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Echocardiography
in Practice
A Case Oriented Approach
by Susan Wiegers, Ted Plappert, and Martin St. John Sutton
Post-infarction Ventricular Septal Defect
Susan E. Wiegers, MD
A 62-year-old woman with rheumatoid arthritis had a long history
of steroid use to control her disease. Four weeks prior to her
current admission she had sustained a large anterior myocardial
infarction which was complicated by atrial fibrillation and congestive
heart failure. She had not received thrombolytic therapy, owing
to delayed presentation to the emergency ward. No post-myocardial
risk assessment was undertaken because the patient was felt
by her treating physicians to be too frail. She was discharged
on a calcium channel blocker to treat her hypertension and a lipid-lowering
agent. One week after discharge she developed
orthopnea and dyspnea on exertion which had not been present
before her infarction. 0n the day of admission,
her visiting nurse found her to be in more significant congestive
heart failure and to be tachycardic. She was brought to her
doctor's office where a loud systolic murmur was noted. She
was in moderate congestive heart failure. She was admitted to
thc coronary care unit and an echocardiogram was performed.
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Figure 70.1
Parasternal long-axis view in systole.
The left atrium (LA) is moderately dilated. The left ventricle
(LV) IS also significantly dilated. The proximal septum appears
to contract but is akinetic beyond that. In fact, comparison
to the diastolic view demonstrates systolic bulging In the
distal septum consistent with aneurysm formation. The ascending
aorta (AO) is normal The interventricular septum in this image
appears to have a normal texture. |
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Figure 70.2
Similar parasternal long-axis view in diastole.
Discontinuity in the mid-anterior interventricular septum (arrows)
is noted. The ventricular septal defect is at the junction between
the contracting and non-contractile myocardium of the septum.
In this view, the ventricular septal defect appears to be approximately
3mm wide. The anterior rnitral valve leaflet is mildly thickened
and mitral annular calcification is noted in the posterior
annulus. The left atrium and left ventricle are again noted
to be enlarged. |
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Figure 70.3
Apical long-axis view with color flow Doppler
imaging in systole. The interventricular septum is on the right
of the image. The turbulent high-velocity jet through the septal
defect is identified by the arrow. The ventricular septal defect
channel follows a seripiginous course through the interventricular
septum as can be seen by the color flow. |
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Figure 70.4
(a) Apical four-chamber view in diastole.
The left atrium (LA) and left ventricle (LV) are markedly enlarged.
The apex is dilated, consistent with aneurysm formation. The
ventricular septal defect is not seen in this image. The right
ventricular cavity is mildly dilated. Compared to the area
of the left ventricular cavity, the right ventricle does not
appear to be enlarged. However, the left ventricle is severely
dilated and judging the size of the right ventricle by comparison
to the left ventricle may lead to erroneous conclusions unless
the left ventricular dilatation is kept in mind. (b) Comparison
of the left ventricular walls in systole demonstrates that
the lateral wall thickens normally, as does the proximal interventricular
septum. However, the septum at the mid-ventricular level is
akinetic and the distal septum and apex bulge In systole which
is diagnostic of an aneurysm. Note that, although the right
ventricle was mildly dilated in the diastolic frame, the systolic
function is hyperdynamic. |
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Figure 70.5
Slightly off-axis apical four-chamber view with
color flow Doppler imaging in a close-up of the interventricular
septum. The high-velocity turbulent jet through the ventricular
septal defect is seen towards the top of the screen. The red
flow on the left ventricular side of the defect indicates that
the initial course of the channel is towards the transducer
at the apex. |
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Figure 70.6
Spectral display of continuous wave
Doppler from the parasternal position across the ventricular
septal defect. In systole, a high-velocity jet from the left
ventricle to the right ventricle is identified. The peak velocity
is 4.2 m/s consistent with a gradient between the right ventricle
and the left lentricle of 71 mmHg (calibration marks represent
1 mm/s). |
Discussion
Two life-threatening complications
of myocardial infarction may present in the first weeks after
the event and be heralded by the development of a new, loud systolic
murmur and the development of heart failure. Acute mitral regurgitation
due to papillary muscle rupture and acute ventricular septal defect
may be extremely difficult to distinguish clinically, especially
in the critically ill patient. Emergency echocardiography is essential
in differentiating the two syndromes. Transthoracic images are
often adequate for diagnosis of both acute mitral regurgitation
and ventricular septal defect. However, transesophageal images
will be necessary if the cause of the murmur and hypotension cannot
be distinguished on the transthoracic study.
