Home SVCC Area: English - Español - Português
Diagnosis, Treatment and Prognosis of
Cardiac Rupture in Acute Myocardial Infarction
Jaume Figueras, MD
Unitat Coronaria, Servei de Cardiologia,
Hospital General Vall d'Hebron,
Left ventricular free wall rupture (FWR) is an infrequent complication in patients with acute myocardial infarction (2-4%) but it carries a high mortality due to sudden death secondary to pericardial tamponade (1-8). Its true incidence remains unknown because most studies refer to autopsy series (4,5,8-11). In addition, most series include also patients with FWR transferred from other centers (4,5,7,8). It is estimated, however that it may account for 5-24% all in-hospital deaths related to AMI (4,6,12,13) and this proportion is clearly higher when we refer to patients with a first ST segment elevation myocardial infarction where it can be 20-30%, particularly among those older than 70 years (14). These figures relate to patients who die of cardiac tamponade or who are operated but it is likely that an imprecise number of patients may present self-limited forms of FWR (8,15) while in others FWR presents as a sudden and unwitnessed death that is erroneously categorized as "asystole or arrhythmic death".
CLINICAL AND ELECTROCARDIOGRAPHIC FEATURES
It is known that FWR is a complication of the elderly patient, generally older than 55 years, with an average age 65-70 years (1,3,4,5,9,16,17), and, in contrast to relatively old reports (9,11,18,19), appears to have no gender preference (3,10,20-22), although it may seem to be more frequent among women because of their lower incidence of AMI (4,5) (). Most patients present a first ST segment elevation myocardial infarction (2,4,9,17,18,20), without clinically apparent heart failure (2,17,18,20) and with an infrequent history of angina pectoris (2,17,20,23). The incidence of diabetes is not particularly high in contrast with the increased incidence of arterial hypertension, which is often higher than 50%, (1,5,6,9,18,20). These patients present a rather prolonged episode of anginal pain, often lasting longer than 6 hours (1,2,4,5,10,11,21,24), or of shorter duration of pain but that has been preceded by other episodes longer than 30-60 minutes (21). Rather frequently they have a delayed hospitalization (2,12,18,21) often because of a misdiagnosis of their AMI or because of a silent AMI presenting as acute pericardial tamponade. Additional triggering factors for development of a FWR are the presence of maintained arterial hypertension (=>150 mm Hg) during the first 10-24 hours of the AMI and/or the performance of undue physical efforts, such as persistent coughing, vomiting or agitation (2,10-12,18,21,25) ( ).
FWR generally develops in patients without previous myocardial infarction, nearly 90% (5,17-20), although histologically the incidence of an old necrosis may be somewhat higher (20). This in part accounts for the infrequent presence of overt heart failure associated with FWR ( 17,18,20) as well as for the fact that infarct size, although variable, is generally not large ( 9,18-20) and may be rather localized in the lateral wall (9,18,19,26,27). On admission, the electrocardiogram is consistent with a transmural AMI with a notably elevated ST segment which tends to persist elevated over the ensuing hours or days (2,10,17).However, patients who present with an electrocardiographically "small" lateral AMI, in whom control of arterial hypertension may not appear to be so important (17) should also deserve especial attention. The presence of left ventricular hypertrophy appears to increase the risk for FWR (1,2,20). Localization of infarction tends to be anterior (4,10,17,28), particularly in the necropsy series (3,4,7,28) and among those who die suddenly of an acute FWR (17), hence excluding cases with subacute FWR (10,15,22,29).
Often, FWR is preceded by chest pain similar to that of the AMI (1,2,5,10,11,19,21,30) and is frequently associated with ST segment re-elevation and/or positivization of flat or negative T waves (2,17,31). Reinfarction may be an explanation for some cases, particularly those with a late rupture (1,18,21,32,33), and some studies have confirmed histologically their existence (18,21,32). Some patients already present recurrence of pain prior to hospitalization, during 2-3 days, which may also be an indication of the stuttering course of the infarction in some cases of FWR. On the other hand, rupture of the necrotic tissue in itself (2,34,35) could also be a mechanism of chest pain, as well as the entrance of blood into the pericardial cavity (1,10). In some cases, the chest pain and ECG changes with hypotension may simply indicate extension of AMI without FWR (36,37). When hypotension develops early after the onset of pain, within few minutes, and particularly when followed by electromechanical dissociation (2,38), however, the possibility of a FWR is highest. More definite diagnosis of FWR, however, requires evidence of pericardial tamponade in the echocardiogram. Moreover, late FWR may often be preceded by symptoms of pericarditis, with or without a friction rub (10).
a) According to time of occurrence.
