Case Report and Brief Review

Percutaneous Closure of Patent Foramen Ovale for Refractory Hypoxemia after HeartMate II Left Ventricular Assist Device Placemen

*Navin K. Kapur, MD, §John V. Conte, MD, *Jon R. Resar, MD
*Navin K. Kapur, MD, §John V. Conte, MD, *Jon R. Resar, MD

During the fourth week of gestation, the primitive atrium divides into right and left atria by forming two septa, the septum primum and secundum. As the septum primum grows from the dorsocranial wall, two openings develop, the foramen primum at the level of the endocardial cushions, and the foramen secundum at the mid-septal level. As the septum primum fuses with the endocardial cushions, the foramen primum is obliterated. During the fifth and sixth weeks of gestation, the septum secundum develops from the ventrocranial wall of the primitive atrium and overlaps the foramen secundum, leaving an incomplete partition known as the foramen ovale. During prenatal life, the foramen ovale allows blood to pass from the right atrium into the left atrium. Higher right atrial pressure prevents return of left atrial blood across the foramen ovale. After birth, as left atrial pressure increases and right atrial pressure decreases, the foramen ovale closes to form a complete intra-atrial septum as the septum primum and secundum fuse.1 By age two, the foramen ovale completely closes in about 75% of individuals. The cause of incomplete closure or a patent foramen ovale (PFO) remains unknown, but is thought to be multifactorial.2

The incidence of probe-patent foramen ovale at autopsy is approximately 27% with slit widths ranging from 1 mm to 19 mm (mean 4.9 mm) in diameter. PFO is a risk factor associated with ischemic strokes, myocardial infarction, decompression sickness and pulmonary embolism.2 In congestive heart failure, elevated left atrial filling pressures can falsely mask the presence of a PFO by pressing the septum primum against the septum secundum and closing the foramen ovale. As a result, diagnostic techniques such as contrast echocardiography with Valsalva maneuvers or catheter-based oximetry measurements may be falsely negative in this population.

In patients with end-stage heart failure requiring mechanical support, implantation of a left ventricular assist device (LVAD) provides hemodynamic support as either a bridge to transplantation or destination therapy.3 Cannulation of the left atrium or left ventricle decreases diastolic filling pressures abruptly and can create a right-to-left pressure gradient across intra-atrial septal defects. Significant shunting can cause profound systemic hypoxemia. Several cases of left-to-right shunting across an intra-atrial septal defect have been reported with pulsatile LVADs.4,5 To date, two cases of transcatheter closure for hypoxemia secondary to a PFO after pulsatile LVAD placement have been reported.6,7 In this case, we describe the first successful PFO closure for refractory hypoxemia after implantation of an axial flow HeartMate II LVAD (Thoratec Corp., Pleasanton, California).

Case Report. A 58-year-old man with Tetralogy of Fallot palliated with a Potts shunt in 1950 and Blalock-Taussig shunt in 1969 underwent implantation of a HeartMate II LVAD for progressive heart failure refractory to optimal medical therapy, continuous inotropes and biventricular pacing. A transesophageal echocardiography (TEE) performed 2 months prior to LVAD implantation showed four-chamber dilatation, biventricular failure, and a PFO by color-flow Doppler. The surgical plan called for LVAD implantation and right atrial exploration for possible PFO closure. Ascending aortic and bicaval cannulation was performed. Outflow graft anastamosis to the ascending aorta was uneventful. The patient was placed on cardiopulmonary bypass for LVAD implantation. A left ventriculotomy for placement of the LVAD apical inflow cannula revealed massive left ventricular blood return, likely via a patent Potts shunt and aortopulmonary collaterals. Adjustments in cardiopulmonary bypass flow and the use of multiple left ventricular vents allowed for LVAD implantation without incident, but precluded right atrial exploration without aortic cross-clamping and circulatory arrest. Given the high likelihood that any period of cardiac arrest would necessitate a right ventricular assist device, right atrial exploration for PFO closure was abandoned with plans to address hypoxic events postoperatively. The patient wassuccessfully weaned off cardiopulmonary bypass with inotropic support and inhaled nitrous oxide (NO). LVAD flows, mixed venous oxygen saturation, and systemic oxygenation were initially excellent. Chest closure was performed uneventfully after aggressive diuresis and weaning of inhaled NO and inotropes.

