Location via proxy:   [ UP ]  
[Report a bug]   [Manage cookies]                

Characteristics and Contemporary Outcome Ventricular Septal Rupture Complicating Acute Myocardial Infarction: Clinical

Download as pdf or txt
Download as pdf or txt
You are on page 1of 8

Ventricular Septal Rupture Complicating Acute Myocardial Infarction: Clinical

Characteristics and Contemporary Outcome


Steen Hvitfeldt Poulsen, Michael Prstholm, Kim Munk, Per Wierup, Henrik Egeblad
and Jens Erik Nielsen-Kudsk
Ann Thorac Surg 2008;85:1591-1596
DOI: 10.1016/j.athoracsur.2008.01.010

The online version of this article, along with updated information and services, is
located on the World Wide Web at:
http://ats.ctsnetjournals.org/cgi/content/full/85/5/1591

The Annals of Thoracic Surgery is the official journal of The Society of Thoracic Surgeons and the
Southern Thoracic Surgical Association. Copyright 2008 by The Society of Thoracic Surgeons.
Print ISSN: 0003-4975; eISSN: 1552-6259.

Downloaded from ats.ctsnetjournals.org by on September 1, 2009

Steen Hvitfeldt Poulsen, MD, DMSci, Michael Prstholm, MD, Kim Munk, MD,
Per Wierup, MD, DMSci, Henrik Egeblad, MD, DMSci, and
Jens Erik Nielsen-Kudsk, MD, DMSci
Departments of Cardiology and Cardiothoracic Surgery, Aarhus University Hospital, Skejby, Denmark

Background. The objective of this paper was to study


the patient characteristics and contemporary short- and
long-term outcome in patients with postinfarct ventricular septal rupture.
Methods. Based on patient files and register data we
performed a review of 64 consecutive patients with
ventricular septal rupture complicating acute myocardial
infarction, admitted to our tertiary center.
Results. The mean age of the patients was 70 7. The
median time was five days from onset of symptoms to the
diagnosis of the ventricular septal rupture. The overall
30-day, one-, and five- year mortalities were 62%, 72%,

and 95%, respectively. Medical treated patients (n 19)


had a 30-day mortality of 100%. Among surgically treated
patients (n 45) the survival at one month, one and five
years was 71%, 48%, and 32%, respectively. History of
hypertension, complicating congestive heart failure, and
age were associated with poor outcome.
Conclusions. Despite improvements in medical and
interventional techniques the early as well as the longterm prognosis remains poor in this contemporary series.

complete in each and every patient. In the GUSTO-I trial,


the patient profile was biased due to the particular
enrolment criteria used in this study [9, 10]. Data from
these selected populations indicate that the overall mortality rates remain high with 73.8% at 30 days in the
GUSTO trial and 87% in the SHOCK trial [9, 10]. Hence,
the aim of this paper was, in a contemporary group of
consecutive patients with postinfarction ventricular septal defect referred to our tertiary center, to study the patient
characteristics, the short and long-term outcomes, and the
influence of different treatment strategies on outcome.

entricular septal rupture in acute myocardial infarction (AMI) is a well-recognized mechanical complication associated with a very high mortality [13]. The
use of thrombolytic agents seems to have reduced the
incidence from 1% to 2% in the prethromobolytic era to
0.2% [1, 2, 4]. In the prethrombolytic era septal rupture
occurred most often in the first week of AMI, typically
three to five days after onset of symptoms [1, 4, 5]. The
outcome after septal rupture in the prethrombolytic era
was extremely poor, with an in-hospital mortality rate of
approximately 45% in surgically treated patients and 90%
in medically managed patients [13]. Predictors of a poor
late outcome in this population included cardiogenic
shock, inferior infarction, and poor right ventricular function [4, 6 8]. After introduction of thrombolysis and
primary percutaneous coronary intervention, the clinical
characteristics and course in unselected postinfarction
ventricular septal defect patients have mainly been examined in relatively small studies or in subgroup analysis. Data in larger selected postinfarction populations are
available from the SHould we emergently revascularize
Occluded Coronaries for cardiogenic shocK? (SHOCK)
registry trial and the Global Utilization of Streptokinase
and TPA for Occluded Coronary Arteries (GUSTO-I) trial
[9, 10]. However, in the SHOCK trial only patients with
manifest shock were included and data were far from
Accepted for publication Jan 2, 2008.
Address correspondence to Dr Munk, Department of Cardiology, Aarhus
University Hospital, Skejby, Brendstrupgaardsvej 100, 8200 Aarhus N, DK
8200, Denmark: e-mail: kim.munk@ki.au.dk.

