Left ventricular assist devices (LVADs) are now established therapy for bridging to cardiac transplantation and as permanent therapy in patients with advanced heart failure.1,2 Left ventricular assist devices very effectively treat pump failure, but ventricular arrhythmia can remain problematic for these patients.3 Previous reports have demonstrated that ventricular arrhythmias are hemodynamically well tolerated in patients with LVADs in situ,4–6 but data on the consequences of more prolonged episodes are not widely available. This case report serves to illustrate the clinical findings in a patient who had likely been in ventricular tachyarrhythmia for several days.
The patient was a 65-year-old male who had undergone implantation of a Heartmate II LVAD as a bridge to cardiac transplantation (Thoratec, Pleasanton, CA) 6 months before for ischemic cardiomyopathy and advanced heart failure. The patient was seen for the evaluation of a 1 week history of fatigue and dyspnea on mild exertion of new onset. The patient also noted new lower extremity swelling and increased his furosemide dosage from 20 mg alternate days to 20 mg daily without any effect. The LVAD pump speed had been stable at 9,600 rpm, but the flows had been reduced at 3.4–3.8 L/min and the pulsatility index (PI) had been considerably lower in the 1.8–2.3 range.
On arrival, the patient was comfortable and in good spirits. Clinical examination revealed the patient to be alert and mentating normally. The patient’s color was normal. Blood pressure was measured at 108 mm Hg by Doppler. The LVAD pump speed was 9,600 rpm. The flow was 3–3.5 L/min, and the PI 1.5–1.8. The patient’s neck veins were distended to the angle of the jaw, and no waveform was discernible. Auscultation of the precordium revealed a continuous mechanical hum, without any variation in frequency. No heart sounds were audible. Mild flank fullness was evident on examination of the abdomen in keeping with ascites. The extremities were warm and well perfused, but there was pitting edema of the lower extremities up to the level of the knees.
The patient was connected to the cardiac monitor, revealing a disorganized broad complex tachyarrhythmia. As the patient was alert and hemodynamically stable, a 12 lead electrocardiogram was recorded to have a permanent record of the arrhythmia (Figure 1), confirming coarse ventricular fibrillation.
Laboratory blood tests drawn on immediate arrival revealed the following: arterial blood gas analysis revealed a pH of 7.42 with Pco2 of 35.4 mm Hg, sodium 140 mmol/L, potassium 3.8 mmol/L, ionized calcium 4.7 mg/dl, glucose 217 mg/dl, and hematocrit 45%. Further laboratory tests demonstrated a serum sodium of 136 mmol/L, potassium 3.6 mmol/L, creatinine 0.9 mg/dl, blood urea nitrogen 18 mg/dl, and bicarbonate 21 mmol/L.
The patient was sedated with 25 mg of fentanyl and 3 mg of midazolam. A single unsynchronized 240 J DC shock cardioverted the patient to atrial fibrillation with a rate of 80–90 beats per minute. Immediately the PI increased to between 4 and 4.5, and flows increased between 4.5 and 5 L/min.
In view of his status as a bridge to transplant, it was decided to load with amiodarone and maintain this therapy until the time of transplantation. Electrolytes were supplemented and corrected and the patient responded well to intravenous diuretic therapy. Inotropic support was not required. He was dismissed from the hospital within 48 hours without any further sequelae. He ultimately proceeded to cardiac transplantation 7 months later, and there were no recurrences of ventricular arrhythmia in the intervening period based on subsequent automatic ICD interrogation.
The patient had an ICD in situ (Medtronic Entrust, Minneapolis, MN), but as was our practice at the time, ventricular tachyarrhythmia therapies were disabled. Unfortunately, detections were also disabled at that time, and therefore, the exact duration and nature of the arrhythmia before presentation could not be specified. Tachyarrhythmia detection was enabled at that point, but therapies remained disabled until the time of transplantation.
This case reports the presentation of an LVAD-supported patient in ventricular fibrillation of uncertain duration, but in the setting of a change in clinical symptoms for the preceding 5–7 days. Although there was evidence of right ventricular failure, with marked jugular venous distension, ascites, and lower extremity edema, the patient was mentating normally, maintaining an adequate systemic pressure, and had no evidence of end-organ impairment.
