Discussion
In 1952, Muller and Dammann described pulmonary artery banding (PAB) for
palliation of congenital heart disease (CHD) with pulmonary hypertension
(PAH).3 As a first step in palliation, PA banding is
the only option, for univentricular physiology patients with
unrestricted pulmonary blood flow. We believe acute regional ischemia,
following PA banding especially in patients with univentricular
physiology, has not been addressed adequately in the literature. Our
patient had ST segment elevation in inferior leads after 3 hours of PA
banding indicating acute ischemia in RCA territory. In majority of
patients with DILV, L - TGA, the systemic vessel arises from the
rudimentary chamber. We hypothesize that sudden shift of preload to the
less compliant rudimentary chamber after PA banding, causes increased
wall stress and hence subendocardial ischemia in the RCA territory.
In the first instance, pressure by the band was thought as a
possibility, since the great vessels were almost antero-posterior
relation. As per the observation of operating surgeon, the band was away
from proximal RCA, since RCA arises from the lateral aspect of anterior
systemic vessel. Pressure by the band can be a possbilty, if RCA arises
posteriorly, making it vulnerable to compression.
Before onset of ischemic changes, there was no hemodynamic aberration
apart from tachycardia. Tachycardia itself can lead to elevation of ST
segment. However, in that case, it should have been global and not
regional, as observed in our case. Rakhi et al reported ST depression in
all the electrocardiographic leads soon after PA banding in a similar
clinical situation.2 These changes persisted despite
elevating the systemic pressures with inotropes and fluid replacement.
We believe decreased myocardial supply is unlikely to be the cause, as
effective PA banding will anyway increase the systemic blood pressure
more than the baseline. We maximized milrinone after acute ischemia in
our case and we believe it helped. Using indilators, to decrease the
ventricular wall stress is more physiological. On the contrary,
vasopressors will increase the myocardial oxygen demand and add to
afterload, hence can compound ischemia.
Echocardiography done at that time revealed mild ventricular dysfunction
and no AV valve regurgitation. Our observation of mild hemodynamic
instability inspite of acute ischemia can be explained by the fact that,
majority of the dominant ventricle is supplied by left coronary. Mild
hemodynamic instability allowed us to pursue aggressive diuresis as
well. We believe, by decreasing end diastolic volumes, by diuretics,
will decrease wall stress and hence improve subendocardial perfusion.
There is a marked decrease in the pulmonary blood flow after banding,
leading to decrease in arterial saturation. This coincides with the
increased oxygen demand immediately after banding. Diuretics can improve
arterial saturation in these high pulmonary blood flow patients, by
removing excess water. Applying PEEP and aggressively treating
atelectasis can prevent intrapulmonary shunting .Optimization of lung
function can substantially mitigate hypoxia, which we believe is an
important compounding factor.
To conclude, ischemia after PA banding in univentricular physiology can
lead to dismal outcome. Use of vasopressors to increase systemic
pressures, will not help. Liberal use of diuretics and inodilators, can
shorten phase of acute remodeling and hence limit ischemia. Once
equilibrium is achieved, ischemia will resolve in a banded single
ventricle.