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69: ASD
Repair after a 10-month treatment with Bosentan in a patient with severe
pulmonary arterial hypertension: A Case Report. Hoetzenecker K, Ankersmit
HJ, Bonderman D, Hoetzenecker W, Seitelberger R, Klepetko W, Lang IM.
Journal of Thoracic and Cardiovascular Surgery.
Introduction
Congenital type II atrial septal defect (ASD II) is associated with
precapillarypulmonary hypertension (PAH) in roughly 10% of cases.
Principally, closure of the shunt lesion is recommended and large ASDs
must be repaired in early childhood to prevent an Eisenmenger’s syndrome.
Once severe pulmonary hypertension or Eisenmenger’s syndrome has
developed, ASD closure is problematic due the increased risk of right
ventricular failure and pulmonary hypertensive crisis. At this stage,
heart-lung transplantation is the only surgical option. Non-surgical
strategies include supplemental oxygen, digitalis, anticoagulation and
vasodilator treatments. In contrast to the traditional rule of
inoperability of an ASD with severe pulmonary hypertension, single case
reports have demonstrated that a surgical correction of an ASD is feasible,
but requires long-time pre- and post-operative treatment with vasodilators.
Endothelin (ET) receptor antagonists are a new class of vasoactive
substances, some of which (e.g. bosentan) are orally active. Bosentan has
been shown to lower pulmonary artery pressure (PAP) and to induce reverse
remodelling of the pulmonary arteries. We report the case of a patient
with ASD II and severe pulmonary hypertension. Successful surgical closure
of the ASD was possible with near-normalized PAPs after ten months of
“conditioning” medication with bosentan.
Clinical Summary
A 71-year-old female was admitted to hospital because of exercise
intolerance and cough. She presented in WHO functional class IV and was
given permanent oxygen. Pneumonia was diagnosed and an antibiotic regimen
was started. Electrocardiography showed a right bundle branch block (RBBB)
with left axis deviation of -130°. Routine echocardiography revealed
severe pulmonary hypertension with a systolic PAP of 89mmHg, and a large
ASD II with a bidirectional shunt. The defect size was 15x36mm, thus too
large for interventional closure. Cardiac catheterization confirmed the
diagnosis of severe PAH with a pulmonary vascular resistance (PVR) over
400dynes.s.cm-5 which is the cut-off for shunt closures at our institution,
and a nitric oxide (NO) non-responder status (Table 1). Surgical repair of
the ASD II deemed impossible because of the degree of PAH with a mean PAP
of 54, high B-Type natriuretic peptide (BNP) and the patient’s severe
physical limitation. Bosentan therapy to condition the patient towards a
later ASD closure was found to be an option by an interdisciplinary
consent. Bosentan was started at a dosage of 125mg/day (2x62.5mg bid) and
was increased to 250mg/day after one month. Laboratory parameters were
controlled monthly, no significant elevation of liver enzymes occurred. 10
months after initiation of bosentan a repeat cardiac catheterization
revealed significantly reduced pulmonary pressures (Table 1) stimulating a
surgical closure of the ASD II with a Dacron patch. In addition the
patient’s tricuspid valve insufficiency was repaired utilizing an
Edwards Lifesience MC3 32mm ring was performed. The patient was extubated
on the first postoperative day, norepinephrine and dobutamine given for
cardiac support could be stopped two days later. During the further
post-operative course recurrent right-sided pleural effusion and a sudden
pericardial tamponade had to be tapped. The patient was discharged from
the hospital on post-operative day 28 under bosentan treatment (250mg/d).
8 months thereafter the patient was in good clinical condition with mild
pulmonary hypertension.
Discussion
In this case report we describe significant hemodynamic improvement under
bosentan therapy, allowing surgical closure of an ASD II 10 months after
bosentan induction, with good clinical outcome 8 months post-operatively.
Treatment options for elderly patients suffering from pulmonary
hypertension are limited. Medical treatment is the standard therapeutic
option as surgical closure of the shunt is associated with an increased
post-operative mortality. The main obstacle for surgical treatment is
right ventricular dysfunction/failure in the presence of severe pulmonary
hypertension after the surgical intervention. However, several recent case
reports have demonstrated that post-operative reduction of PAP
significantly reduces the risk of right heart failure, making surgical
closure a possible treatment option.
Recently, Frost et al. reported a vasodilatative “conditioning”
therapy in a patient suffering from Eisenmenger's syndrome that was
initially considered inoperable. The ASD II in this case could be closed
after 4 years of epoprostenol therapy. 8 years after surgical intervention
the patient is clinically stable with near-normal pulmonary pressures.We
now present a similar case treated with bosentan. Bosentan has several
advantages compared to epoprostenol. Because it is an oral drug, there are
no complications related to an intravenous delivery system which are
common under prostaglandin therapy. Furthermore, adverse side effects of
epoprostenol including headache, diarrhoea and rash are avoided. By
contrast, the side effect profile of oral bosentan includes elevated liver
enzymes in 7% of cases. Fortunately, no clinically relevant increases of
transaminases occurred in the patient during 16 months of follow-up.
In the described case bosentan was continued because of the 8 months
hemodynamic data together with the assumption that a pulmonary vascular
disease is present. As the clinical outcome in this elderly patient is
excellent further invasive diagnostic procedures re-evaluating bosentan
therapy were abandoned. We conclude that bosentan treatment of a patient
with ASD II and severe pulmonary hypertension results in an amelioration
of pulmonary hypertension that may allow surgical correction according to
standard operating procedures of pulmonary hypertension units.
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