Elderly patients,
particularly those on steroids and perhaps women, are more likely
to sustain acute free-wall rupture and interventricular septal
rupture after infarction. There has been some suggestion that
the use of thrombolytic agents has contributed to an increased
incidence of these complications, although this remains controversial.1 Ventricular
septal rupture is equally common after anterior and inferior myocardial
infarctions.2 Infarct expansion and extensive myocardial
thinning may lead to intolerable wall stress, particularly at areas
with marked distortions in normal geometry, as in this patient.3 The
average time to development of a ventricular septal defect is approximately
5 days and the defect may range from very small to a 1-cm hole
in the septum.4 The ventricular septal defect
may take a winding course through the necrotic myocardium, leading
to an exit into the right ventricle far displaced from the left
ventricular site of the defect. Color flow within the inter- ventricular
septum, or high-velocity, turbulent flow in the right ventricular
apex may provide echocardiographic clues to the diagnosis. The
hemodynamic consequences of the defect depend on the degree of
shunt flow, residual right ventricular function and response to
the volume overload as well as to the extent of coronary artery
obstruction. In this patient, the right ventricular function was
hyperdynamic and the gradient between the left and right ventricle
was high, indicating that the defect was restrictive, at least
on presentation. The modified Bernoulli equation (pressure gradient
= 4v2, where v is the velocity of the ventricular septal
defect jet measured by continuous-wave Doppler) can be used to
calculate the pressure difference between the two ventricles. In
this patient, the velocity of the ventricular septal defect jet
was 4.2 m/s which, when substituted into the equation, yields a
71-mmHg gradient between the ventricles. The systolic blood pressure
by cuff was 1 10 mmHg. Therefore, the peak systolic pressure in
the right ventricle, and by extrapolation the peak pulmonary
artery systolic pressure is obtained by subtracting the gradient
between the ventricles from the cuff pressure. In this patient,
the peak pulmonary artery pressure can be estimated as 39 mmHg.
In the critically ill patient, stabilization with intra-aortic
balloon counterpulsation should be attempted, but deterioration
in the hemodynamic status frequently demands emergency surgery.
Transesophageal echocardiography is essential in the course of the
operative repair. The distortion
of the left ventricular geometry induced by the repair
may lead to the development of mitral regurgitation, which
should be addressed in the operating room. The right
ventricular systolic function is an important determinant of
the outcome of the surgery. The tissue which contains the
ventricular septal defect is usually highly necrotic with little
tensile strength, and residual shunts are not uncommon.
Echocardiographic imaging will help determine the size of
any residual shunt flow and aid in the decision to return to
the operating room. It is no longer the practice to delay
surgery, as the interim mortality was unacceptable. Rather,
intervention should be undertaken as soon as possible using
one of the recently described techniques.
This patient deteriorated hemodynamically over the
course of 12 hours. An intra-aortic balloon was placed and
she was taken to the operating room. An extensive
ventricular septal defect was repaired using a bovine
pericardial patch to exclude the infarcted septum from the
left ventricular cavity.5 Saphenous vein grafts were placed
to the right coronary artery and a large obtuse marginal.
The patient did well with the exception of a surgical infection of
the venous harvest site. She was discharged on the 18th postoperative
day.
References
1. Kinn JW, O'Neill WW, Renzuly KH, et al. Primary angioplasty
reduces risk of myocardial rupture compared to thrombolysis for
acute myocardial infarction. Cathet Cardiovasc Diagn 1997;42:151-7.
2. Mann IM, Roberts WC. Cardiac morphologic observations after
operative closure of acquired ventricular septal defect during
acute myocardial infarction: analysis of 16 necropsy patients.
Am J Cardiol 1987;60:981-7.
3. Jugdutt BJ, Michorowski EL. Role
of infarct expansion in rupture of the ventricular septum after
acute myocardial infarction: a two- dimensional echocardiographic
study. Clin Cardiol 1987;10:641-52.
4. 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 1997;38:589-93.
5. David TE. Operative management
of postinfarction ventricular septal defect. Semin Thorac Cardiovasc
Surg 1995;7:208-13.
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