Original Contribution

Percutaneous Right Ventricular Assist Device Using the TandemHeart ProtekDuo: Real-World Experience

Estefania Oliveros, MD, MSc1; Fareed M. Collado, MD2; Marie F. Poulin, MD4; Christopher W. Seder, MD3; Robert March, MD3; Clifford J. Kavinsky, MD, PhD2

Estefania Oliveros, MD, MSc1; Fareed M. Collado, MD2; Marie F. Poulin, MD4; Christopher W. Seder, MD3; Robert March, MD3; Clifford J. Kavinsky, MD, PhD2


Background. Acute right ventricular (RV) failure is challenging to treat and mechanical circulatory support devices are limited. The TandemHeart ProtekDuo (THPD; TandemLife) is a novel percutaneous RV assist device that can provide 4.0 liters per minute of blood flow through venovenous extracorporeal life support. It allows venous drainage from the right atrium and reinfusion of blood into the main pulmonary artery via internal jugular vein access. We aim to provide real-world insight into disease characteristics resulting in the use of THPD for mechanical support and enhance knowledge of best practice regarding clinical management weaning and removal/exit strategies. Methods. We retrospectively collected data of consecutive patients who received a THPD device at our center for acute RV failure between August 2015 and February 2018. Results. Eleven patients were diagnosed with acute RV failure and required placement of THPD. The hospital length of stay ranged from 12 to 223 days. The average length of support ranged from 11 to 154 days. We observed complications such as stroke (18.2%), sepsis (63.6%), massive gastrointestinal bleed (45.5%), and heparin-induced thrombocytopenia (54.5%). These patients received on average 85 units of blood products. Survival was 82% at 30 days and 72% at 180 days. Six of the patients were successfully weaned from the THPD devices and 1 patient required venovenous extracorporeal life support. Conclusions. This real-world experience, despite high morbidity, continues to suggest benefits of THPD for patients with severe acute RV failure.

J INVASIVE CARDIOL 2021 March 22 (Ahead of Issue).

Key words: mechanical assist devices, ProtekDuo, right ventricular failure, TandemHeart

Right ventricular (RV) failure is challenging to treat, and mechanical circulatory support devices applicable to acute RV failure are limited. Mortality has been reported to be as high as 50% for patients with RV failure.1,2 The TandemHeart ProtekDuo (THPD; TandemLife) was recently introduced as a mechanical adjunct for acute RV failure that can provide venovenous extracorporeal life support (VV-ECLS). The THPD is a 29 Fr, dual-lumen cannula that is inserted percutaneously through the right internal jugular vein under fluoroscopic and ultrasound guidance. The distal end of the cannula is positioned in the main pulmonary artery over a stiff guidewire. The inflow ports are positioned in the right atrium and the distal outflow ports in the main pulmonary artery. The procedure can take place in the cardiac catheterization laboratory or in the operating room. This system is connected to the Centrimag TandemHeart pump (TandemLife). It provides flow up to 3.9 L/min for RV support. There is venous drainage and reinfusion of blood to the pulmonary artery resulting in the offload of the RV, henceforth decreasing the work of the chamber. It can be combined with an external oxygenator, thus replacing the lungs. In one large, randomized controlled clinical trial of 180 adults with acute respiratory distress syndrome (ARDS), the use of advanced VV-ECLS therapy reduced the rate of death and disability by 31% compared with conventional management with mechanical ventilation.3

The purpose of this study was to provide insight into real-world use of the THPD device. We aim to describe the circumstances leading to the clinical decision of using a mechanical RV assist device for support, as well as to enhance knowledge of best practices regarding clinical management, weaning, and removal strategies for the THPD device.


This is a single-center, retrospective study of patients treated between August 1, 2015, and February 1, 2018. We reviewed medical records of consecutive adult patients who received a THPD device for acute RV failure. Baseline demographics were obtained for all participants, as well as details of the present illness, medications, hemodynamic values when available, and biochemical parameters. The primary endpoints were: survival following THPD removal with myocardial and/or pulmonary recovery; need for durable ventricular assist device implant; transition to another mechanical support device; cardiac and/or lung transplant; survival at 30 and 180 days; and serious adverse events related to the THPD while on support. Other measurements included hospital length of stay, use of blood products, and need for renal support (chronic renal replacement therapy or dialysis). RV failure was defined as the inability of the RV to maintain sufficient blood flow through the pulmonary circulation to achieve adequate left ventricular (LV) filling. RV failure was diagnosed clinically by the treating advanced heart failure cardiologist or cardiothoracic surgeon, as well as by echocardiography.

Statistical analysis. Continuous variables are expressed as mean ± standard deviation, whereas dichotomous variables are expressed as frequency (%). SPSS, version 25 software (IBM) was used for statistical analysis. The study was approved by the institutional review board of Rush University Medical Center.


