Changes In Plasma Viscosity Research Articles

Sex-differential downregulation of methotrexate on plasma viscosity and whole blood viscosity in psoriasis.

Psoriasis is associated with an increased risk for cardiovascular disease (CVD). Methotrexate (MTX) is often used as a first-line system therapy and there is a need to determine its effect on whole blood viscosity (WBV) and plasma viscosity (PV) in psoriasis.METHODSA prospective, single-center, interventional study with a total of 111 psoriatic patients who received MTX therapy from October 22, 2018, to December 28, 2019, and 111 age- and sex-matched healthy controls. Changes in WBV, PV, blood counts, liver and renal function were evaluated.RESULTSPsoriatic patients had significantly higher levels of WBV and relative viscosity (RV) at low shear rate (LSR), erythrocyte aggregation index (EAI), and PV than sex and age-matched healthy controls. PV was positively correlated with erythrocyte sedimentation rate (ESR), ESR was positively correlated with high sensitive C-reactive protein (hCRP). But only hCRP was positively associated with psoriasis area severity index (PASI) score. MTX significantly decreased the levels of PV, ESR, hCRP, and blood pressure (BP) in male patients, and the level of WBV in female patients. Sex-specific downregulation of MTX on WBV, PV, hCRP, and BP, indicating that the effect of MTX on the risk of cardiovascular disease was related with sex.

Plasma viscosity during normal pregnancy

The changes in plasma viscosity and plasma proteins were serially measured in 14 nulli- and 10 multiparae, during their normal pregnancies. As compared to the non-pregnant value plasma viscosity decreased in the first trimester, but increased during the second and third trimester until term. At 37 weeks, the plasma viscosity value exceeded the non-pregnant value, the difference being statistically significant. The increase in plasma viscosity during the second and third trimester of pregnancy was determined by the rise in fibrinogen concentration, which overruled the plasma viscosity lowering influence of the falling total serum protein concentration

Menopause-related change in plasma viscosity

Menopause-related change in plasma viscosity

Impact of fluid resuscitation with hypertonic-hydroxyethyl starch versus lactated ringer on hemorheology and microcirculation in hemorrhagic shock

The choice of volume expander for fluid resuscitation in hemorrhagic shock is still debated. Changes in plasma viscosity (PV) are barely investigated while PV modulates functional capillary density, microcirculation and organ function. The present study evaluated the impact of 2 strategies of fluid resuscitation in hemorrhagic shock in pigs. Ten pigs were subjected to hemorrhagic shock and randomly assigned to a low viscosity fluid regimen (Lactated Ringer's, LR) group or a high viscosity regimen (hypertonic-hydroxyethyl starch, HES) for volume resuscitation. Sublingual microcirculatory flow and tissue oxygen tension were assessed together with macro- and microcirculatory, biochemical and rheological variables at baseline, 30 minutes after hemorrhagic shock, immediately after reaching resuscitation endpoints (R-0), and 60 minutes after resuscitation (R-60). PV decreased similarly in both groups following resuscitation (from 1.36 [1.32-1.38] to 1.21 [1.21-1.23] for LR, and from 1.32 [1.31-1.32] to 1.20 [1.17-1.21] mPa.s for HES). No differences were found between the groups for other rheological variables, microcirculatory flow or tissue oxygen tension at R-0 and R-60. Despite a 6-fold difference in the volumes required to achieve blood flow endpoints, commercially available volume expanders had similar effects on rheological and microcirculatory variables, irrespective of their viscosity. Our findings are consistent with the absence of clinically relevant differences between crystalloid and colloid resuscitation of hemorrhagic shock.