These findings are in keeping with the reports of other authors who have reported similar clinical findings in the setting of prolonged ventricular tachyarrhythmia (up to 12 days) with pulsatile ventricular assist devices.6 In these cases, similar findings of a reduction in LVAD flow and an increase in central venous pressure in keeping with right ventricular dysfunction were described. In all ambulatory patients described, there was no syncope or change in mentation, although most patients reported lethargy. This finding is further supported by more recent reports,4,7 the latter in a patient supported by a continuous flow device.
The present report is additive to this collective experience and describes the clinical sequelae of what was most likely several days of ventricular tachyarrhythmia. It is however the first report to describe an ambulatory patient presenting in ventricular fibrillation. It is probable that the initial arrhythmia was a monomorphic or polymorphic ventricular tachycardia, which degenerated into ventricular fibrillation, but the absence of ICD detection data before presentation precludes further elaboration.
The reason for tolerance of ventricular fibrillation with LVAD support in these cases likely relates to the creation of a Fontan-like physiology in the LVAD-supported patient with right ventricular dysfunction (Figure 2). Where the pulmonary vascular resistance is sufficiently low, even in the setting of poor, or even absent contractile function in the right ventricle, the off-loading of the left ventricle by the LVAD can result in indirect off-loading of the right ventricle across the pulmonary vasculature. The degree to which this may occur is largely dependent on the pulmonary vascular resistance. Although pulmonary vascular resistance decreases in most patients after LVAD support due to the effects of LV off-loading, the amount of reduction is variable and dependent on the degree of fixed pulmonary vascular disease, intrinsic pulmonary disease, and the efficacy of off-loading of the LV by the LVAD. Therefore, the degree of hemodynamic tolerance of ventricular tachyarrhythmias by LVAD-supported patients is also likely to be very variable.
In that regard, our decision to keep therapies inactive after this event was controversial. However, to date, no strict guidelines are yet available on the management of ICDs in LVAD-supported patients. In the majority, ventricular arrhythmias are well tolerated, but prolonged ventricular tachyarrhythmias are likely to lead to negative clinical consequences if not treated. Where the PVR is high, ventricular arrhythmia of even short duration is not likely to be well tolerated. Recommendations have since been made that given that ventricular arrhythmias remain common after LVAD implantation, the prophylactic ICD implantation should be considered.3,8 Therefore, our current practice is to implant an ICD where an indication would otherwise exist based on current guidelines9 and where an ICD has already been implanted, to keep therapies active, but keeping detection intervals longer to reduce shock burden. In this respect, recent recommendations regarding strategic ICD programming in patients receiving ICDs for primary prevention are helpful.10 However, frequent ICD shocks in heart failure patients have been shown to have a negative impact on long-term outcome,11 and this appears to be the case even where pump failure is effectively treated by a LVAD.12 It needs to be understood that the role of an ICD in the LVAD-supported patient is no longer to prevent sudden cardiac death, but rather to terminate ventricular arrhythmia which may lead to decompensation in clinical status. Our recent findings that outcomes in patients with ICD therapies active or inactive are similar post-LVAD implant13 underline that this is an issue that continues to require ongoing study and streamlining of the appropriate use of ICD technology in these patients. In practice, ICD therapies need to be individualized taking into account the preimplant arrhythmia history of each patient, and based on clinical judgment, how well ventricular tachyarrhythmias are likely to be tolerated after LVAD implantation.
No invasive hemodynamic data were available at the time of presentation, and an echocardiogram was not undertaken in the interests of proceeding to DC cardioversion as expeditiously as possible. Furthermore, the absence of ICD detection data from the time of LVAD implantation up to the time of presentation in ventricular fibrillation is a major limitation in accurately assessing the duration of ventricular fibrillation and the mechanism of onset.
Ventricular tachyarrhythmia such as ventricular fibrillation, which would usually be considered life threatening, may be tolerated for some time in LVAD recipients. Implantable cardioverter defibrillator shocks are therefore more likely to be experienced while awake by patients after LVAD implantation, and emerging data raise concerns regarding the effect or recurrent ICD shocks on overall outcome. These findings underline the need for ongoing study regarding the appropriate role of ICD therapy in these patients and the need for strategic programming of tachyarrhythmia therapies. The variability in hemodynamic tolerance of ventricular arrhythmia in LVAD recipients likely implies that such strategic programming will need to be individualized on a case-by-case basis.
The authors acknowledge the assistance of our secretarial staff with preparation of this manuscript, in particular Ms. Patra A. Baker.
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