The subsequent postoperative course was complicated by profound arterial hypoxemia and inability to wean the patient from a fraction of inspired oxygen (FiO2) of 100%. Before LVAD implantation, the inter-atrial pressure gradient was 17 mmHg (LA pressure: 38 mmHg, RA pressure: 21 mmHg) with an arterial pO2 of 219 torr (FiO2 40%). Total pulmonary-to-systemic flow ratio (Qp/Qs) measured 1.45 L/minute. After LVAD placement, the patient was brought to the cardiac catheterization lab on post-operative day 6, where intracardiac echocardiography (ICE) demonstrated a PFO (Figure 1) with predominantly right-to-left shunting. The PFO diameter measured 8 mm. The inter-atrial gradient had decreased to 0.0 (LA pressure: 13 mmHg, RA pressure: 13 mmHg) with an arterial PO2 of 76 torr (FiO2 100%). Qp/Qs decreased to 0.91 L/minute. A 28 mm CardioSeal Septal Occlusion Device device (NMT Medical Inc., Boston, Massachusetts) was deployed percutaneously. The patient’s saturation immediately improved to 100% with an arterial PO2 of 303 torr (FiO2 100%). Within 3 days of PFO closure, the patient was successfully weaned off mechanical ventilation. Hemodynamically, the patient remained stable with good systemic perfusion and LVAD flows of 5.5 to 6.0 L/minute. Seven days after PFO closure, a right atrial thrombus was observed extending from a right atrial pacing lead without evidence of systemic or pulmonary embolization. Unfortunately, the patient experienced respiratory arrest secondary to an aspiration event and died.

Discussion. The diagnosis of PFO remains elusive in the preoperative assessment of patients undergoing LVAD placement. Elevated left atrial filling pressures associated with endstage cardiomyopathy may attenuate the hemodynamic effects of provocative maneuvers such as Valsalva during echocardiography and catheter-based oximetry. Sensitivity and specificity for diagnosis of a PFO are 89% and 100%, respectively, for contrast TEE, and both 100% for color Doppler TEE.8 A recent report suggests that partial occlusion of the pulmonary artery intraoperatively can safely increaseright atrial pressure, decrease left atrial pressure and identify a subclinical PFO with right-to-left shunting using color flow Doppler and bubble study.9 Given the increased risk of systemic hypoxemia with right-to-left shunting, identification and management of PFO in patients undergoing LVAD placement is of paramount importance.

LVAD implantation generally includes TEE assessment to evaluate for the presence of a PFO, management of intracardiac air, and monitoring of ventricular function. Management of a PFO during LVAD placement generally involves suture-based closure at the time of initial cannulation. However, masked PFOs and intra-operative conditions may preclude surgical PFO closure. While percutaneous PFO closure has been successfully described in the literature with pulsatile LVADs. In this study, we describe the first case report of successful PFO closure for profound hypoxemia after implantation of an axial flow HeartMate II LVAD.

In the case of pulsatile LVADs, synchronous counterpulsation allows for LVAD filling during ventricular systole and mechanical ejection during ventricular diastole, resulting in maximal LV unloading. Synchronous mode could therefore exacerbate right-to-left shunting across a septal defect. Asynchronous mode (fill-to-empty mode) intermittently allows for LVAD ejection during ventricular systole leading to increased LV afterload, preventing continuous right-to-left shunting across a septal defect.5 Axial flow LVADs have been shown to induce partial unloading of the left ventricle with lower overall mean arterial pressures compared to pulsatile LVADs,10 Despite, partial LV unloading associated with axial flow devices, this case illustrates the possibility that profound right to-left shunting across inter-atrial septal defects may remain a persistent issue in this emerging patient population.

References

References

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