Intravenous immunoglobulin increases plasma viscosity without parallel rise in blood pressure

Intravenous immunoglobulin (IVIg) is a commonly used therapy for autoimmune disease, but may cause chronic hypertension and thrombosis. We determined whether: (i) IVIg systematically affects blood pressure in the short term; (ii) acute changes in plasma viscosity because of IVIg correlate with blood pressure effects; (iii) effects of IVIg on acute blood pressure are related to baseline blood pressure or hypertension status and (iv) IVIg influences plasma markers of inflammation, anticardiolipin antibodies and homocysteine as additional putative prothrombotic risk factors. Twenty adults with autoimmune neurological disease who received a course of IVIg were evaluated immediately before and after each infusion, on every day of the course. Blood pressure, pulse and the following haematological parameters were determined: plasma viscosity, erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), haematocrit, fibrinogen, interleukin-6 (IL-6), homocysteine and anticardiolipin positivity. Intravenous immunoglobulin caused both acute and cumulative rises in plasma viscosity across a treatment course, but no concordant changes in blood pressure. There was also no correlation between individual blood pressure changes and viscosity, baseline blood pressure or hypertension status. Levels of IL-6 rose across the course of therapy, but the acute-phase reactants CRP and fibrinogen did not. One patient developed anticardiolipin antibodies during therapy. Individual courses of IVIg do not systematically raise blood pressure. Where IVIg is found to cause hypertension, this does not appear to be due to a direct effect of IVIg on plasma viscosity.

Effects of posture and ergometer-specific exercise modality on plasma viscosity and plasma fibrinogen: The role of plasma volume changes

The aim of the present study was ascertain the effects posture and exercise modality on the main determinants of blood rheology. Thirteen subjects performed two exercise trials, in random order, at approximately 70% VO(2) max for 45-min. One trial was performed on a motorized treadmill at an intensity corresponding to 70% VO(2) max, while the other was performed on a stationary pike at an intensity corresponding to 70% VO(2) max. In the cycling trial subjects stood for 30-min, followed by sitting for 30-min then cycled for 30-min at 70% VO(2) max. In the treadmill trial, subjects sat for 30-min followed by standing for 30-min then ran on the treadmill for 30-min at 70% VO(2) max. Variations of body postures prior to exercise were associated with opposite changes in plasma volume, plasma viscosity and plasma fibrinogen. When post exercise raw data were not adjusted for plasma volume changes, a significant increase (p < 0.05) in plasma viscosity and plasma fibrinogen was found with no difference between the cycling and running trials. However, the increase in plasma viscosity and fibrinogen were no longer apparent when the raw data post exercises were adjusted for plasma volume changes. Changing body posture from standing to sitting and vice versa were associated with opposite changes in plasma volume and mirrored the changes in plasma viscosity and fibrinogen. In addition, ergometer-specific vigorous exercises at the same relative intensity, irrespective of its modality, transiently increased plasma viscosity and plasma fibrinogen mainly due to exercise-associated haemoconcentration.

Effect of changes in the intravascular volume during hemodialysis on blood viscoelasticity

Adoption of high rate of ultrafiltration (UF) during hemodialysis (HD) may affect the hemorhelogical blood profile, by changing Hematocrit (Hct) and the concentration of plasma proteins, which may in turn interfere with tissue perfusion. The aim of this work is to examine the effect of acute volume change during dialysis on the hemorheological variables. The study included 21 hemodialysis patients. Hematocrit (Hct) and percent decrease in blood volume (BV) were recorded by blood volume monitor. Blood samples were taken before and at the end of dialysis, for measuring plasma fibrinogen and haemorheological variables, which included blood viscosity, plasma viscosity, red cells elasticity and aggregation. The UF volume was 3.52±1.54 L. Hct increased from 34.2±6.1 to 42.1±7.3% (P<0.001), and blood volume (BV) decreased to 85.5±6.4% (P<0.001). Blood and plasma viscosity significantly increased from 3.28±0.69 to 5.48±0.85 mPa.s (P<0.001), and from 1.24 ± 0.16 to 1.65±0.24 mPa.s (P<0.001), respectively. Changes in plasma viscosity were correlated to changes in plasma fibrinogen (r=0.63, P<0.05), while the increase in blood viscosity was correlated to the percent reduction in blood volume (r=0.85, P<0.005). Red cells elasticity increased from 0.26±0.12 to 0.48±0.18 mPa.s (P<0.05), and the aggregation index rose from 0.86±0.31 to 1.25±0.26 (P<0.01). This combination of increased plasma viscosity and red cell aggregability may lower the velocity of erythrocyte transfer inside the tissue capillaries after HD, which may affect tissue perfusion. Moreover, increased elasticity may require more energy from the heart to disaggregate the cells, and this may induce problems in the patients with cardiac dysfunction. In conclusion, the hemorheological variables change after dialysis in the direction which may impede the flow inside the microvessels.