2008 by The Society of Thoracic Surgeons


Published by Elsevier Inc

(Ann Thorac Surg 2008;85:1591 6)


2008 by The Society of Thoracic Surgeons

Patients and Methods


We reviewed the medical records of 64 consecutive patients
admitted to our tertiary cardiac center with ventricular
septal rupture complicating AMI during the period from
January 1993 to December 2002. Data were collected retrospectively. Individual consent for participation was therefore not obtained. This approach was approved by the local
ethical committee. The diagnosis of AMI was based on
typical clinical symptoms, electrocardiographic signs of
infarction, and a documented elevation of cardiac enzymes
(creatine kinase and creatine kinase MB fraction) to at least
twice the upper normal limits. The ventricular septal rupture was diagnosed by echocardiography (disrupted ventricular septum with evidence of left-to-right shunt by color
Doppler) in all cases.
Demographic data, medical history, electrocardiographic patterns, Killip class, hemodynamic data, and
0003-4975/08/$34.00
doi:10.1016/j.athoracsur.2008.01.010

Downloaded from ats.ctsnetjournals.org by on September 1, 2009

ADULT CARDIAC

Ventricular Septal Rupture Complicating Acute


Myocardial Infarction: Clinical Characteristics and
Contemporary Outcome

1592
ADULT CARDIAC

POULSEN ET AL
PROGNOSIS IN POSTINFARCT VENTRICULAR SEPTAL RUPTURE

Table 1. Patient Characteristics

Ann Thorac Surg


2008;85:1591 6

Table 2. Hemodynamic Profile of Patients

Number
Age (yrs) (range)
Gender M/F
Hypertension
Diabetes mellitus
Previous angina
Previous AMI
Smoker
VSD localization (anterior/posterior)
Peak CKMB (g/L)
Peak TNT (g/L)
Peak CKB (g/L)

64
70 7 (5384)
35/29 (55/45)
18 (28)
7 (11)
17 (27)
9 (14)
41 (64)
32/32 (50/50)
242 198
2.75 3.99
79 68

Values are given as mean one standard deviation for continuous


variables and for categoric variables as numbers (%).
AMI acute myocardial infarction;
CKB creatine kinase B;
CKMB creatine kinase MB;
VSD ventricular septal defect.

angiographic and echocardiographic findings were obtained for each patient. Medical treatment and scheduled
timing of surgery were noted. Two-dimensional Doppler
echocardiography was performed in all patients to assess
left ventricular systolic function, location and character of
the ventricular septal defect, Doppler pressure gradient,
and systolic pulmonary artery pressure.
The overall strategy of the department throughout the
study period was to delay surgical repair for at least 3 to
14 days according to each surgeons preference, in the
hope that the septal muscle would become sturdier over
time. All patients were operated with a uniform technique, using a single Dacron patch (Bard Medical,
Tempe, AZ).
A division between early (2 days from diagnosis of
ventricular septal defect) and late (2 days) surgery was
used to distinguish those who needed acute-subacute
operation because they were decompensated or were
judged to be too unstable at the time of diagnosis from
those who underwent scheduled surgery.

Heart rate (beats/minute)


Systolic blood pressure (mm Hg)
Diastolic blood pressure (mm Hg)
Killip class (I-IV)
LVEF
Ventricular septal defect Doppler gradient
(mm Hg)
Tricuspid valve regurgitation Doppler gradient
(mm Hg)
Mitral valve regurgitation (none, mild, moderate,
severe)

101 20
98 18
61 13
25/34/5/0
0.44 0.1
52 18
44 15
44/16/4/0

Values are given as mean SD for continuous variables and for categoric
data as numbers.
LVEF left ventricular ejection fraction.