Depending on the time of its development, FWR may be early, when it occurs within the first 48 hours, or late, when it occurs beyond the second day (
). Early FWR represents 40-50% of cases (1,5,17,20,39) but its proportion is likely to be higher when considering also those patients who die suddenly outside of the hospital (16,40). In this initial presentation, factors such as a persistent strain in the infarcted zone due to sustained arterial hypertension (2,9,17-19,41) or to maintenance of ambulatory activities (11,18,21,25), appear to be of importance. Autopsy studies have revealed that in patients with an early FWR there is hardly any thinning of the infarcted area whereas in late FWR the infarcted tissue has already expanded (17,25,39). Moreover, even though late FWR appears to be less affected by arterial hypertension, undue physical exercise (2,18,21) can also contribute to this lethal complication. As indicated, infarct extension may also be an alternative trigger of late FWR by completing the transmurality of the infarction (18,32).
b) According to its clinical presentation.
When considering the clinical and hemodynamic manifestations, FWR may be considered acute or subacute (). There is agreement that the acute form is associated with sudden cardiac arrest caused by electromechanical dissociation secondary to acute pericardial tamponade (3,4,5,10,17). This is accompanied by severe cyanosis of the neck and face and intense jugular ingurgitation. Less clear, however, is the definition of the subacute form, term coined by O'Rourke some years ago in a report of 3 cases (42). This concept initially implied cases with acute tamponade manifested by severe hypotension or electromechanical dissociation that was temporarily reversed by resuscitative maneuvers which allowed a surgical repair (42,43). Provided that there is no apparent mechanistic difference between an acute or a subacute FWR that presents as electromechanical dissociation, we propose that the term subacute FWR be reserved for cases presenting with hypotension of different severity. In contrast, the term acute should be limited to FWR causing a cardiac arrest by electromechanical dissociation. This definition, therefore, implies that even though both presentations may be initially successfully managed medically, the subacute form is clearly less severe and, hence, more likely to recover. In addition, this distinction would help to encompass the different severities among the subacute forms, which may range from severe hypotension and syncope to forms with little or negligible hemodynamic impairment (15,43).
The presence of the subacute form has been increasingly recognized and may account for up to 30% of all in-hospital FWR (1,5,11,12,15,24,30,42-44). However, the existence of a subset of patients with a "mild" subacute FWR has received little attention (43). These patients, who meet the basic FWR clinical profile, that is, age >55 years, first transmural AMI with persistent ST segment elevation without overt heart failure, present with a moderate to severe pericardial effusion but without hemodynamic compromise and that is usually identified by a routine postinfarction echocardiogram. According to our experience, this condition should clearly alert to the possibility of a "silent" subacute FWR for we have witnessed some cases in whom the possibility of a subacute FWR was not contemplated and who subsequently died of a re-rupture with tamponade confirmed in a necropsy study. Hypothetically, however, some of these hemopericardiums, particularly those linked to mild forms of subacute FWR, could be attributed to others causes, such as an hemorrhagic infarction or an hemorrhagic pericarditis (30,42,45,46). Necropsy documentations of this kind of hemopericardiums, however, are very scanty (45,46) and existing reports refer to cases, with or without tamponade, that have been operated and in whom no apparent FWR was observed (30,42,43). Notwithstanding these interpretations (30,44-46), however, we consider that at least in a number of these surgical cases the possibility of an overlooked healed FWR as the responsible cause, should have been contemplated. In fact, there exist some necropsy studies of AMI with hemopericardium in which a FWR that was not apparent macroscopically (4,17,18,44) corresponded, histologically, to a thrombosed myocardial dissection (44,47). Moreover, some of these operated cases apparently unrelated to a FWR, later developed a left ventricular pseudoaneurysm (48,49).
Therefore, it is our contention that some self-limited FWR are rather small and probably become open temporarily only during bursts of arterial hypertension or increased myocardial strain. Some of them may even just represent a stuttering oozing through a narrow fissure (22,44). The subsequent organization of the hematoma would lead to an initial healing by fibrin deposits that would progressively evolve to a definite healing by pericardial adhesions.
