Clinical Hemorheology and Microcirculation - Volume 55, issue 1

Authors: Meiselman, Herbert J.

Article Type: Other

DOI: 10.3233/CH-131757

Citation: Clinical Hemorheology and Microcirculation, vol. 55, no. 1, pp. 1-3, 2013

Authors: Baskurt, Oguz K.

Article Type: Other

DOI: 10.3233/CH-131683

Citation: Clinical Hemorheology and Microcirculation, vol. 55, no. 1, pp. 5-5, 2013

Authors: Hardeman, Max R.

Article Type: Research Article

DOI: 10.3233/CH-131684

Citation: Clinical Hemorheology and Microcirculation, vol. 55, no. 1, pp. 7-14, 2013

Authors: Brun, Jean-Frédéric | Varlet-Marie, Emmanuelle | Romain, Ahmed-Jérôme | Guiraudou, M. | Raynaud de Mauverger, Eric

Article Type: Research Article

Abstract: Classic studies on exercise hemorheology evidenced that blood fluidity is impaired during exercise (short term exercise-induced hyperviscosity) and is improved as a result of regular exercise practice (hemorheologic fitness). Extensive description of these events led to the concepts of “the triphasic effects of exercise”, “the paradox of hematocrit”, and “the hemorheological paradox of lactate”. However, some results obtained in training studies do not fit with this classical picture and cannot be explained by a simplistic paradigm based on the Hagen-Poiseuille law. Taking into account the non-linearity of the effects of viscosity factors on blood flow and oxygen delivery helps to …elaborate another picture. For example, moderately high values of hematocrit and erythrocyte rigidity induced by high intensity exercise are likely to trigger a physiological vasodilation improving circulatory adaptation (rather than limiting performance as was previously assumed). This may apply to the acute rise in red cell rigidity observed during strenuous exercise, and also to the paradoxical rise in hematocrit or red cell rigidity observed after some training protocols and that did not fit with the previous (simplistic) paradigms. The “healthy primitive lifestyle” hypothesis assumes that evolution has selected genetic polymorphisms leading to insulin resistance as an adaptative strategy to cope with continuous low intensity physical activity and a special alimentation based on lean meat and wild herbs (i.e., moderately high in protein, rich in low glycemic index carbohydrates, and poor in saturated fat). We propose here that this model may help to explain on an evolutionary perspective these apparently inconsistent findings. The pivotal explanation is that the true physiological picture would be that of an individual whose exercise and nutritional habits are close from this lifestyle, both sedentary subjects and trained athletes representing situations on the edge of this model. Show more

Keywords: Insulin resistance, exercise, training, metabolic syndrome, far mass, fat-free mass, body fluids, hematocrit, blood viscosity, plasma viscosity, hemorheology, erythrocyte aggregation, erythrocyte deformability

DOI: 10.3233/CH-131686

Citation: Clinical Hemorheology and Microcirculation, vol. 55, no. 1, pp. 15-27, 2013

Authors: Tripette, Julien | Hardy-Dessources, Marie-Dominique | Romana, Marc | Hue, Olivier | Diaw, Mor | Samb, Abdoulaye | Diop, Saliou | Connes, Philippe

Article Type: Research Article

Abstract: This review presents the epidemiological data regarding the exercise-related complication in exercising sickle cell trait carriers, and focuses on the different potential mechanisms that could be involved in these adverse events, such as hemorheological alterations, inflammation, vascular adhesion of circulating blood cells, oxidative stress and impaired nitric oxide metabolism. We also discuss the effects of different modulating factors such as vascular function, environment (hot temperature), hydration status, physical fitness, exercise intensity and genetic factors.

Keywords: Sickle cell trait, exercise-related sudden death, hemorheology, inflammation, vascular function

DOI: 10.3233/CH-131687

Citation: Clinical Hemorheology and Microcirculation, vol. 55, no. 1, pp. 29-37, 2013

Authors: Varlet-Marie, Emmanuelle | Guiraudou, Marie | Fédou, Christine | Raynaud de Mauverger, Eric | Durand, Fabienne | Brun, Jean-Frédéric

