High dietary intake of fats has been thought to be one of the major risk factors for the development of CVD. Less is known about the possible influence of fats from various sources on haemorheological abnormalities, which are considered an important factor in the pathogenesis of these diseases. The goal of the present study was to investigate effects of high-fat diets enriched in unsaturated fatty acids (USFA), SFA or trans-fatty acids (TFA), respectively, on haemorheological parameters in rats. Wistar female rats were divided into four groups and fed diets based on the AIN-93M formulation containing approximately 10 % energy from soyabean oil (control group) or 40 % energy from soyabean oil (USFA), palm oil (SFA) and vegetable shortening (TFA) for 8 weeks. The results showed that rats fed high-fat diets exhibited significant increases in serum TAG levels (P < 0·01), plasma viscosity (P < 0·01), whole blood viscosity (P < 0·01) and internal viscosity (P < 0·01) compared to the controls. The TFA group showed a significant decrease in erythrocyte deformability (P < 0·01) and increase in internal viscosity (P < 0·01) compared with the other groups. In addition, a significant increase in blood levels of free radicals (P < 0·01) was found in the TFA group, suggesting that the attack of oxygen-free radicals could be responsible for the impaired erythrocyte deformability. These impairments could be partly responsible for the development of various circulatory disorders. The present haemorheological study provides additional insights into the potential adverse effects of trans-fat and high-fat diets on haemorheological parameters.

Observational data have suggested that increased water intake decreases the risk of CHD. A postulated mechanism is that increased water ingestion reduces blood viscosity. The aim of the present study was to assess the effect of increased fluid intake on blood viscosity. Men (n 67) and postmenopausal women (n 27) with one or more risk factors for CVD who reported intake of ≤ 0·5 litres water daily were randomised to a control group (n 31), an intervention group (n 32) that increased their daily water intake by 1 litre/d and an intervention group (n 31) that ingested 1 litre blueberry juice/d. All were encouraged to continue their usual diet and lifestyle. Whole-blood viscosity and blood and urine chemistries were measured by standard techniques after 2 and 4 weeks. Urine volume increased (by a median of 872 and 725 ml in the water and blueberry juice groups, respectively, v. 10 ml in the control group; P ≤ 0·002), confirming the subjects' adherence to the protocol. Urine osmolality and urinary levels of Na, K and creatinine decreased in the water and blueberry juice groups v. the controls (P < 0·05). No change was seen in whole-blood viscosity or in levels of fibrinogen, total protein, lipids, glucose, insulin, C-peptide or other chemistry and haematology variables. In conclusion, a postulated protective effect of increased water or fluid intake is not explained by a change in blood viscosity and increased fluid intake does not influence CVD risk factors in the short term.

Background: Acute renal failure is an occasional complication after cardiopulmonary bypass in infants. Whereas it is well known that postoperative hemodynamics inflict acute renal failure, the influence of extra-corporeal circulation on the kidney is less clear. Moreover, changes in blood viscosity occur during and after surgery, which may influence renal dysfunction. For this reason, we investigated the impact of blood viscosity on renal function during cardiopulmonary bypass. Methods: In 34 patients weighting less than 10 kg, we performed repeated analysis of urine, blood, and plasma viscosity. Results: Polyuria and proteinuria that appeared during cardiopulmonary bypass indicated an elevated transglomerular filtration gradient, which recovered within 24 hours. The appearance of N-acetyl-β-D-glucosaminidase in the urine, and elevated excretion of sodium, were additionally indicative of mild tubular damage. Elevation of blood viscosity during hypothermic perfusion showed a statistical correlation with proteinuria and N-acetyl-β-D-glucosaminidaseuria. With hypothermia, the relation of blood viscosity to plasma viscosity became stronger, while the relation to the hematocrit decreased compared to normothermia. Conclusions: During cardiopulmonary bypass perfusion, the kidney can be stressed by proteinuria and mild tubular damage. Our data provide evidence that the kidneys can be protected by improved blood viscosity during cardioplegia, but this needs confirmation in a prospective interventional study.

Sudden sensorineural hearing loss that presents as the initial sign of haematological disease is very rare. Chronic myelogenous leukaemia has been implicated as a causative factor of sudden sensorineural hearing loss.

A 49-year-old male presented with unilateral sudden sensorineural hearing loss. The patient was found to have chronic myelogenous leukaemia during a work-up for his hearing loss. We present a case of a chronic myelogenous leukaemia patient whose first manifestation was sudden sensorineural hearing loss. We presume that cochlear vessel occlusion as a result of elevated blood viscosity was responsible for this patient’s hearing loss. Early onset of sudden deafness in a chronic myelogenous leukaemia patient may be due to the hyperviscosity syndrome and it may be possible to reverse hearing loss through early leukapheresis.