Up until recently the only possible treatment for FWR was urgent (often desperate) surgery for cases that could barely survived an acute tamponade (21,30,43,44,50,51). Since the eighties, however, there have been several reports demonstrating that application of a large dacron pad sutured or glued to the epicardial surface could substantially improved the surgical results (43,52-54). Moreover, the favorable experience from our own institution with medical management in a selected group of these patients, also confirmed by some isolated reports (8,51,55,56), with strict blood pressure control mostly with beta blockers and extending the period of hospital rest for several days, has also contribute to broaden the therapeutic spectrum for this complication.
Although FWR is the most frequent cause of hemopericardium during AMI, particularly when the patient's clinical profile conforms that of recognized risk for this complication, definite clinical diagnosis of FWR can only be obtained, with some limitations (44,47-49), through a thoracotomy or, occasionally, through the echocardiographic (15,51) or angiographic (26,29,30,51,56) demonstration of blood leaking to the pericardial cavity. This is the reason why, conceptually, we will consider management of hemopericardium rather than FWR. We will distinguish hemopericardium with or without hemodynamic compromise.
1) HEMOPERICARDIUM WITH HEMODYNAMIC COMPROMISE
a) Initial treatment:
Patients who fulfill the clinical profile of risk for FWR and who experience a sudden non-arrhythmic hypotension unrelated to administration of betablockers or vasodilators associated with sinus bradycardia or nodal rhythm and jugular distension, should be considered as presenting tamponade and will be treated with fluid replacement with colloidal solutions and Dobutamine at 5-10 micg/Kg/min. As soon as possible, an echocardiogram should be performed to assess the presence of a pericardial effusion, with or without signs of right atrial compression. If hemodynamic recovery is readily achieved, a maintenance protocol (see below) will be followed and the cardiac surgical team will be informed of the existence of a probable FWR and the possibility to intervene if hemodynamic stabilization is not maintained. If there is no cardiac surgery available the patient should be transferred to another center with these facilities. If the patient remains hypotensive with signs of peripheral hypoperfusion, a pericardiocentesis should be carried out to withdraw a small quantity of pericardial fluid (10-50 ml), enough to achieve hemodynamic recovery and an adequate urine output. A second pericardiocentesis can be performed if recovery is partial or absent, or if tamponade recurs. If following pericardiocentesis recovery is achieved and sustained the maintenance protocol may be followed, but if recovery is unsuccessful after two pericardiocentesis, an emergent thoracotomy should be undertaken. Surgical treatment applying a teflon (43,52,54,57) or a pericardial (58) patch to the epicardial surface of the ruptured site with cyanoacrylate glue (54), preferably without the use of cardiopulmonary bypass, would be the optimal choice. This may be more difficult if active bleeding is present after opening the pericardium. In this case cardiopulmonary bypass may facilitate patch application. Infartectomy of the rupture zone followed by a teflon-buttressed suture (53), on the other hand, should be limited to cases in whom the use of the patch is unsuccessful, because it may reduce excessively the size of the ventricular cavity.
When tamponade is complicated by a cardiac
arrest due to electromechanical dissociation, cardiac massage may be necessary
to regain adequate pulse besides the previously referred measures. In these
instances, endotracheal intubation and mechanical ventilation may also be mandatory,
and pericardiocentesis will be frequently required before an echocardiogram
can be performed. If there is no hemodynamic recovery with all these measures,
which may also include administration of epinephrine, a desperate surgical treatment
should be attempted because it may be lifesaving in some instances (21,30,43,44,53).
In patients with a slow recovery, particularly in those with large infarcts,
it may be necessary to monitor the right and left ventricular filling pressures
through a Swan-Ganz catheter to assess the hemodynamic response to therapy and
the possible reappearance of tamponade.
b) Maintenance treatment
Once hemodynamic recovery has been attained, a conservative approach may follow. This includes maintenance of blood pressure between 100-120 mm Hg to avoid undue myocardial wall strain and to preserve urine output. In some patients with large AMI, and because of myocardial hypocontractility, use of dobutamine with or without furosemide may still be necessary for several hours o days to maintain adequate urine output in the absence of tamponade. As soon as possible, however, inotropic support should be withdrawn and replaced by beta blocking agents, initially propranolol because its easier titration, as tolerated, to reduce myocardial work as much as possible. To further avoid excessive myocardial tension, patients bed rest should be extended to 4-8 days and undue physical efforts, such as excessive strain during use of a commode or other isometric exercise, repetitive vomiting or coughing, should be avoided. The routine postinfarction discharge exercise test should be postponed for the first two months. Anticoagulant therapy should be withheld but antiaggregant therapy with low dose aspirin may probably be continued.