Body composition and exercise performance as determinants of blood rheology in middle-aged patients exhibiting the metabolic syndrome

Aerobic capacity and performance are associated with increased blood fluidity, while sedentarity leads to decreased exercise performance, and blood hyperviscosity. We aimed at investigating the relationships among body composition, blood rheology and exercise performance in this situation. In 46 sedentary subjects (53.09 ± 1.79 yr old; BMI = 32,35 ± 0,80) attending our unit for an exercise prescription we performed an exercise test to assess aerobic capacity, together with blood lipid profile and blood viscosity (MT 90 viscometer, Myrenne erythroaggregometer). The maximal aerobic capacity VO2max was not correlated to blood rheology but its changes were negatively correlated to those of plasma viscosity (r = -0.679) and pre-training VO2max values were negatively correlated to the BMI (r = -0.45873; p = 0.00430) and fatness (waist circumference r = -0.53476; p = 0.00406). Hemorheological parameters were as expected correlated to blood lipids. The main determinant of the RBC rigidity index Tk was HDL-cholesterol (r = -0.70026; p = 0.00121). The main determinant of M1 is HDL-cholesterol (r = -0.5157; p = 0.0238). RBC aggregability "M" is negatively correlated to total cholesterol (r = -0.758932; p = 0.000105); HDL-cholesterol (r = -0.62232; p = 0.00444); LDL-cholesterol (r = -0.64486; p = 0.00386). Whole blood viscosity is correlated to triglycerides (r = 0.8569; p = 0.00000140) and negatively correlated to HDL-cholesterol (r = -0.5622; p = 0.0122). Waist circumference (an index of abdominal fatness) is correlated to blood viscosity (r = 0.597; p = 0.00888). The waist to hip ratio is correlated to Hct (r = 0.70075 p = 0.00120) and to blood viscosity (r = 0.8124334; p = 0.0000420). Fat-free mass is correlated to blood viscosity (r = 0.66528; p = 0.00137) and hematocrit (r = 0.64350; p = 0.00220). Hip circumference is negatively correlated to plasma viscosity (r = -0.5007; p = 0.0290). Therefore, this study confirms that hemorheological parameters are influenced by blood lipids, that changes in plasma viscosity are correlated to those of aerobic capacity, and that abdominal fat mass is associated with a worsening of blood rheology and of exercise performance. By contrast, gluteal fat (a factor associated with favorable lipid profile and high insulin sensitivity) is associated with a decrease in plasma viscosity, and fat-free mass is associated with higher blood viscosity and hematocrit, consistent with recent literature linking its size in abdominal obesity with a deleterious metabolic profile.

Effects of plasma viscosity modulation on cardiac function during moderate hemodilution