Mortality
Causes of death and survival information for the entire
population were obtained from medical records and
through the Danish Central Personnel Register, where all
deaths in the country are recorded within two weeks. The
survival information was obtained in February 2003.

Statistical Analysis
Continuous variables were summarized as mean SD
and the rank sum test was used for comparisons. Categoric
variables were compared by the 2 test. Survival rates were
plotted according to the Kaplan-Meier method and comparison of survival rates between subgroups were tested
with the log-rank test. A multivariate Cox proportional
hazard analysis was performed to identify independent
predictors of cardiac death. Variables included were age,
heart rate, a history of hypertension, diabetes mellitus,
Killip class, infarct location, systolic blood pressure, ejection
fraction, and previous myocardial infarction. A p value of
less than 0.05 was considered significant. SPSS version 10.0
(SPSS Inc, Chicago, IL) was used for calculations.

Results
Clinical Characteristics
Table 1 displays the baseline characteristics for the 64
patients. Median time from debut of AMI symptoms to
diagnosis of the ventricular septal rupture was five days
(range, 0 to 195 days). Twenty-seven percent and 64% of
the cases were diagnosed within two days, respectively, one
week after the reported onset of AMI symptoms (Fig 1).
Based on electrocardiographic (ECG) findings, the index myocardial infarction was inferior in 29 patients,
anterior in 30 patients, and combined anterior and inferior in 3. The index myocardial infarction was characterized by ST-segment elevation and (or) Q-waves in 97% of
cases. Two patients presented with left bundle branch
block. Based on echocardiography, the location of the
septal rupture was equally distributed between an anterior and inferior-posterior location.

Angiographic and Hemodynamic Data


Fig 1. The time course from onset of symptoms to diagnosis of the
left ventricular septal rupture.

Coronary angiography was performed in 55 patients


(86%). The majority had single-vessel or double-vessel

Downloaded from ats.ctsnetjournals.org by on September 1, 2009

POULSEN ET AL
PROGNOSIS IN POSTINFARCT VENTRICULAR SEPTAL RUPTURE

Table 3. Profile of Medical or Surgically Treated Patients


Characteristics

Nonoperated Operated p Value

Number
Age (yrs)
Hypertension
Diabetes mellitus
Prior myocardial infarction
Heart rate (beats per min)
Systolic BP (mm Hg)
Anterior infarction
Killip class I
LVEF

19
73 6
10 (53)
3 (16)
4 (21)
99 32
94 26
10 (52)
15 (79)
0.44 0.10

45
68 7
7 (16)
4 (9)
5 (11)
102 14
100 14
22 (49)
24 (53)
0.45 0.10

0.03
0.002
0.42
0.43
0.35
0.38
0.78
0.09
0.91

Values are given as mean one standard deviation for continuous


variables and for categoric variables as numbers (%).
BP blood pressure;

LVEF left ventricular ejection fraction.

coronary artery disease (51% and 31%, respectively)


while the remaining 18% had triple-vessel disease. The
left anterior descending artery was identified as the
infarct-related artery in 23 patients (42%), the right coronary artery in 29 patients (53%), and the left circumflex
artery in only 3 patients (5%).
Hemodynamic characteristics are shown in Table 2. At
admission, 32% and 59% of the patients demonstrated a
systolic blood pressure less than 90 mm Hg and less than
100 mm Hg, respectively. A heart rate greater than 100
beats per minute was noted in 41% of all cases. The mean
left ventricular ejection fraction was mildly reduced
(mean, 0.44 0.1; range, 0.25 to 0.65) and was significantly higher in inferior infarcts compared with anterior
infarcts (0.47 0.09 vs 0.41 0.09, p 0.02). None of the
patients demonstrated severe mitral valve regurgitation.
Consistent with the presence of a left-to-right shunt, the
pulmonary systolic pressure was elevated as assessed by
Doppler measurements of tricuspid valve regurgitation
jets (Table 2).

