Calf Muscle Characteristics, Strength Measures, and Mortality in Peripheral Arterial Disease

McDermott, Mary M.; Liu, Kiang; Tian, Lu; Guralnik, Jack M.; Criqui, Michael H.; Liao, Yihua; Ferrucci, Luigi

doi:10.1016/j.jacc.2011.12.019

Cited by 105 publications

(113 citation statements)

References 21 publications

(58 reference statements)

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“…25, 26 Patients with severe PAD are likely to have muscle sarcopenia due to intermittent claudication, rest pain, and CLI. 27 In the present study, PAD severity was significantly associated with muscle sarcopenia, as measured with FFMI. Therefore, it is possible that eGFRcys is superior to eGFRcr for evaluating kidney function Tables 1,2. …”

Section: Gfr and Muscle Sarcopeniasupporting

confidence: 53%

Cystatin C-Based eGFR Is a Superior Prognostic Parameter to Creatinine-Based eGFR in Post-Endovascular Therapy Peripheral Artery Disease Patients

Otaki

Takahashi

Watanabe

et al. 2015

Circ J

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Section: Gfr and Muscle Sarcopeniasupporting

confidence: 53%

Cystatin C-Based eGFR Is a Superior Prognostic Parameter to Creatinine-Based eGFR in Post-Endovascular Therapy Peripheral Artery Disease Patients

Otaki

Takahashi

Watanabe

et al. 2015

Circ J

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“…131 Overall leg strength has also been shown to associate with mortality in men, but not women, with PAD. 132 Taken together, these findings suggest that the morphological changes in calf muscle predispose to significant functional decline and may be an additional marker for increased risk among patients with symptomatic PAD.…”

Section: Skeletal Muscle Structural Abnormalitiesmentioning

confidence: 99%

Pathogenesis of the Limb Manifestations and Exercise Limitations in Peripheral Artery Disease

Hiatt¹,

Armstrong²,

Larson³

et al. 2015

Circulation Research

133

118

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P eripheral artery disease (PAD) is initiated by atherogenic mechanisms common to all major vascular territories but encompasses several distinctly important clinical sequelae.1 The global burden of PAD is large and rising, with substantial morbidity and mortality found in high-, middle-, and low-income countries. 2 The atherosclerotic occlusive disease underlying PAD is associated with an exercise limitation in the majority of patients, whereas the classic symptoms of intermittent claudication, ischemic rest pain, and ischemic ulceration are less common manifestations. 3 Patients with PAD are also at increased risk of myocardial infarction, ischemic stroke, heart failure, renovascular hypertension, and vascular death reflecting the systemic atherosclerotic burden. [4][5][6] The epidemiology of Peripheral Artery Disease Compendium© 2015 American Heart Association, Inc. The diagnosis of PAD can be ascertained by simple hemodynamic measurements, in particular, the ankle-brachial index (ABI), a test performed by measuring the systolic blood pressure in each arm and the dorsalis pedis and posterior tibial arteries of each ankle. The highest of the dorsalis pedis or posterior tibial artery pressures is the numerator of the ABI specific to each leg, whereas the highest arm pressure on either side is the denominator. A ratio of <0.90 in either leg is considered hemodynamic evidence of PAD. 16 When imaged, PAD can be characterized as one or more arterial stenoses or occlusions involving the distal aorta, iliac, femoral, popliteal, or tibial arteries. 17The underlying mechanisms responsible for the functional limitations in PAD are hemodynamic in origin, which affects the supply of oxygen and substrates to metabolically active tissue: skeletal muscle in the case of intermittent claudication and skin and subcutaneous tissues in the case of critical leg ischemia. However, additional pathophysiologic mechanisms contribute to the limb manifestations, where a reduction in blood flow alone does not fully account for the exercise limitation. Recent research into the pathophysiology of this exercise limitation has identified several important sequelae resultant from the chronic hemodynamic deficit. These changes affecting the vasculature and skeletal muscle distal to the primary hemodynamic lesions likely contribute to the mechanisms of exercise limitation in PAD. These advances are reviewed here with an additional focus on identifying possible future therapeutic strategies. Symptomatic Manifestations and Exercise Limitations in PADIn the coronary circulation, plaque rupture leading to acute ischemic events is a common clinical presentation; in PAD, progressive atherosclerosis leading to chronic stenosis and occlusion, often in series, in the arteries supplying the lower extremities dominates the symptomatic manifestations.6 Limb SymptomsPatients with PAD may present with a range of limb symptoms. Most patients are either asymptomatic or have atypical limb symptoms during exercise, whereas only a third have typical symptoms of c...

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“…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). Furthermore, worsening of the myopathy is associated with progression of PAD from claudication to rest pain and tissue loss (Cluff et al 2013;Weiss et al 2013).…”

Section: Introductionmentioning

confidence: 99%

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

Koutakis¹,

Miserlis

Myers

et al. 2015

J Histochem Cytochem.

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SummaryPatients with peripheral artery disease (PAD) develop a myopathy in their ischemic lower extremities, which is characterized by myofiber degeneration, mitochondrial dysfunction and impaired limb function. Desmin, a protein of the cytoskeleton, is central to maintenance of the structure, shape and function of the myofiber and its organelles, especially the mitochondria, and to translation of sarcomere contraction into muscle contraction. In this study, we investigated the hypothesis that disruption of the desmin network occurs in gastrocnemius myofibers of PAD patients and correlates with altered myofiber morphology, mitochondrial dysfunction, and impaired limb function. Using fluorescence microscopy, we evaluated desmin organization and quantified myofiber content in the gastrocnemius of PAD and control patients. Desmin was highly disorganized in PAD but not control muscles and myofiber content was increased significantly in PAD compared to control muscles. By qPCR, we found that desmin gene transcripts were increased in the gastrocnemius of PAD patients as compared with control patients. Increased desmin and desmin gene transcripts in PAD muscles correlated with altered myofiber morphology, decreased mitochondrial respiration, reduced calf muscle strength and decreased walking performance. In conclusion, our studies identified disruption of the desmin system in gastrocnemius myofibers as an index of the myopathy and limitation of muscle function in patients with PAD. (J Histochem Cytochem 63:256-269, 2015)

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Calf Muscle Characteristics, Strength Measures, and Mortality in Peripheral Arterial Disease

Cited by 105 publications

References 21 publications

Cystatin C-Based eGFR Is a Superior Prognostic Parameter to Creatinine-Based eGFR in Post-Endovascular Therapy Peripheral Artery Disease Patients

Cystatin C-Based eGFR Is a Superior Prognostic Parameter to Creatinine-Based eGFR in Post-Endovascular Therapy Peripheral Artery Disease Patients

Pathogenesis of the Limb Manifestations and Exercise Limitations in Peripheral Artery Disease

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

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