Download Ventricular free wall rupture after myocardial infarction

Hong Kong Journal of Emergency Medicine
Ventricular free wall rupture after myocardial infarction
F Lateef and N Nimbkar
Patients with their first myocardial infarction (MI), who present to the emergency department many hours
after the onset of chest pain, who appear to be improving but suddenly develop new chest pain and
unexpected hypotension (with or without signs of cardiac tamponade), should be suspected of having
ventricular free wall rupture (VFWR). The mainstay of treatment is surgery. These patients may be managed
with the administration of fluids, cautious use of inotropes and echocardiographic scanning, which should
be performed on an emergent basis, while being prepared to be moved to the emergency surgical suite.
However, at no cost should surgery be delayed. This paper reviews the current literature of VFWR after
MI, a condition which remains difficult to diagnose, in many aspects, to this day. The review examines the
historical background, incidence, postulated risk factors, clinical presentation, investigations and
management. (Hong Kong j.emerg.med. 2003;10:238-246)
Keywords: Cardiac tamponade, cardiogenic shock, echocardiography, electrocardiography, post-infarction
heart rupture
"It seems that a person dies from a broken heart,
not in young adult life from a great grief or
emotion, but usually in old age, on account of
diseased coronaries…"
Krumbhaar and Crowell 1
Background
Current awareness of the health care profession in
treating arrhythmias after myocardial infarction (MI)
and the effectiveness of their treatment have brought
myocardial pump failure and cardiac rupture to
prominence, as causes of early mortality. Myocardial
pump failure is more common than cardiac rupture.
Sh o r t o f m e c h a n i c a l d e v i c e s a n d / o r c a rd i a c
transplantation the prognosis of post-infarct early
Correspondence to:
Fatimah Lateef, MBBS, FRCSEd
Singapore General Hospital, Department of Emergency
Medicine, Outram Road, Singapore 169608
Email: [email protected]
Uniformed Services University of Health Sciences, Bethesda,
Maryland, USA
Narayan Nimbkar, MS, FRCSEd, FACS
heart failure is not significantly improved by
treatment. Rupture of cardiac muscle can manifest as
perforation of the inter-ventricular septum, papillary
muscle rupture or ventricular free wall rupture
(VFWR), with the left being more common than the
right. Early and successful treatment of left ventricular
free wall rupture (LVFWR) has a distinct salutary
effect on the overall prognosis of MI.
William Harvey in 1647 described cardiac rupture as
a finding at autopsy of a knight who suffered severe
chest pain. 2 Morgagni, who had the misfortune of
dying from this malady, had collected 10 cases by
1765.3 An English Surgeon Joseph Hodgron, in 1850,
first suggested an association of coronary artery
obstruction and cardiac rupture. 4 This was quickly
followed by the landmark observations of Malmsten
(1861), 5 Winsor (1880) 6 and Steven (1884). 7
Krumbhaar and Crowell et al1 in 1925 cited 564 cases
from the literature, including one of their own.
Davenport,8 in 1928, reported references to 734 cases
in the world literature. The reports of surgical repair
of LVFWR started appearing in the literature around
1970. 9-11 Raitt et al 12 in their publication in 1993
tabulated 72 long-term survivors of myocardial free
wall rupture treated by surgery.