BackgroundPrevious studies have found that increasing plasma viscosity as whole blood viscosity decrease has beneficial effects in microvascular hemodynamics. As the heart couples with systemic vascular network, changes in plasma and blood viscosity during hemodilution determine vascular pressure drop and flow rate, which influence cardiac function. This study aimed to investigate how changes in plasma viscosity affect on cardiac function during acute isovolemic hemodilution.Materials and MethodsPlasma viscosity was modulated by hemodilution of 40% of blood volume with three different plasma expanders (PEs). Dextran 2000 kDa (Dx2M, 6.3 cP) and dextran 70 kDa (Dx70, 3.0 cP) were used as high and moderate viscogenic PEs, respectively. Polyethylene glycol conjugated with human serum albumin (PEG-HSA, 2.2 cP) was used as low viscogenic PE. The cardiac function was assessed using a miniaturized pressure-volume conductance catheter.ResultsAfter hemodilution, pressure dropped to 84%, 79%, and 78% of baseline for Dx2M, Dx70 and PEG-HSA, respectively. Cardiac output markedly increased for Dx2M and PEG-HSA. Dx2M significantly produced higher stroke work relative to baseline and compared to Dx70.ConclusionAcute hemodilution with PEG-HSA without increasing plasma viscosity provided beneficial effects on cardiac function compared to Dx70, and similar to those measured with Dx2M. Potentially negative effects of increasing peripheral vascular resistance due to the increase in plasma viscosity were prevented.

Plasma Viscosity Changes in Patients with Liver Cirrhosis

Plasma viscosity (PV) is a major determinant of capillary blood flow through the microcirculation, which, if impaired, can result in potentially important clinical sequelae. The objectives of this study were to investigate the alterations of PV values in different stages of cirrhosis, and to determine if any change in PV correlates with Child score or Model for End-Stage Liver Disease (MELD) score or has any prognostic significance. The study included 92 patients with cirrhosis and 28 healthy volunteers. Upper endoscopic and ultrasonographic examinations of the patients were obtained. Serum biochemistry fibrinogen, complete blood count, C-reactive protein (CRP), and lipid profile were performed. PV was determined using a rotational viscosimeter. PV decreased with the progression in Child scores (Child A: 1.46 +/- 0.20 mPa-s, Child B: 1.33 +/- 0.21 mPa-s, Child C: 1.12 +/- 0.15 mPa-s), (P < 0.001). A similar change was detected between the MELD score and PV (P < 0.001). There was a positive correlation between the total protein, albumin and plasma viscosity in the control group, but a similar relationship was not found in cirrhotic patients. History of hepatic encephalopathy (30 of 92 patients) was independently associated with decreased PV (P = 0.003). We observed that increasing Child and MELD scores were significantly associated with lower PV levels irrespective of biochemical and hematologic values. These observations support the concept that hemorheologic changes in cirrhotic patients might be either the cause or the result of a pathophysiological process, and it may not be easy to distinguish between these two possibilities.

Increased blood viscosity: Disease, adaptation or treatment?

The editorial by Forconi and Gori [1] challenges a cornerstone of cardiovascular physiology in questioning the interpretation of Hagen–Poiseuille’s law for viscous liquid flow in tubes in making the link between the fluid mechanical properties of blood and how these translate into physiological effects, which ultimately set peripheral vascular resistance, blood pressure and cardiac output. Application of this law is deceptively simple: it characterizes cardiovascular regulation through the relationship between the viscosity of blood, and the diameter of the vessels through which it flows, which determine the flow resistance to the delivery of oxygenated blood by the heart. However, this simplicity is now irremediably broken since we know that in the circulation geometry (vessel diameter) is a function of blood viscosity, or more correctly vessel wall shear stress, directly related to the product of blood viscosity and blood flow. The relationship between vessel diameter and blood viscosity and shear stress is governed by the shear stress dependant release of vasoactive mediator such as prostacyclin and nitric oxide (NO). These effects mostly seen in endothelial cell cultures and as the reaction of the inhibition to the production of NO in intact vascular beds, have now been demonstrated in intact organisms, and even man. In essence we are presented with the counterintuitive concept that increasing blood viscosity in an intact organism may lower systemic vascular resistance. A minor acute increase in hematocrit, and therefore blood viscosity significantly reduces blood pressure and increases cardiac output, an effect not related to the improvement of oxygen carrying capacity [2]. A corollary to the prevailing view of the consequences Hagen–Poiseuille’s law is that increased blood viscosity is necessarily detrimental, since it increases vascular resistance. Again Forconi and Gori [1], challenge this concept pointing out that the opposite, namely lowering blood viscosity via for instance hemodilution, has not been demonstrated to provide a benefit. In fact the tendency to anemia, at levels that do not impact oxygen carrying capacity is shown to be associated with risk of hypertension [3], while erythrocytosis consequent to adaptation to altitude, does little to change oxygen carrying capacity, but may be involved in providing significant compensatory vasodilatation. These considerations lead to the emergence of increased viscosity as an adaptive mechanism, particularly effective on the healthy individual exposed to unusual challenges. We refer in general to changes in blood viscosity, a process that has two components, one the changes in blood itself, and the second the changes in plasma viscosity. It is comparatively simple to lower blood viscosity by hemodilution, and blood transfusion restore blood viscosity providing beneficial effects

