Author + information
- Received April 10, 2003
- Revision received November 18, 2003
- Accepted November 24, 2003
- Published online May 5, 2004.
- Steven C. Horton, MD, FACC†,‡,* (, )
- Reza Khodaverdian, MD*,
- Amanda Powers, BS†,
- James Revenaugh, MD, FACC†,‡,
- Dale G. Renlund, MD, FACC†,‡,
- Stephanie A. Moore, MD, FACC*,†,
- Brad Rasmusson, MD*,†,
- Karl E. Nelson, BS, MBA† and
- James W. Long, MD, PhD*,‡
- ↵*Reprint requests and correspondence:
Dr. Steven C. Horton, 324 10th Avenue, Suite 206, Salt Lake City, Utah 84103, USA.
Objectives A protocol was designed to diagnose the common malfunctions of a left ventricular assist device (LVAD).
Background Mechanical circulatory support, primarily with an LVAD, is increasingly used for treatment of advanced heart failure (HF). Left ventricular assist device dysfunction is a recognized complication; but heretofore, a systematic method to accurately diagnose LVAD dysfunction has not been thoroughly described.
Methods We developed a catheter-based protocol designed to characterize a normally functioning LVAD and diagnose multiple types of dysfunction. A total of 15 studies of 10 patients supported with an LVAD were reviewed. All patients had been evaluated due to concerns regarding LVAD dysfunction.
Results Of 15 examinations performed, 11 documented severe LVAD inflow valve regurgitation. One of these cases proved to have coexistent severe mitral valve regurgitation. One case was diagnosed with distortion of the LVAD outflow graft. One case of suspected embolization from the pumping chamber excluded the outflow graft as the source of emboli. One study had aortic insufficiency.
Conclusions As LVAD use for treatment of end-stage HF becomes widespread and durations of support are extended, dysfunction will be increasingly prevalent. This catheter-based protocol provided a practical method to diagnose multiple causes of LVAD dysfunction.
Mechanical circulatory support, primarily with a left ventricular assist device (LVAD), is increasingly used to treat advanced heart failure (HF). Short-term LVADs are highly successful in bridging patients with end-stage HF to transplantation (1,2). Additionally, the Randomized Evaluation of Mechanical Assistance for the Treatment of Congestive Heart Failure (REMATCH) trial showed that patients with New York Heart Association functional class IV congestive HF, who were ineligible for heart transplantation, received a longer-term survival benefit from the LVAD than from optimal medical therapy (3). Thus, LVAD technology has also been proven to be effective for long-term HF treatment, frequently referred to as “destination therapy.” Given the substantial number of patients with end-stage HF, as well as the potential benefits offered by mechanical circulatory support, it seems likely that LVAD use will become a more widespread, mainstream treatment.
As LVAD use becomes more commonplace, the care of LVAD patients will gradually shift away from surgeons toward cardiologists. This follows the pattern that emerged as heart transplantation became widely accepted and as surgical complications were minimized. While the initial surgery remains under the proper purview of surgeons, ever more cardiologists are asked to manage patients who have LVADs. These cardiologists and others who treat these patients must, therefore, also deal with the inherent risks in LVAD use, sometimes complications beyond their immediate expertise. One primary concern is LVAD device failure, the second leading cause of death in the REMATCH study (3).
We sought to better understand the normal physiology of LVADs, troubleshoot dysfunctional devices, and diagnose the most common modes of dysfunction. To date, only a few catheter-based case reports have been published (4,5). Using a systematized approach based on cardiac catheterization, we evaluated patients with the HeartMate LVAD (Thoratec Corp., Pleasanton, California), used either as bridge to transplant or as destination therapy. The protocol we developed helped characterize a normally functioning LVAD and diagnosed multiple types of dysfunction, including LVAD inflow valve regurgitation (IVR), outflow graft distortion, aortic insufficiency, and possible sources of device-associated embolization. The protocol offers a useful tool for cardiologists and others in managing LVAD patients.
Our pool of patients were all those who had received the HeartMate VE or XVE LVAD since September 1999. Demographic details of those studied are summarized Table 1. Of these, six had received the LVAD as a bridge to transplant; four had received the LVAD as destination therapy. All evaluations occurred between June 2000 and July 2002.
Overall, 15 studies using 10 patients on HeartMate LVADs were reviewed. All patients were evaluated for suspected LVAD dysfunction. The function of each LVAD was tested according to our catheterization laboratory protocol for assessing LVAD function, combining catheterization data with angiography. The protocol is summarized in Table 2.
All patients were simultaneously evaluated by echocardiography (6).
