A Muto

FWH Sutherland

Halil Basel

Hasan Ekim

J Herlitz

J Iemura

JM Padro

KD Hutchins

L Nunez

M Kudo

MH McMullan

MJ Reardon

Mustafa Tuncer

O Amir

R Pretre

RC Becker

V Mantovani

WM Park

English

PubMed

Springer - Publisher Connector

BioMed CentralCases Journal
ssOpen AcceCase Report
Repair of ventricle free wall rupture after acute myocardial 
infarction: a case report
Hasan Ekim*1, Mustafa Tuncer2 and Halil Basel1
Address: 1Yüzüncü Yil University, Department of Cardiovascular Surgery, Van, Turkey and 2Yüzüncü Yil University, Department of Cardiology, 
Van, Turkey
Email: Hasan Ekim* - drhasanekim@yahoo.com; Mustafa Tuncer - drmtuncer66@yahoo.com; Halil Basel - hbasel@mynet.com
* Corresponding author    
Abstract
Introduction: Acute myocardial infarction (AMI) may culminate in sudden death by ventricular
fibrillation, cardiogenic shock, and cardiac rupture. We present a case of postinfarction rupture
treated by direct closure and coronary artery bypass grafting after thrombolytic therapy.
Case report: A 67-year-old woman with cardiac risk factors of hypertension, diabetes mellitus,
and being post-menopausal was admitted complaining of chest pain and sweating. Thrombolytic
therapy with streptokinase was started due to acute myocardial infarction. But, reperfusion criteria
were not achieved. Echocardiography revealed a moderate pericardial effusion with mild right
chamber collapse and pericardial thrombus. Cardiac catheterization revealed totally occluded left
anterior descending (LAD) and circumflex coronary arteries. She was taken to the operating-room
immediately. The pericardium was opened and a large amount of blood with thrombus was
removed. Her hemodynamic indices improved immediately. There was active bleeding from
multiple sites with a 4 mm rupture. Cardiopulmonary bypass was established. Direct closure of
rupture was carried out. Reversed autogenous saphenous vein bypass grafts were placed to the
LAD and second obtuse margin coronary arteries. Postoperative recovery was uneventful and she
was discharged from hospital in good condition. She remained asymptomatic during first year
following the surgery.
Conclusion: This case demonstrates that left ventricular free wall rupture is not always fatal and
that early diagnosis and emergency surgical therapy may be successful. The combination of surgical
repair with revascularization should be considered, because 80% of patients who experience
LVFWR have multivessel coronary artery disease.
Introduction
Acute myocardial infarction (AMI) may culminate in sud-
den death by ventricular fibrillation, cardiogenic shock,
and cardiac rupture. Cardiac rupture may involve the free
wall of ventricle, the interventricular septum, or papillary
muscle [1]. Ventricular free wall rupture is an important
but underrecognized cause of death after myocardial inf-
arction. The real incidence is unknown [2]. Although sur-
gical management is essential, the most appropriate
surgical management remains controversial, because the
experience of any surgeon or surgical group seems to be
quite small [3]. However, survival without operative inter-
vention has been described but appears to be an uncom-
mon event [4]. We present a case of postinfarction rupture
Published: 27 November 2009
Cases Journal 2009, 2:9099 doi:10.1186/1757-1626-2-9099
Received: 19 September 2009
Accepted: 27 November 2009
This article is available from: http://www.casesjournal.com/content/2/1/9099
© 2009 Ekim et al; licensee BioMed Central Ltd. 
This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), 
which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.Page 1 of 4
(page number not for citation purposes)
Cases Journal 2009, 2:9099 http://www.casesjournal.com/content/2/1/9099treated by direct closure and coronary artery bypass graft-
ing after thrombolytic therapy.
Case report
A 67-year-old woman with cardiac risk factors of hyper-
tension, diabetes mellitus, and being post-menopausal
was admitted complaining of chest pain and sweating.
Her blood pressure was 80/60 mmHg, her heart rate was
120 beats/min. Auscultation revealed no murmurs. There
was ST elevation in leads D1, AVL, D2, D3, aVF, V6 and ST
depression with dominant R waves in leads V1 and V2 in
12-lead electrocardiography. Oral aspirin, intravenous
nitroglycerin and heparin were given. The chest radio-
graph was unremarkable. With the diagnosis of acute
inferoposterolateral myocardial infarction, thrombolytic
therapy was started. The choice of thrombolytic was strep-
tokinase since tPA was not available and primary PCI was
not possible within an acceptable time period. Reper-
fusion criteria were not achieved within four hours of
thrombolytic therapy. Blood pressure was lowered gradu-
ally and there was dyspnea and sweating with blurred con-
scious. Echocardiography revealed a moderate pericardial
effusion with mild right chamber collapse and pericardial
thrombus. There was a turbulant flow between poster-
oapical left ventricular free wall and pericardial sack on
color Doppler. Cardiac catheterization revealed totally
occluded left anterior descending (LAD) and circumflex
coronary arteries and normal right coronary artery (Figure
1, 2).
She was taken to the operating-room immediately.
Median sternotomy was performed and the pericardium
was opened. A large amount of blood with thrombus was
removed. Her hemodynamic indices improved immedi-
ately. When the heart was lifted carefully, the area of
necrosis was inspected (approximately 3 cm in diameter)
in the distribution of the obtuse marginal coronary artery
and was found to be extremely friable. There was active
bleeding from multiple sites with a 4 mm rupture. Cardi-
opulmonary bypass was established by cannulation of the
ascending aorta and dual stage venous cannulation
through the right atrium. Moderate hypothermia was used
and a left ventricular vent was inserted through the right
superior pulmonary vein. Myocardial protection was
achieved by means of isothermic blood cardioplegia
delivered in an antegrade manner through the ascending
aorta. Direct closure of rupture was carried out by two
mattress sutures with Teflon felt. Reversed autogenous
saphenous vein bypass grafts were placed to the LAD and
second obtuse margin coronary arteries. The patient was
weaned from cardiopulmonary bypass with dobutamine
support. The cardiopulmonary bypass time and aortic
cross-clamping time were 104 and 88 minutes, respec-
tively. The chest was closed and drained in the usual man-
ner.
Coronary angiography showing total occlusion of the left anterior descending and circumflex c ronary arteriesFigure 1
Coronary angiography showing total occlusion of the 
left anterior descending and circumflex coronary 
arteries.
Coronary angiography showing normal right coronary arteryFigure 2
Coronary angiography showing normal right coro-
nary artery.Page 2 of 4
(page number not for citation purposes)
Cases Journal 2009, 2:9099 http://www.casesjournal.com/content/2/1/9099The patient was transferred to the open heart recovery
room in stable condition with inotropic support. Postop-