Treatment
Thrombolytic therapy had been administrated in 28 patients (44%) while seven of the patients (11%) underwent

1593

Table 4. Comparison of Patients Managed With Early or


Late Surgical Repair
Characteristics

Early
Operation

Late
Operation

Number
Age (yrs)
Gender (M/F)
Hypertension
Diabetes mellitus
Previous AMI
Anterior AMI
Systolic BP (mm Hg)
Diastolic BP (mm Hg)
Heart rate (beats/min)
Killip class 1
LVEF

14
69 6
6/8
3 (21)
0 (0)
1 (7)
6 (43)
89 14
59 14
102 14
8 (57)
0.42 0.09

31
68 8
19/12
5 (16)
4 (13)
4 (13)
14 (45)
105 11
67 12
102 14
16 (52)
0.46 0.10

0.67
0.25
0.67
0.29
0.96
0.89
0.0001
0.05
0.97
0.73
0.23

Values are given as mean one standard deviation for continuous


variables and for categoric variables as numbers (%).
Early operation: day 12;

Late operation day 3.

AMI acute myocardial infarction;


left ventricular ejection fraction.

BP blood pressure;

LVEF

primary angioplasty. Vasopressor therapy was given in


38 patients (59%) combined with intraaortic balloon
counter pulsation therapy (IABP) in 35 patients (55%).
Acute severe renal failure developed during the first 24
hours in 6 patients. They were treated with hemodialysis.
Ventricular septal rupture repair was performed in 45
patients (70%) and patients with more than one-vessel
disease had concomitant coronary artery bypass grafting
(42%). Patients treated medically were significantly older,
and a history of hypertension and advanced heart failure
were more frequently present compared with patients
who underwent surgery (Table 3). The median time from
the diagnosis of ventricular septal rupture to surgery
was six days (interquartile range, 1.5 to 12 days).
Surgery was performed within 48 hours in 14 patients.
Five patients who were scheduled for surgery after two to
three days had to be operated on an earlier basis due to
worsening of the clinical and hemodynamic status. Baseline characteristics in patients who had early surgery
were comparable to patients with late surgery except
from a significantly lower blood pressure (Table 4).

Short- and Long-Term Outcome

Fig 2. Short-term cumulative survival in medically and surgically


treated patients.

The overall 30-day, 1-, and 5-year mortality rates were


62%, 72%, and 95%, respectively. The median survival
time was 32 days (interquartile range, 6 to 649 days).
None of the medically treated patients survived 30 days
while patients treated surgically had a 30-day survival
rate of 71% (Fig 2). The long-term survival rate in the
surgically treated group was 48% after one year and 32%
after five years. In the surgically treated patients with an
age 75 years or greater (n 7) the one-year survival rate
was 0% compared with 52% in patients with an age less
than 75 years. The highest one-year survival rate among
the surgically treated group was found in patients with
an age less than 65 years (n 12) as compared with

Downloaded from ats.ctsnetjournals.org by on September 1, 2009

ADULT CARDIAC

Ann Thorac Surg


2008;85:1591 6

1594
ADULT CARDIAC

POULSEN ET AL
PROGNOSIS IN POSTINFARCT VENTRICULAR SEPTAL RUPTURE

Ann Thorac Surg


2008;85:1591 6

Table 5. Multivariate Cox Regression Analysis for Predictors


of All Cause Mortality After One Year
Predictors
Hypertension
Killip class 1
Heart rate (beats/min)
Diabetes mellitus
Systolic BP (mm Hg)
LVEF (5)
Age (yrs)
Infarct location
Previous AMI
AMI acute myocardial infarction;
left ventricular ejection fraction.

Wald 2

p Value

7.46
4.02
3.69
1.17
0.99
0.87
0.08
0.01
0.01

0.006
0.04
0.05
0.28
0.32
0.35
0.78
0.98
0.98

BP blood pressure;

LVEF

patients with an age of 65 to 74 years (n 26) (83% and


38%, respectively, p 0.05) (Fig 4). Patients who underwent late (2 days) or early (2 days) surgical repair had
one-year survival rates of 64% and 38%, respectively (p
0.05) (Fig 3). In patients who underwent late surgery (2
days after the diagnosis), no statistical difference between
the AMI treatment strategies (fast revascularization, conservative treatment) and mortality were found (p 0.62).
However, there was a tendency toward better one-year
survival among patients treated with percutaneous angioplasty or thrombolysis (71%) compared with patients
without revascularization (59%).
A multivariate regression analysis was performed to
identify factors associated with one-year mortality (Table 5).
History of hypertension, high Killip class at admission,
and heart rate were identified as independent predictors
of mortality.