Article Type: Research Article

Abstract: Body composition and nutrition have been reported to be correlated with blood rheology. However, in sedentary and in physically active individuals these relationships seem to be not exactly similar. This study investigated whether exercise training status influences these relationships. 32 athletes (ATH) (age: 25 ± 0.7 yr; body mass index (BMI): 23.75 ± 0.23 kg/m2 ) were compared to 21 sedentary subjects (SED) (age: 45.19 ± 2.90; BMI = 33.41 ± 1.33) with nutritional assessment (autoquestionnaire), bioelectrical impedancemetry, viscometry at high shear rate (MT90) and Myrenne aggregometer. Subjects differ according to age, weight and adiposity parameters. Their eating behavior is …different: ATH eat a higher percentage of protein (p < 0.005), a lower percentage of lipid (p < 0.05), and a higher total amount of carbohydrate (+31% p < 0.02). Their viscosity factors are similar except plasma viscosity which is higher in SED than ATH (1.51 ± 0.03 vs 1.43 ± 0.02 mPa.s, p < 0.05). In both ATH and SED, abdominal obesity (waist-to-hip ratio or WHR) is associated with impairments in blood rheology, but not exactly the same. In ATH, WHR is associated with an increase in hematocrit (r = 0.647; p = 0.009), plasma viscosity (r = 0.723; p = 0.002), and caloric (and CHO) intake moderately increase RBC rigidity (r = 0.5405; p = 0.0251) and aggregability (r = 0.3366 p = 0.0596). In SED the picture is different, adiposity increases hematocrit (r = 0.460; p = 0.048), abdominal fatness increases blood viscosity independent of hematocrit, and CHO intake is associated with lower RBC aggregability (r = −0.493; p = 0.0319). Show more

Keywords: Nutrition, carbohydrates, exercise, fat mass, hematocrit, blood viscosity, plasma viscosity, hemorheology, erythrocyte aggregation

DOI: 10.3233/CH-131688

Citation: Clinical Hemorheology and Microcirculation, vol. 55, no. 1, pp. 39-54, 2013

Authors: Baskurt, Oguz K. | Meiselman, Herbert J.

Article Type: Research Article

Abstract: Red blood cells (RBC) are exposed to various levels of shear stress (SS) during their flow in the circulatory system, yet no significant damage occurs if their mechanical stability is not impaired. Alternatively, normal RBC may be damaged during flow in non-physiological environments and under extreme SS (e.g., extracorporeal circulation, ventricular assist devices). The shear-induced damage may result in hemolysis or in altered mechanical properties of RBC that, in turn, reduces the ability of RBC to withstand further damage by SS. An ektacytometer employing a Couette shearing system was used to apply SS at a constant level of 100 Pa …for 300 seconds as a model of sub-hemolytic mechanical stress. The degree of cellular damage during and after the application was assessed by diffraction pattern analysis. The area of the diffraction pattern was found to correlate with the number of RBC in the sheared suspension. Monitoring the ellipse area during the application of gradually increasing SS provides the concentration of the remaining intact RBC and can therefore be used to estimate the hemolytic threshold as a measure of RBC mechanical stability. The hemolytic threshold determined after the mechanical stress application was found to be ~150 Pa, while it was ~250 Pa in the same samples before the SS application. Additionally, SS-elongation index curves recorded before and after the application of the sub-hemolytic SS significantly differed from each other, indicating the impairment in deformability following the mechanical stress. The Couette type ektacytometer can be used as a tool to assess the sub-hemolytic damage to RBC in testing the biomedical equipment. Show more

Keywords: Erythrocyte mechanical stability, artificial organs, left ventricular assist device, ektacytometry, hemolyic threshold

DOI: 10.3233/CH-131689

Citation: Clinical Hemorheology and Microcirculation, vol. 55, no. 1, pp. 55-62, 2013

Authors: Guiraudou, Marie | Varlet-Marie, Emmanuelle | Raynaud de Mauverger, Eric | Brun, Jean-Frédéric

Article Type: Research Article

Abstract: In a precedent study we observed that overall adiposity evaluated with the body mass index (BMI) was correlated with plasma viscosity and red blood cells (RBC) aggregation while abdominal obesity as assessed with the waist to hip ratio (WHR) was correlated with hematocrit. We investigated this issue in 129 women (age 15–65 years, BMI: 15 to 44 kg/m2 , WHR: 0.65 to 1.13, fatness: 12–58%) who were divided into fatness groups: 17 underweight women (BMI <18.5), 75 normal weigh (BMI 18.5–24.9), 11 overweight (BMI 25–29.9), and 26 obese (BMI >30) divided according to WHR into 13 lower body and 13 …upper body obese women. Whole blood viscosity significantly increases across obesity classes, and is higher in upper body than in lower body obesity (2.84 ± 0.08 vs 3.29 ± 0.09 mPa.s, p < 0.05). The correlations between whole blood viscosity and BMI (r = 0.383 p < 0.01) and WHR (r = 0.364 p < 0.01) are found again. The former is explained by correlations of BMI with plasma viscosity (r = 0.303 p < 0.01) and red cell rigidity (r = 0.356 p < 0.01) and the latter is only explained by a correlation between WHR and hematocrit (r = 0.524 p < 0.01). BMI is also correlated with RBC aggregation parameters. Actually, when total fatness is evaluated with the percentage of fat (%fat) given by bioimpedance analysis (BIA), the picture is slightly different, since %fat is correlated with whole blood viscosity and RBC aggregation parameters but not with hematocrit, plasma viscosity and red cell rigidity. Fat free mass is also correlated with whole blood viscosity (r = 0.227 p < 0.02) due to a correlation with hematocrit (r = 0.483 p < 0.01) but neither RBC rheology nor plasma viscosity. This study shows that fatness by its own is associated with increased red cell aggregation, that abdominal fat increases blood viscosity due to a rise in hematocrit, and that overall body size as assessed with the BMI is associated with increased plasma viscosity and red cell rigidity. Show more

