Cardiovasc Pathol Vol. 1, No.

3 199
July-September 1992:19%203

Pathogenesis of a Double Rupture (Septal and Free Wall Rupture)

After Acute Myocardial Infarction
Richard S. Larson, MD, PhD, Ethan J. Haskel, MD, and Julio E. Perez, MD

From the Departments of Pathobgy and Medicine, Washington University School of Medicine, St. Louis, Missouri

Rupture of both the ventricular septum and free wall (double rupture) is an unusual and,
typically fatal, post-myocardial infarction complication. We report here the sequence of
events leading to the formation of a double rupture.

Rupture of either the ventricular septum or free wall
of the heart occurs in 1% to 10% of patients after myo-
cardial infarction (MI) and carries a high mortality (l-
3). Typically, rupture develops within 14 days after the
onset of infarction, but approximately 25% of cases of
cardiac rupture occur within the first 24 hours (3,4).
Cardiac rupture occurs more frequently in patients
without previous angina and typically follows first myo-
cardial infarctions (1). Ruptures also occur most fre-
quently in patients with inferior MIS with ST segment
elevation or Q wave infarction (24).
Rupture of both the ventricular septum and free
wall (double rupture) has been reported in a small
number of patients following an acute MI (45). How-
ever, the sequence of events leading to formation of a
double rupture has not been elucidated. The present
case documents the clinical events in the evolution of
a double rupture.
Case Summary
A 65-year-old man was admitted to Barnes Hospital
after suffering an acute myocardial infarction. He had
complained of back pain during the preceding month.
Cardiac risk factors included cigarette smoking (50
pack-years) and hypercholesterolemia (240-250 mg/dl).
Two weeks prior to admission he developed acute
chest pain radiating to both arms, which lasted for 45
Manuscript received July 1, 1991; accepted February 3, 1992.
Address for reprints: Richard S. Larson, Department of Pathol-
ogy, Box 8118, Washington University, 660 S. Euclid Avenue, St.
Louis, MO 63110.
minutes and was accompanied by fever. A week prior
to admission he experienced a sudden “snap” in his
midback followed by right shoulder pain radiating to
both arms. He became acutely dyspneic.
The pain subsided but dyspnea persisted, and the
patient was admitted to an outside hospital two days
prior to admission at Barnes Hospital. At the outside
hospital the blood pressure was 90/60 mmHg, and a
systolic murmur was noted. Arterial blood pH was Pcot
was 25 mmHg, and PO, was 94 mmHg on 2 liters forced
inspiratory 0,. Venous blood creatine kinase and lac-
tate dehydrogenase concentrations were normal. Elec-
trocardiogram (EKG) demonstrated an acute inferior
MI. Swan-Ganz catheterization revealed a pulmonary
capillary wedge pressure of 30 mmHg. Echocardio-
graphy demonstrated satisfactory left ventricular func-
tion as well as mild thickening of the aortic and mitral
valve leaflets. The ventricular septum was not well
visualized. Nitrates, furosemide, and enteric-coated
aspirin were administered with some symptomatic
improvement.
The patient was transferred to Barnes Hospital,
where he was noted to be tachypneic. The blood pres-
sure was 94/30 mm/Hg, and the pulse was 90/min and
regular. A systolic murmur was best heard at the left
sternal border, and an S4 and S3 gallop were noted.
The EKG was unchanged. Swan-Ganz catheterization
revealed central venous pressure of 15 mmHg, pul-
monary wedge pressure of 25 mmHg, and pulmonary
artery pressure of 58/35 mmHg. Two-dimensional and
Doppler echocardiography demonstrated a ventricular
septal defect with left-to-right shunt flow (Fig. 1). Mi-

01992 by Elsevier Science Publishing Co., Inc. 1054-8807/92/$5,00

200 LARSON ET AL. Cardiovaac Pathol Vol. I, No. 3
DOUBLE RUPTURE AFTER ACUTE MI July-September 1992: 199-203

Figure 1. Mid-diastolic still frame, A (above), and schematic

representation, B (below), of the patient’s left ventricle ob-
tained from the parasternal short axis view at the level be-
tween the papillary muscles and the mitral valve. A definitive
discontinuity of the posterior septal-inferior segment is dem-
onstrated (A: arrowhead; B: asterisk), consistent with ven-
tricular septal rupture. (LV: left ventricle; RV: right
ventricle.) The septal myocardium corresponding to the
darkened area on the schematic was mobile. Part of this flail
pennisula of tissue is indicated in Figure 2A (asterisk).