Comment
In a relatively large consecutive and contemporary series of
patients with AMI complicated with ventricular septal rup-

Fig 3. Long-term survival in patients treated with early (2 days)


or late surgery (2 days).

Fig 4. Long-term survival in surgically treated patients according


to age.

ture, the present study demonstrates that the overall shortand long-term mortality remains high in the reperfusion
era. It is notable that, due to the Danish socialized medicine
practice, this material represents unselected patients from a
defined geographic area within a defined time period.

Patient Characteristics
The average age in our study was 70 years, which appears
consistent with the GUSTO-I trial and SHOCK trial but
higher than observed in the prethrombolytic studies
[6 10]. The increased age seems to be consistent with the
increased age of the general population but may also
reflect enhanced confidence to surgical treatment in the
referring hospitals, even in elderly patients. The majority
of our patients were men. This is in accordance with
earlier studies but in contrast to the findings in the
GUSTO-I and SHOCK trials, where a predominance of
females was noted [9 13]. The median time from debut of
AMI to ventricular septal rupture diagnosis was five days
in our study and more than one-fourth of the patients
developed the rupture within two days. This observation
and data from the GUSTO-I trial may indicate that
rupture might occur sooner than described in prethrombolytic studies [1, 5, 9, 13]. Although thrombolytic therapy
reduces infarct size, reperfusion may potentially promote
hemorrhage and dissection in the myocardium, thus
accelerating the risk of rupture. Rupture was also seen
within one to two days in the smaller group of patients
treated with primary angioplasty. It should be noted,
however, that the early recognition of septal rupture
merely may reflect that access to echocardiography in the
primary hospitals is facilitated nowadays.
As shown by others we found a predominance of
one-vessel disease with a total occlusion of the infarctrelated coronary artery in approximately 50% of patients.
Anterior infarcts have in some studies been associated
with a more frequent development of septal rupture than

Downloaded from ats.ctsnetjournals.org by on September 1, 2009

POULSEN ET AL
PROGNOSIS IN POSTINFARCT VENTRICULAR SEPTAL RUPTURE

1595

inferior-posterior infarcts [5, 1315]. In the present study,


the ECG location of the AMI and the location of the
septal rupture by echocardiography were equally distributed between anterior and inferior-posterior locations in
accordance with other patient series [16].

the first four months after surgery. However, the strongest predictor of long-term outcome was a history of
hypertension. Hypertension is a recognized predictor for
septal rupture in AMI but has not previously been
associated with long-term prognosis [17, 18].

Treatment and Prognosis

Strategy for Management

Congestive heart failure was noted in 61% of the patients


on admission with approximately one-third being in
cardiogenic shock. Nearly two-thirds received inotropic
support and diuretics and preoperative IABP was used in
55% of cases, which is in accordance with other reports
[9, 15]. Although no definite documentation exists that
IABP improves survival the use is widely accepted as a
favorable support in the treatment of myocardial septal
rupture. The IABP decreases left ventricular afterload,
reduces the magnitude of the left-to-right shunt, and
increases the coronary perfusion. Thus, IABP may stabilize and improve the clinical and hemodynamic condition
in a number of patients. Severe hemodynamic deterioration developed in five initially stable patients. In these
patients, who were scheduled for later operation, urgent
need for surgical closure of the defect suddenly occurred.
Deterioration before surgery and cardiogenic shock at
admission are known strong predictors of early mortality
and in accordance with these observations none of the
five patients survived for 30 days [9, 15]. In accordance
with previous reports we have demonstrated that clinical
signs of heart failure, such as increased Killip class and
increased heart rate, were independent predictors of
long-term mortality [9, 12, 15].
Hospital survival in the United Kingdom during the
period 1988 to 1999 was 31% to 47% in patients with
ventricular septal rupture and for surgically treated patients in the SHOCK trial and GUSTO-I trial it was 19%
and 53%, respectively. In the present study, the 30-day
survival in surgically treated patients was as high as 76%.
For patients who survive surgery, the long-term prognosis is relatively good. In the GUSTO-I trial, one-year
survival was 47% in surgically treated patients. Similar to
these results, we found a one-year survival of 48%.
Furthermore, the five-year survival was 32% in our study,
which is reasonably comparable with the 41% found by
Deja and colleagues [15]. However, the mean age was
only 65 years in the study by Deja and colleagues
compared with a mean age in the present study of 70
years. This difference might indeed affect survival with
younger patients displaying a more favorable prognosis
than elderly as also illustrated in the present study. As in
the prethrombolytic era, the prognosis in medically
treated patients remains extremely poor with an inhospital mortality of 94% in the GUSTO-I trial, 96% in the
SHOCK Registry, and 100% in the present study [9, 10].
In the present report, the medically treated patients were
significantly older compared with the surgically treated
patients, otherwise they seemed comparable. As shown
previously and emphasized by the present study, advanced age is associated with poor outcome. In this
regard, it is also noteworthy that none of our surgically
treated patients with an age of 75 years or more survived