Keywords: Metabolic syndrome, hematocrit, blood viscosity, plasma viscosity, hemorheology, erythrocyte aggregation, fat mass, fat-free mass, gluteal fat

DOI: 10.3233/CH-131690

Citation: Clinical Hemorheology and Microcirculation, vol. 55, no. 1, pp. 63-73, 2013

Authors: Kwaan, Hau C.

Article Type: Review Article

Abstract: Plasma cell dyscrasias are characterized by a malignant clonal proliferation of plasma cells. Due to the excessive production of abnormal clonal gammaglobulins, or paraproteins, there are major hemorheologic changes in the circulation. As a result, clinical manifestations of the hyperviscosity syndrome become a major cause of morbidity and mortality. Pathogenic factors for the hyperviscosity are due both to increased plasma viscosity and to increased erythrocyte aggregation, leading to increased whole blood viscosity. These changes are dependent on the plasma concentration as well as the molecular size of the paraprotein with the threshold for onset of hyperviscosity for IgG >15 g/dl, …for polymerized IgG3 >4–5 g/dl, for IgA >10–11 g/dl; for polymerized IgA >6–7 g/dl and for IgM >3 g/dl. Correspondingly, the incidence of symptomatic hyperviscosity in Waldenstrom's macroglobulinemia is 10–30%, while that in IgG myeloma is 2–6%. Clinically, the syndrome has neurologic features of headache and dizziness, visual changes, renal failure, and cardiac failure from increased plasma volume. Thrombotic complications are frequent. Paradoxically, there can be bleeding complications due to impairment of platelet function. Removal of the paraprotein by plasma exchange (plasmapheresis) can effectively reduce the hyperviscosity. Long-term control of paraprotein production can be achieved by chemotherapy. The early recognition of the symptoms of hyperviscosity, confirmed by laboratory findings of increased paraproteins and of increased blood viscosity, is essential for the proper management of this group of disorders. Show more

Keywords: Hyperviscosity, plasma cell dyscrasias, myeloma, Waldenstrom's macroglobulinemia, plasmapheresis

DOI: 10.3233/CH-131691

Citation: Clinical Hemorheology and Microcirculation, vol. 55, no. 1, pp. 75-83, 2013

Authors: Lee, Sang-Rok | Jung, Jin-Mu | Jung, Lae-Young | Lee, Ju-Hyung | Lee, Sun-Hwa | Rhee, Kyoung-Suk | Chae, Jei Keon | Kim, Won Ho | Ko, Jae Ki | Lee, Dong-Hwan | Rosenson, Robert S.

Article Type: Research Article

Abstract: OBJECTIVES: As most clinical studies measure whole blood viscosity (WBV) from peripheral samples, potential differences in WBV obtained from the coronary arteries are often ignored. This study investigated differences in WBV measured from coronary artery specimens in patients with and without acute coronary syndrome (ACS). METHODS AND RESULTS: Consecutive patients with chest pain who underwent diagnostic coronary angiography were divided into two groups [non-ACS (n = 16), ACS (n = 22)]. The ACS group consisted of unstable angina (n = 13) and acute myocardial infarction (n = 9) patients. Two blood samples were obtained from each patient at the both …coronary artery ostia prior to coronary angiography. Low-shear and high-shear blood viscosities (BVs) were measured at shear rates of 1 and 300 s−1 , respectively, by a scanning capillary tube viscometer (Bio-Visco Inc., SouthKorea). Both low-shear and high-shear BVs obtained from peripheral, left and right coronary arteries were not different in both groups. Mean coronary low-shear WBV values obtained in ACS group were 29.2% higher than those in non-ACS group (295.3 ± 87.2 mP vs. 228.5 ± 69.2 mP, p = 0.016). Mean coronary high-shear WBV values obtained in ACS group were 15.6% higher than those in non-ACS group (42.9 ± 10.0 mP vs. 37.1 ± 4.6 mP, p = 0.036). CONCLUSIONS: Direct measurement of WBV from the coronary artery showed no differences with peripheral samples. Future larger studies are needed to clarify our results. Show more

Keywords: Acute coronary syndrome, blood viscosity, wall shear stress, coronary vessels

DOI: 10.3233/CH-131692

Citation: Clinical Hemorheology and Microcirculation, vol. 55, no. 1, pp. 85-94, 2013