The indications for placement of THPD were determined by ongoing elevation of right atrial pressure despite aggressive pulmonary vasodilator, diuretic, or inotropic support, inability to wean inotrope support or vasopressor during continuous flow left ventricular assist device (LVAD) support despite acceptable LV filling pressure and LVAD functions, and clinical signs of RV dysfunction including hepatic congestion, lower-extremity edema, and cardiohepatic or cardiorenal syndrome. Eleven patients were diagnosed with acute RV failure, requiring vasopressors and inotropes, and had placement of THPD. Baseline characteristics and laboratory values are presented in Tables 1 and 2, respectively. Hemodynamic data at the time of insertion of THPD was only available in 4 patients (Table 3).

The different scenarios behind RV failure in our cohort were the following (Figure 1):

Post lung resection: 4 patients in our cohort had lung cancer requiring right-sided lobectomy by video-assisted thorascopic surgery. None of these individuals had evidence of RV failure prior to surgery. The evidence of RV failure was seen in the immediate postsurgical setting within 24-48 hours, and during this period the THPD was placed. All 4 patients developed atrial arrhythmias. They were all successfully weaned and survived.

Acute respiratory distress syndrome: 2 patients had a complicated hospital course with multiorgan failure and cardiac arrest. THPD was placed after cardiac arrest within 48 hours. One of the patients did not survive when he acquired nosocomial pneumonia.

Post durable LVAD placement: 1 patient had no evidence of RV failure prior to LVAD placement for destination therapy. Unfortunately, despite escalation of support with the THPD to improve RV failure, the patient did not survive.

Post partum cardiomyopathy leading to biventricular failure: 1 patient was placed on venoarterial (VA)-ECMO and required simultaneous RV support with THPD, with an excellent outcome and appropriately weaning the RV support followed by LV support.

Massive pulmonary embolism: 1 patient received systemic thrombolysis and required THPD placement due to evidence of persistent RV failure. Due to lack of improvement and persistent hypoxemia after 2 days, the patient required central cannulation with VV-ECMO, leading to a prolonged hospital course but successful decannulation and survival.

Late presentation of right coronary artery acute myocardial infarction: 1 patient with RV infarct and failure requiring THPD placement for support. The patient’s family ultimately decided to place the patient on hospice and he expired.

Post cardiothoracic surgery: 1 patient with mitral valve regurgitation, heart failure with reduced ejection fraction of 25%, and evidence of pulmonary hypertension underwent mitral valve replacement and developed severe RV failure postoperatively. THPD was placed 1 day after valvular surgery. The hospital course was complicated by septic shock and death.

The mean THDP settings were 3258 ± 1548 rpm and flow of 3.89 ± 0.71 L/min at the time of insertion. The mean amount of blood products transfused was 85 units (range, 0-243 units). Mortality was seen in 36.4%; in all cases, patients died after families opted to provide comfort care and discontinue mechanical support. Complications (Figure 2), outcomes (Figure 3), and survival (Figure 4) are shown. None of the complications were related to device insertion. The mean hospital length of stay was 103 ± 67 days (range, 12-223 days). The mean duration of mechanical support was 58 ± 47 days (range, 11-154 days). Survival was 82% and 72% at 30 and 180 days, respectively. Six of the devices were successfully weaned. No predictors of successful weaning could be identified, which was likely due to the small cohort size.


THPD has 2 main goals: RV recovery and increased end-organ perfusion. The right atrial ports drain blood from the atrial cavity and decrease the RV end-diastolic pressure and volume, as well as central venous pressure. The result is a reduction in the right atrial and RV wall tension and microvascular resistance, leading to lower mechanical work and oxygen demand. The outflow tip of the THPD in the pulmonary artery increases pulmonary blood flow and left-sided filling pressures, and reduces ventricular interdependence as well as leftward septal shifting. Hence, cardiac output and coronary blood flow improve.

Hypoxemia causes pulmonary vasoconstriction and increases RV pressure overload. In cases of acute respiratory distress syndrome (ARDS), the management of RV pressure overload is critical.4 Currently, there are histopathologic reports to describe the damage that takes place when there is evidence of RV overload. At a cellular level, there are remodeling responses to RV and LV pressure overload that are similar, but it appears that the RV is more vulnerable to oxidative stress, has decreased angiogenic response, and tends to activate cell death pathways in a larger magnitude than the LV.5 Placement of an oxygenator connected to the THPD may be a plausible alternative to alleviate hypoxemia and manage the RV pressure overload.

