Morphological, histochemical, and interstitial pressure changes in the tibialis anterior muscle before and after aortofemoral bypass in patients with peripheral arterial occlusive disease

Albani, Maria; Megalopoulos, Angelos; Kiskinis, Dimitrios; Parashos, Sotirios A.; Grigoriadis, Nikolaos; Guiba-Tziampiri, Olympia

doi:10.1186/1471-2474-3-8

Cited by 8 publications

(9 citation statements)

References 34 publications

(46 reference statements)

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“…Previous studies have demonstrated necrosis, inflammation and phagocytocis, myocyte internal nuclei, and endomysial fibrosis in the skeletal muscle of patients with peripheral arterial disease. These changes were accompanied by concomitant neuropathic changes with evidence of significant atrophy and denervation . Our observations are in concordance with these findings.…”

Section: Discussionsupporting

confidence: 92%

Histopathological changes in skeletal muscle associated with chronic ischaemia

Roos

Fyhr

Sunnerhagen

et al. 2016

APMIS

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Muscle biopsy is an essential part in the diagnostic workup in patients with suspected neuromuscular disorders. It is therefore important to be aware of morphological alterations that can be caused by systemic factors or natural ageing. Chronic limb ischaemia is frequent in elderly individuals. This study was performed to examine histopathological and mitochondrial changes in muscle in patients with chronic critical limb ischaemia. Muscle biopsy of skeletal muscle of the lower limb of patients with chronic ischaemia leading to amputation was performed and compared with muscle biopsies of healthy, age-matched controls. The histopathological abnormalities included fibrosis, necrosis, atrophy, glycogen depletion, internal nuclei, rimmed vacuoles, fibre type grouping, cytochrome c oxidase deficient fibres, MHC-I upregulation, and signs of microangiopathy. The only alteration found in age-matched controls was a few cytochrome c oxidase deficient fibres. There were also increased levels of multiple mitochondrial DNA deletions in ischaemic muscles compared with controls. Critical limb ischaemia is associated with significant histopathological changes in muscle tissue and also increased levels of mitochondrial DNA deletions. Since the alterations mimic different primary myopathic changes, chronic ischaemia is important to consider as a differential diagnosis in elderly individuals, investigated with muscle biopsy for muscle disease.

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Section: Discussionsupporting

confidence: 92%

Histopathological changes in skeletal muscle associated with chronic ischaemia

Roos

Fyhr

Sunnerhagen

et al. 2016

APMIS

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“…Exercise evokes repeated episodes of demand ischemia due to insufficient arterial supply, which may lead to myopathy and muscle fatigue [6]. Our present finding of myofiber atrophy (Figure 2) in demand ischemia has been observed in limb muscle biopsies from PAD patients [28]. Altered myofiber morphology has been correlated with diminished calf muscle strength and reduced maximum walking distance [4].…”

Section: Discussionmentioning

confidence: 54%

Revascularization and muscle adaptation to limb demand ischemia in diet-induced obese mice

Albadawi

Tzika

Rask‐Madsen

et al. 2016

Journal of Surgical Research

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Background Obesity and type 2 diabetes are major risk factors for peripheral arterial disease (PAD) in humans which can result in lower limb demand ischemia and exercise intolerance. Exercise triggers skeletal muscle adaptation including increased vasculogenesis. The goal of this study was to determine whether demand ischemia modulates revascularization, fiber size, and signaling pathways in the ischemic hind limb muscles of mice with diet-induced obesity (DIO). Materials and Methods DIO mice (n=7) underwent unilateral femoral artery ligation (FAL) and recovered for 2-weeks followed by 4-weeks with daily treadmill exercise to induce demand ischemia. A parallel sedentary ischemia group (n=7) had FAL without exercise. The contralateral limb muscles of sedentary ischemia served as control. Muscles were examined for capillary density, myofiber cross-sectional area (CSA), cytokine levels, and phosphorylation of STAT3 and ERK1/2. Results Exercise significantly enhanced capillary density (p<0.01) and markedly lowered CSA (p<0.001) in demand ischemia compared to sedentary ischemia. These findings coincided with a significant increase in G-CSF (p<0.001) and IL-7 (p<0.01) levels. In addition, phosphorylation of STAT3 and ERK1/2 (p<0.01) were increased while UCP-1 and MCP-1 protein levels were lower (p<0.05) without altering VEGF and TNFα protein levels. Demand ischemia increased the PGC1α mRNA (p<0.001) without augmenting PGC1α protein levels. Conclusions Exercise induced limb demands ischemia in the setting of DIO causes myofiber atrophy despite an increase in muscle capillary density. The combination of persistent increase in TNFα, lower VEGF and failure to increase PGC1α protein may reflect a deficient adaption to demand ischemia in DIO.

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“…The lack of full agreement between the results of Cioni et al and the present study can be explained by the fact that different rules that describe the behavior of PSDF parameters relate to muscles with different characteristics. Fiber type I proportion in the tibialis anterior muscle, which Cioni et al studied, is on average about 70% (Albani et al, 2002), since in muscle TP and ED it is respectively 60% and 47% (Larsson et al, 2001;Lindman et al, 1990). This shows a similar proportion in muscle tibialis and TP.…”

Section: Psdf Frequency Bandsmentioning

confidence: 62%