Capillary microscopy and hemorheology in children during antiepileptic monotherapy with carbamazepine and valproate

The interactions of epilepsy and antiepileptic therapy an one hand and cardiovascular system on the other hand are multiple and complex. Antiepileptic drugs (AEDs) cause alterations of serum lipids and of the fatty acid composition of the membranes. Homocystein, known to induce vascular endothelial damage was found to be elevated in patients on valproate (VPA) and carbamazepine (CBZ) therapy. Marked coronary artherosclerosis and myocardial infarction may already occur in children treated with CBZ. Community based studies corroborated a higher incidence of myocardial infarction, peripheral vascular diseases hypercholesterinemia, left ventricle hypertrophy and stroke in patients with epilepsy. In this context, we wanted to elevate changes of microcirculation related to AEDs commonly prescribed such as VPA and CBZ. Capillary microscopy is a non-invasive technique for measuring the velocity of red blood cells and for determining nutritional blood flow in the capillaries of the skin. It can easily be performed in children. The aim of this study was to look for possible effects an antiepileptic monotherapy with carbamazepine or valproate has on the peripheral microcirculation in epileptic children. We were able to examine 14 children with CBZ and 24 children with VPA, recruited in our neuropediatric Unit. The results were compared to normative values, determined in former analyses of 207 healthy children. We found significant differences in capillary density, tortuous index of the capillaries, capillary diameter and flow rate of erythrocytes for both antiepileptic drugs. Additionally, there were changes in plasma viscosity and the aggregation of erythrocytes. These microcapillary effects could be of special interest in the relationship of a long-term antiepileptic therapy and the development of vascular diseases. We suggest that the influence of AEDs on microcirculation should also be considered in further studies on cardiovascular changes in patients with antiepileptic long-term medication.

The procoagulant potential of environmental particles (PM10)

Background and Aims: Epidemiology studies have shown that cardiovascular (CV) disease is primarily responsible for the mortality associated with increased pulmonary environmental particle (PM10) exposure. The mechanisms involved in PM10...

Eritrosit sedimentasyon hızı Derleme

Erythrocyte sedimentation rate ESR increases in pathological conditions such as infection inflammation neoplasm and tissue damage and this increase is generally parellel to the activation of the illness Increased ESR is also found in fat adults and children without any other health problem ESR is affected by facrors such as acute phase proteins mainly fibrinogen alpha beta globulins and albumin and number shape deformability of erythrocytes and changes in plasma viscosity The best known method to measure and to distinguish high and low levels of ESR is the “Westergreen method” Although ESR is not reliable as a disease marker its simplicity cheapness and widely usability still makes it a practical mathod in the diagnosis and follow up of disease Key words: Erythrocyte sedimentation rate child