During cardiac surgery, acute RV failure can be caused by hypoxia, myocardial ischemia, microemboli, air emboli leading to myocardial infarction, arrhythmias, and excessive volume loading. Twenty percent or more of patients undergoing isolated LVAD implantation experience acute RV failure, which is a leading cause of morbidity and mortality.6 Four of our patients underwent lung resection, which has been determined to be a cause of RV failure from primary respiratory disease (ie, hypoxemia) or the surgical procedure. Studies have shown that RV function can be impaired after lung resection.7 Lung cancer is the most common indication for major lung resection, and it is rarely associated with pulmonary hypertension.8 In the postoperative period, the marked reduction of pulmonary vascular bed after lung resection can lead to pulmonary hypertension, followed by RV failure. The anatomical changes in the thoracic cavity can alter the normal heart position, and nerve injuries can affect cardiac performance.8 RV dilation has been described after pneumonectomy.7 The increment of dead space to the alveolar space ratio, decrease of diffusion surface, and mechanical limitations in the postsurgical setting augment the oxygen demand, cardiac work, and myocardial oxygen anatomic consumption. The etiology of RV failure after pulmonary resection may be multifactorial in the presence of arrhythmias seen in the immediate postoperative period, changes in the RV afterload, chamber dilation, thoracic cavity changes, etc.9,10

After the patient has been hemodynamically stabilized on THPD support, weaning off the device takes place. The initial step is the reduction of the sweep, followed by the reduction of flow and assessment of clinical parameters.11,12 Many investigators have proposed and validated the use of hemodynamic formulas to assess RV function and predict failure, such as pulmonary artery pulsatility index,13 transpulmonary gradients,14,15 right atrial pressure/pulmonary capillary wedge pressure ratio, tricuspid annular plane systolic excursion/pulmonary artery systolic pressure,16 pulmonary vascular resistance,14 diastolic pulmonary gradient, RV stroke work index,17 pulmonary artery compliance, and pulmonary artery elastance.18 These values were not documented in all 11 cases from our cohort, but for future studies it would be useful to use this information as markers of diagnosis and assessment, and possibly as weaning tools.

One advantage of THPD is that it allows the patient to ambulate early and helps minimize deconditioning. Allowing the patients to be extubated earlier may be beneficial because positive pressure ventilation can impede RV preload by increasing intrathoracic pressure and decreasing RV transmural filling pressure.19

In our study, we observed that there was a significant amount of blood products that were transfused in the setting of acute RV failure. The blood transfusions took place in the setting of liver failure, coagulopathy, and gastrointestinal bleeding. There was no evidence of hemolysis related to the THPD. An increase in the RV preload with blood transfusions would cause RV dilation, free-wall tension, and oxygen demand.19

Acute RV failure has a reported mortality of 50%;1,2 interestingly, the overall survival rate in our cohort was 81.8% at 30 days (9 patients) and 72.7% at 180 days, as seen in our Kaplan-Meier curves, which suggests a benefit with mechanical support.

The first publication about THPD was 3 years ago.11 Nicolais et al20 reported the use of THPD in a small series of patients as a bridge to heart or lung transplant, for severe pulmonary hypertension, acute myocarditis, and post heart transplant RV failure. The only device complication reported was related to severe tricuspid regurgitation due to leaflet tethering that resolved after device removal. In our cohort, patients did not have direct complications related to the device; instead, they were related to the high morbidity associated with RV failure. Other series have reported the use of THPD post LVAD.12 Our cohort is unique because it reports the use after lung resection, pulmonary embolism, and acute myocardial infarction with right coronary artery involvement.

Study limitations. This study included a small number of patients, and data were retrospectively collected. This observational study was designed to collect data for informational and descriptive purposes and has not been powered to evaluate a hypothesis. The manuscript is expected to provide information to help understand clinical results that may lead to improvements in patient management, as well as device weaning and removal strategies. Additionally, only 4 of the 11 patients had hemodynamic data, which limits the use of right heart catheterization values for further assessment and weaning of patients with THPD. The echocardiographic data were incomplete in the reports due to the difficulty of obtaining good windows in postsurgical patients.

The THEME (TandemHeart Experiences and MEthods) registry will provide some insight into the use of the device.21 Other devices such as the Impella RP, Tandem RVAD, and ECMO provide RV support and could be a plausible alternative to be considered in cases of RV shock.


THPD is an option for mechanical support in RV failure and should be considered as a viable strategy in this high morbidity and mortality scenario. THPD can be used in conjunction with optimal medical therapy. Appropriate application can maximize the possibility of myocardial recovery. 

From the 1Division of Cardiology, Department of Medicine, 2Department of Medicine, Section of Cardiovascular Diseases, and 3Department of Cardiovascular and Thoracic Surgery, Rush University Medical Center, Chicago, Illinois; and the 4Division of Cardiovascular Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts.

Disclosure: The authors have completed and returned the ICMJE Form for Disclosure of Potential Conflicts of Interest. The authors report no conflicts of interest regarding the content herein.

Manuscript accepted July 27, 2020.

