Acute right heart failure (RHF) because of pulmonary vascular diseases is frequently encountered and is associated with a high mortality.1 , 2 Underlying causes are severe pulmonary embolism (PE) and the final pathway of pulmonary hypertension (PH) of various etiologies.3 This leads to secondary RHF frequently accompanied by systemic hypoxia. Consequently, RHF is the main cause of death in patients with pulmonary arterial hypertension.4
If pharmacological treatment fails, mechanical circulatory support is the last resort.5 In this situation, retrograde/peripheral venoarterial extracorporeal membrane oxygenation (vaECMO) is a reliable bailout strategy to reduce central venous and right atrial pressure and improve right ventricular (RV) hemodynamics through a reduction of pulmonary blood flow. Initially, vaECMO also supports the systemic circulation. However, vaECMO raises aortic blood flow, thereby increasing mean and diastolic arterial pressure, that is, systemic afterload. This may lead to increased left ventricular (LV) volumes and reduced LV ejection fraction and stroke work and finally LV failure. Retrograde vaECMO is beneficial in these situations for a short period of time only. RV support with a cannula placed in the main pulmonary artery to preserve pulmonary blood flow and to avoid the hemodynamic complications of retrograde vaECMO might be more physiologic. So far, percutaneous RVADs have primarily been used in patients with RHF because of ischemic heart disease but not in those with PH. We present the proof-of-concept of such a novel approach in four patients with RHF because of PH, in which we used an ECMO-based oxygenation RVAD, previously termed “oxyRVAD” by Wang et al,6 , 7 in which the returning cannula was placed in the main pulmonary artery, hence, bypassing the RV.
Four patients with PH-related RHF were treated in our institution in 2016. The baseline characteristics of these patients are shown in Table 1. The necessity for informed consent was waived by the ethics committee (Ärztekammer des Saarlandes) because of the retrospective nature of the study. All patients, except one, were primarily treated with retrograde vaECMO using the femoral vein and artery as standard cannula entry sites. As standard oxygenator, a 7.0 L-HLS or Quadrox-I primed with physiological saline solution on the Maquet CardioHelp (Getinge, Rastatt, Germany) platform was used. Usually, we used 23 F draining cannulas and 17 F returning cannulas (Getinge, Rastatt, Germany) with heparin coating. Cannulation for vaECMO was done percutaneously under ultrasound guidance by the staff intensivists. Two patients were cannulated in external hospitals by our mobile ECMO Team and transported to our institution by helicopter.
As RHF progressed and/or signs and symptoms of left heart failure as a consequence of vaECMO appeared, patients were put on an oxyRVAD. The first report for the placement of a pulmonary artery cannula using the internal jugular vein (IJV) was from Kiernan et al.8 We modified the technique for a more convenient cannula placement as described below:
- Under ultrasound guidance, a 7 F introducer (Edwards, CA) was inserted into the right IJV.
- Under fluoroscopic guidance, a double lumen Swan-Ganz catheter compatible with up to 0.038″ guidewires (Teleflex, Morrisville, NC) or a 6 F internal mammary artery (IMA) angiographic catheter (Medtronic, Minneapolis, MN) with a soft guidewire was advanced to the main pulmonary artery.
- A 0.035″ Amplatz Super Stiff guidewire (Boston Scientific, MA) was exchanged over the Swan-Ganz or the IMA catheter with the tip advanced to a pulmonary artery controlled under fluoroscopy.
- Serial dilatations of the IJV were performed using a standard vascular dilation set (Maquet, Rastatt, Germany).
- Under fluoroscopic guidance, a Carmeda-coated Biomedicus cannula of up to 21 F diameter (Medtronic, Minneapolis, MN) was advanced to the pulmonary artery trunk.
- In vaECMO patients, the femoral artery cannula was clamped, and the pulmonary artery cannula was connected to the returning tube changing the circuit from vaECMO to oxyRVAD. In veno-venous ECMO patients cannulated via the right IJV, the left IJV was used for oxyRVAD or the present cannula was exchanged over the wire.
