Delayed Presentation of Ventricular Septal Rupture – A Case Report Case Reports

Case Reports
Delayed Presentation of Ventricular Septal
Rupture – A Case Report
M Ullah, L A Sayami, SK Chakrabarty, AAS Majumder
Department of Cardiology, NICVD, Dhaka
Abstract:
Keywords:
Ventricular septal
rupture,
Myocardial
infarction.
Ventricular septal rupture (VSR) is a devastating complication of acute MI. In GUSTO trial about
0.2% patient developed VSR.1 The mortality rate among patients with septal rupture who are treated
conservatively without mechanical closure is approximately 24 percent in the first 24 hours, 46
percent at one week, and 67 to 82 percent at two months. We are reporting a case of VSR with MI who
presented with heart failure after 14 months of index MI.
Case Report:
Mr. X a 75 years old farmer presented with
shortness of breath and swelling of both lower
limbs for two months. According to his statement
he was reasonably well about two months back.
Then he developed severe respiratory distress
which is of NYHA II grade with edema of both
lower limbs. It was not associated with any chest
pain. His shortness of breath increased in last two
days. He was normotensive, nondiabetic and exsmoker. He gave history of sudden severe chest
pain about 14 months back. At that time he took
some medication (name of the drugs and other
documents not available) and continued for few
days. Chest pain subsided after the initial 24 hours.
After that he continued his usual activities without
any limitation.
(Cardiovasc. j. 2009; 2(1) : 91-94)
sided pleural effusion. Echocardiogram revealed
aneurysm in the posterior part of the basal portion
of the IVS with rupture in the RV. It was a type
III variety of ventricular septal rupture. Cardiac
catheterization showed significant step up of
oxygen saturation in the RV with QP/QS ratio of
2: 1. Coronary angiogram revealed 100% stenosis
of the RCA. Distal RCA and PDA are visualized
by collaterals from LAD. LAD and LCX were
normal. Patient was treated with diuretics,
vasodilator, antiplatelet and antilipid drugs and
was referred for surgical closure of VSR with
CABG.
On examination, his blood pressure was normal,
but he had tachycardia, dependant oedema and
raised JVP. His apex beat was shifted. There was
pansystolic murmur of Grade 3/6 in left lower
parasternal area. He had hepatomegaly and
bilateral basal crepitations in lungs. There was no
feature suggestive of deep vein thrombosis (DVT)
of lower limbs.
ECG shows Q wave in II,III & aVF without any
change in ST – segment. Cardiac markers were
normal. X-ray showed cardiomegaly with right
Fig.-1: Aneurysmal dilatation of IVS.
Address of Correspondence : Dr. Mohammad Ullah, Assistant Professor, Dept. of Cardiology, National Institute of
Cardiovascular Diseases, Dhaka, Bangladesh.
Cardiovascular Journal
Volume 2, No. 1, 2009
Discussion:
Acute myocardial infarction (AMI) may be
associated with devastating mechanical
complications. Rupture of the interventricular
septum (VSR) is one of them. In the era before
reperfusion therapy, septal rupture complicated 1
to 3 percent of AMI.2-6 In GUSTO -1 trial (41,021
patients with thrombolytic therapy) VSR was
suspected in 0.3% cases and confirmed in 0.2%
cases.1 thus reperfusion therapy has reduced the
incidence of VSR.
VSR was first reported by Latham in 1846. 7
Without reperfusion therapy VSR usually occurs
in the first week. 3,5, 8,9,10 The median time from
the onset of symptoms of AMI to rupture is
generally 24 hours or less in patients who are
receiving thrombolysis.22
Fig.-2: Aneurysmal dilatation of IVS.
VSR occurs more frequently in anterior than other
types of AMI.2, 6, 8,11,12. In our patient it was an
inferior MI. Risk factors for VSR in the era before
thrombolytic therapy included HTN,13,14 advanced
age (60 to 69 years),11 female sex,13,15 and the
absence pf history of angina or MI.1, 2, 16–18 Angina
or infarction may lead to myocardial
preconditioning as well as to the development of
coronary collaterals, both of which reduce the
likelihood of septal rupture. 18 In patients
undergoing thrombolysis, advanced age, female sex
and the absence of smoking are often associated
with an increased incidence of septal rupture,6
whereas the absence of antecedent angina has not
been associated with an increased risk.11 Our
patient was an elderly patient of 75 yrs age.
Fig.-3: Color flow from aneurysm to RV.
Becker and van Mantgem classified the
morphology of free-wall rupture into three types,
which are also relevant to ventricular septal
rupture19 : in type I there is an ruptures have an
abrupt tear in the wall without thinning; in type
II, the infarcted myocardium erodes before rupture
occurs and is covered by a thrombus; and type III
has marked thinning of the myocardium, secondary
formation of an aneurysm, and perforation in the
central portion of the aneurysm. In our patient it
was a type III VSR.
The size of septal rupture ranges from millimeters
to several centimeters. Morphologically, septal
rupture is categorized as simple or complex.
Simple septal rupture has a discrete defect and a
Fig.-4: Color flow from aneurysm to RV.
92
Delayed Presentation of Ventricular Septal Rupture – A Case Report
direct through-and-through communication across
the septum. The perforation is at the same level
on both sides of the septum. Extensive hemorrhage
with irregular, serpiginous tracts within necrotic
tissue characterizes complex septal rupture. 7,16
Septal ruptures in patients with anterior
myocardial infarction are generally apical and
simple . Conversely, in patients with inferior
myocardial infarction, septal ruptures involve the
basal inferoposterior septum and are often
complex. In our patient the VSR was in
inferoposterior and basal portion of IVS.