Lateef et al./Ventricular free wall rupture
Incidence
The incidence of LVFWR is difficult to compute
because the denominators used in different studies
were dissimilar. Some studies might not have utilised
the appropriate denominator. For example, scientific
papers based on autopsy studies presented the data as
the number of VFWR expressed as a percentage of
the total number of autopsies. This kind of data would
give the prevalence of VFWR among those who died
of myocardial infarction (MI), but would not tell the
frequency of the complication in patients suffering
from acute MI. Incidence of myocardial rupture in
published autopsy series of MI varied from 5.0% to
24.0%.13-35 Some studies utilised the cohort of patients
with MI and cardiogenic shock (CS). In this selected
group of patients, the incidence of VFWR varied
between 2.7% to 10.5%.11,36 Figueras et al encountered
81 (5.4%) patients with VFWR among 1,487 patients
with first MI, with Killip I and II status.37
In studies where the cohorts were smaller, even
without selectivity (e.g. CS, Killip classification), the
incidence of VFWR was high viz., from 2.4% to
6.6% 38-42 with the exception of the study by Park et
al, where in a small cohort the rate was less than 1.0%.43
An earlier exception to this was a population-based
study with high (95%) autopsy rate from Sweden. 44
In this study there were 2,477 "attacks" (i.e. MI) of
which 858 were fatal. One hundred and four (4.2%)
of them had cardiac rupture and haemopericardium.
Considering the apparently high mortality rate (34.6%),
one may suspect that the total number of MI patients
was actually more than 2,477 or that Swedes were
more likely to develop VFWR. When studies with a
large cohort of MI patients were evaluated for the
frequency of VFWR, the incidence seemed to be
around 1.0%. 45-47 Colletti et al found that LVFWR
contributed to about 24.0 % in hospital mortality after
acute MI and it was present in 40.0% of patients who
died of acute MI in the first week.48 It is evident that
the incidence of VFWR is not well defined in its scope.
There is a suggestion that it may be increasing as a
cause of death among victims with MI. This increase
may be more apparent than real as other causes of
death have become less common. 49-52 In a study from
239
Vienna, the rate of myocardial rupture was unchanged
over a recent 16-year period.53 A reasonable estimate
of the incidence of LVFWR after MI seems to be closer
to 1.0%. 54 The often-quoted figure of annual death
rate of 25,000 persons in the USA from cardiorhexis
(myocardial rupture) comes from the article by Bates
et al. 55 There was, however, no mention as to how
this figure was arrived at.
Risk factors
T h e t y p i c a l p a t i e n t w i t h LV F W R i s u s u a l l y
described as an older female, with no previous MI,
no left ventricular hypertrophy, who has never
experienced myocardial ischaemic symptoms or had
only minor symptoms previously and who has acute
transmural myocardial infarction, without mural
thrombus. In the Thrombolysis and thrombin
Inhibition in Myocardial Infarction (TIMI) 9A and
9B trial, the patients with VFWR were of lower
body weight and smaller stature. 54 When age and
other covariates were taken into consideration as
independent variables, females were not markedly
more at risk than males of the same age. The odds
ratio for females to have cardiac rupture, adjusted
for age and other covariates, drops from the unadjusted
ratio of 2.41 to 1.62. 46 Chandra et al showed that
women, age for age, had higher mortality from all
causes after MI. 48 Weaver et al found that after
a d j u s t i n g f o r a l l t h e d i f f e re n c e s i n b a s e l i n e
characteristics, known to be important for prognosis,
there was a slight excess in the risk of mortality for
women (relative risk=1.15) after MI. 56 Patients with
VFWR (or tamponade presumed to be from rupture)
usually have significantly less prior history of MI or
angina.36,55,57 Often, VFWR is a complication of first
MI.34,57 These patients are less likely to have diabetes
mellitus and peripheral vascular disease, 36,54 both
conditions are associated with the development of