The patient will be followed in the Coronary Care Unit for the first 7-10 days depending upon the severity of the initial hypotension, the presence of an electromechanical dissociation, the magnitude of pericardial effusion, the overall hemodynamic status and the difficulty to control of blood pressure. An echocardiogram should be repeated every 2-4 days, depending on the hemodynamic course, to assess changes in the pericardial effusion. If the patient presents a second episode of tamponade but arterial hypotension is not severe, a new pericardiocentesis may be performed and if satisfactory results are obtained, maintenance treatment may be resumed. This option could be particularly contemplated in patients with high risk surgery because of old age, morbidity factors such as severe diabetes, peripheral vascular disease, advanced renal or chronic pulmonary disease, previous cerebrovascular accident, large infarction, especially of posterior localization, etc. On the other hand, if these relative contraindications are not present and the recurrence of tamponade is severe or not readily reversed, the surgical treatment is indicated following a new pericardiocentesis, which again should be limited to 10-40 ml, as an attempt to stabilize the hemodynamic condition prior to the operation.
c) Early follow-up treatment
During the first 2 months after hospital discharge, the patient should be allowed to walk but to avoid relatively strenuous exercise, particularly isometric stress, to strictly control his o her blood pressure (=< 120/80 mm Hg) and to receive betablocker therapy as tolerated. An echocardiographic control at one month to assess the course of pericardial effusion is advisable. In our series, of 35 patients with a strongly suspected FWR who were managed without a surgical repair and survived the hospitalization period did not develop a left ventricular pseudoaneurysm during a mean follow-up of 72 months and among the 5 long-term non survivors all had a non cardiac death except for one who presented progressive heart failure.
2) HEMOPERICARDIUM WITHOUT HEMODYNAMIC
According to our experience, their therapeutical approach may follow the maintenance treatment and the early follow-up treatment alluded above. A diagnostic pericardiocentesis may be useful to confirm the existence of an hemopericardium.
Even though ours is the first prospective series of a conservative approach to FWR, that includes some patients previously referred (15), there have been isolated reports of other cases who have also survived without surgery (8,51,55,56). Thus, some patients with a strongly suspected FWR may be successfully managed without operation although, clearly, in a considerable proportion of cases with FWR surgical treatment is still the only alternative.
The first case of FWR that was operated was reported in 1969 by Lillehei (50) and ever since there have been several reports describing successful interventions in few cases, the majority in emergent and rather extreme conditions (6,30,43,52,53). They represented, however, the very tip of the iceberg for most FWR would die without operation or would be mistakenly interpreted as "arrhythmic", "asystolic" or "unwitnessed" sudden deaths. Recognition of the subacute form since 1972 and the progressive awareness that a less dramatic form of presentation may account for up to 30 % of all hospitalized cases of FWR (1,5,11,12,15,24,42,43), however, has notably improved the prospects of survival of this mechanical complication. Moreover, use of teflon patches (52,54,57) has resulted in a much better surgical outcome in part because of its simplicity, often sparing the use of extracorporeal pump, and because the remarkable limitation of myocardial damage by avoiding infarctectomy and/or the practice of deep sutures that are often a potential source of subsequent tears and tamponade. Most importantly, identification of a subset of patients who may be successfully treated without operation has additionally improved the overall survival perspective. In our most recent experience over the last 5 years (1996-2000), of 50 consecutive patients prospectively evaluated that developed a moderate to severe pericardial effusion shortly after an acute ST segment elevation myocardial infarction, 34 presented tamponade and 6 were managed surgically and 28 medically. Twenty one survived (62%), 4 after a surgical repair (teflon patch) and 17 after medical treatment. The remaining 16 did not present tamponade and all survived under medical management. However, we believe that to achieve these or better results is of paramount importance to have a high level of suspicion and to have readily available echocardiographic facilities to explore those patients with a high risk clinical profile for FWR to detect early moderate or even mild pericardial effusion that might herald subsequent tamponade and death due to re-rupture. In addition, early hospital admission and strict control of hypertension mostly by early administration of beta blockers is likely to reduce the incidence of this complication. Overall, use of thrombolytic agents within the first 6 hours after the onset of infarction also tends to reduced the incidence of FWR (33,59) and, according to some preliminary evaluation, a more relevant benefit may be derived from an early primary angioplasty (60).
