Patients with peripheral arterial disease exhibit reduced joint powers compared to velocity-matched controls

Abstract

Previous studies have shown major deficits in gait for individuals with peripheral arterial disease before and after the onset of pain. However, these studies did not have subjects ambulate at similar velocities and potential exists that the differences in joint powers may have been due to differences in walking velocity. The purpose of this study was to examine the joint moments and powers of peripheral arterial disease limbs for subjects walking at similar self-selected walking velocities as healthy controls prior to onset of any symptoms. Results revealed peripheral arterial disease patients have reduced peak hip power absorption in midstance (p = 0.017), reduced peak knee power absorption in early and late stance (p = 0.037 and p = 0.020 respectively), and reduced peak ankle power generation in late stance (p = 0.021). This study reveals that the gait of patients with peripheral arterial disease walking prior to the onset of any leg symptoms is characterized by failure of specific and identifiable muscle groups needed to perform normal walking and that these gait deficits are independent of reduced gait velocity.

Introduction

Peripheral arterial disease (PAD) is the result of thickening and hardening of the arterial walls [1]. Intermittent claudication (IC) is the most common symptom of PAD, characterized by pain, cramping, aching and tiredness [2]. It is exacerbated by activities such as walking and relieved upon rest [2], [3]. IC is associated with decreased physical activity, poor health outcomes, and increased dependence [1], [4], [5]. Spatial and temporal measures of gait in PAD patients are abnormal. Specifically, PAD patients walk slower, take shorter and wider steps, and spend more time in double support than their healthy counterparts [3], [6], [7], [8], [9], [10], [11]. Recently, our group has shown that PAD patients walk with altered gait kinematics and kinetics prior to the onset of pain [3], [6], [7], [12]. Specifically, the ankle takes longer to reach maximum dorsiflexion in late stance [8]. This limits the time for plantar flexion during propulsion. In addition, the ankle is unable to generate the power burst needed during push-off [3], [7]. Decreases in ground reaction forces [6], [13] as well as peak ankle plantar flexor moments and powers [3], [14] have been documented, providing evidence of the inability of PAD patients to propel themselves at the end of the gait cycle. Further alterations in the gait cycle [9] demonstrate the significant gait impairment of PAD patients prior to the onset of pain, even in the unaffected legs of patients with unilateral disease [3], [7].

These studies have provided valuable insight into the gait of PAD patients. However, these studies had PAD patients and healthy controls walking at their self-selected walking velocities, which were different between groups [3], [6], [7], [13], [14]. This provided the benefit of capturing the mechanics that the subjects would typically ambulate with, however, since walking velocity was significantly reduced for PAD patients in all of these studies, the true effect of walking velocity is not known. It is well established that the biomechanics of gait are dependent on the walking velocity [15], [16], [17]. Consequently, it is not entirely clear whether the alterations found in PAD gait are due to actual impairments in the lower limbs or an effect of a reduced walking velocity.

A similar issue has been present in the aging related research where elderly individuals walk with altered moments and powers at the hip, knee, and ankle joints compared to their healthy, younger counterparts [17], [17], [18], [19], [20], [21], [22]; but they also ambulate at slower velocities [20], [23]. Devita and Hortobagyi [17] addressed the issue of walking velocity as a possible confounder of elderly gait alterations by having subjects walk at a controlled velocity. They found that ankle kinetics were reduced while the hip kinetics had slight increases, demonstrating a redistribution of forces from distal to proximal musculature. However, they had all subjects walk at a controlled velocity, which likely would not have been the natural speed for all individuals, thus causing possible altered mechanics from their natural gait.

The purpose of this study was to compare joint moments and powers of healthy controls and PAD patients walking at a similar self-selected walking velocity. We hypothesized that despite ambulating at the same velocity as healthy controls, differences in peak joint moments and powers in PAD patients would persist.