collateral circulation, which is thought to decrease the
likelihood of rupture. 36 (Table 1) However, it is likely
that diabetes mellitus has neither a protective nor a
deleterious effect on VFWR. 58 It is also possible that
diabetics tend to present late because of absence of
pain or atypical pain symptoms.59
240
Table 1. Factors indicating increased risk for VFWR
Demographics
Older age
Female
Coronary risk factors
Non-diabetic
Hypertension
Vascular risk factors
First myocardial infarction
No peripheral vascular disease
No left ventricular hypertrophy
No history or only a very recent history of angina
Patient factors
Low body weight/small stature
Within 5 days of MI
Recurrent chest pain with no ECG changes suggestive of
re-infarction or infarct extension
The role of hypertension as an etiologic factor is
controversial. Some authors found enough evidence to
blame hypertension for facilitating rupture.16,18,26,30,34,54,60
Recent literature, which included prospective studies,
showed a similar incidence of hypertension among
those with or without rupture. 17,32,33,35,36,42,51,52,57
Figueras et al noted that hypertension at presentation
after MI, was seen in those patients who had early
rupture, but not in those who had late rupture. 61
Exertion, documented as such or presumptively so,
by late presentation to hospital after the infarction
(presuming that hospital admission would have
rendered them with bed rest), seemed to increase the
incidence of VFWR. 18,62 Solodky et al in a stepwise
logistic regression model, found that advanced age,
female gender, Killip class >1, tachycardia (>100 beats/
min), hypotension on admission and the use of
thrombolytics to be independently associated with
cardiac rupture. The more the number of these adverse
variables present in a patient, the greater was the risk
of cardiac rupture.39
A retrospective study from Portugal showed no
difference in incidence of cardiac rupture with or
without thrombolysis. 63 Nakamura et al detected a
slight advantage (1.7% Vs 2.7%) in favour of
thrombolysis. 64 Early thrombolytic therapy appeared
to improve survival and decreased the risk of cardiac
Hong Kong j. emerg. med. Vol. 10(4) Oct 2003
rupture. 65,66 One other group of agents used in the
treatment of MI is nitrates. In a case controlled
retrospective study, Pollak et al showed a beneficial
effect of administration of nitrates, intravenously or
orally, on the incidence of VFWR. 67
Pathology
A patient with myocardial rupture is more likely to
have the culprit infarction as her first infarction. After
the MI, the weakened infarcted segment of cardiac
muscle gives way under the strain of intraventricular
pressure and the pressure gradient created. Thus, if
there is a septal infarct, left to right pressure gradient
could cause ventricular septal perforation. Intraventricular
pressure is always more than intrapericardial pressure.
However, in terms of pressure gradient, the right
ventricle is not subject to strain comparable to the
left ventricle, and hence the much lower frequency of
right ventricular rupture. This is not the only factor
which protects the right ventricle. The right ventricle
has better collateral circulation and also thinner wall,
allowing better perfusion of myocardium and
decreasing the likelihood of transmural infarction.
Myocardial free wall rupture of atrial chambers has
not been reported. Between the two ventricles, the
left is almost always the one that ruptures. Right
ventricular free wall rupture is rare, as exemplified by
the first case of Cobbs et al, 10 three in the study by
Lopez-Sendon et al38 and one by Sherer et al.68 Anterior
and lateral wall ruptures of the left ventricle are much
more prevalent than posterior wall ruptures, probably
because of the protection afforded by the adherent
pericardium. The rupture is consistently in the
infarcted area, somewhat eccentrically located and
often near the junction of infarcted and viable
myocardium.55,69 The sites are categorised according
to whether it is near the atrioventricular groove (basal),
near the apex (apical) or in between (middle) and
whether it is on the anterior, lateral or inferior surface.
