Skeletal muscle carnitine metabolism in patients with unilateral peripheral arterial disease

1992 ◽  
Vol 73 (1) ◽  
pp. 346-353 ◽  
Author(s):  
W. R. Hiatt ◽  
E. E. Wolfel ◽  
J. G. Regensteiner ◽  
E. P. Brass
Keyword(s):  
Peripheral Arterial Disease ◽  
Lactate Threshold ◽  
Normal Subjects ◽  
Arterial Disease ◽  
Short Chain ◽  
Peak Exercise ◽  
Muscle Lactate ◽  
Control Subjects ◽  
Carnitine Metabolism ◽  
Peripheral Arterial

Patients with peripheral arterial disease (PAD) have abnormalities of carnitine metabolism that may contribute to their functional impairment. To test the hypothesis that muscle acylcarnitine generation (intermediates in oxidative metabolism) in patients with PAD provides a marker of the muscle dysfunction, 10 patients with unilateral PAD and 6 age-matched control subjects were studied at rest, and the patients were studied during exercise. At rest, biopsies of the gastrocnemius muscle in the patients' nonsymptomatic leg revealed a normal carnitine pool and lactate content compared with control subjects. In contrast, the patients' diseased leg had higher contents of lactate and long-chain acylcarnitines than controls. The muscle short-chain acylcarnitine content in the patients' diseased leg at rest was inversely correlated with peak exercise performance (r = -0.75, P less than 0.05). With graded treadmill exercise, only patients who exceeded their individual lactate threshold had an increase in muscle short-chain acylcarnitine content in the nonsymptomatic leg, which was identical to the muscle carnitine response in normal subjects. In the patients' diseased leg, muscle short-chain acylcarnitine content increased with exercise from 440 +/- 130 to 900 +/- 200 (SE) nmol/g (P less than 0.05). In contrast to the nonsymptomatic leg, there was no increase in muscle lactate content in the diseased leg with exercise, and the change in muscle carnitine metabolism was correlated with exercise duration (r = 0.82, P less than 0.01) and not with the lactate threshold. We conclude that energy metabolism in ischemic muscle of patients with PAD is characterized by the accumulation of acylcarnitines.(ABSTRACT TRUNCATED AT 250 WORDS)

Activation Products of the Haemostatic System in Coronary, Cerebrovascular and Peripheral Arterial Disease

2001 ◽  
Vol 85 (02) ◽  
pp. 234-239 ◽  
Author(s):  
M. L. Bots ◽  
F. Haverkate ◽  
P. Meijer ◽  
A. Hofman ◽  
C. Kluft ◽  
...  
Keyword(s):  
Peripheral Arterial Disease ◽  
Transient Ischemic Attack ◽  
Pressure Ratio ◽  
Arterial Disease ◽  
Population Based ◽  
Control Subjects ◽  
History Of ◽  
Ischemic Attack ◽  
Peripheral Arterial ◽  
D Dimer

SummaryTo determine the presence of a ‘hypercoagulable state’ as assessed by indices of thrombin and plasmin generation and of the amount of fibrin that is lysed, in patients with stable coronary, cerebral and peripheral arterial disease a population-based cross-sectional study was performed. From a population-based cohort comprising 7983 men and women aged 55 years and over, we randomly selected 127 subjects with a history of myocardial infarction, 124 with a history of stroke and/or transient ischemic attack, 131 patients with peripheral arterial disease and 263 control subjects in the same age group without arterial disease. Subjects using anticoagulant drugs were not selected. F1+2, TAT, and PAP were not associated with a history of cardiovascular events, nor with peripheral arterial disease. In contrast, positive associations were found for D-Dimer. Mean D-Dimer level was 40 μg/l (95% CI 35,44) in control subjects; 53 μg/l (47, 61) in those with a history of myocar-dial infarction and 51 μg/l (45, 58) in those with a history of stroke and or transient ischemic attack. D-Dimer increased gradually with increasing severity of peripheral atherosclerosis; a decrease in ankle/arm systolic blood pressure ratio of 0.1 was associated with an increase in D-Dimer of 3.9 μg/l (p<0.01). This was more pronounced in subjects with higher F1+2, TAT and PAP concentration. In conclusion, the markers of onset of coagulation F1+2, TAT and PAP are not associated with the presence of arterial disease, but increased levels of these markers are necessary for the positive association between D-Dimer and arterial disease.

