Abnormal joint powers before and after the onset of claudication symptoms

Abstract

Objective Claudication is the most common manifestation of peripheral arterial disease, producing significant ambulatory compromise. The purpose of our study was to evaluate patients with bilateral lower limb claudication and characterize their gait abnormality based on advanced biomechanical analysis using joint torques and powers. Methods Twenty patients with bilateral claudication (ten with isolated aortoiliac disease and ten with combined aortoiliac and femoropopliteal disease) and sixteen matched controls ambulated on a walkway while three dimensional biomechanical data were collected. Patients walked before and after onset of claudication pain. Joint torques and powers at early-, mid-, and late-stance for the hip, knee and ankle joints were calculated for claudicating patients before and after the onset of claudication pain, and were compared to control subjects. Results Claudicating patients exhibited significantly reduced hip and knee power at early-stance (weight acceptance phase) due to decreased torques produced by the hip and knee extensors. In mid-stance (single limb support phase), patients had significantly reduced knee and hip power due to the decreased torques produced by the knee extensors and the hip flexors. In late-stance (propulsion phase), reduced propulsion was noted with significant reduction in ankle plantar flexor torques and power. These differences were present before and after the onset of pain with certain parameters worsening in association with pain. Conclusions The gait of claudication is characterized by failure of specific and identifiable muscle groups needed to perform normal walking (weight acceptance, single limb support and propulsion). Parameters of gait are abnormal with the first steps taken, in the absence of pain, and certain of these parameters worsen after the onset of claudication pain.

Abnormal myofiber morphology and limb dysfunction in claudication

“…A widely held view concerning the pathophysiology of claudication has been that limb dysfunction and walking limitation of claudicating patients are produced exclusively by exercise-induced ischemia in the muscles of the lower limb. Published work from our group and others [4–6,21] has revised this view by documenting the presence of a myopathy in leg muscles of patients with PAD and demonstrating a constellation of baseline, gait abnormalities of rested patients, before the onset of claudication [10,11,22–25], when tissue oxygen levels [26] and blood flow [13] in the leg are similar to (and sometimes even higher than) those of controls. Furthermore, measurements of muscle strength in PAD patients determined as 5-s maximal isometric strength, a blood flow-independent assessment [12], demonstrated that muscle strength in PAD patients is significantly reduced compared with that of controls.…”

Abnormal Accumulation of Desmin in Gastrocnemius Myofibers of Patients with Peripheral Artery Disease

“…Dalakas et al (2000) proposed that accumulation of damaged desmin in association with disruption of the filamentous network weakens the sarcomere and causes increased mechanical stress within and between myofibrils, myofiber fragility, Z-disc disintegration and myofibrillar damage. Similarly, the accumulation and abnormal distribution of desmin in PAD myofibers, which signal damage to the cytoskeleton, may contribute to decreased strength of leg muscles, impaired limb function and decreased activity in patients with PAD (Hedberg et al 1988b;Koutakis et al 2010a;Koutakis et al 2010b;McDermott et al 2004;McDermott et al 2007;McDermott et al 2001;Regensteiner et al 1993). Myofibers, in long skeletal muscles, are much shorter than the muscle length and, as a result, most of them start and finish without attaching themselves to either tendon (Gaunt and Gans 1990;Schejter and Baylies 2010;Trotter 2002).…”

“…Work from several laboratories including our own has demonstrated a myopathy in the affected lower extremities of patients with PAD, which is characterized by mitochondrial dysfunction, increased oxidative damage, myofiber degeneration, muscle fibrosis and decreased muscle force production (Brass and Hiatt 2000;Cluff et al 2013;Hedberg et al 1989;Hedberg et al 1988b; Koutakis et al 2010a;Makitie and Teravainen 1977;Makris et al 2007;Marbini et al 1986;McDermott et al 2004;McDermott et al 2012;Pipinos et al 2007;Pipinos et al 2003;Regensteiner et al 1993;Weiss et al 2013). This myopathy is closely related to leg function, daily activity, quality of life and even mortality of patients with PAD (Anderson et al 2009;Brass 1996;Evans et al 2011;Gardner et al 2013;Garg et al 2011;McDermott et al 2009;McDermott et al 2012; Thompson et al 2014).…”

Muscle strength and control characteristics are altered by peripheral artery disease

“…2–9 The myopathic changes are associated with decreased quality of life, 10 leg function, 11–12 poor health outcomes and mortality in patients with PAD. 12–13 Furthermore, the functional effects of the myopathy are most clearly seen in the gait alterations 14–22 claudicating patients demonstrate from the first step they take before they experience any exercise-induced ischemia or pain. 14–16,18–19 The altered gait profile found in PAD patients presents as decreased muscle power contributions at the ankle, knee, and hip joints.…”

“…Among these findings, the compromised biomechanics at the ankle joint are the most consistent deficits seen in patients with PAD compared with Controls. 15,18,21–22 These alterations include a lack of controlling the downward, plantar flexion motion of the foot upon heel strike, 19 decreased ankle power generation during push off, 22 decreased plantar flexion impulse, 16 decreased energy output during the push-off phase of gait, 15 and altered ankle angle variability. 14 These findings equate to an overall reduced ability for a patient with PAD to propel themselves forward during the late stance phase of gait and are present from the first step the patients take while they become exacerbated after the onset of claudication pain.…”