Thus, there are nine different sites, i.e. anterior basal,
lateral basal, inferior basal, anterior middle, lateral
middle, inferior middle, anterior apical, lateral apical
and inferior apical. (Table 2) Out of these possible
Lateef et al./Ventricular free wall rupture
241
Table 2. Sites of VFWR and their frequencies
haemopericardium and cardiogenic shock leading
quickly to death.42,80-82 Subacute or stuttering ruptures
imply gradual or incomplete ruptures of the infarcted
area with slow and/or repetitive bleeding in the
pericardial sac causing progressive or recurrent cardiac
tamponade producing waxing and waning of
symptoms and signs indicating haemodynamic
instability. The chronic course is where there is
d e v e l o p m e n t o f ve n t r i c u l a r p s e u d o a n e u r y s m
detected at surgery or autopsy. This is generally
asymptomatic. 83
Positions
Basal
Middle
Apical
Anterior
++
+++
++
Inferior
+
++
+
Lateral
++
+++
++
+++ indicates the most common type
+ indicates the least common type
rupture sites, the anterior and lateral middle sites
together made up 58% of all ruptures.69 In the study
by Batts et al, 66% of the rupture sites were in the
middle location and 48% of the total were in anterior
and lateral middle sites. 34 (Table 2) Although interventricular septal rupture and ventricular free wall
rupture are two distinct anatomical entities, there are
patients who suffer both ruptures simultaneously.70
Purcaro et al described six pathologic types of ruptures
encountered in their series of 28 patients.42 They were:
(1) through and through straight rupture of normal
thickness myocardium (Perdigao71 Type I); (2) similar
b u t t h r o u g h t h e t h i n n e c r o t i c m y o c a rd i u m ;
(3) multiple small perforations (Perdigao Type II);
(4) rupture of outer layer only (Perdigao Type IV);
(5) subepicardial haematoma without free rupture into
the pericardial sac; and (6) haemorrhagic infarct with
wall integrity but leaking surface. Their classification
covers all the cases described in the literature except
type III of Perdigao et al in which the orifice of rupture
is protected either by thrombus on the ventricular side
or by pericardial symphysis.71
The size of the rupture varied from not detectable
(leaking surface) 42 to 70 mm. 55 Some studies found
that larger infarcts were more prone to LVFWR.27,55,57
Others reported that smaller infarcts were often found
in association with LVFWR. 12,17,33,72,73 Extensive
coronary artery disease was noted by Bates et al55 but
most of the authors found that the disease was limited
to only one vessel.15,17,32,71,73-79
Clinical features
Clinically, there are acute, subacute and chronic
VFWR. Acute or blow out rupture is a sudden
transmural rupture of the infarcted area causing
VFWR occurs within twenty-four hours of MI in 20.0%
to 30.0% of those who eventually rupture in any given
series30,41 and within one week in 80.0% to 100.0%.34,41,57
Only the series by Purcaro et al showed a substantially
higher incidence of VFWR (53.6%) on the first day.42
Ventricular free wall rupture should be suspected when
a patient recovering from acute myocardial infarction
experiences chest pain and cardiovascular collapse. 79
Rupture may occur in patients doing well after their
first MI. Acute electromechanical dissociation (EMD)
is a specific and very suggestive sign of VFWR in a
patient with first MI without cardiac failure.35 This
criterion alone, however, may still be due to other
possible diagnoses such as massive pulmonar y
embolism post-MI. In practical terms, no harm is
likely to be done by this mistake, as these misdiagnosed
patients are likely to have massive MI not amenable
to any treatment. The association of bradycardia,
distended neck veins, and cyanosis of head and neck
has also been noted as a significant manifestation.
Lopez-Sendon et al on a prospective study of more
than 1,400 patients concluded that of all variables
studied, hypotension, haemodynamic cardiac
tamponade, pericardial effusion >5 mm at end-diastole
on echocardiogram, echocardiographic abnormalities
of haemopericardium and cardiac tamponade taken
together have high predictive value.38 Hypotension as
such is not diagnostic but the fact that every patient
who developed VFWR has hypotension makes it
imperative to use other studies to exclude VFWR.
Symptoms distinct from the initial chest pain and
other symptoms of acute MI were present consistently
in patients who subsequently developed LVFWR. 42
Presence of at least two out of three symptoms from a
symptom triad of (1) positional pleuritic chest pain
242
with or without a rub or recurrent uncharacterised
chest pain; (2) single or repetitive large volume
unprovoked emesis; and (3) unexplained restlessness
or agitation, was consistently noted in 84% of patients.69
Physical examination will reveal evidence of
hypoperfusion of organs. Signs of pericardial tamponade
will be evident to a variable extent but classical signs
may not always be present. Unconsciousness and agonal
respiration will be a manifestation of reduced brain
perfusion. Patients with subacute rupture may show
improvement in between hypotensive episodes.