Besides a surgical strategy, the predominant medical


strategy prior to surgery is to reduce left ventricular (LV)
filling pressures and afterload. This involves the following: (1) IABP treatment- inotropics (or both in combination) in cases with signs of heart failure or cardiogenic
shock (blood pressure below 90 mm Hg); (2) diuretics;
and (3) dialysis in cases with an oliguria. After surgery,
the medical strategy is based on standard cardiac care
involving diuretics to decrease LV filling pressures, angiotensin-converting enzyme inhibitors, and beta blockers to diminish LV wall stress and afterload. The treatment strategy in this study has provided results
comparable with the majority of previously published
papers. Still, our 30-day mortality is 24%! How can we
improve outcome? In accordance with our expectations
we found in the present study that patients who were
operated early (2 days after diagnosis) had a more
adverse outcome compared with patients who underwent late surgery. This observation is likely to be explained by selection bias with more advanced stages of
heart failure with significant lower baseline blood pressures (Table 4). The fragile necrotic myocardium is a
major concern while operating on an urgent basis. Therefore, from a technical perspective the best time to perform surgery is after fibrotic healing of the necrotic
muscle. However, in a histologic study it was demonstrated that proliferation of connective tissue was not
present until the third week after infarction [19]. Furthermore, in a large proportion of patients it is not possible to
postpone surgery because they develop severe heart
failure and multiorgan dysfunction. A sudden hemodynamic deterioration between admission and scheduled
later operation carried 100% mortality in our population,
a result similar to findings of other reports [15]. A logical
measure to avoid further hemodynamic deterioration
should be to operate upon the patients immediately after
establishment of the diagnosis when a coronary angiography has been performed. A surgical technique with
infarct exclusion by means of a large endocardial patch
has permitted early operation. This technique was described by Deja and colleagues [15] and by David and
colleagues [20] who reported a 30-day mortality of 14%.
Their strategy was to operate all patients expeditiously.
Presently, we have adopted this technique and are operating the vast majority emergently.
In patients who are severely hemodynamically compromised, it may be considered to use a ventricular assist
device to bridge the patient to surgery with closure of the
septal defect or to heart transplantation. The latter strategy
has recently been reported with excellent outcome [21].
In this study, medically treated patients showed 100%
mortality after 30 days. Therefore, the overall strategy is to
correct the ventricular septal defect. In the elderly patients