eratively, she was electively sedated and ventilated for 8
hours, during which time inotropic support was with-
drawn. The patient recovered uneventfully and was dis-
charged on the 16th postoperative day. At the 1-year
follow-up visit, she was free from angina and in New York
Heart Association Functional class l.
Discussion
A cardiac rupture in patients with AMI is the second most
common cause of hospital death, after pump failure. The
incidence of ventricular free wall rupture after myocardial
infarction has been accurately and consistently defined. It
complicates approximately 4% of myocardial infarctions
and accounts for 12% to 21% of deaths after infarction
[5]. Four patterns of ruptures on a left ventricle have been
described [5]. Type 1 exhibits an almost direct trajectory
with little dissection or bloody infiltration of the myocar-
dium. Type ll has a multicanalicular trajectory with exten-
sive myocardial dissection and bloody infiltration. In type
lll, the orifice of rupture is protected either by a thrombus
or by a pericardial symphysis. Type lV is an incomplete
rupture, indicating that the trajectory does not extend
completely through the muscle. The terms pseudoaneu-
rysm, simple or complex, and blow-out or ooze ruptures
used in the literature describe the same pathologic condi-
tion and can easily be fitted into this classification.
In practice, it is usual that an operation is conducted
within a few days after onset of AMI and low cardiac out-
put greatly increases the surgical risk when the operation
under the cardiac arrest is conducted. Moreover, repair of
perforation by suture techniques raises the difficulty of
sewing fragile myocardium [6]. Fortunately, as our case
was active bleeding from multiple sites with a 4 mm rent,
suture repair was feasible.
Sudden hypotension and bradycardia, often with cyanosis
and loss of consciousness, is a frequent indicator of
impending rupture. It is provoked by the entry of blood in
the pericardial cavity and is often transient because the
resultant small hemopericardium acts as a tampon to pre-
vent further egress of blood [7]. The onset of rupture may
be heralded by chest pain [8], which may be resistant to
opiates, or by the classic features of cardiac tamponade,
namely, shock with hypotension, pulsus paradoxus, ele-
vated venous pressure, quiet heart sounds, sinus bradycar-
dia, or frank electromechanical dissociation [5].
Intra-aortic balloon pump (IABP) support is a widely
accepted treatment for ventricular septal rupture compli-
cating AMI. However, its role in patients with left ventricu-
lar free wall rupture (LVFWR) is less clear. It is used
infrequently in patients with LVFWR [9]. Older age,
female sex, hypertension, and a 1st lateral or anterior wall
AMI constitute traditional risk factors for LVFWR [9]. The
rupture occurs typically between 1 and 7 days after the inf-
arction. It might present suddenly with profound cardio-
genic shock and cardiac tamponade [2]. There may be a
predilection to first infarctions and even single vessel dis-
ease because of the paucity of collateral vessels [10].
LVFWR can be treated more conservatively by direct mat-
tress suture buttressed with Teflon felt with or without car-
diopulmonary bypass. In both techniques, the suture line
must be along the nonischemic area and transmural
stitches are required. Furthermore, if the sutures are
placed in the necrotic myocardium, tearing could occur,
particularly in the posterior wall of the left ventricle [11].
Nunez et al. [12] reported the application of a patch cov-
ering the area of infarction and anchored to normal myo-
cardium with continuous running sutures. Because the
anchoring sutures are placed only in the epicardium and
shallow surface of the myocardium, myocardial damage
with this technique is minimal. More recently, sutureless
techniques using fibrin glue and collagen hemostats with
the patch have been developed with some degree of suc-
cess [13]. However, there is a caution associated with the
sutureless technique. If reoperation for coronary artery
bypass grafting needs to be performed, identification and
exposure of the coronary artery might be difficult due to
the widely and deeply piled collagen hemostats [11]. The
other possible problems associated with a sutureless patch
technique include the risk of recurrent rupture, pseudoan-
eurysm formation, and mitral valve regurgitation due to
ischemic cardiomyopathy [3].
Anterior and inferoapical ruptures are easily accessed
through a sternotomy, while lateral and inferobasal rup-
tures require mobilization of the heart and, often, unload-
ing of the heart. The ease with which bleeding can be
controlled on a beating and working heart with epicardial
patching makes us wonder if the principle of avoiding car-
diopulmonary bypass should not be extended to lateral
and posterior rupture by directly approaching them
through a left thoracotomy, especially in patients with
reduced ventricular function [7]. Principles of repair of
LVFWR are to stop the bleeding, anchor the repair on
healthy tissue, minimize distortion of heart geometry
[14], and revascularization if necessary. Association of
VFWR with thrombolytic treatment has been proposed,
since plasmin, activated by thrombolytic drugs, has the
known effect of breaking down collagen [2]. However, the
influence of thrombolysis on the incidence of rupture
remains controversial, but it appears rupture occurs earlier
in the course when compared with the prethrombolytic
era [4].Page 3 of 4
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Becker et al. [15] suggest that beginning late treatment
with rt-PA is not associated with an increased risk for rup-
ture. However, these data may not hold true for other
thrombolytic agents that are not as specific as rt-PA [4].
There was a beneficial effect with a reduction in cardiac
rupture rate in patients treated with streptokinase within
5 hours of symptom onset. Afterward, a significantly
increased rupture rate developed in those patients who
underwent delayed treatment [14]. ACC/AHA guidelines
(2004) and ESC guidelines (2008) related to myocardial
infarction recommend thrombolytic therapy (SKZ or tPA)
in patients with true posterior myocardial infarction.
Therefore, SKZ was used in our case.
Conclusion
This case demonstrates that left ventricular free wall rup-
ture is not always fatal and that early diagnosis and emer-
gency surgical therapy may be successful. The
combination of surgical repair with revascularization
should be considered, because 80% of patients who expe-
rience LVFWR have multivessel coronary artery disease
[4].
Consent
Informed written consent was obtained for publication of
the manuscript and figures.
Competing interests
The authors declare that they have no competing interests.
Authors' contributions
The authors performed a literature search, and wrote and
approved the final manuscript.
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Repair of ventricle free wall rupture after acute myocardial infarction: a case report