CHANGES IN HEMORHEOLOGICAL PROFILE OF MEN WITH CHD ENTERING A PHASE I/II CARDIAC REHABILITATION PROGRAM

The purpose of this study was to determine if several hemorheological parameters remained constant for older men entering a phase I/II cardiac rehabilitation program. Ten nonsmoking men with known ischemic heart disease (IHD) not taking diuretics (mean age = 60.2 ± 11.6 yrs) volunteered to participate in this study. Initial blood samples were taken during the cardiac rehabilitation admission clinic and analyzed for plasma fibrinogen concentration (FIB)(3.2 ± 0.5 g/l), hematocrit (HC) (39.2 ± 3.5), and plasma viscosity (PV)(1.28 ± 0.09 mPa's). Subjects were returned to the community while they waited to start the formal cardiac rehabilitation classes. During this time (mean interval = 39.1 ± 13.0 days) no formal exercise prescription was followed nor was there any significant change to their pharmacological therapy. Subjects were then re-tested for FIB (3.1 ± 0.5 g/l), HC (36.7 ± 4.6) and PV (1.21 ± 0.7 mPa · s) just prior to starting the cardiac rehabilitation classes. Two tailed, paired t-test revealed a significant change to PV (p < 0.01) and HC (p < 0.01) but no significant change to FIB (p = 0.41). Further analysis revealed a significant correlation between the change in PV and the change in FIB (r = 0.71, p < 0.01), and a significant correlation between the change in PV and the change in HC (r = 0.51, p = 0.05). The findings suggest: 1) PV and HC did not remain constant over the time period, 2) a significant relationship indicates the change in PV can be accounted for by the change in FIB, 3) the common decrease in HC and FIB (both concentration measures) suggest that there was a change in plasma volume.

Effects of acute exercise on hemorheological, endothelial, and platelet markers in patients with chronic heart failure in sinus rhythm.

Chronic heart failure (CHF) is associated with an increased risk of thrombosis and thromboembolic events, including stroke and venous thromboembolism. which may be related to a prothrombotic or hypercoagulable state. Acute vigorous exercise has been associated with activation of hemostasis, and this risk may well be particularly increased in patients with CHF. The study was undertaken to determine whether acute exercise would adversely affect abnormalities of hemorheological (fibrinogen, plasma viscosity, hematocrit), endothelial (von Willebrand factor), and platelet markers (soluble P selectin) in patients with CHF. We studied 22 ambulant outpatients (17 men; mean age 65+/-9 years) with stable CHF (New York Heart Association class II-III and a left ventricular ejection fraction of < or =40%) who were exercised to exhaustion on a treadmill. Results were compared with 20 hospital controls (patients with vascular disease, but free of CHF) and 20 healthy controls. Baseline von Willebrand factor (p = 0.01) and soluble P-selectin (p = 0.006) levels were significantly elevated in patients with CHF when compared with controls. In the patients with CHF who were exercised, plasma viscosity, fibrinogen, and hematocrit levels increased significantly, both immediately post exercise and at 20 min into the recovery period (repeated measures analysis of variance, all p<0.05). There was a positive correlation between exercise workload and the maximal changes in plasma viscosity in the patients with CHF (Spearman r = 0.5, p = 0.02). Plasma viscosity levels increased with exercise in the hospital control group, although no other exercise-induced changes were noted in this group. The present study indicates that the hemorheological indices. fibrinogen, and hematocrit specifically increase during acute exercise in patients with CHF. Although moderate exercise should be encouraged in patients with CHF, vigorous exercise should probably be avoided in view of its potential prothrombotic effects in this high-risk group of patients.

Haemorheological adaptation during pregnancy in a Latin American population.

To investigate haemorheological changes during pregnancy in a Latin American population and compare to previously published data from Caucasian populations. Cross-sectional study. 75 pregnant women at 10-36 wk of gestation and 17 non-pregnant female controls in Lima, Peru. All the women and their ancestors for three generations were born and lived at sea level. Viscosity, haematocrit and plasma fibrinogen, albumin and total protein concentrations were determined in blood samples obtained after an overnight period of fasting. At 10 wk of gestation, total protein concentration and plasma viscosity were above non-pregnant levels by about 15% and subsequently decreased linearly with gestation. Fibrinogen concentration was increased in the first trimester; it then decreased to a nadir at about 20 wk and subsequently increased. Albumin concentration decreased linearly with gestation. Haematocrit decreased from pre-pregnancy levels at 10 wk to a nadir at about 26 wk. Blood viscosity increased in the first trimester and then decreased with gestation to a nadir at about 26 wk. In the first trimester of pregnancy blood and plasma viscosity are increased and they subsequently fall with advancing gestation. Plasma viscosity reflects the changes in total protein concentration, and blood viscosity is dependent on the interplay of changes in plasma viscosity and haematocrit.