the septum and posterior wall were markedly thinned

in the area of rupture (0.3 cm and 0.6 cm, respectively).
The mitral and aortic leaflets were mildly thickened
and calcified, but not to a degree that would have
caused significant valvular dysfunction. Microscopic
tral and aortic valve function was essentially normal evaluation of the heart demonstrated an infarct involv-
and the pericardial space was free of fluid. Within ing the entire thickness of the myocardium. Myocytes
minutes of this study, the patient suddenly developed located at the peripheral area of the infarction had
apnea while eating dinner and was immediately found been completely replaced. Eosinophilic necrotic myo-
to be in electromechanical dissociation. Cardiopulmo- cytes were still present within the central area of the
nary resuscitation was unsuccessful. infarction. A significant fibroblastic cell proliferation
At autopsy, 550 ml of blood was found in the peri- and monocytic cell infiltrate was appreciated. Masson
cardial sac. The heart had a transmural infarct of the trichrome staining demonstrated the presence of a
posterior free wall of the left ventricle and the poste- modest amount of collagen formation. A reticulin stain
rior third of the ventricular septum. Severe atheroscle- failed to demonstrate a fibrous network in the granu-
rosis (90% luminal area narrowing) was observed in lation tissue. These findings are consistent with a his-
the right coronary artery 1.5 cm from its origin. tological infarct age of 14 to 21 days, which is in close
whereas the left coronary system was unremarkable. agreement with the clinical impression of approxi-
Luminal thrombus was not identified. A 1.1 X 0.9 cm mately two weeks. Several vascular structures were
communicating orifice was noted in the ventricular sep- identified within the epicardial adipose tissue and myo-
tum (Fig. 2A), and a 2.4 cm transverse perforation in cardium. Significant small vessel disease was not
the posterior wall of the heart was seen (Fig. 2B). Both identified.
Cardiovasc Pathol Vol. I, NO. 3
July-September 1992:199-203
Figure 2. Gross transverse sections of
the cardiac ventricles. The left ventricle
(LV) with the site of the septal wall rup-
ture, A (above), and posterior wall rup-
ture, B (below), are indicated (arrows).
The white, firm areas located along the
septum and posterior wall demarcate the
extent of the myocardial infarction and
the relatively central locations of the
ruptures.
Discussion
This patient’s post-MI course was complicated by the
development of a double rupture. The laboratory find-
ings, clinical history, and microscopic findings indicate
that the MI occurred 14 to 21 days prior to death. Rup-
ture of the septum probably occurred one week prior
to admission and caused the acute onset of dyspnea
and back pain. The resultant left-to-right shunting led
to continued dyspnea and the systolic murmur. We es-
timate that approximately one week after rupture of
the ventricular septum, the posterior free wall of the
left ventricle ruptured acutely, causing tamponade and
sudden death.
After an infarction, a reparative inflammatory proc-
ess occurs that leads to the formation of fibrous scar
tissue. Initially polymorphonuclear cells, followed by
mononuclear cells, infiltrate the periphery and perivas-
cular areas of the infarction. Prior to the formation of
scar tissue, these cells proteolytically digest and phag-
ocytose the infarcted myocytes and associated extra-
cellular matrix before advancing to the more central
areas of infarction. Because the areas of most active
LARSON ET AL. 201
DOUBLE RUPTURE AFI’ER ACUTE MI
degradation and proteolysis would not have an intact
extracellular matrix or cellular elements, these areas
would be expected to have lower tensile strength than
that of fibrous tissue or necrotic myocytes. The free
wall rupture occurred in a thinned area of the posterior
wall and septum in which viable myocytes were absent
and fibrotic tissue had not yet formed (Fig. 3). It is
interesting that the free wall rupture in this case-as
well as in several cases of single free wall rupture (6)-
occurred at the border of an area of more well formed
fibrosis and an area of continuing and ongoing repair,
the area expected to have the lowest tensile strength.
Double rupture after myocardial infarct is rare.
However, two anatomical types of double ruptures,
true and junctional, have been described (5). These
types are distinguished by the location of the ventric-
ular rupture relative to the septal rupture. In a true
double rupture, two distinct rupture sites are anatom-
ically apparent. In a junctional rupture, a single rupture
site in the left ventricle communicates with both the
right ventricle and pericardial space. Anatomically, it
has been impossible to distinguish whether a junctional
rupture is a double rupture or a single rupture that
202 LARSON ET AL. Cardiovasc Pathol Vol. I, NO. 3
DOUBLE RUPTURE AFTER ACUTE MI July-September 1992: 199-203