Crossref

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A: Prediction of rupture in acute myocardial infarction. Clin Cardiol

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Aris A: Subacute cardiac rupture: repair with sutureless technique. Ann Thorac Surg

Gregoric ID, Smart FW: Left ventricular free wall rupture in acute myocardial infarction. Tex Heart Inst J

H: A surgical case of ventricular septal perforation after repairing left ventricular free wall rupture. Ann Thorac Cardiovasc Surg

JC: Ischemic left ventricular free wall rupture: prediction, diagnosis, and treatment. Ann Thorac Surg

JL: Diagnosis and treatment of subacute free wall ventricular rupture after infarction. Ann Thorac Surg

Kaneda T: Surgical strategy for left ventricular free wall rupture after acute myocardial infarction. Ann Thorac Surg

Natarajan GA: Cardiac rupture in acute myocardial infarction.

SH: Surgical experience with left ventricular free wall rupture. Ann Thorac Surg

SK: Postinfarction ventricular free wall rupture: strategies for diagnosis and treatment. Ann Thorac Surg

Sutureless repair with TachoComb sheets for oozing type postinfarction cardiac rupture. Ann Thorac Surg

Topol EJ: Cardiac rupture associated with thrombolytic therapy: impact of time to therapy in the late assessment of thrombolytic efficacy (LATE) study.

Turina MI: Experience with postinfarction left ventricular free wall rupture. Ann Thorac Surg

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Repair of ventricle free wall rupture after acute myocardial infarction: a case report

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