FWR is strongly suspected when a patient with an high risk profile, namely, age > 55 years with a first myocardial infarction with persistent ST segment elevation, absence of overt heart failure and prolonged pain suddenly presents hypotension or electromechanical dissociation associated with jugular ingurgitation and a moderate to severe pericardial effusion. The term acute FWR should be restricted to patients with cardiac arrest by electromechanical dissociation, and that of subacute should be applied to those presenting systemic hypotension of variable severity. In patients with cardiac arrest has occurred, management includes cardiac massage, ventilatory support, administration of inotropic agents and colloids, and practice of a pericardiocentesis. If recovery is not attained, emergency thoracotomy with repair of the ruptured site is performed with application of a Teflon patch glued to the epicardium, preferably without the use of cardiopulmonary by pass. If recovery is readily achieved, however, a conservative management with blood pressure control and avoidance of physical stress may be implemented with a close surveillance of the case by the surgical team. In patients with hypotension, initial management will contemplate colloid infusion and dobutamine infusion and performance of a pericardiocentesis aimed to withdraw 10-50 ml, enough to restore hemodynamic competence and urine output, and to proceed with conservative management thereafter. If hemodynamic recovery can not be attained, the surgical treatment should be performed.
The conservative strategy implies, in addition, that bed rest should be extended for 5-7 days after diagnosis of FWR has been suspected and that beta blockade therapy be instituted as soon as possible. This approach would be particularly indicated in patients with important co-morbidity factors that greatly increase the surgical risk, such as severe chronic lung disease, renal failure, extensive myocardial infarction, serious peripheral vascular disease, etc... However, this modality of therapy should only be adopted in a center with surgical facilities needs to be confirmed by careful experiences from different institutions.
1. London RE, London SB. Rupture of the heart. A critical analysis of 47 consecutive autopsy cases. Circulation 1965; 31:202-208.
2. Friedman HS, Kuhn LA, Katz AM. Clinical and electrocardiographic features of cardiac rupture following acute myocardial infarction. Am J Med 1971; 50:709-720.
3. Bates R, Beutler S, Resnekov L, Anagnostopoulos C. Cardiac rupture - challenge in diagnosis and management. Am J Cardiol 1977; 40: 429-437.
4. Rasmussen S, Leth A, Kjoller E, Pedersen A. Cardiac rupture in acute myocardial infarction. A review of 72 consecutive cases. Acta Med Scand 1979; 205:11-16.
5. Dellborg M, Held P, Swedberg K, Vedin A. Rupture of the myocardium. Occurrence and risk factors. Br Heart J 1985; 54:11-16
6. Shapira I, Isakow A, Burke M, Almog C. Cardiac rupture in patients with acute myocardial infarction. Chest 1987; 92:219-223.
7. 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.
8. Blinc A, Noc M, Pohar B, Cernic N, Horvat M. Subacute rupture of the left ventricular free wall after acute myocardial infarction. Three cases of long-term survival without emergency surgery. Chest 1996;109:565-567.
9. Naeim F, De la Maza LM, Robbins SL. Cardiac rupture during myocardial infarction. A review of 44 cases. Circulation 1972; 45:1231-1239.
10. Oliva PO, Hammill SC, Edwards WE. Cardiac rupture, a clinically predictable complication of acute myocardial infarction: Report of 70 cases with clinicopathologic correlations. J Am Coll Cardiol 1993; 22:720-726
11. Feneley MP, Chang VP, O'Rourke MF. Myocardial rupture after acute myocardial infarction. Ten year review. Br Heart J 1983; 49.550-556.
12. Lewis AJ, Burchell HB, Titus JL. Clinical and pathologic features of post-infarction cardiac rupture. Am J Cardiol 1969;23:43-53.
13. Reddy SG, Roberts 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.
14. Maggioni AP, Maseri A, Fresco C, Franzosi MG, Mauri F, Santoro E, Tognoni G. GISSIII. Age-related increase in mortality among patients with a first myocardial infarctions treated with thrombolysis. N Engl J Med 1993;329:1442-1448.
