Suggested Methodology

Left Atrial Septostomy as a Stress Test for Right Ventricular Function to Determine LVAD Candidacy

Roy B. Mukku1, MD, Joseph A. Walsh1, MD, MSc, Brett Sheridan2, MD, David V. Daniels1, MD

Roy B. Mukku1, MD, Joseph A. Walsh1, MD, MSc, Brett Sheridan2, MD, David V. Daniels1, MD

Extracorporeal membrane oxygenation is used in patients with severe left ventricular (LV) dysfunction as circulatory support during bridge to durable ventricular assist device implantation or transplantation.1 A known complication of extracorporeal membrane oxygenation (ECMO) is the development of pulmonary edema and hemorrhage, and subsequent right ventricular (RV) distension and/or failure. In patients who develop evidence of right heart failure, an important challenge is determining whether or not RV function will return with the implantation of a left ventricular assist device (LVAD); that is, whether or not these patients have primary RV failure that will not recover after the left ventricle is offloaded. One management strategy for bridging patients from ECMO to LVAD involves the placement of a temporary LVAD, such as an Impella (Abiomed), with further observation in order to determine any change in right heart hemodynamics and function. Yet placement of such a temporary ventricular assist device is not without significant cost and risk for complications. Balloon atrial septostomy (BAS) has been well described as a strategy to decompress the LV and aid in recovery of function.2 In this case, we report a possible method of using BAS to identify patients with biventricular failure who may have the potential for RV recovery by decreasing the burden of pulmonary edema and improving hemodynamics.

Case Presentation

A 47-year-old man with a past medical history of non-ischemic cardiomyopathy with severely reduced LV systolic function, atrial fibrillation (on rivaroxaban), and asthma presented to an affiliate hospital with nausea, vomiting, diarrhea, and poor PO intake. In the emergency department, he was normotensive and an initial electrocardiogram (EKG) showed atrial fibrillation with rapid ventricular response at a rate of 129 bpm. Initial labs were notable for new-onset renal failure. A chest x-ray showed a mild degree of congestive heart failure, but no frank pulmonary edema. He was given metoprolol and digoxin IV for rate control, along with normal saline and empiric antibiotics, and subsequently admitted to the intensive care unit for close monitoring. Over the next 3 hours, he experienced persistent hypotension that was not responsive to IV fluids and developed respiratory distress that ultimately resulted in hemodynamic collapse and pulseless electrical activity. The patient underwent three rounds of cardiopulmonary resuscitation and was intubated with subsequent achievement of return of spontaneous circulation. He was started on vasopressor support with norepinephrine for shock that was thought to be from a mixed etiology of cardiogenic shock (known LV and RV dysfunction) and sepsis. A transthoracic echocardiogram was obtained and showed biventricular failure with a LV ejection fraction (LVEF) of 10%. The patient was subsequently placed on inotropic support with dobutamine and cannulated for VA-ECMO using a 16 French (Fr) sheath in the right femoral artery and 23 Fr sheath in the left femoral vein. Initial right heart catheterization showed a pulmonary arterial (PA) pressure of 45/34 mmHg (Figure 1).

After successful VA-ECMO cannulation and Swan-Ganz catheter placement, the patient was subsequently transferred to our institution for further management and LVAD consideration. While on ECMO, he was maintained on anticoagulation with an unfractionated heparin infusion.

Upon transfer to our facility, his clinical status improved, with end organ function moving to near baseline, and inotropic support began to be weaned with stabilization of his hemodynamics. Unfortunately, the patient again developed persistent hypotension and was restarted on inotropic support with milrinone and vasopressor support with norepinephrine. Despite stabilization with VA-ECMO, the patient continued to have hypoxic respiratory failure from recurrent pulmonary edema, which was thought to be likely secondary to VA-ECMO, and thus, left atrium venting using balloon atrial septostomy was considered.

The patient underwent uncomplicated atrial septostomy using an 18 mm Tyshak II balloon (B. Braun Interventional Systems). Pre-septostomy mean left atrial (LA) pressure was 37 mmHg with a v-wave to 49 mmHg. Post-septostomy mean LA pressure was 11 mmHg with a v-wave to 12 mmHg. Given the dramatic drop in LA pressure, diuresis was discontinued in order to facilitate renal perfusion. Following BAS, the patient was noted to have return of a pulsatile waveform with a normal PA pulse pressure (55/17 mmHg, mean 30 mmHg [Figure 2]). The PA pulsatility was maintained following the procedure, suggesting recovery of right ventricular contractility.

Discussion

RV failure is a frequent complication following LVAD implantation, with an incidence ranging from 9-44%.3 The presence of left heart failure and resulting pulmonary hypertension can lead to RV hypertrophy, which, over time, can lead to RV dilatation and reduced cardiac output, ultimately resulting in right heart failure. Echocardiography remains the primary imaging modality for assessing cardiac function in heart failure patients, and although cardiac magnetic resonance imaging (MRI) has emerged as the gold standard, its use in clinical practice is limited.4 Pressure reduction of the left atrium, in theory, may benefit RV function; however, following implantation of an LVAD, increased venous return and leftward interventricular septum (IVS) shift may lead to RV dysfunction.5 Several pre-operative risk factors for post operative right heart failure have been identified and include existence of pre-operative circulatory failure requiring mechanical circulatory support6, severe RV systolic dysfunction, and RV strain as demonstrated on pre-operative transthoracic echocardiography7. In our practice, prior to proceeding with LVAD implantation, use of a temporary ventricular assist device prior to durable LVAD implantation for a patient on ECMO has been used as a means to assess RV hemodynamics and viability. This method could provide insight as to whether a patient can tolerate LVAD implantation from a right heart perspective, as there are limited options for biventricular assist devices available at this time. In patients who are on VA-ECMO, the development of pulmonary edema and elevated pulmonary pressures can lead to RV failure. In our patient, the use of BAS for LA venting showed return of RV contractility by a pulsatile PA waveform. We hypothesize that in patients with biventricular failure, using BAS for LV venting could be a surrogate method to assess the potential return of RV function. By identifying patients with potentially preserved RV contractility, patients who are better candidates for LVAD implantation from the standpoint of RV function could be better identified and thereby forgo implantation of a temporary LVAD (e.g., Impella). One consideration for this method would be closure of the iatrogenic right-to-left shunt following LVAD implantation, as the reduction in RV afterload following LVAD implantation would likely lead to hypoxemia resulting from the right-to-left shunt. This type of closure has been reported through transcatheter methods.8-10

Conclusion

In patients on VA-ECMO who develop pulmonary edema with resulting RV distension and failure, the use of balloon atrial septostomy for left heart decompression may be used as a “stress test” to assess the viability and functionality of the RV. Identifying hemodynamically viable RVs by the use of this method may assist clinicians in identifying patients who are likely to tolerate the transition to a more durable mechanical circulatory support such as an LVAD. Using this novel application of balloon septostomy to assess RV function offers a possible approach to better patient selection for durable mechanical circulatory support, with an accompanying potential for improved resource allocation and an overall net cost savings. 

1Division of Cardiovascular Disease, Sutter California Pacific Medical Center, San Francisco, California; 2Division of Cardiothoracic Surgery, Sutter California Pacific Medical Center, San Francisco, California

Disclosure: The authors report no conflicts of interest regarding the content herein.

The authors can be contacted via Roy B. Mukku, MD, at mukkurb@sutterhealth.org.

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