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.