Investigations
Patients who are prone to develop VFWR may show
certain characteristic findings on their electrocardiogram
(ECG). In one study, deviation of ST segment or T
wave or both, from expected evolutionary pattern
during the first 72 hours after onset of MI, was
observed consistently in all patients. 69 In another
study, sinus tachycardia defined as a regular rate over
100/min was noted on the admission ECG of all
patients who eventually developed LVFWR. If there
was inferior wall MI leading to LVFWR, then the sum
total of ST-segment deviation in all 12 leads was
significantly higher in those with rupture. Other ECG
findings noted with anterior and inferior wall rupture
following MI were R wave duration of 20 ms in aVR84
and ST-elevation ≥0.1 mV in Lead II. With inferior
wall MI, in addition to tachycardia (>100/min), there
were R wave duration >20 ms in aVR and V6; ST
elevation ≥0.1 mV in leads II, aVF, V4 to V6; and T
wave negativity in leads II, III, aVF and aVR.
Combined criteria of tachycardia and ST elevation in
V5 for inferior MI were useful predictors of inferior
wall rupture with 92% specificity. 85 The combined
criteria of tachycardia and ST elevation in lead II were
useful predictors of anterior wall rupture with 58%
specificity. 85 Yoshino et al also observed that ST
elevation in lead aVL in acute anterior MI was the
only independent predictor of VFWR (odds ratio 12.1).85
In the study by Figueras et al, patients with anterior
acute MI who had high ST elevation (6-7 mm) on
the admission ECG were at higher risk of LVFWR.61
Sudden increase in amplitude of T wave or reversal to
upright of previously inverted T wave is highly
Hong Kong j. emerg. med. Vol. 10(4) Oct 2003
suggestive of haemopericardium and hence of VFWR.
Mir described an ECG finding of a monophasic RS
complex with an upright T wave and progressive ST
segment elevation, called an "M complex" which was
seen in patients who went on to develop VFWR. 86
Notwithstanding the findings of these authors, Purcaro
et al in their prospective study attached so little
importance to ECG findings that it was not even
mentioned. In the discussion, they concluded that the
ECG findings of rupture were confusing.42 Other studies
drew similar conclusions that none of the ECG findings
were sensitive or specific or pathognomonic for predicting
cardiac rupture.12,38,81 Abrupt transient hypotension and
bradycardia followed by EMD are invariably the signs
of bleeding into the pericardial sac. Sudden EMD
without overt heart failure in a patient with the first MI
has a predictive accuracy of 97.6% for the diagnosis of
VFWR. 35 The haemopericardium causes pericardial
tamponade and associated manifestations such as
cyanosis, jugular venous distension and altered
sensorium. This may be a terminal event but occasionally
the patient may improve spontaneously, transiently or
even permanently. Where there is a high clinical suspicion
of VFWR and conditions permit, an echocardiogram
should be performed. Echocardiography is the best way
to confirm the diagnosis. Presence of liquid in the
pericardial sac especially with evidence of solid clot by
high acoustic intrapericardial echoes together with
diastolic compression of the right ventricle is diagnostic.
If the leak into the pericardial cavity is demonstrated,
the diagnosis is confirmed beyond any doubt.
Cardiac catheterisation is an unwarranted procedure.
It can be performed later if indicated. 42,81 If a SwanGanz catheter happens to be already inserted, the
multiple level pressure measurements show the
diastolic equalisation of right atrial, pulmonary artery,
and pulmonary capillary wedge pressures. Other
findings include right atrial pressure with deep
x descent and a shallow y descent, decrease in the pulse
pressure in the pulmonary artery, inspiratory elevation
of right atrial pressure and pulsus paradoxus.
Pericardiocentesis with aspiration of fluid, especially
blood, clinches the diagnosis and also alleviates the
adverse pathophysiology of tamponade. However,
negative pericardiocentesis does not exclude VFWR.
