Gait deficiencies associated with peripheral artery disease are different than chronic obstructive pulmonary disease

Abstract

Objective: Previous studies have indicated that patients with peripheral artery disease (PAD), display significant differences in their kinetic and kinematic gait characteristics when compared to healthy, aged-matched controls. The ability of patients with chronic obstructive pulmonary disease (COPD) to ambulate is also limited. These limitations are likely due to pathology-driven muscle morphology and physiology alterations establish in PAD and COP, respectively. Gait changes in PAD were compared to gait changes due to COPD to further understand how altered limb muscle due to disease can alter walking patterns. Both groups were independently compared to healthy controls. It was hypothesized that both patients with PAD and COPD would demonstrate similar differences in gait when compared to healthy controls.

Methods: Patients with PAD (n=25), patients with COPD (n=16), and healthy older control subjects (n=25) performed five walking trials at self-selected speeds. Sagittal plane joint kinematic and kinetic group means were compared.

Results: Peak values for hip flexion angle, braking impulse, and propulsive impulse were significantly reduced in patients with symptomatic PAD compared to patients with COPD. After adjusting for walking velocity, significant reductions (p<0.05) in the peak values for hip flexion angle, dorsiflexor moment, ankle power generation, propulsion force, braking impulse, and propulsive impulse were found in patients with PAD compared to healthy controls. No significant differences were observed between patients with COPD and controls.

Conclusions: The results of this study demonstrate that while gait patterns are impaired for patients with PAD, this is not apparent for patients with COPD (without PAD). PAD (without COPD) causes changes to the muscle function of the lower limbs that affects gait even when subjects walk from a fully rested state. Altered muscle function in patients with COPD does not have a similar effect.

Keywords: Chronic obstructive pulmonary disease; Gait; Kinematics; Kinetics; Peripheral artery disease; Vascular disease.

Fig. 1

Ensemble average stance phase curves showing angles, moments, and powers in the sagittal plane of the ankle, knee and hip and the vertical, braking-propulsion, and medial-lateral forces. Labels for peaks are as follows: PFA – peak plantarflexion angle; DFA – peak dorsiflexion angle; KFA – Peak knee flexion angle; KEA – peak knee extension angle; HFA – peak hip flexion angle; HEA – peak hip flexion angle; DFM – peak dorsiflexor moment; PFM – peak plantarflexor moment; KFM – peak knee flexor moment; KEM – peak knee extensor moment; HFM – peak hip flexor moment; A1–peak ankle power absorption during early stance; A2–peak ankle power absorption during mid to late stance; A3–peak ankle power generation; K1–peak knee power absorption during early stance; K2–peak knee power generation during mid stance; K3–peak knee power absorption during late stance; H1–peak hip power generation during early stance; H2–peak hip power absorption during mid to late stance; H3–peak hip power generation during late stance; VF1–peak vertical force during early stance; VF2–minimum vertical force during midstance; VF3–peak vertical force during late stance; BF – peak braking force; PF – peak propulsive force; MF – peak medial force; LF – peak lateral force. Variable which were significantly different between groups for ANCOVA are indicated by an asterisk (*) next to the name.

Fig. 2

Peak braking and propulsive impulses during stance phase for control subjects and patients with PAD and COPD after adjustment for self-selected walking speed. Significant differences * (p < 0.01).