Evaluation of patient differences for cardiac output, LVAD flow, and related factors are presented for patients with and without IVR. Values are presented as means with standard deviation, and Student ttest was used to evaluate the significance of differences between inflow valve groups, with two-tailed p values and 0.05 considered nominally significant.
After compiling the assessments, we were able to define a normally functioning LVAD, depicted in Figure 1. Any normally functioning LVAD in the auto mode (rate automatically adapted by the device according to the blood volume available) has all of the following seven characteristics:
1) Pulmonary capillary wedge pressure (PCWP) is normal. The right heart pressures reflect a well-decompressed left ventricle (LV). For the PCWP to be considered normal, it must be normal in the auto mode or, after being converted from the “fixed-rate” mode, the PCWP must normalize within 5 min after conversion.
2) Cardiac output as indicated in the LVAD monitor is approximately the same as the thermodilution-derived cardiac output as long as no native LV ejection is occurring through the aortic valve.
3) Aortic blood tracings do not display any significant beat-to-beat variability. In the absence of a native LV contribution, aortic pressure is purely mechanical. It should, therefore, be “clockwork regular.”
4) There is no pressure gradient within the LVAD outflow graft; there is no significant systolic gradient across the LVAD outflow valve. These correspond to the pressures measured in condition 2, 3, 4, and 5 checked in the catheterization laboratory protocol (Table 2).
5) The outflow graft appears smooth without distortion (Fig. 2).
6) There is no regurgitation of the LVAD outflow valve on angiography.
7) Left ventricular pressures typically remain less than aortic pressures. The LV pressures vary related to their timing with the LVAD cardiac cycle. Hemodynamic parameters from a normal study are shown in Table 3.
Using this definition of normal function as a baseline, we sought to diagnose several types of LVAD dysfunction: LVAD IVR, outflow graft distortion, embolization from LVAD pumping chamber, and acquired aortic valve disease. Our findings with respect to each type of malfunction are discussed in detail in the following text.
LVAD inflow valve regurgitation
Inflow valve regurgitation causes ineffective decompression of the LV, and a volume overloaded state, which eventually renders the LVAD unable to completely decompress the LV. Inflow valve regurgitation can be caused by a torn cusp or commisure dehiscence of the prosthetic valve. This can be the result of high pump chamber pressure. Conditions that can more rapidly lead to this IVR include significant hypertension and outflow graft twisting or distortion (7).
Clinically, these patients typically presented with prolonged, excessively fast LVAD rates (115 to 120 beats/min) when placed in the auto mode. This produces the condition colloquially known as “runaway VAD.” Of 31 VE-LVAD patients implanted between 1999 and 2001, we diagnosed 11 with significant IVR (32%). The average time from implantation to first onset was six months. The earliest onset was 2 months after implantation; the latest onset was 15 months after surgery.
Of our 15 angiographic examinations, 11 were diagnosed with severe IVR. One experienced coexistent severe mitral valve regurgitation. At angiography, the LV became opaque when radiocontrast dye was regurgitated into the LV after injection into the LVAD beyond the inflow valve. This correlated well with observations made simultaneously with echo-Doppler studies (8). Hemodynamically, patients with IVR differed from normal in the following ways:
1) Right heart pressures reflect a non-decompressed LV. The PCWP is elevated in the fixed mode and rarely returns to normal in the auto mode. This is observed upon insertion of the thermodilution catheter and in conditions 7 and 8 of our protocol.
2) The actual cardiac output, as measured by thermodilution or Fick methods, is significantly less than those displayed on the LVAD system monitor, indicative of the degree of ineffective cycling of blood.
3) The LVAD rate accelerates and remains at maximal rates in the auto mode.
4) Aortic blood pressures may vary significantly over many consecutive beats and follow a periodic pattern. Examples of this variability are shown in Figure 3.
5) Simultaneous LV and aortic pressure tracings reveal elevated aortic pressures when left ventricular systole and LVAD systole occur synchronously. When the systoles occur non-synchronously, the aortic pressures are decreased (Figs. 3 and 4). ⇓
6) Because of the regurgitant volume, LV diastolic pressures (IVR wave) are more elevated during asynchronous periods of LVAD pumping. Figure 4illustrates this wave pattern.
7) Angiography reveals regurgitation of radiocontrast dye into the LV with injection beyond the LVAD inflow valve.
8) In patients with coexistent mitral regurgitation, significant v waves are present in the PCWP tracing.
In patients without IVR, cardiac output exceeded LVAD flow by an average of 11% (range, 0% to 11.4%). In patients with LVAD IVR, the mean LVAD flow was, on average, 32.6% higher (range, 16.3% to 38.9%). When compared with patients without IVR, patients with IVR showed significantly lower cardiac output, higher LVAD flows and rates, and a greater difference between cardiac output and pump flow (p < 0.001). This data is summarized in Table 4.
