PubMed · 3574577
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L O Simpson, B I Shand, R J Olds. 1987. IgA nephropathy.. https://doi.org/10.1159/000184131
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Exercise training has recently become an accepted therapeutic modality in chronic heart failure after myocardial infarction. Because the therapeutic mechanism behind it is controversial and not well understood, we analyzed the influence of exercise training on blood viscosity. Twenty-five patients with chronic heart failure (ejection fraction < 40%) after myocardial infarction were randomly assigned to either an 8-week intensive exercise program at a residential rehabilitation center or 8 weeks of sedentary life at home. Exercise consisted of two 1-hour walking sessions per day and four intensive bicycle ergometer training sessions of 40 minutes at 70% to 80% peak exercise capacity per week. Whole blood viscosity, viscosity at standardized hematocrit of 45% (P45) at high and low shear rates, and plasma viscosity were measured in a Couette-type viscometer before, during, and at the end of the study period. Exercise training, which significantly increased maximal cardiac output and oxygen uptake, did not change plasma viscosity, whole blood viscosity, and P45 significantly. Sedentary controls, however, had a higher whole blood viscosity and P45 after 8 weeks. No statistical difference was found, however, between the two groups. We conclude that blood rheology remains unaffected by exercise training in patients with chronic heart failure. The improvement of blood viscosity remains an interesting therapeutic option for the symptoms of these patients, which must be achieved by methods other than exercise training.
PURPOSE: The purpose of the current study was to determine whether hemostatic and rheologic factors are associated with the deterioration of peripheral arterial disease in patients with intermittent claudication and the influence of smoking and severity of underlying disease on these relationships. METHODS: We conducted a prospective cohort study with a 6-year follow-up period of a consecutive series of 607 patients with uncomplicated intermittent claudication. The study setting was the Peripheral Vascular Clinic, Royal Infirmary of Edinburgh. The main outcome measures were peripheral vascular intervention or onset of severe chronic leg ischemia (rest pain, ulceration, gangrene). RESULTS: A total of 210 patients died during follow-up. Two hundred three patients did not have a vascular event or deterioration of limb ischemia, 45 patients underwent a peripheral vascular intervention, and 64 progressed to severe chronic leg ischemia. Median levels (interquartile ranges) of whole blood viscosity were significantly higher in the vascular intervention group (3.75 mPa/sec; range, 3.38 to 4.13 mPa/sec) than in those who did not deteriorate 3.48 mPa/sec; range, 3.06 to 3.83 mPa/sec) (p < or = 0.05), and plasma von Willebrand factor was higher in those with severe chronic leg ischemia (154.0 IU/dl; range, 122.0 to 187.0 IU/dl) than in those who did not deteriorate (131.0 IU/dl; range, 106.0 to 165.0 IU/dl) (p < or = 0.01). After adjustment for age, sex, cigarette smoking, and ankle brachial pressure index, the levels of plasma fibrinogen and blood and plasma viscosities were each associated with an increased risk of vascular intervention (all p < or = 0.05). There were no significant associations between any of the hemorheologic factors and the risk of severe chronic leg ischemia on multivariate analyses. CONCLUSION: Elevations in rheologic factors may have important effects on further reduction of blood flow in the legs of patients with claudication and promote worsening ischemia and clinical progression of symptoms.
The objective of this study was to investigate the effects of obstructive sleep apnoea on: (i) PaCO2 levels; (ii) coagulation systems (plasma fibrinogen levels and whole blood viscosity); and (iii) heat shock proteins (HSPs) levels, which are also called stress proteins, in patients with obstructive sleep apnoea syndrome (OSAS). Patients treated with or without nasal continuous positive airway pressure (NCPAP) had arterial blood gases, plasma fibrinogen, haematocrit, serum total protein and changes in PaCO2 (estimated by transcutaneous PaCO2) measured before and after polysomnography. Heat shock protein 72 levels in peripheral blood mononuclear cells were also measured during sleep with and without NCPAP. OSAS patients with hypercapnia demonstrated significant increases in PaCO2 in the morning compared with the previous night. In such OSAS patients, treatment with NCPAP resulted in a normalization of the 20 mg/dL increase in fibrinogen levels which had been seen previously in the morning after sleep. Basal HSP 72 levels (08.00 pm before sleep) were high in OSAS patients compared to normal subjects and progressively decreased during sleep in the absence of NCPAP therapy. NCPAP relieved disabling day-to-day symptoms in addition to improving cardiovascular morbidity in patients with OSAS. Therefore it is important to understand the effects of OSAS on various organ systems as the prevalence of patients with OSAS is high.