Diabetes and smoking are more important for prognosis of patients with peripheral arterial disease than some genetic polymorphisms

VASA ◽  
2019 ◽  
Vol 48 (3) ◽  
pp. 229-235
Author(s):  
Vinko Boc ◽  
Mojca Božic Mijovski ◽  
Maja Pohar Perme ◽  
Ales Blinc
Keyword(s):  
Adverse Events ◽  
Peripheral Arterial Disease ◽  
Arterial Disease ◽  
Cardiovascular Death ◽  
Event Free Survival ◽  
Free Survival ◽  
Control Subjects ◽  
Peripheral Arterial ◽  
Major Adverse Events

Abstract. Background: The role of genetic polymorphisms in peripheral arterial disease (PAD) is incompletely understood. We tested whether selected single nucleotide polymorphisms (SNPs) were associated with PAD and with adverse events in an observational study cohort. Also, the role of diabetes and smoking was studied. Patients and methods: 742 patients with PAD and 713 age- and gender-matched control subjects were subjected to yearly physical and laboratory investigations and were managed for 5 years according to the European guidelines on cardiovascular disease prevention. The occurrence of all-cause death, cardiovascular death, non-fatal myocardial infarction, ischemic stroke or critical limb ischemia (major events) and revascularization procedures (minor events) was recorded. In 655 patients with PAD and 612 control subjects the following SNPs were determined: rs1466408, rs13428968 and rs12803 of NR4A2 gene, rs10499563 of IL6 gene, rs668 and rs12953 of PECAM1 gene, and rs10861032 of Chr12 locus. Results: The distribution of selected SNPs did not differ between patients with PAD and control subjects, and neither between subjects with or without major adverse events. In contrast, diabetes and smoking affected survival and event-free survival. Among patients with PAD, diabetes doubled the hazard ratio (HR) for cardiovascular death and smoking doubled the HR for death or major event. The 5-year survival of diabetics with PAD was 0.80 (CI 0.75–0.85) and of non-diabetics with PAD 0.87 (CI 0.84–0.90), p = 0.045. The 5-year survival of active smokers with PA D was 0.80 (CI 0.75–0.62), of former smokers 0.83 (CI 0.79–0.88), and of never-smokers 0.89 (CI 0.86–0.93), p = 0.024. Conclusions: SNPs of NR4A2, IL6, PECAM1 and Chr12 were not associated with PAD or with major adverse events. However, diabetes and smoking were associated with worse survival and event-free survival in patients with PAD.

scholarly journals Angiogenic response to passive movement and active exercise in individuals with peripheral arterial disease

2013 ◽  
Vol 115 (12) ◽  
pp. 1777-1787 ◽  
Author(s):  
B. Hoier ◽  
M. Walker ◽  
M. Passos ◽  
P. J. Walker ◽  
A. Green ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Peripheral Arterial Disease ◽  
Arterial Disease ◽  
Passive Movement ◽  
Vegf Receptor ◽  
Tissue Samples ◽  
Angiogenic Response ◽  
Control Subjects ◽  
Thrombospondin 1 ◽  
Peripheral Arterial

Peripheral arterial disease (PAD) is caused by atherosclerosis and is associated with microcirculatory impairments in skeletal muscle. The present study evaluated the angiogenic response to exercise and passive movement in skeletal muscle of PAD patients compared with healthy control subjects. Twenty-one PAD patients and 17 aged control subjects were randomly assigned to either a passive movement or an active exercise study. Interstitial fluid microdialysate and tissue samples were obtained from the thigh skeletal muscle. Muscle dialysate vascular endothelial growth factor (VEGF) levels were modestly increased in response to either passive movement or active exercise in both subject groups. The basal muscle dialysate level of the angiostatic factor thrombospondin-1 protein was markedly higher ( P < 0.05) in PAD patients compared with the control subjects, whereas soluble VEGF receptor-1 dialysate levels were similar in the two groups. The basal VEGF protein content in the muscle tissue samples was ∼27% lower ( P < 0.05) in the PAD patients compared with the control subjects. Analysis of mRNA expression for a range of angiogenic and angiostatic factors revealed a modest change with active exercise and passive movement in both groups, except for an increase ( P < 0.05) in the ratio of angiopoietin-2 to angiopoietin-1 mRNA in the PAD group with both interventions. PAD patients and aged individuals showed a similar limited angiogenic response to active exercise and passive movement. The limited increase in muscle extracellular VEGF combined with an elevated basal level of thrombospondin-1 in muscle extracellular fluid of PAD patients may restrict capillary growth in these patients.

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