Downloaded from ats.ctsnetjournals.org by on September 1, 2009

ADULT CARDIAC

Ann Thorac Surg


2008;85:1591 6

1596
ADULT CARDIAC

POULSEN ET AL
PROGNOSIS IN POSTINFARCT VENTRICULAR SEPTAL RUPTURE

(75 years), the prognosis with surgery is extremely grave


and surgical treatment should probably only be offered
in selected cases. In this particular group it may also be
appropriate to consider the use of a transcatheter closure
device; particularly if the patient is not considered for
concomitant coronary artery bypass surgery, if the ventricular septal defect has a simple structure (predominantly anterior located), and if it is not located close to the
mitral valve apparatus. Only case reports and small
series have documented the yield of these devices that
may change into significant future treatment options
[2224]. In this context, an 83-year-old patient with septal
rupture was recently treated in our department with an
Amplatz occluder and the outcome was successful.
Another controversial question is the need for concomitant coronary bypass surgery. Some series indicate that
concomitant revascularization may improve late survival
[25, 26], whereas others have failed to show any definitive
benefit of concomitant bypass surgery [27, 28]. In the
present study coronary grafting was only performed in
patients with multivessel disease to ensure optimal conditions for the left and right ventricular performance in
the postoperative phase.
In summary, the mean age of the patient with ventricular
septal defects is higher than described in prethrombolytic
series. Clinical signs of congestive heart failure on admission, advanced age, and a history of hypertension were
associated with poor long-term outcome. Despite improvements in medical and interventional techniques the early as
well as the long-term overall prognosis remained poor in
this contemporary series. However, a more favorable prognosis was found in surgically treated patients who were
younger than 75 years. The potential benefit of early transcatheter intervention in selected patients or by modified
surgical techniques needs further exploration.

References
1. Topaz O, Taylor AL. Interventricular septal rupture complicating acute myocardial infarction: from pathophysiologic
features to the role of invasive and noninvasive diagnostic
modalities in current management. Am J Med 1992;93:683 8.
2. Heitmiller R, Jacobs ML, Daggett WM. Surgical management of postinfarction ventricular septal rupture. Ann Thorac Surg 1986;41:68391.
3. Davies RH, Dawkins KD, Skillington PD, et al. Late functional results after surgical closure of acquired ventricular
septal defect. J Thorac Cardiovasc Surg 1993;106:592 8.
4. Moore CA, Nygaard TW, Kaiser DL, Cooper AA, Gibson RS.
Postinfarction ventricular septal rupture: the importance of
location of infarction and right ventricular function in determining survival. Circulation 1986;74:4555.
5. Edwards BS, Edwards WD, Edwards JE. Ventricular septal
rupture complicating acute myocardial infarction: identification of simple and complex types in 53 autopsied hearts.
Am J Cardiol 1984;54:12015.
6. Cummings RG, Califf R, Jones RN, Reimer KA, Kong YH, Lowe
JE. Correlates of survival in patients with postinfarction ventricular septal defect. Ann Thorac Surg 1989;47:824 30.
7. Held AC, Cole PL, Lipton B, et al. Rupture of the interventricular septum complicating acute myocardial infarction: a
multicenter analysis of clinical findings and outcome. Am
Heart J 1988;116:1330 6.

