1Surgery, University of Florida, Gainesville,
FL, 2Surgery, University of Florida, Jacksonville, FL,3Medicine, University of Florida, Gainesville, FL,
Introduction: Cardiogenic shock is a state of low cardiac
output resulting in life threatening end organ hypoperfusion and
hypoxia.1 Mechanical circulatory support is often a
necessary therapy for those who fail medical
management.2,3 While durable LVAD is a sustainable
option for many patients,4,5 the pitfalls of these
therapies should be described to offer solutions to potentially
recurring problems. Only through optimizing medical and surgical
management options, can we continue to improve the lives of the patients
on the continuum of cardiogenic shock and end-stage heart failure.
Methods: Pericardial release through a left mini anterior
thoracotomy.
Results: LS is a 39-year-old woman with a medical history
significant for systolic heart failure secondary to viral myocarditis.
She was medically managed by the heart failure team for over a year, and
her heart function stabilized with left ventricular ejection fraction
(LVEF) greater than 40%. When she became pregnant in 2018, her LVEF
declined to 10-15%. Six months after an uneventful cesarean section she
presented in ambulatory cardiogenic shock, with a 40 lb weight gain,
jugular venous distention to the level of the mandible, and acute renal
injury.
She was started on inotropes, underwent aggressive diuresis, and had an
axillary intra-aortic balloon pump (IABP) placed. LS was discussed at
the Medical Review Board and listed for orthotropic heart transplant
(OHTx). Despite two weeks of ambulatory IABP support, LS progressively
deteriorated, and so we elected to bridge-to-transplant with a
pericardial placed Heartware (Medtronic, Minneapolis, MN) LVAD via
sternotomy.
LS did well post-operatively with flows averaging 4-5 L/min. However,
over the next four weeks, her LVAD intermittently experienced low flow
alarms to 2.5 L/min with MAPs greater than 90mmHg. TTE evaluation
demonstrated a midline septum and the aortic valve opening with every
beat, so the RPMs were increased in addition to continue afterload
reduction. Despite these interventions, LS had progressively worsening
low flow alarms, and was now flowing consistently at 1.5 L/min (Figure
1). On postoperative day 34, we elected for surgical reintervention. We
proceeded with a left mini anterior thoracotomy for pericardial release.
With the pericardium exposed, an incision in the pericardium was made
superior and parallel to the phrenic nerve 3cm cranial and caudal to the
LVAD. It was clear that the LVAD had been displaced in the pericardium
superiorly and anteriorly with the inflow cannula now directed at the
septum. By reangling the LVAD inflow, pump flows immediately improved to
>4.5 liter/min. Two 0-prolenes were used to anchor the pump
to the chest wall (Figure 2).
Postoperatively, LS experienced normalization of her right atrial,
pulmonary artery and wedge pressures. She recovered well following the
pericardial release. Nine months later, she underwent an uneventful OHTx
and has been discharged home.
Conclusion: The LVAD device pocket can undergo contraction in
the postoperative period changing the angle of the inflow or outflow
cannula.6 This has been described previously in
pre-peritoneal placed LVADs, but is not well known in pericardial placed
LVADs. In patient LS, we noticed a steady decline in LVAD flows over a
five week interval due to a progressive device migration. In order to
optimize end-organ support and to prevent pump thrombosis we employed a
pericardial release and device anchor along the chest wall. We were able
to utilize this as a durable solution for LVAD malalignment, and
successfully bridge this patient to OHTx.