In recent years, the population of patients implanted with a left ventricular assist device has been increasing. Ventricular arrhythmias are the most interesting and most deadly complications among patients with these implants. Ventricular arrhythmias may cause cardiovascular collapse and death in some cases, whereas they may be asymptomatic or less symptomatic in others. In the case described here, we present the therapeutic approach to a patient with a left ventricular assist device who had ventricular fibrillation and the pathophysiology of his clinical condition.
Key words : Heart failure, Mechanical circulatory support system, Ventricular arrhythmia
Heart failure (HF) has a poor prognosis and is a common cause of death in human populations.1 Despite the introduction of new drug regimens and high-risk cardiac surgery, many patients with HF with reduced ejection fraction progress to end-stage disease. Cardiac transplant is the first-line therapy for selected patients with end-stage HF.2 However, cardiac transplant has always been limited therapy option, and there is always need for alternative options. Patients with end-stage HF who cannot be stabilized with medical therapy can be treated by mechanical circulatory support systems (CSSs) to unload the failing ventricle and to maintain sufficient end-organ perfusion. The left ventricular assist device (LVADs) is one of the CSSs commonly used for patients with chronic HF. Although CSSs provide survival benefits, bleeding, thromboembolism (both of which can cause stroke), pump thrombosis, driveline infections, and device failure remain significant problems and can affect the long-term outcomes of patients with LVADs.3,4
One of the most common problems in patients with LVADs is ventricular arrhythmias. The Interagency Registry for Mechanical Circulatory Support study found that arrythmias were the third most common adverse event in patients with LVAD implants (0.9 events per patient-year), after infection (2.1 events per patient-year) and bleeding (2.0 events per patient-year).5 The increased number of LVAD implants are reflected in the literature as case reports of survivors with long-standing ventricular arrhythmia.6,7
In this case report, we present a patient with longer-term ventricular fibrillation survival after LVAD implantation. The patient provided permission to publish features of his history, and patient identity has been protected.
A 58-year-old male patient was admitted to our hospital with low-flow alarm on LVAD, with the implantable cardiac defibrillator providing 6 shocks and the patient having dizziness when he stood up. He had end-stage ischemic cardiomyopathy, hypertension, and diabetes mellitus in his medical history. Ventricular fibrillation was detected on his electrocardiogram (Figure 1). In interrogation of data from the implantable cardiac defibrillator, we noted 6 incidences of shock therapy, 12 hours of ventricular fibrillation, and no remaining battery life. Pacing, sensing functions, and impedances were normal. The patient had undergone LVAD implantation 2 years previously.
Patients with LVADs undergo annual right heart catheterization (RHC) in our clinic. The case patient underwent his last RHC 1 month before presentation. His results showed pulmonary capillary wedge pressure of 3 mm Hg, pulmonary artery pressure of 12 mm Hg, and pulmonary vascular resistance of 2.69 Wood units. The patient’s laboratory findings were unremarkable except for anemia (hemoglobin level of 10 mg/dL) and high-sensitivity troponin levels that were slightly above normal values.
Bedside transthoracic echocardiography was administered. The aortic valve was not opening, and the right ventricle and left ventricle were fibrillating. The Glasgow coma score of the patient was 15. Although the right ventricle was not working, the circulation system was completed by the LVAD. Blood was flowing from the right ventricle to the left atrium with support of the CSS.
The patient was hospitalized in the coronary intensive care unit. Amiodarone infusion was administered as a 300-mg bolus and 50 mg/h intravenous infusion was started. The patient was defibrillated with 200 J, resulting in cardiac rhythm returning to sinus rhythm (Figure 2). A battery replacement procedure was performed, and the patient was added to the emergency transplant wait list.
Our present case report demonstrated the life-saving benefit of LVADs while in a persistent ventricular fibrillation. This case is important because it suggests that LVAD supports a continuous circulation system while ventricles are fibrillating. Both our present case and the literature showed that low pulmonary artery pressure and pulmonary vascular resistance are linked with low mortality in patients with LVAD implants and ventricular fibrillation.8 In the management of patients with LVAD, regular RHCs are needed to allow modifications in revolutions per minute and doses of medications (eg, diuretics, vasodilators) so that patients can be protected from increased mortality after ventricular fibrillation.
Ventricular arrhythmias are a known adverse effect of LVADs; however, their overall incidence is low.8 So far, there are no consistent results about the mortality effects of ventricular arrhythmias in patients with LVADs. In a meta-analysis of observational studies, ventricular arrhythmias were shown to be associated with mortality.9 Another study showed that ventricular arrhythmias conferred a mortality rate as high as 33% compared with a mortality rate of 18% in LVAD recipients without ventricular arrhythmias.10 Although sustained ventricular fibrillation may be a lethal arrhythmia for patients supported by an LVAD, ventricular arrhythmias also seem to be well tolerated with symptoms of weakness or palpitation.9 The literature is also not consistent about the treatment and inadequate on suggestions to save patients with LVAD who present with ventricular fibrillations.10
In patients with low pulmonary vascular resistance threatened by LVAD, loss of right ventricular contractility is well tolerated, similar to that shown in our patient.9,10 We suggest that underlying pathophysiologies leading to survival include low pulmonary pressure (pulmonary vasculare resistance, pulmonary capillary wedge pressure, and pulmonary arterial pressure) and high central venous pressure. Although contractility may not occur in the right ventricle, LVAD may have enough preload for system circulation in patients with low pulmonary pressure and high central venous pressure. However, this does not mean that ventricular arrhythmias are not a life-threatening condition and do not need treatment. In patients with LVAD, ventricular arrhythmias can lead to death with cardiovascular collapse or end-stage organ damage.
After any LVAD implantation, we recommend placement of an implantable cardiac defibrillator, close monitoring, and early and repeated RHC procedures, with adjustment to LVAD parameters and medication doses as needed per RHC results. During sustained ventricular fibrillation, saline infusion and low-dose norepinephrine may be considered to increase central venous pressure and medical or electrical cardioversion is suggested. Finally, early cardiac transplant should be considered for ventricular fibrillation survival in patients with LVAD.
Although ventricular fibrillation can result in patient death, LVADs can save patients from death during ventricular fibrillation for hours or days. We suggest that ventricular fibrillation should be treated as we did, even when asymptomatic. Close monitoring and lower pulmonary pressure may save more lives in patients with LVADs.
DOI : 10.6002/ect.2021.0405
From the 1Department of Cardiology, 29 Mayis State Hospital; the 2Department of Cardiovascular Surgery; and the 3Department of Cardiology, Ankara Hospital, Başkent University Faculty of Medicine, Ankara, Turkey
Acknowledgements: The authors have not received any funding or grants in support of the presented research or for the preparation of this work and have no declarations of potential conflicts of interest.
Corresponding author: Ersin Doğanözü, 29 Mayis State Hospital, Department of Cardiology, Aydınlar, Dikmen Cd. No:312, 06105 Çankaya/Ankara, Turkey
Phone: +90 5325615870
Figure 1. Patient Electrocardiogram Showing Ventricular Fibrillation
Figure 2. Patient Electrocardiogram Showing Return to Cardiac Rhythm of Atrial Fibrillation