Ventricular septal ruptures associated with an
inferior or anterior myocardial infarction generally
involve right ventricular infarction.15
M Ullah et al.
reported a mortality rate of only 6 percent among
patients who survived the first 30 days after
surgery.7 Among 60 patients who survived surgical
repair, the 5-year survival rate was 69 percent,
the 10-year survival rate was 50 percent, and the
14-year survival rate was 37 percent.22 Eighty-two
percent of these patients were in New York Heart
Association class I or II at follow-up, and angina
and other medical problems were not prevalent.
The development of a residual or recurrent septal
defect is reported in up to 28 percent of patients
who survive repair and is associated with high
mortality.21
References:
Some studies have found that septal rupture is
associated with multivessel coronary artery
disease.2, 8 However, others found a high prevalence
(54 percent) of single-vessel disease among patients
with ventricular septal rupture.11,20 Ventricular
septal rupture is likely to be associated with total
occlusion of the infarct- related artery.3,6,11 In
our patient it was total occlusion of the RCA and
LAD & LCX were normal. In the GUSTO-I study,
total occlusion of the infarct-related artery was
documented in 57 percent of patients with
ventricular septal rupture, as compared with 18
percent of those without ventricular septal
rupture.6 Collaterals are less often evident in
patients with ventricular septal rupture,2, 11, 18
supporting the hypothesis that collateral
circulation reduces the risk of rupture of the cardiac
free wall as well as septal rupture.18
The mortality rate among patients with septal
rupture who are treated conservatively without
mechanical closure is approximately 24 percent in
the first 24 hours, 46 percent at one week, and 67
to 82 percent at two months. 3,4 Lemery et al.
reported a 30-day survival rate of 24 percent among
medically treated patients, as compared with a rate
of 47 percent among those treated surgically.20
Our patient survived 14 months after the MI having
some medication only during the initial few months.
To the best of our knowledge, this is the first
reported case of VSR in our country who survived
for such a long period with conservative treatment
For patients who survive surgery, the long-term
prognosis is relatively good.7, 21Crenshaw et al.
93
1.
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: 27-32.
2.
Pohjola-Sintonen S, Muller JE, Stone PH, et al.
Ventricular septal and free wall rupture complicating
acute myocardial infarction: experience in the
Multicenter Investigation of Limitation of Infarct Size.
Am Heart J 1989; 117: 809-18.
3.
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: 545-53.
4.
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.
5.
Hutchins GM. Rupture of the interventricular septum
complicating myocardial infarction: pathological analysis
of 10 patients with clinically diagnosed perforations.
Am Heart J 1979; 97: 165-73.
6.
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:
45-55.
7.
Latham PM, Lectures on subjects connected with clinical
medicine comprising disease of the heart. London:
Longmans, Brown, Green and Longmans II 1846: 16876
8.
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: 1201-5.
9.
Gray RJ, Sethna D, Matloff JM. The role of cardiac surgery
in acute myocardial infarction. I. With mechanical
complications. Am Heart J 1983; 106: 723-8.
Cardiovascular Journal
Volume 2, No. 1, 2009
10. Fox AC, Glassman E, Isom OW. Surgically remediable
complications of myocardial infarction. Prog Cardiovasc
Dis 1979; 21: 461-84.
50 unoperated necropsy patients without rupture. Am
J Cardiol 1988; 62: 8-19.
17. Figueras J, Cortadellas J, Soler-Soler J. Comparison of
ventricular septal and left ventricular free wall rupture
in acute myocardial infarction. Am J Cardiol 1998; 81:
495-7.
11. Skehan JD, Carey C, Norrell MS, de Belder M, Balcon
R, Mills PG. Patterns of coronary artery disease in postinfarction ventricular septal rupture. Br Heart J 1989;
62: 268-72.
18. Prêtre R, Rickli H, Ye Q, Benedikt P, Turina MI.
Frequency of collateral blood flow in the infarct-related
coronary artery in rupture of the ventricular septum
after acute myocardial infarction. Am J Cardiol 2000;
85: 497-9.
12. Birnbaum Y, Wagner GS, Gates KB, et al. Clinical and
electrocardiographic variables associated with increased
risk of ventricular septal defect in acute anterior
myocardial infarction. Am J Cardiol 2000; 86: 830-4.
13. Shapira I, Isakov A, Burke M, Almog CH. Cardiac
rupture in patients with acute myocardial infarction.
Chest 1987; 92: 219-23.
19. Becker AE, van Mantgem JP. Cardiac tamponade: a
study of 50 hearts. Eur J Cardiol 1975; 3: 349-58.
20. 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: 147-51.
14. 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: 953-5.
21. Blanche C, Khan SS, Chaux A, Matloff JM. Postinfarction
ventricular septal defect in the elderly: analysis and
results. Ann Thorac Surg 1994; 57: 1244-7.
15. Cummings RG, Reimer KA, Califf R, Hackel D, Boswick
J, Lowe JE. Quantitative analysis of right and left
ventricular infarction in the presence of postinfarction
ventricular septal defect. Circulation 1988; 77: 33-42.
22. Hochman JS, Buller CE, Sleeper LA, et al. Cardiogenic
shock complicating acute myocardial infarction —
etiologies, management and outcome: a report from
the SHOCK Trial Registry. J Am Coll Cardiol 2000; 36:
Suppl A: 1063-70.
16. Mann JM, Roberts WC. Acquired ventricular septal
defect during acute myocardial infarction: analysis of
38 unoperated necropsy patients and comparison with
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