ruptured through the posterior septum and free wall
concurrently. The present case represents a junctional
type of double rupture and clearly demonstrates that
the rupture of the septal wall occurred prior to ven-
tricular wall rupture.
An alternative classification system based on histo-
logical and anatomical findings recognizes three types
of cardiac rupture: blowout, hemorrhagic-dissecting,
and thinning-with-rupture. A blowout rupture is an
abrupt tear occurring within the area of infarction
without an appreciable decrease in wall thickness. A
hemorrhagic-dissecting rupture is characterized by
multiple, hemorrhagic endocardial ulcers from which
fissures extend into the myocardium. The free wall rup-
ture in this case is an example of the third type of rup-
ture, thinning-with-rupture. This type of rupture is
expected to occur one to three weeks after MI and
typically is located in the more central areas of the in-
Cardiovasc Pathol Vol. I, No. 3
July-September1992:199-203
farction, as are both of the ruptures in this case (Fig.
2).
The events documented in this case report suggest,
as do previous studies (Z-.5), that cardiac rupture oc-
curs in an area of myocardium undergoing active repair
following a transmural-more likely, posterior wall-
infarct. To our knowledge this case is the first docu-
mentation of sequential formation of cardiac ruptures.
As a corollary, this case demonstrates that after a sin-
gle rupture patients are still at risk for a second rup-
ture. An association between systemic hypertension
and cardiac rupture had been shown initially. However,
more recent and controlled studies have not demon-
strated this association (3), and the patient in this case
was not hypertensive. It is interesting to speculate that
exertion or catecholamine release may have led to in-
creased ventricular pressures, thereby contributing to
the production of either the first or second ruptures.
Supported in part by SCOR in Ischemic Heart Disease (NIH-H2-
17646).
LARSON ET AL. 203
DOUBLERUFIIJRE AmR ACUTEMI
Figure 3. Microscopic sections stained with hematoxylin and
eosin at the site of posterior wall rupture (A, X20, B, X40).
The left ventricle (LV) with the site of posterior free wall
rupture (A) is indicated. The septal rupture occurred superior
and proximal to the area of the septum indicated (S). Indi-
cated areas (*) contain significant numbers of remaining ne-
crotic myocytes. Bordering on these areas are regions of
fibroblastic cell proliferation, monocytic cell infiltration, and
early collagen formation (0). Microscopic demonstration of
the infarct age (C, X200) shows an organizing infarction with
necrotic myocytes, among fibroblastic cell proliferation and
monocytic cell infiltration.
References
1. Stevenson WG, Linssen GCM, Havenith MG, Brugada P, Wellens
HJJ. Spectrum of death after myocardial infarction: a necropsy
study. Am Heart J 1989;118:1182-1188.
2. Mann JM, Roberts WC. Acquired ventricular septal defects dur-
ing acute myocardial infarction: analysis of 138 unoperated nec-
ropsy patients and comparison with 50 unoperated necropsy
patients without rupture. Am J Cardiol 1988;62:8-19.
3. Pohjola-Stintonen S, Muller JE, Stone PH, et al. Ventricular sep-
tal 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.
4. Edwards BS, Edwards WD, Edwards JE. Ventricular septal rup-
ture complicating acute myocardial infarction: identification of
simple and complex types in 53 autopsied hearts. Am J Cardiol
1984;54:1201-1205.
5. Mann JM, Roberts WC. Ventricular free wall and septal rupture
(double rupture) in patients with acute myocardial infarction. Am
J Cardiol 1987;60:722-725.
6. Sugiura M, Okada R. Myocardial rupture in old age. Geriatrics
1970;25:13c139.
7. Shozawa T, Masuda H, Sageshima M, Kawamura K, Okada E,
Saito N. Classification of cardiac rupture complicated in myocar-
dial infarction. Acta Pathol Jpn 1987;37(6):871-886.