The procedure was done in general anesthesia using total intravenous anesthetics or volatile anesthetics. Patients were immediately extubated in the operating room or after the procedure on intensive care unit. No procedure-related complications occurred. ECMO circuits and oxygenators were checked for clots and functional performance on a daily basis. Partial thromboplastin time was aimed at 45–55 s. Daily interruption of sedation was mandatory, except in hemodynamically unstable patients. RASS 0 was the goal of sedation in all patients. The hemodynamic situation was monitored by echocardiography and an arterial line only because of the unreliable data obtained by a pulmonary artery catheter under oxyRVAD. Patients were weaned off vasopressors whenever possible.
Upon presentation, qualitative echocardiography of the RV and invasive hemodynamic assessment revealed severe right ventricular impairment in all patients. Peak N-terminal prohormone of brain natriuretic peptide (NT-proBNP) levels were significantly elevated (21,734 ± 10,318 pg/mL; cutoff < 62.9 pg/mL), indicating severe myocardial wall stress, according to the imaging probably originating from the RV. Additionally, patients presented with moderate to severe renal impairment according to their estimated glomerular filtration rate. All but one patient had continuous renal replacement therapy. Further, all patients had signs and symptoms of congestive hepatopathy. One patient was twice on oxyRVAD, as the RV worsened again after oxyRVAD removal. Functional parameters and pharmacological treatment are displayed in Table 2.
Hemodynamic improvement on oxyRVAD implantation was primarily judged by the decline in NT-proBNP levels (Figure 1A) and conventional chest x-rays over time (Figure 1B). On oxyRVAD, multiorgan failure steadily improved over time by increased cardiac output (e.g., monitored by bilirubin, transaminases, renal and neurological function as appropriate). However, as RHF was a secondary problem of underlying pulmonary vascular diseases, the patients’ oxyRVAD support was intended as bridging technique until the causative etiology was effectively treated. This could be achieved in two patients who finally made a full recovery, that is, 1) a patient with massive PE and heparin-induced thrombocytopenia; and 2) a patient with chronic thromboembolic PH who underwent surgical pulmonary thrombectomy. The patient with heparin-induced thrombocytopenia was treated with the direct thrombin inhibitor argatroban and an albumin-pretreated Quadrox-I oxygenator. Later, this was changed to a phosphatidyl cholin-coated 7 L oxygenator (Eurosets; Medolla, Italy).
Two patients eventually died, one of septic shock on day 11 and the other because of pulmonary hemorrhage on day six.
Our series shows the feasibility of an ECMO-based RVAD approach in these patients as a temporary treatment modality. Mortality in RV failure is high if volume resuscitation or pharmacological therapies fail. Lung transplantation (or pulmonary thrombendartherectomy in case of chronic thromboembolic PH) is the only viable long-term option.9 As these patients are INTERMACS level 1 or 2, mechanical circulatory support is urgently required to buy time. Retrograde/ peripheral vaECMO is a feasible bailout strategy but may lead over time to left heart failure. Further, the reported run time in patients with, for example, massive PE is around 5 days,10 which is mostly too short for a successful bridging to transplant according to our previous experience.11 Additionally, oxyRVAD might have physiological advantages: antegrade blood flow preventing LV distension, preserved pulmonary circulation, the prevention of arterial cannulation complications (e.g., limb ischemia), and the “north-south syndrome”.12 Probably the most important advantage of this approach is the avoidance of a thoracotomy.
A major concern of this technique is the indwelling catheter causing injury of valves or chordae. In this small series, we could not find relevant alterations of valvular function post oxyRVAD. This issue needs special attention in the future as it is conceivable that a large bore cannula causes injury to the delicate valvular apparatus. Of similar concern is the development of thromboses along the cannula and especially in the RV because of altered blood flow. In the present series, we did not encounter this problem; however, thrombosis and thromboembolism is a threat in prolonged extracorporeal support.13
Mechanical circulatory support using a modified veno-venous ECMO with a cannula in the pulmonary artery (“oxyRVAD”) provides an effective treatment to patients with severe RHF not responding sufficiently to other medical interventions. The deployment of a pulmonary artery cannula under fluoroscopy using a modification of previously described techniques was a safe and fast procedure. OxyRVAD is a promising tool for PH patients that may be used for prolonged periods as bridging technique until a causative treatment of the patient’s underlying disease is carried out.
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