**1. Introduction**

Heart failure (HF) is a general acute and chronic disease expressing the advanced stage of various types of heart disease, and its prevalence is increasing year by year [1]. As the risk of HF increases with age [2], elderly patients occupy more than four-fifth of all patients with HF. HF may reduce organ and physical functional capacity and their daily life performance in patients. HF greatly affects physical function as well as body composition of skeletal muscle, which is greatly correlated with high rates of morbidity, hospitalization, and mortality [3, 4].

Sarcopenia is a syndrome characterized by general skeletal muscle mass loss and strength, which is related to poor outcomes and high mortality in patients with a

variety of underlying diseases [5]. Although sarcopenia has been first defined as an age-related syndrome, it was also frequently associated with serious complications in even younger patients with advanced stage of HF [6, 7]. The alteration in the skeletal muscle system in patients with HF plays the main role in developing many signs and symptoms related to HF [8, 9]. Then, sarcopenia may significantly greatly attribute to the poor prognosis in patients with HF than in those of the same age without HF [8]. The rate of sarcopenia in a patient with HF is reported to be higher at 19.5% than that in healthy individuals of the same age [10]. Although sarcopenia is more frequently associated with increasing age, an even higher prevalence of 47% has been reported in patients younger than 55 years with dilated cardiomyopathy [11]. Therefore, the patient population with end-stage HF requiring ventricular assist device (VAD) or heart transplantation (HTx) may be different from those with less advanced HF.

Even in younger patients with end-stage HF, metabolic abnormalities related to sarcopenia develop and affect renal and hepatic function [11]. Skeletal muscle, which is the greatest reservoir of protein, is easily wasted in catabolic illness including end-stage HF. However, therapeutic interventions to reverse progressive local and systemic catabolism in advanced HF are limited. Growth hormone (GH) administration and aerobic exercise rehabilitation are known to increase insulinlike growth factor (IGF)-1 level in the blood and increase skeletal muscle volume in HF [12–14]. VAD implantation for bridge-to-transplantation (BTT) and destination therapy (DT) improves local and systemic metabolism probably due to corrected hemodynamics and tissue perfusion in patients with end-stage HF [15, 16]. Multiple literatures have reported that advanced strategies for HF, such as VAD implantation and HTx, provide optimal hemodynamic support and improve local and systemic metabolism, resulting in improvement of other organ function as well as physical capacity [17, 18].

Due to the great development in the field of left VAD (LVAD) in the past two decades, patients referred to this therapy are greatly increased. Although great advances in methodology and increased clinical experience in LVAD therapy had improved patient survival with end-stage HF over time, a certain amount of patients still has a high prevalence of mortality, comorbidity, and hospitalization after LVAD implantation, even in clinical trial settings [19]. As patients for DT are older and have more commodities before LVAD implantation than those for BTT, the use of LVAD for DT recently approved clinically worldwide may lead to higher mortality and morbidity in patients implanted with LVAD.

In this article, we review the impacts of both VAD and HTx on variables associated with sarcopenia as well as malnutrition in patients with end-stage HF and vice versa and discuss therapeutic interventions to reverse sarcopenia before and after LVAD implantation.

### **2. Diagnosis of sarcopenia**

According to the consensus on definition and diagnosis by the European Working Group on Sarcopenia in Older People (EWGSOP), sarcopenia is defined by the presence of both reduced skeletal muscle mass and function as well as reduced physical performance (**Figure 1**) [20]. Skeletal muscle strength is assessed by handgrip strength (HGS), whereas physical performance is assessed by usual gait speed. In the presence of reduced skeletal muscle function, defined by a reduced gait speed (<0.8 m/s) and/or a reduced HGS (<26–30 kg for men and <16–20 kg for women), the diagnosis requires verification of reduced skeletal muscle mass. Currently, magnetic resonance imaging (MRI) and computed tomography (CT)

*Sarcopenia in Patients with End-Stage Cardiac Failure Requiring Ventricular Assist Device or… DOI: http://dx.doi.org/10.5772/intechopen.100612*

**Figure 1.** *Sarcopenia assessment algorithm.*

have been the gold standard to accurately measure the mass of a skeletal muscle as well as its density and fatty infiltration.

The HGS is an easy and simple tool but suffers from that peripheral muscle strength and function might improve after LVAD implantation and HTx as previously described [21, 22]. To resolve these limitations, investigators in the field of mechanical circulatory support and HTx have begun to estimate the grade of sarcopenia by evaluating the mass of skeletal muscles, such as psoas and pectoralis muscles with clinical prognosis. Positive results have been reported in patients undergoing invasive thoracic and abdominal surgeries [23–26] as well as in those with advanced HF [27–29]. CT scans provide precise identification and quantification of individual skeletal muscle and fat tissue components [30–32].

Creatinine excretion rate index (CER index) in 24-hour urine collection is an easily measurable and less invasive classic marker of total-body skeletal muscle mass [33] and a reliable biomarker even in patients with advanced HF [34, 35]. Iwasaki et al. [36] reported that the CER index in patients with continuous-flow implantable LVAD (CF-LVAD) was significantly correlated with psoas and pectoralis muscles mass measured by CT scan.