Ann Thorac Surg


2008;85:1591 6

8. Feneley MP, Chang VP, ORourke MF. Myocardial rupture


after acute myocardial infarction. Ten year review. Br Heart J
1983;49:550 6.
9. Crenshaw BS, Granger CB, Birnbaum Y, et al. Risk factors,
angiographic patterns, and outcomes in patients with ventricular septal defect complicating acute myocardial infarction. Circulation 2000;101:2732.
10. Menon V, Webb JG, Hillis LD, et al. 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 6.
11. Radford MJ, Johnson RA, Daggett WM Jr, et al. Ventricular
septal rupture: a review of clinical and physiologic features
and an analysis of survival. Circulation 1981;64:54553.
12. Deville C, Fontan F, Chevalier JM, Madonna F, Ebner A,
Besse P. Surgery of post-infarction ventricular septal defect:
risk factors for hospital death and long-term results. Eur
J Cardiothorac Surg 1991;5:16775.
13. Lemery 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;70:14751.
14. Skehan JD, Carey C, Norrell MS, de Belder M, Balcon R, Mills
PG. Patterns of coronary artery disease in post-infarction ventricular septal rupture. Br Heart J 1989;62:268 72.
15. Deja MA, Szostek J, Widenka K, et al. Post infarction
ventricular septal defect - can we do better? Eur J Cardiothorac Surg 2000;18:194 201.
16. Di Summa M, Actis Dato GM, Centofanti P, et al. Ventricular
septal rupture after a myocardial infarction: clinical features and
long term survival. J Cardiovasc Surg (Torino) 1997;38:58993.
17. Shapira I, Isakov A, Burke M, et al. Cardiac rupture in patients
with acute myocardial infarction. Chest 1987;92:219 23.
18. Oskoui R, Van Voorhees LB, DiBianco R, Kiernan JM, Lee F,
Lindsay J Jr. Timing of ventricular septal rupture after acute
myocardial infarction and its relation to thrombolytic therapy. Am J Cardiol 1996;78:9535.
19. Fishbein MC, Maclean D, Maroko PR. The histopathologic
evolution of myocardial infarction. Chest 1978;73:8439.
20. David TE, Dale L, Sun Z. Postinfarction ventricular septal
rupture: repair by endocardial patch with infarct exclusion.
J Thorac Cardiovasc Surg 1995;110:131522.
21. Faber C, McCarthy PM, Smedira NG, Young JB, Starling RC,
Hoercher KJ. Implantable left ventricular assist device for
patients with postinfarction ventricular septal defect. J Thorac Cardiovasc Surg 2002;124:400 1.
22. Lee EM, Roberts DH, Walsh KP. Transcatheter closure of a
residual postmyocardial infarction ventricular septal defect
with the Amplatzer septal occluder. Heart 1998;80:522 4.
23. Benton JP, Barker KS. Transcatheter closure of ventricular
septal defect: a nonsurgical approach to the care of the
patient with acute ventricular septal rupture. Heart Lung
1992;21:356 64.
24. Szkutnik M, Bialkowski J, Kusa J, et al. Postinfarction ventricular septal defect closure with Amplatzer occluders. Eur
J Cardiothorac Surg 2003;23:323327.
25. Muehrcke DD, Daggett WM Jr, Buckley MJ, Akins CW,
Hilgenberg AD, Austen WG. Postinfarct ventricular septal
defect repair: effect of coronary artery bypass grafting. Ann
Thorac Surg 1992;54:876 83.
26. Cox FF, Plokker HW, Morshuis WJ, Kelder JC, Vermeulen
FE. Importance of coronary revascularization for late survival after postinfarction ventricular septal rupture. A reason
to perform coronary angiography prior to surgery. Eur
Heart J 1996;17:18415.
27. Dalrymple-Hay MJ, Monro JL, Livesey SA, Lamb RK. Postinfarction ventricular septal rupture: the Wessex experience.
Semin Thorac Cardiovasc Surg 1998;10:111 6.
28. Loisance DY, Lordez JM, Deleuze PH, Dubois-Rande JL,
Lellouche D, Cachera JP. Acute postinfarction septal rupture: long-term results. Ann Thorac Surg 1991;52:474 8.

Downloaded from ats.ctsnetjournals.org by on September 1, 2009

Ventricular Septal Rupture Complicating Acute Myocardial Infarction: Clinical


Characteristics and Contemporary Outcome
Steen Hvitfeldt Poulsen, Michael Prstholm, Kim Munk, Per Wierup, Henrik Egeblad
and Jens Erik Nielsen-Kudsk
Ann Thorac Surg 2008;85:1591-1596
DOI: 10.1016/j.athoracsur.2008.01.010
Updated Information
& Services

including high-resolution figures, can be found at:


http://ats.ctsnetjournals.org/cgi/content/full/85/5/1591

References

This article cites 28 articles, 18 of which you can access for free at:
http://ats.ctsnetjournals.org/cgi/content/full/85/5/1591#BIBL

Citations

This article has been cited by 3 HighWire-hosted articles:


http://ats.ctsnetjournals.org/cgi/content/full/85/5/1591#otherarticle
s

Subspecialty Collections

This article, along with others on similar topics, appears in the


following collection(s):
Myocardial infarction
http://ats.ctsnetjournals.org/cgi/collection/myocardial_infarction

Permissions & Licensing

Requests about reproducing this article in parts (figures, tables) or


in its entirety should be submitted to:
http://www.us.elsevierhealth.com/Licensing/permissions.jsp or
email: healthpermissions@elsevier.com.

Reprints

For information about ordering reprints, please email:


reprints@elsevier.com

Downloaded from ats.ctsnetjournals.org by on September 1, 2009

You might also like