Management of Continuous Flow Left Ventricular Assist Device Patients in the Cardiac Catheterization Laboratory

Introduction 

In the United States, nearly 6 million individuals have been diagnosed with heart failure. Of these, an estimated 550,000 patients are in advanced heart failure (HF), defined as New York Heart Association (NYHA) Class IIIb or Class IV.¹ Historically, these patients slowly drifted into a category of medical futility with no option for meaningful recovery despite optimal medical therapy. 

In the modern era, the use of surgically implanted left ventricular assist devices  (LVADs) as a bridge therapy to either recovery or cardiac transplantation has shed light at the end of the HF tunnel. More recently, the use of LVADs as ‘destination therapy’ has further illuminated a future for patients with end-stage HF. 

Over 2000 LVADs are implanted annually in the United States alone.² In the modern era, LVADs have evolved from large, bulky pulsatile systems to smaller, compact, fully implantable continuous flow (CF) pumps that generate minimally pulsatile blood flow when functioning optimally. These CF-LVADs use rotodynamic pumps to transfer kinetic energy from a circulating impeller to the bloodstream, thereby generating forward flow. CF-LVADs can be divided into two categories: axial-flow and centrifugal-flow pumps. In both cases, blood is pulled into the impeller of the pump via an inlet cannula connected to the left ventricular apex and delivered to the systemic circulation via an outflow cannula connected to either the ascending or descending aorta (Figure 1). 

The physiology of axial versus centrifugal flow pumps was recently reviewed by Moazami and Starling et al in 2013.³ Briefly, several primary determinants of flow through a CF-LVAD include the speed of the rotor, the caliber of the inflow and outflow conduits, and the gradient of pressure across the pump from the inflow to outflow segments. When LVADs become dysfunctional, each of these three determinants of flow must be examined carefully. Rotor speed can become impaired by obstruction anywhere along the inflow to outflow segment. Obstruction can be caused by thrombus formation, kinking of an inflow or outflow conduit, or by pannus formation around the inflow ostium. Since flow is determined by a gradient of pressure across the inflow and outflow segments, CF-LVADs are highly sensitive to changes in preload and afterload. Decreased preload or increased afterload can reduce LVAD flows (Figure 2). For example, right ventricular failure may reduce left ventricular preload and lead to reduced LVAD flows. When LVADs become dysfunctional, physicians will evaluate the patient’s symptoms, laboratory values, device parameters, valvular function and hemodynamic status. When bedside examination, laboratory testing, echocardiography or other imaging studies fail to identify a cause for LVAD dysfunction, an invasive hemodynamic assessment may be necessary. 

Invasive diagnostic evaluation of patients with LVADs

The most common indications for diagnostic evaluation of LVAD dysfunction in the cardiac catheterization laboratory include: 1) signs and symptoms of left heart failure, 2) signs and symptoms of right heart failure, 3) chest pain, 4) abnormal LVAD alarms, 5) recurrent arrhythmia, or 6) hypotension (Table 1). Each of these clinical presentations carries a list of possible differential diagnoses that can often be narrowed after invasive hemodynamic assessment.

Evaluation in the catheterization laboratory begins with an assessment of right heart hemodynamics to determine cardiac filling pressures, total cardiac output, pulmonary pressures, right ventricular function and evidence of right-sided valvular disease. To further evaluate pump function, a ‘ramp’ study can be performed by measuring hemodynamic variables and LVAD parameters at incremental levels of flow through the device. Ramp studies can also be performed non-invasively and are used to optimize LVAD settings and to identify subclinical LVAD dysfunction.⁴ 

One of the most common causes of LVAD dysfunction is pump thrombosis. The incidence of CF-LVAD thrombosis is approximately 8% and is most commonly due to thrombosis of the pump bearings.^5,6 Signs of possible CF-LVAD thrombosis include clinical evidence of decompensated heart failure, changes in device parameters including power spikes and low flow alarms, laboratory evidence of hemolysis, failure to unload the left ventricle on an echocardiographic ramp study, and/or visualization of a filling defect in inflow or outflow cannulas on computed tomography (CT) angiography. However, confirming the diagnosis remains challenging and invasive hemodynamic assessment may be considered. Right heart catheterization often demonstrates a reduced cardiac output as measured by the Fick method in the setting of CF-LVAD thrombosis. In some cases, right heart catheterization alone may be insufficient to clarify a diagnosis and left heart catheterization may be required. In these cases, left ventriculography can be used to opacify inflow and outflow conduits, and intracavitary hemodynamics can be used to evaluate LVAD function. When CF-LVADs are functioning properly, both LV pressure and volume should be reduced, hence the term LV ‘unloading’. Therefore, under optimal pump conditions, LV systolic pressure should be lower than aortic systolic pressure.  