15. Figueras J, Cortadellas J, Evangelista A, Soler-Soler J. Medical management of selected patients of left venrticular free wall rupture during acute myocardial infarction. J Am Coll Cardiol 1997;29:512-518.
16. Batts K, Ackermann DM, Edwards WD. Postinfarction rupture of the left ventricular free wall: Clinicopathologic correlates in 100 consecutive autopsy case. Hum Pathol 1990; 21:530-535.
17. Figueras J, Curos A, Cortadellas J, Sans M, Soler-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.
18. Wessler S, Zoll PM, Schlesinger MJ. The pathogenesis of spontaneous cardiac rupture. Circulation 1952; 6:334-351.
19. Edmonson HA, Hoxie HJ. Hypertension and cardiac rupture. A clinical and pathologic study of seventy-two cases in thirteen of which rupture of the interventricular septum occurred. Am Heart J 1942;24:719-733
20. 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.
21. Figueras J, Cortadellas J, Calvo F, Soler-Soler J. Relevance of delayed hospital admission on development of cardiac rupture during acute myocardial infarction. Study in 225 patients with free wall, septal or papillary muscle rupture. J Am Coll Cardiol 1998;32:135-139.
22. 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.
23. Nakano M, Konishi T, Takezawa H. Potential prevention of myocardial rupture resulting from acute myocardial infarction. Clin Cardiol 1985; 8: 199-204.
24. Jetter WW, White PD. Rupture of the heart in patients in mental institution. Ann Int Med 1944;21:783-794.
25. Lautsch FV, Lanks KW. Pathogenesis of cardiac rupture. Arch Pathol 1967; 84:264-271.
26. Schuster EH, Bulkley BH. Expansion of transmural myocardial infarction: a pathophysiologic factor in cardiac rupture. Circulation 1979; 60:1532-1538.
27. Saffitz JE, Fredrickson RC, Roberts WC. Relation of size of transmural acute myocardial infarct to mode of death, interval between infarction and death and frequency of coronary arterial thrombi. Am J Cardiol 1986; 57:1249-1254.
28. Perdigao C, Andrade A, Ribeiro C. Rupture cardiaque dans l'infarctus aigu du myocarde. Differents types clinico-anatomiques de 42 cas récents observés en 30 mois. Arch Mal Coeur 1987;80:336-344.
29. Grollier G, Seanu P, Babatasi G, Agostini D, Lécluse E, Saloux E, Valette B, Maïza D, Khayat A, Potier JC. Rupture subaiguës de la paroi libre du coeur. Aspects cliniques, échocardiographiques et anatomiques à propos de 10 cas. Arch Mal Coeur 1993; 86: 1729-1738.
30. Windsor HM, Chang VP, Shanahan MX. Postinfarction cardiac rupture. J Thorac Cardiovasc Surg 1982; 84:755-761.
31. Mir MA. Prognostic value of an electrocardiographic sign in acute myocardial infarction. Am Heart J 1972; 84:182-188.
32. Silvestri F, Stanta G, Constantinides F, Peruzzo P. La rottura di cuore come complicanza dell'infarto acuto del miocardio. Considerazioni anatomoistopatologiche sulla base di 154 osservazionei autopiche. Pathologica 1980; 72: 491-500.
33. 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.
34. Datta BN, Bowes VF, Silver MD. Incomplete rupture of the heart with diverticulum formation. Pathology 1975;7:179-185.
35. Freeman WJ. The histologic patterns of ruptured myocardial infarcts. Arch Pathol 1958;65:646-653.
36. Figueras J, Cinca J, Valle V, Rius J. Prognostic implications of early spontaneous angina after acute transmural myocardial infarction. Int J Cardiol 1983;4:261-272.
37. Bosch X, Theroux P, Waters DD,Pelletier GB, Roy D. Early postinfarction ischemia: Clinical, angiographic and prognostic significance. Circulation 1987;75:988-995.
38. 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.
39. Van Tassel RA, Edwards JE. Rupture of heart complicating myocardial infarction. Analysis of 40 cases including nine examples of left ventricular false aneurysm. Chest 1972;61:104-116.
40. Shirani J, Berezowski K, Roberts WC. Out-of-hospital sudden death from left ventricular free wall rupture during acute myocardial infarction as the first and only manifestation of atherosclerotic coronary artery disease. Am J Cardiol 1994; 73:88-92.