Address for correspondence: Clifford J. Kavinsky, MD, PhD, Rush University Medical Center, 1717 West Congress Parkway, Suite 307 Kellogg, Chicago, IL 60612. Email: clifford_j_kavinsky@rush.edu

  1. Melenovsky V, Hwang SJ, Lin G, Redfield MM, Borlaug BA. Right heart dysfunction in heart failure with preserved ejection fraction. Eur Heart J. 2014;35:3452-3462.
  2. Konstam MA, Kiernan MS, Bernstein D, et al. Evaluation and management of right-sided heart failure: a scientific statement from the American Heart Association. Circulation. 2018;137:e578-e622.
  3. Parekh M, Abrams D, Brodie D. Extracorporeal techniques in acute respiratory distress syndrome. Ann Transl Med. 2017;5:296.
  4. Lahm T, Douglas IS, Archer SL, et al. Assessment of Right Ventricular Function in the Research Setting: Knowledge Gaps and Pathways Forward. An Official American Thoracic Society Research Statement. Am J Respir Crit Care Med. 2018;198:e15-e43.
  5. Reddy S, Bernstein D. Molecular mechanisms of right ventricular failure. Circulation. 2015;132:1734-1742.
  6. Dunlay SM, Strand JJ, Wordingham SE, et al. Dying with a left ventricular assist device as destination therapy. Circ Heart Fail. 2016;9:e003096.
  7. Kowalewski J, Brocki M, Dryjanski T, Kapron K, Barcikowski S. Right ventricular morphology and function after pulmonary resection. Eur J Cardiothorac Surg. 1999;15:444-448.
  8. Wang Z, Yuan J, Chu W, Kou Y, Zhang X. Evaluation of left and right ventricular myocardial function after lung resection using speckle tracking echocardiography. Medicine (Baltimore). 2016;95:e4290.
  9. Okada M, Okada M, Ishii N, et al. Right ventricular ejection fraction in the preoperative risk evaluation of candidates for pulmonary resection. J Thorac Cardiovasc Surg. 1996;112:364-370.
  10. Okada M, Ota T, Okada M, Matsuda H, Okada K, Ishii N. Right ventricular dysfunction after major pulmonary resection. J Thorac Cardiovasc Surg. 1994;108:503-511.
  11. Aggarwal V, Einhorn BN, Cohen HA. Current status of percutaneous right ventricular assist devices: first-in-man use of a novel dual lumen cannula. Catheter Cardiovasc Interv. 2016;88:390-396.
  12. Ravichandran AK, Baran DA, Stelling K, Cowger JA, Salerno CT. Outcomes with the Tandem ProtekDuo dual-lumen percutaneous right ventricular assist device. ASAIO J. 2018;64:570-572.
  13. Mazimba S, Welch TS, Mwansa H, et al. Haemodynamically derived pulmonary artery pulsatility index predicts mortality in pulmonary arterial hypertension. Heart Lung Circ. 2019;28:752-760.
  14. Handoko ML, De Man FS, Oosterveer FP, Bogaard HJ, Vonk-Noordegraaf A, Westerhof N. A critical appraisal of transpulmonary and diastolic pressure gradients. Physiol Rep. 2016;4:e12910.
  15. Naeije R, Gerges M, Vachiery JL, Caravita S, Gerges C, Lang IM. Hemodynamic phenotyping of pulmonary hypertension in left heart failure. Circ Heart Fail. 2017;10:e004082.
  16. Ghio S, Temporelli PL, Klersy C, et al. Prognostic relevance of a non-invasive evaluation of right ventricular function and pulmonary artery pressure in patients with chronic heart failure. Eur J Heart Fail. 2013;15:408-414.
  17. Frea S, Bovolo V, Bergerone S, et al. Echocardiographic evaluation of right ventricular stroke work index in advanced heart failure: a new index? J Card Fail. 2012;18:886-893.
  18. Harjola VP, Mebazaa A, Celutkiene J, et al. Contemporary management of acute right ventricular failure: a statement from the Heart Failure Association and the Working Group on Pulmonary Circulation and Right Ventricular Function of the European Society of Cardiology. Eur J Heart Fail. 2016;18:226-241.
  19. Ventetuolo CE, Klinger JR. Management of acute right ventricular failure in the intensive care unit. Ann Am Thorac Soc. 2014;11:811-822.
  20. Nicolais CD, Suryapalam M, O’Murchu B, et al. Use of ProtekDuo TandemHeart for percutaneous right ventricular support in various clinical settings: a case series. J Am Coll Cardiol. 2018;71:A1314.
  21. Bermudez C CS, Coletti AT, O’Neill BP, et al. Percutaneous right ventricular support: initial experience from the Tandemheart experiences and methods (THEME) registry. ASAIO J. 2018;64.