Other causes of CF-LVAD dysfunction include obstruction of inflow or outflow conduits, and valvular heart disease. Obstruction may be due to kinking, which can occur as some CF-LVADs shifts position within the chest cavity over time. The diagnosis of conduit obstruction can often be made by CT angiography. In the catheterization laboratory, ventriculography and intravascular ultrasound (IVUS) interrogation of the graft confirm the presence of an obstruction. Valvular heart disease such as aortic insufficiency and mitral regurgitation are important causes of CF-LVAD dysfunction. Echocardiography is sufficient to make the diagnosis of valvular disease in most cases. However invasive hemodynamics, aortography, and ventriculography can be used if non-invasive imaging is insufficient. 

Right heart failure can occur in 5-10% of patients after LVAD implantation.⁷ Echocardiographic parameters suggestive of right ventricular (RV) failure include RV dilatation, reduced RV ejection fraction, reduced excursion of the tricuspid annulus assessed by tissue Doppler imaging, and tricuspid regurgitation. Hemodynamic variables consistent with RV failure while on LVAD support include a right atrial pressure (RAP) of > 15 mmHg, RAP to pulmonary capillary wedge pressure (PCWP) ratio of > 0.6, and pulmonary artery pulsatility index (PaPi) score of < 1.⁸

Chest pain on LVAD support is a complex presentation that is most commonly due to non-cardiac causes. The true incidence of ischemic chest pain during LVAD support remains unknown. Acute myocardial infarction (AMI) can occur in LVAD patients and may be due to coronary plaque rupture. Other possible causes for AMI include paradoxical thromboembolism from a deep venous thrombosis, thromboembolism from an intracavitary thrombus in the left ventricle or from the aortic root, and LVAD failure leading to elevated LV filling pressures and impaired myocardial perfusion. Left heart catheterization should be performed only after carefully weighing the risks versus potential benefits (see Contraindications). Potential benefits of coronary intervention for patients with LVAD include 1) symptom relief, 2) prevention of arrhythmia, 3) reducing ongoing myocardial damage, and 4) supporting RV function. Future studies are required to evaluate the benefit of revascularization in the setting of LVAD support, especially as the number of patients receiving ‘destination therapy’ LVADs continues to grow. 

Contraindications to invasive hemodynamic testing in patients with LVADs

The same contraindications for cardiac catheterization apply to LVAD as in non-LVAD patients, with a few noteworthy considerations. First, arterial access under direct visualization may be facilitated by the use of ultrasound and the micropuncture technique, given that arterial flow is non-pulsatile in patients with CF-LVADs, who are often chronically anti-coagulated. Second, as the LVAD inflow cannula is positioned at the cardiac apex, every attempt to prevent catheter or wire entrapment in the LVAD should be taken. Catheter or wire entrapment could be fatal. Third, nearly 50-75% of LVAD patients develop some degree of commissural fusion of the aortic valve.⁹ Furthermore, aortic root thrombus can develop due to stasis when a CF-LVAD is fully functional. For these reasons, visualization of the aortic root to rule out thrombus and to evaluate aortic valve opening should be performed in advance of left heart catheterization or coronary angiography (Figure 3). Finally, prior to cardiac catheterization, all patients should be evaluated by an interventional cardiologist, heart failure/transplant specialist, and cardiac surgeon. This multidisciplinary approach is the best way to avoid complications and unnecessary procedures. 

Percutaneous interventions for patient with LVADs

As the number of patients with LVADs continues to grow, awareness of potential complications while on mechanical support are becoming more apparent. An evolving field in interventional cardiology is the development of techniques to percutaneously manage some of these complications. A few examples are listed below. 

Percutaneous left ventricular support: LVAD patients presenting with acute HF and hemodynamic instability due to device malfunction or LVAD thrombosis may require temporary circulatory support, either with an intra-aortic balloon pump, a percutaneous LVAD (i.e., TandemHeart (CardiacAssist)], or veno-arterial extra-corporeal membrane oxygenation (VA-ECMO). 

Percutaneous right ventricular support: Patients with RV failure refractory to volume resuscitation and pharmacologic support may benefit from short-term percutaneous mechanical support with either the Impella RP device (Abiomed) or right-sided TandemHeart until recovery or surgical RVAD placement.

