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The Texas Heart Institute Journal logoLink to The Texas Heart Institute Journal
. 2006;33(4):487–489.

Use of a Percutaneous Ventricular Assist Device for Treatment of Cardiogenic Shock due to Critical Aortic Stenosis

Christopher M Frank 1, Nanthini Palanichamy 1, Biswajit Kar 1, James M Wilson 1, Igor D Gregoric 1, Pranav Loyalka 1, Andrew B Civitello 1
PMCID: PMC1764950  PMID: 17215976

Abstract

We present the case of a 72-year-old woman who was transferred to our institution in cardiogenic shock and with multiple-organ failure, due to critical aortic stenosis. She was considered too high-risk to undergo aortic valve replacement. A TandemHeart® percutaneous ventricular assist device was used to stabilize the patient's condition before surgery, and she subsequently underwent successful aortic valve replacement. To our knowledge, this is the 1st report in the literature of this particular application of the TandemHeart device.

Key words: Angioplasty, transluminal, percutaneous coronary; aortic valve stenosis/complications/surgery; heart assist devices; heart bypass, left; heart valve prosthesis; multiple organ failure; shock, cardiogenic; stents

The TandemHeart® percutaneous ventricular assist device (pVAD) (Cardiac Assist, Inc.; Pittsburgh, Pa) has been used in more than 500 patients, either for temporary cardiac support during high-risk percutaneous coronary interventions,1–4 or as a bridge to emergency coronary bypass grafting, cardiac transplantation, or surgically implanted left ventricular assist device. The TandemHeart pVAD comprises an inflow cannula (placed in the left atrium via a transseptal approach from the femoral vein), a centrifugal continuous-flow pump, and an outflow cannula (placed in the descending aorta via the femoral artery). The TandemHeart is placed percutaneously under fluoroscopic guidance in the cardiac catheterization laboratory. The pump can provide a cardiac output of up to 4 L/min.1 With appropriate anticoagulation, patients can be supported for up to 2 weeks with this device in the intensive care unit (ICU).

Case Report

In May 2005, a 72-year-old woman in cardiogenic shock was transferred to our institution for possible emergency aortic valve replacement. Two years earlier, she had undergone coronary artery bypass grafting (with bilateral mammary artery grafts) at another institution. At that time, the patient was known to have moderate aortic stenosis, but valve replacement was deferred because of the small size of her aortic root. Her medical history also included hypertension, rheumatoid arthritis with associated pulmonary fibrosis, depression, irritable bowel syndrome, fibromyalgia, and esophageal reflux disease.

During the 6 months before admission to our institution, the patient had been hospitalized repeatedly for symptoms of congestive heart failure. Elective valve replacement had been recommended, but she was reluctant to undergo surgery. One month before admission, the patient was hospitalized for a skin rash and fever. After 3 of 11 blood cultures were positive for coagulase-negative staphylococcus, a presumptive diagnosis of aortic valve endocarditis was made, and a course of intravenous vancomycin was initiated. She became afebrile but developed progressive hemodynamic compromise and was therefore transferred to our institution.

During the transfer, the patient's condition became progressively unstable, and she required noninvasive positive pressure ventilation to manage her pulmonary edema. Within hours of her arrival, she required endotracheal intubation to maintain oxygenation; she developed shock that necessitated norepinephrine, vasopressin, dopamine, and sodium bicarbonate administration; and she became anuric, despite high doses of intravenous diuretic agents. Her blood urea nitrogen level was 65 mg/dL; creatinine, 2.8 mg/dL; total bilirubin, 4.1 mg/dL; alanine aminotransferase, 2,058 mg/dL; aspartate aminotransferase, 799 mg/dL; and arterial lactate, 106 mg/dL. Oxygen saturation levels were 92% despite 100% oxygen administration via an endotracheal tube. An echocardiogram showed mild left ventricular hypertrophy and mildly depressed systolic function (ejection fraction, 0.40–0.44), with global hypokinesis. The peak and mean gradients across the aortic valve (49 and 28 mmHg, respectively) and the calculated aortic valve area (0.7 cm2) indicated severe aortic stenosis. Emergency valve replacement was considered; however, given her clinical status, it was determined that the risk of death was unacceptably high. After discussion with the patient's family, it was decided to attempt a percutaneous intervention.

The patient was brought to the cardiac catheter-ization laboratory, where a TandemHeart pVAD was inserted. Intravenous heparin was administered to maintain an activated clotting time (ACT) >250 sec. The pump was started at 3,000 rpm, producing a flow rate of 1.7 L/min, and was titrated up to 5,000 rpm, producing a flow rate of 3 L/min. Within 15 minutes of device placement, the patient's oxygen saturation improved to 100%, and arterial blood pressures returned to normal. She was weaned completely from vasopressin and norepinephrine and was hemodynamically stable on dopamine alone (10 μg/kg per min). She also began producing urine at rates in excess of 100 cc/hr.

