Case Report and Brief Review

Use of Tandem Heart‚Ñ¢ as a Temporary Hemodynamic Support
Option for Severe Pulmonary Artery Hypertension Complicated
by Cardiog

Sanjay Rajdev, MD, Raymond Benza, MD, Vijay Misra, MD
Sanjay Rajdev, MD, Raymond Benza, MD, Vijay Misra, MD

The TandemHeart device (Cardiac Assist, Inc., Pittsburg, Pennsylvania), a percutaneous nonpulsatile centrifugal left ventricular (LV) assist device, is a recent introduction to the armamentarium of periprocedural hemodynamic stability tools. It has been used to support the poorly functional left heart in a variety of high-risk interventional procedures. TandemHeart has been used to assist the left ventricle while complicated interventional procedures like left main coronary artery stenting are carried out.1 It also has been found useful to allow the heart to recover from cardiogenic shock2 and myocarditis, postcardiotomy cardiac failure3 and during percutaneous aortic valve replacement in an animal model.4 However, its application thus far to support a poorly functioning right ventricle (RV) in the setting of severe pulmonary hypertension has not been described. We report our experience with the use of the TandemHeart device as a temporary hemodynamic support option for a critically ill young female with severe pulmonary artery hypertension complicated by cardiogenic shock.

Case Report. The patient was a 26-year-old African-American female who was referred to the department of cardiovascular thoracic surgery at the University of Alabama at Birmingham for evaluation of severe pulmonary artery hypertension. The patient had history of progressive worsening dyspnea over the past month which had progressed to NYHA class III at the time of her hospital presentation. Her past medical history was significant for an episode of viral illness manifesting as nausea, vomiting and diarrhea before the start of her worsening symptoms. She occasionally complained of migraine headaches. There was no history of tobacco, alcohol or drug abuse. Her grandmother died of dilated cardiomyopathy, and her sister had a trait for sickle cell. She had no history of syncope or diagnosed congenital heart disorder.

On examination, the patient had a heart rate of 124 beats/minute and her blood pressure was 129/82 mmHg. The central venous pressure was 9 cm of H20 with large V-waves and no hepatospleenomegaly. A pansystolic murmur was audible at the left lateral sternal border with a loud second heart sound. A RV S4 gallop was audible. The electrocardiogram showed evidence of tall, peaked P-waves (P pulmonale) with right-axis deviation and incomplete right bundle-branch block. Her body mass index was determined to be 1.82 m2. Blood workup and cultures for bacteremia, viremia and protozoa were negative. She tested negative for hypercoagulable states. A workup for pulmonary thromboembolism and connective tissue disorders was negative. A two-dimensional transthoracic echocardiography revealed a normal LV ejection fraction, but a reduced RV ejection fraction (35%). There was moderate-to-severe tricuspid regurgitation with severe pulmonary artery hypertension and moderate-to-severe pulmonary regurgitation. The estimated pulmonary artery systolic pressure by tricuspid regurgitation jet was 85 mmHg. A bubble study was carried out, which confirmed the presence of a patent foramen ovale with right-to-left shunt. Left and right heart catheterization confirmed a high pulmonary artery pressure of 90/35/54 mmHg. Her arterial blood pressure was 88/50/58 mmHg (Figure 1), and her cardiac index was 1.4 L/minute. The patient’s coronary arteries were normal.

A presumptive diagnosis of pulmonary hypertension of uncertain etiology was made, and the patient was started on intravenous dobutamine, digoxin, ramipril, carvedilol, aspirin, subcutaneous enoxaparin and inhaled nitric oxide at 10 ppm. Subsequently, pulmonary vascular reactivity testing was carried out using an infusion of intravenous epoprostenol sodium (Flolan), which was progressively increased from 2 ng/kg/min to 8 ng/kg/min. No change was observed in the hemodynamic variables assessed. A Swan-Ganz catheter was inserted through the right internal jugular vein for hemodynamic monitoring.

The condition of the patient deteriorated over the course of the next few days and she had worsening of dyspnea to NYHAClass IV with falling arterial saturation that was unresponsive even to escalating doses of inhaled nitric oxide (80 ppm) and intravenous epoprostenol (17 ng/kg/min). The dobutamine infusion was increased to 10 ug/kg/min and intravenous inotropes vasopressin and norepinephrine were started. The patient was electively intubated and mechanically ventilated. The patient’s relatives were thoroughly informed of the possible interventional options including an atrial septostomy, but opted for an experimental TandemHeart device.

Procedure. The patient was sedated and transferred to the cardiac catheterization laboratory. A 6 Fr canula was introduced into the right femoral vein and a Berman catheter was advanced into the pulmonary artery. An intravenous heparin bolus of 70 U/kg was administered. The patient’s cardiac output and index were 2.3 L/min and 1.26 L/min/m2, respectively. The systemic and pulmonary vascular resistances were both equal, at 2,468 dynes-sec/cm5. The systolic, diastolic and mean values for pulmonary and arterial blood pressure were 81/28/45 and 83/45/56 mmHg, respectively. The mean central venous pressure and pulmonary capillary wedge pressures were 17 and 6 mmHg, respectively (Table 1). The Berman catheter was then exchanged over a 0.038 inch J-tip double-length guidewire for a 6 Fr multipurpose catheter. The multipurpose catheter was then advanced into the main pulmonary artery through which a 0.038 inch J-tip 260 cm Amplatz Super Stiff guidewire (Meditech, Westwood, Massachusetts) was placed in the pulmonary artery. A 14 x 21 Fr twostage dilator was then used to dilate the proximal common femoral vein at the site of venous access. The 21 Fr TandemHeart transseptal canula was advanced along with the 13 Fr obturator over the Amplatz Super Stiff guidewire into the pulmonary artery up to the 60 cm mark, and its position was confirmed with an intracardiac echocardiography probe (Figure 2). The left common femoral vein was similarly dilated using the 14 x 21 Fr two-stage dilator, and then another 21 Fr TandemHeart transseptal canula along with its 13 Fr obturator was advanced up to the 44 cm mark until the right atrial/inferior vena caval junction was reached (Figure 3).

The peripheral ends of the canulae were sutured to the patient’s thigh and clamped. The right femoral venous canula was connected to the outflow conduit, and the left femoral vein canula was connected to the inflow conduit of the TandemHeart pump after performing de-airing, per the specified protocol. Thus, two wet-to-wet connections were performed attaching the TandemHeart pump to both of the transseptal canulae. The pump was started at 3,000 revolutions per minute (rpm), the clamps were removed and the pump speed was increased to 4,750 rpm, yielding 1.7 liters of blood flow. The speed of the TandemHeart pump was adjusted and titrated using the pump controller switch on the console to obtain optimal hemodynamics. Finally, the output was adjusted to 1.9 L/min with a pump speed of 4,900 rpm. Postprocedure, the patient’s cardiac output and index increased to 4.7 L/min and 2.58 L/min/m2, respectively. The systemic and pulmonary vascular resistance decreased to 1,548 and 1,424 dynes-sec/cm5, respectively. The values for pulmonary and arterial blood pressure increased to 104/34/52 and 87/57/68 mmHg, respectively, while the mean central venous pressure and pulmonary capillary wedge pressure changed slightly to 18 and 6 mmHg, respectively. The left and right heart work indices also showed dramatic improvement postprocedure (Table 1). The patient’s arterial blood gas saturation improved from 92% preprocedure to 99% postprocedure. The patient tolerated the procedure well and there were no procedure- related complications. The patient was transferred to the interventional intensive care unit for further care.

Hospital Course. The patient was hemodynamically stable and showed signs of improvement post TandemHeart deployment. A heparin infusion was started to keep the target activated clotting time (ACT) value at > 250 seconds. The TandemHeart pump speed was adjusted to 5,500 rpm, corresponding to a flow of 1.8 L/min. The patient’s cardiac output improved, with maximal pulmonary and arterial blood pressures of 109/33/53 and 115/68/85 mmHg, respectively, recorded during a 48-hour period postprocedure. Her pulmonary capillary wedge pressure increased to 11 mmHg and her arterial blood saturations rose to 99%. Unfortunately, attempts to wean her from hemodynamic and inotropic support were unsuccessful, and the patient expired 56 hours after the procedure.

Discussion. Available therapeutic options for primary pulmonary hypertension include vasodilators (oxygen, calcium channel-blockers, inhaled nitric oxide, adenosine and prostacyclin analogues), anticoagulants, digoxin and diuretics. Lung transplantation or combined heart and lung transplantation constitutes the definitive therapeutic modality for primary pulmonary hypertension. Given the rapid nature of progression of the disease and a median survival rate of only 2.5 years after diagnosis,5 patients with primary pulmonary hypertension are unlikely to survive until the organ becomes available. Atrial septostomy, a palliative treatment modality for primary pulmonary hypertension, has been associated with high mortality rates of up to 16%.6 The predictors for increased mortality include patients with impending death and patients with severe RV failure on maximal cardiorespiratory support.6 Hence, the benefits of atrial septostomy are best realized when done early in the course of the disease, since patients with severe right heart failure and impending death derive little benefit, if at all.7 This notion is supported by the recently published ACCP evidence-based clinical practice guidelines, which suggest that patients with the most advanced pulmonary artery hypertension, as defined by a very high pulmonary vascular resistance and low cardiac output, fare worse and are more likely to die after atrial septostomy.8 Moreover, the mortality rate is even higher if the procedure is performed at a center where the operators are inexperienced.9,10

The reason for not performing an atrial septostomy in our patient was three-fold. First, the patient was considered to be too high-risk for the procedure because of advanced primary pulmonary hypertension with extremely high pulmonary vascular resistance and pulmonary vascular resistance index, cardiogenic shock on inotropic and mechanical ventilatory support and impending death. Secondly, the procedure is not routinelyperformed in our cardiac catheterization laboratory, hence the risk of the patient dying was considered prohibitively high. The third and most important reason was the unwillingness of the patient’s relatives to give permission for the procedure.

While there has been some evidence that performing atrial septostomy in a select subset of patients does provide symptomatic relief and some survival benefit,11 the disease process per se, if unaffected by atrial septostomy, and the long-term effects are considered palliative at best.6 The hemodynamic consequences of the right-to-left shunt created by atrial septostomy are an increase in left heart cardiac output, a drop in right atrial pressure and a drop in arterial blood saturation. Contemporary studies of atrial septostomy for pulmonary hypertension7,9,10 have reported a modest rise in cardiac index (15–58%), a reduction of right atrial pressure (0–41%) and a reduction in arterial saturation (8–15%) postprocedure, while no change was observed in the pulmonary vascular resistance in these studies. In contrast, the insertion of a TandemHeart device in our patient led to a remarkable increase in her cardiac index (104%), an increase in arterial saturation (6%) and an impressive decrease in pulmonary vascular resistance (58%). Her mean arterial and pulmonary blood pressure both increased (Table 2). The elevation in pulmonary artery pressure was due to an increased amount of blood delivered via the TandemHeart pump to the pulmonary vasculature; however, it was of questionable physiological significance, since the ratio of systemic-to-pulmonary vascular resistance was favorably affected.

In addition, the cardiac work indices, which have not been reported in earlier studies, showed a favorable response postprocedure. There was a significant reduction in systemic vascular resistance and an improvement in mean arterial blood pressure postprocedure. The patient’s arterial saturation postprocedure increased to 99%, which was an improvement over her preprocedure saturation. This constitutes an important distinction from the atrial septostomy procedures previously reported that showed a definitive drop in arterial blood gas saturation due to a right-to-left shunt at the atrial level. Therefore, the use of the TandemHeart device led to a unique set of favorable hemodynamic parameters not obtained thus far in any previous attempt with atrial septostomy. Use of the TandemHeart device to provide hemodynamic support in right heart failure has not been reported in the literature. Our attempt to employ this device to temporarily provide hemodynamic support to the failing right ventricle was a last resort option for a “no-option” patient. Despite the patient having almost fixed pulmonary artery hypertension, we tested the device and observed that the patient was able to tolerate the increased volume of blood delivered through the device into the pulmonary vascular bed. The unique ability of the TandemHeart device to regulate the amount of blood delivered (by adjusting the pump speed and hence cardiac output) to the pulmonary vascular bed can be used to obtain the optimal set of hemodynamic variables for patients.

This is the first experience with the use of the Tandem-Heart device in a patient with primary pulmonary hypertension that showed favorable hemodynamics postimplantation. It provides a new therapeutic addition to the present strategies to treat primary pulmonary hypertension. Based on the encouraging hemodynamic data, we believe that this device should be further tested early in the course of the disease as a bridge to lung or combined heart-lung transplantation.




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