Catheter-based LVAD thrombolysis:  Intracavitary thrombolysis to resolve LVAD thrombosis has been used in select patients deemed inoperable candidates for pump exchange or urgent transplantation (Figure 4). This approach may be considered in patients with: 1) continued evidence of hemodynamically significant LVAD thrombosis despite aggressive antiplatelet and antithrombotic therapy; 2) evidence of end-organ dysfunction; or 3) hemodynamic compromise.^10-14 Though data is limited, the potential advantages of intracavitary over systemic infusion of thrombolytics may include the ability to monitor changes in left ventricular hemodynamics, a reduction in the total dose of thrombolytic required, and a potentially lower risk of bleeding complications.¹⁵ 

Outflow graft stenting: Outflow graft balloon angioplasty and stenting offers an attractive therapeutic intervention for management of LVAD outflow obstruction without the need for a surgical intervention. Figure 5 illustrates successful deployment of a 10 mm x 37 mm Express LD balloon-expandable stent (Boston Scientific).¹⁶ 

Coronary revascularization: Data regarding coronary revascularization at the time of LVAD implantation or after LVAD implantation are lacking. Less than 5% of LVADs are explanted in the U.S. for LV recovery.¹⁷ Whether coronary revascularization in LVAD patients with severely depressed LV systolic function who demonstrate myocardial viability impacts clinical outcomes remains unknown. Specifically, whether revascularization can improve LV function while on LVAD support to the point of promoting LVAD explantation is poorly understood. All patients on CF-LVAD support being referred for percutaneous coronary intervention should be reviewed on a case-by-case basis by a multidisciplinary team. 

Percutaneous aortic valve therapy: Moderate to severe aortic insufficiency occurs in approximately 11% of the CF-LVAD population within 4 years of implantation. Several reports described an incidence ranging between 7 to 46% within the first 3 years of CF-LVAD implantation.¹⁸ Aortic insufficiency most commonly develops due to commissural fusion of the aortic valve leaflets while on CF-LVAD support. Once present, moderate to severe aortic insufficiency can reduce systemic perfusion and lead to worsening left heart failure. Treatment options include surgical repair or replacement of the aortic valve, LVAD exchange, and cardiac transplantation. Percutaneous closure and replacement of the aortic valve has been described and should be considered in poor candidates for operative repair or patients being supported by CF-LVADs as destination therapy.^19-23

Ventricular tachycardia ablation: Analogous to the management approach of non-LVAD patients, catheter ablation for ventricular tachycardia (VT) should be considered in CF-LVAD patients with incessant VT or in those receiving recurrent implantable cardioverter-defibrillator (ICD) shocks not manageable by reprogramming and antiarrhythmic therapy. Despite the advantage of full LV support in CF-LVAD patients during catheter ablation, sustained and frequent VT can cause hemodynamic instability and shock due to RV dysfunction, loss of atrioventricular synchrony, and impaired left ventricular filling. 

Contrary to previous case reports, intrinsic myocardial scar, rather than the apical inflow cannulation site, appears to be the dominant substrate as noted in one recent report that included 21 patients referred for VT ablation.²⁴ Left ventricular access for electroanatomic mapping using the Carto navigational system (Johnson & Johnson, Biosense-Webster) or EnSite NavX (St. Jude Medical) often requires a trans-septal approach as retrograde LV access via the aortic valve may be prohibited by a closed aortic valve in some patients with CF-LVAD.²⁵ Operators should avoid insertion of mapping and ablation catheters into the inflow cannula; however, data with respect to tendency of mapping catheters to be drawn into the inflow cannula remains limited.^24-26 Finally, due to limited catheter maneuverability in the fully unloaded LV, a lower success rate of VT ablation is possible.

Conclusions

In 2001, a prophetic editorial by James Fang, MD, accompanied one of the first reports describing the potential long-term benefits of LVAD therapy in advanced heart failure and was appropriately titled ‘Rise of the Machines’.²⁷ The rising use of machines to support heart function has led to increased awareness of device-associated complications. The cardiac catheterization lab offers a platform for invasive hemodynamic assessment to diagnose a variety of those complications in addition to an emerging number of therapeutic interventions. Larger studies are needed to better define the role of such advanced therapeutics in the treatment algorithm of device malfunction. As we move forward in time, rise of the machines will now include a rising tide of mechanics to improve the quality and quantity of life for patients living with LVADs.

Disclosure: Dr. Kapur reports he is a consultant to Thoratec Inc. and Heartware Inc., and receives research support from Heartware Inc. Dr. Jumean reports no conflicts of interest regarding the content herein.

The authors can be contacted via Dr. Navin Kapur at: nkapur@tuftsmedicalcenter.org

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