After TandemHeart implantation, a coronary angiogram showed a patent graft from the left internal mammary artery to an obtuse marginal artery, and a patent graft from the right internal mammary artery to the posterior descending artery. The left main coronary artery was 95% occluded at the ostium, and the left anterior descending artery was filling via the obtuse marginal artery. In an attempt to optimize coronary perfusion, percutaneous transluminal coronary angioplasty of the left main coronary artery was performed with a 3.0- × 9-mm angioplasty balloon (Maverick, Boston Scientific Corporation; Natick, Mass), followed by placement of a 3.0- × 13-mm sirolimus-eluting stent (Cypher, Cordis Corporation, a Johnson & Johnson company; Miami Lakes, Fla). Postdilation was performed with a 4.0- × 9-mm noncompliant balloon (Quantum Maverick, Boston Scientific Corporation) at 19 atm. An excellent angiographic result was achieved.

After 6 days in the ICU, the patient's condition stabilized. She was weaned from all inotropic support, and her renal and hepatic function normalized. She was then sufficiently stable to undergo aortic valve replacement with a 21-mm stentless aortic root bioprosthesis (Medtronic Freestyle, Medtronic, Inc.; Minneapolis, Minn) through a minimally invasive partial sternotomy. The pVAD support was discontinued during the surgical procedure and was successfully restored after the patient was weaned from cardiopulmonary bypass. The TandemHeart was removed 2 days later. The patient's postoperative course was prolonged and complicated by mediastinal bleeding that required repeat surgery for hematoma evacuation, ventilator dependence requiring tracheostomy, a urinary tract infection, drug-related thrombocytopenia, postoperative atrial fibrillation, and acute gout.

The patient was discharged to a rehabilitation facility 2 months after admission. At that time, she was ambulatory and breathing via a tracheostomy collar. Her mental status was normal, as were her renal and hepatic functions. An echocardiogram obtained 6 weeks after valve replacement surgery showed the systolic function to be at the lower limits of normal (ejection fraction, 50%). The peak gradient across the prosthetic valve was 27 mmHg and the mean gradient was 14 mmHg, which indicated that the bioprosthetic valve was functioning normally. Eighteen months after the procedure, the patient was living independently, had mild exertional dyspnea (New York Heart Association functional class I), and had no angina pectoris.

Discussion

To our knowledge, this is the first reported use of a pVAD in a patient in cardiogenic shock due, at least in part, to critical aortic stenosis. A recent report,5 however, described the use of a pVAD for support of a high-risk patient who had an unstable coronary syndrome and severe aortic stenosis and was undergoing a percutaneous coronary intervention. Unlike our case, that patient did not have multiple-organ failure and was not in shock. We believe that the pVAD is ideally suited for patients with aortic stenosis who are in cardiogenic shock, because the device provides hemodynamic benefits by lowering left atrial and left ventricular pressures while maintaining cardiac output. The hemodynamic benefits can be dramatic, as they were for our patient, in whom there was an almost immediate reversal of multiple-organ failure despite her moribund state and her expected operative mortality risk of nearly 100%.

The prognosis is extremely poor for patients who are in cardiogenic shock and have critical aortic stenosis and multiple-organ failure. Although there have been reports of such patients surviving emergency valve replacement surgery,6 surgeons are understandably reluctant to operate on patients with such a high risk of perioperative death. Percutaneous balloon aortic val-vuloplasty is another approach,7 but it is associated with an extremely high periprocedural mortality rate and provides only modest and transient improvement in symptoms and mortality rates.8–14 Although aortic valve replacement has been performed with the aid of percutaneous cardiopulmonary support,15,16 historically this approach has been used infrequently because of the morbidity and mortality rates associated with large arterial cannulae, hemolysis, thromboembolism, incomplete unloading, and because of the need for perfusionists and anesthesiologists.17,18

Patients with critical aortic stenosis who can safely undergo surgical replacement of the valve should do so; however, we believe that there may be a small number of high-risk patients ineligible for immediate surgery (for example, those with irreversible disease or in whom death is imminent) whose conditions can be successfully stabilized with the TandemHeart pVAD before they undergo aortic valve replacement.

Footnotes

Address for reprints: Andrew B. Civitello, MD, 1200 Binz, Suite 1290, Houston, TX 77004. E-mail: acivi@swbell.net

References

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