41. Christensen D, Fond M, Reading J, Castle H. Effect of hypertension on myocardial rupture after acute myocardial infarction. Chest 1977; 72: 618-622.
42. O'Rourke MF. Subacute heart rupture following myocardial infarction: clinical features of a correctable condition. Lancet 1973;2:124-126.
43. Lopez-Sendon J, Gonzalez A, Lopez de Sa E, et al.. 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.
44. Balakumaran K, Verbaan CJ, Essed CE, et al.. Ventricular free wall rupture: sudden, subacute, slow, sealed and stabilized varieties. Eur Heart J 1984; 5: 282-288.
45. Lange HF, Aarseth S. The influence of anticoagulant therapy on the occurrence of cardiac rupture and hemopericardium following heart infarction.II. A controlled study of a selected treated group based on 1044 autopsies. Am Heart J 1958;56:257-263.
46. Barbour HB, Jhirst AE, Johns VJ. Nontraumatic hemopericardium. An analysis of 105 cases. Am J Cardiol 1961;8:102-108.
47. Torp-Pedersen C, Hansen FS, Pedersen A. Relation of left ventricular free wall rupture in acute myocardial infarction to forced immobilization. Am J Cardiol 1988;61:910-912.
48. Shabbo FP, Dymond DS, Rees GM, Hill IM. Surgical treatment of false aneurysm of the left ventricle after myocardial infarction. Thorax 1983; 38:25-30.
49. Kolibash AJ, Magorien RD, Bush CA, Vasko JS. Long-term survival following cardiac rupture with subsequent development of left ventricular pseudoaneurysm. Cathet Cardiovasc Diagn 1982; 8:409-417
50. Lillehei CW, Lande AJ, Rassman WR, Tanaka S, Bloch JH. Surgical management of myocardial infarction. Some promising concepts utilizing revascularization, mechanical circulatory asistance, operative treatment of severe complications, and cardiac replacement. Circulation 1969;39:IV:315- 33.
51. Raitt MH, Kraft CD, Gardner CJ, Pearlman AS, Otto CM. Subacute ventricular free wall rupture complicating myocardial infarction. Am Heart J 1993;126:946-955.
52. Cobbs BW, Hatcher CR, Robinson PH. Cardiac rupture: Two long-term survivals. JAMA 1973;223:532-535.
53. Padró JM, Mesa JM, Silvestre J et al.. Subacute cardiac rupture: repair with a sutureless technique. Ann Thorac Surg 1993;55:20-24.
54. Griffith GC, Hegde B, Oblath RW. Factors in myocardial rupture. An analysis of two hundred and four cases at Los Angeles County Hospital between 1924 and 1959. Am J Cardiol 1961;8;792-798.
55. Vasilomanolakis EC, Famularo MA, Kozlowski J, Schrager B, Licht JR, Ellestad MH. Catheter Cardiovasc Diagn 1983;9:291-296.
56. John LCH, O'Riordan JB. Peri-infarct pursestring for repair of subacute cardiac rupture. Ann Thorac Surh 1996;61:728-730.
57. Almdahl SM, Hotvedt R, Larsen U, Sorlie DG. Postinfarction rupture of left ventricular free wall repaired with a glued-on pericardial patch. Case report. Scand J Thorac Cardiovasc Surg 1993;27:105-107.
58. Honan MB, Harrell FE, Reimer KA, et al. Cardiac rupture, mortality and the timing of thrombolytic therapy. A meta-analysis. J Am Coll Cardiol 1990;16:359-367.
59. Garcia E, Elízaga J, Perez-Castellano N, Serrano JA, Soriano J, Abeytua M, Botas J, Rubio R, Lopez de Sá, López-Sendón JL, Delcan JL. Primary angioplasty versus systemic thrombolysis in anterior myocardial infarction. J Am Coll Cardiol 1999;33:605-611.
Your questions, contributions and commentaries
will be answered
by the lecturer or experts on the subject in the Ischemic Heart Disease list.
Please fill in the form (in Spanish, Portuguese or English) and press the "Send" button.
2nd Virtual Congress of Cardiology
Dr. Florencio Garófalo
Dr. Raúl Bretal
Dr. Armando Pacher
Technical Committee - CETIFAC
Copyright© 1999-2001 Argentine Federation of Cardiology
All rights reserved
This company contributed to the Congress: