion: an important contribution to the improvement of regional and global left ventricular function. Circulation. 1999; 99: 36–43.
31. Shapira I, Isakow A, Burke M, Almog C. Cardiac rupture in patients with acute myocardial infarction. Chest. 1987; 92: 219–223.[CrossRef][Medline] [Order article via Infotrieve]
32. White HD, Norris RM, Brown MA, Takayama M, Maslowski A, Bass NM, Ormiston JA, Whitlock T. Effect of intravenous streptokinase on left ventricular function and early survival after acute myocardial infarction. N Engl J Med. 1987; 317: 850–855.[Abstract]
33. Christensen D, Fond M, Reading J, Castle H. Effect of hypertension on myocardial rupture after acute myocardial infarction. Chest. 1977; 72: 618–622.[CrossRef][Medline] [Order article via Infotrieve]
34. Schuster EH, Bulkley BH. Expansion of transmural myocardial infarction: a pathophysiologic factor in cardiac rupture. Circulation. 1979; 60: 1532–1538.
35. Purcaro A, Constantini C, Ciampani N, Mozzanti M, Silenzi C, Gili A, Belardinelli R, Astolfi D. Diagnostic criteria and management of subacute ventricular free wall rupture complicating acute myocardial infarction. Am J Cardiol. 1997; 80: 397–405.[CrossRef][Medline] [Order article via Infotrieve]
36. Canovas SJ, Lim E, Dalmau MJ, Bueno M, Buendia J, Hornero F, Gil O, Garcia R, Paya R, Perez J, Echanove I, Montero J. Midterm clinical and echocardiographic results with patch glue repair of left ventricular free wall rupture. Circulation. 2003; 108 (suppl II): II-237–II-240.
37. Lemeri R, Smith HC, Giuliani ER, Gersh BJ. Prognosis in rupture of the ventricular septum after acute myocardial infarction and role of early surgical intervention. Am J Cardiol. 1992; 70: 147–151.[Medline] [Order article via Infotrieve]
38. Menon V, Webb JG, Hillis LD, Sleeper LA, Abboud R, Dzavik V, Slater JN, Forman R, Monrad ES, Talley JD, Hochman JS. Outcome and profile of ventricular septal rupture with cardiogenic shock after myocardial infarction: a report from the SHOCK Trial Registry: Should We Emergently Revascularize Occluded Coronaries in Cardiogenic Shock? J Am Coll Cardiol. 2000; 36: 1110–1116.
39. Crenshaw BS, Granger CB, Birnbaum Y, Pieper KS, Morris DC, Kleiman NS, Vahanian A, Califf RM, Topol EJ. Risk factors, angiographic patterns, and outcomes in patients with ventricular septal defect complicating acute myocardial infarction. Circulation. 2000; 101: 27–32.
Related Article:
CLINICAL PERSPECTIVE
The incidence of cardiac rupture and its rate of death were investigated in 6678 consecutive ST-elevation myocardial infarction patients during a 30-year period (1977 to 2006). A total of 425 patients experienced a free wall or septal rupture. After the exclusion of referrals from other centers (n=44), the incidence of definite cardiac rupture declined progressively (6.2% in 1977 to 1982 to 3.2% in 2001 to 2006) in parallel with a progressive use of reperfusion therapy (0% to 75.1%). In addition, among patients with cardiac rupture, there was a progressive fall in mortality rates (94% to 75%) in conjunction with a better control of systolic blood pressure; an increased use of reperfusion therapy (0% to 59%), β-blockers (0% to 45%), angiotensin-converting enzyme inhibitors (0% to 38%), and aspirin (0% to 96%); and a lower use of heparin (99% to 67%). Although cardiac rupture continues to be a frequent cause of death in ST-elevation myocardial infarction patients in the reperfusion era, our findings disclose that its incidence and rate of death have declined over the last 30 years. Although we recognized that the origin of this improvement is multifactorial, it is likely that it was associated in part with the progressive use of reperfusion therapy, particularly mechanical, and β-blockers, angiotensin-converting enzyme inhibitors, and aspirin. Thus, our results further stress the need for early implementation of these therapeutic measures that may potentially prevent mechanical complications, particularly in high-risk patients such as those with a first ST-elevation myocardial infarction, >60 years of age, without overt heart failure, and without ST-segment resolution.
Circulation 2008 118: 2667-2668.
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