Two other conditions that could lead to discrepancies between measured cardiac output and LVAD flow rates are aortic insufficiency and LVAD outflow valve insufficiency. We did not detect any cases with these problems.
This protocol was not designed for detection of inflow valve obstructions that could occur in the setting of hypertrophic cardiomyopathy, vegetations, or other impingements of the inflow cannula. Detection of that would require introduction of two pressure catheters, one in the LV and one in the body of the LVAD, with simultaneous pressure measurements.
Outflow graft distortion
One of our patients was diagnosed with distortion of the LVAD outflow graft resulting from LVAD displacement in a morbidly obese patient. Clinically, this patient presented with hemolytic anemia. His alarms indicated his LVAD was pumping against high pressures. Systolic pressure obtained within the LVAD pumping chamber (condition 10) was 324 mm Hg. At angiography, the outflow graft demonstrated an acute angle bend, making it impossible for a guide wire to pass beyond the kinked graft. This distortion was confirmed at the time of surgery.
One of our patients was diagnosed with embolization from the pumping chamber of a failed LVAD as a diagnosis of exclusion. He presented with acute bilateral leg pain. Angiography revealed a clot at the aortoiliac bifurcation. Because angiography of the outflow graft excluded the graft as the source of the thrombus, we were able to choose an abdominal approach to replace only the LVAD pump. After explant, we confirmed that a thrombus was within the LVAD chamber. On review, this patient had been exposed, without anticoagulation, to a long period of sub-optimal flow dynamics with inadequate filling and emptying while his LVAD was activated pneumatically.
Acquired aortic valve disease
Both acquired aortic stenosis and insufficiency are known to develop during LVAD therapy (9,10). One of our patients had minimal, asymptomatic aortic insufficiency. Angiography performed in condition 3 of the protocol offers adequate opacification of the ascending aorta to test for this condition. If high-grade aortic stenosis was suspected, then detection would be improved by dropping LVAD rates to low levels in order to adequately detect a gradient, because gradients are directly proportional to native ventricular outflow across the native valve. However, detection of aortic stenosis is not usually clinically necessary because an LVAD can function normally in the setting of aortic stenosis (11). Aortic stenosis would be very relevant in the setting of LVAD failure, or when the LVAD is used as a bridge to recovery.
No serious complications occurred using our protocol. There were no complications of bleeding, infection, vascular trauma, or stroke.
Two patients experienced transient arrhythmias. Most arrhythmias are tolerated with a well-functioning LVAD. One patient developed ventricular fibrillation during catheterization. The patient remained hemodynamically stable on LVAD support and was easily cardioverted back into normal sinus rhythm. This arrhythmia is illustrated in Figure 7.
A unique rhythm situation arose when exchange guide wires were used to place a multi-purpose catheter across the inflow valve within a VE-LVAD. We believe these guide wires transmitted a small electrical current that was sensed by the surface electrocardiogram leads. While in normal sinus rhythm, one patient's defibrillator interpreted the otherwise benign current as ventricular fibrillation and issued defibrillating shocks. The electrocardiograms that resulted are depicted in Figure 8. To avoid this situation, the protocol now calls for defibrillators and pacemakers to be appropriately reprogrammed during catheterization.
Left ventricular assist device malfunction is an important cause of morbidity and mortality (3). The incidence of device malfunction will increase in the future as durations of support exceed the life expectancy of current generation LVADs. As cardiologists provide care for an increasing number of LVAD patients, it is particularly important that they be able to accurately diagnose and successfully troubleshoot a dysfunctional device. This paper presents a catheter-based protocol designed to meet that need. By using this diagnostic tool, cardiologists and others who care for LVAD patients should be able to successfully identify most malfunctions of the LVAD.
The authors gratefully appreciate the assistance of Ashley Renlund and Patricia Horton in preparation of the manuscript, and the care given to our patients by Brandi Porter, RN.
- heart failure
- inflow valve regurgitation
- left ventricle/ventricular
- left ventricular assist device
- pulmonary capillary wedge pressure
- Randomized Evaluation of Mechanical Assistance for the Treatment of Congestive Heart Failure
- Received April 10, 2003.
- Revision received November 18, 2003.
- Accepted November 24, 2003.
- American College of Cardiology Foundation
- ↵Ferns J, Dowling R, Bhat G. Evaluation of a patient with left ventricular assist device dysfunction. ASAIO J 2001:47696–8.
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