Lateef et al./Ventricular free wall rupture
Treatment
The treatment of subacute cardiac free wall rupture
is surgical irrespective of the clinical status of the
patient. 11,12,38,42,43,48,52,57,79-82,87 Acute or blow out
rupture is generally not amenable to surgery because
the course of events is so rapid that it is not feasible in
most institutions to take these patients to a surgical
suite in time to undergo surgery. McMullan et al
believe that EMD is a diagnostic sign and should be
followed by an echocardiogram if available and
feasible. In the event of progression to cardiogenic
shock or cardiorespiratory arrest, immediate surgery
is warranted. 82 The mortality rate for surgery in acute
ruptures is high but the mortality rate without surgery
is virtually 100%.12,49,55 As time is of the essence and
diagnostic certainty might not be possible, surgery is
sometimes justified on the basis of a strong clinical
suspicion. This is especially so as there have been no
reported operative deaths in patients who were
explored but found not to have myocardial rupture.12,38
The operation should preferably be done in a hospital
which has full facilities for cardiopulmonary bypass.
In hospitals with no facility for cardiopulmonary
bypass, patients with anterior or lateral infarction may
still have a chance of survival because these ruptures
can be repaired with sutures buttressed with felt,
without cardiopulmonary bypass. 4 Temporising with
modalities such as administration of inotropes and
fluids, pericardiocentesis, intra-aortic balloon pump
insertion or even bedside cardiopulmonary resuscitation
wastes valuable time in a patient with acute rupture.
Even in subacute rupture (stuttering rupture), cardiac
catheterisation is not indicated. 11,12,42,45,81,82 It can be
performed later if indicated.
After categorically stating that the treatment of VFWR
is surgical, it should be pointed out that there are more
than occasional descriptions of patients who survived
the non-operative treatment, sometimes even with no
specific treatment. 36,37,40,68,88 If, for any reason, a
decision is made to treat a patient medically and for
those patients awaiting surgery, the first objective is
to obtain and maintain haemodynamic stability. This
is best achieved by rapid infusion of fluids and
inotropic support. Pericardiocentesis if successful may
243
help to relieve the impact of tamponade. Intra-aortic
balloon pump is an adjunct worth considering under
appropriate circumstances. Pharmacological afterload
reduction may also be considered.
Prognosis
Dramatic as the presentation and treatment of
LVFWR is, surgery would not be justified if the results
were not correspondingly dramatic. Acute LVFWR
usually results in death within 30 minutes of
cardiovascular collapse and hence it is unlikely to be
amenable to surgery. If surgery can be performed
before death, the occasional survivor is worth the
effort. Subacute rupture is a different issue. Padro et
al had 100% long-term survival rate after surgery. 81
No other group had shown such remarkable results,
but the results were still encouraging, e.g. 48.5% longterm survivors from the series by Lopez-Sendon et al.38
Purcaro et al had 16 out of 24 surgically operated
patients discharged well from the hospital. Eleven
(45.8%) of these were living normal lives at home. 42
These were three series with relatively large number
of patients. One multicenter, multinational study had
38% survival.36 For a small number of operations, Park
et al had four out of four survivors. 43 McMullan et al
had also successfully operated on acute (blow out)
LVFWR with long-term survival.82 Other centres with
only small numbers of patients have also shown
remarkable successes with long-term survival after
surgery. 10,11,12,87,89-95
Summary
VFWR is a catastrophic complication that occurs
within 7 days, in 1-4% of patients with acute MI. It
can manifest as cardiogenic shock or circulatory
collapse. It often occurs in older females with their
first, small, transmural acute MI.
Acute onset of shortness of breath, cardiac arrest,
shock, diaphoresis, unexplained emesis or syncope may
herald the onset of VFWR. A high index of suspicion
is essential.
244
Resuscitation with fluid, cautious use of inotropes and
pericardiocentesis can only offer temporary support
at best. Without prompt surgical repair, mortality
remains very high.
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