Plasma viscosity and cerebral blood flow

We hypothesized that the response of cerebral blood flow (CBF) to changing viscosity would be dependent on "baseline" CBF, with a greater influence of viscosity during high-flow conditions. Plasma viscosity was adjusted to 1.0 or 3.0 cP in rats by exchange transfusion with red blood cells diluted in lactated Ringer solution or with dextran. Cortical CBF was measured by H(2) clearance. Two groups of animals remained normoxic and normocarbic and served as controls. Other groups were made anemic, hypercapnic, or hypoxic to increase CBF. Under baseline conditions before intervention, CBF did not differ between groups and averaged 49.4 +/- 10.2 ml. 100 g(-1). min(-1) (+/-SD). In control animals, changing plasma viscosity to 1. 0 or 3.0 cP resulted in CBF of 55.9 +/- 8.6 and 42.5 +/- 12.7 ml. 100 g(-1). min(-1), respectively (not significant). During hemodilution, hypercapnia, and hypoxia with a plasma viscosity of 1. 0 cP, CBF varied from 98 to 115 ml. 100 g(-1). min(-1). When plasma viscosity was 3.0 cP during hemodilution, hypercapnia, and hypoxia, CBF ranged from 56 to 58 ml. 100 g(-1). min(-1) and was significantly reduced in each case (P < 0.05). These results support the hypothesis that viscosity has a greater role in regulation of CBF when CBF is increased. In addition, because CBF more closely followed changes in plasma viscosity (rather than whole blood viscosity), we believe that plasma viscosity may be the more important factor in controlling CBF.

Effect of atorvastatin on hemorheologic-hemostatic parameters and serum fibrinogen levels in hyperlipidemic patients

Plasma fibrinogen and hemorheologic-hemostatic factors contribute to dyslipidemia-induced morbidity. Some of these parameters can be favorably affected when abnormal serum lipoprotein levels are corrected. Thus, we investigated whether treatment with atorvastatin would result in changes in plasma viscosity and other hemorheologic and hemostatic parameters. Twenty-two hyperlipidemic men at a university lipid clinic were treated single-blinded with atorvastatin 80 mg/day for 12 weeks to determine hemostatic-hemorheologic parameters including blood viscosity, fibrinogen levels, whole blood platelet aggregation, tissue plasminogen activator antigen, hematocrit, plasminogen activator inhibitor activity, factor VII activity, red blood cell (RBC) deformity and lipid ratio, sedimentation rate, and fasting serum lipoprotein levels. Atorvastatin treatment provided significant lowering of serum lipoprotein levels: low-density lipoprotein −53% (p = 0.0001), very low density lipoprotein −43% (p = 0.0001), and triglycerides −35% (p <0.0001). These effects were accompanied by changes in plasma viscosity −10% (p = 0.0007), arachidonic acid-induced whole blood platelet aggregation −11% (p = 0.006), factor VII −8% (p = 0.001), RBC lipid composition +5% (p = 0.0003), and RBC sedimentation −33% (p = 0.0002). Plasma fibrinogen levels were not affected. Thus, atorvastatin 80 mg/day produced marked reductions in serum low-density lipoproteiin cholesterol (−53%), very low density lipoprotein cholesterol (−43%), and triglycerides levels (−35%), and significant changes in plasma viscosity as well as other hemorheologic-hemostatic parameters, but no changes in plasma fibrinogen levels.

Disorders of microcirculation in coronary heart disease

Disturbances of microcirculation in coronary artery disease can be seen in the presence of critical stenosis of epicardial coronary arteries, as a result of endothelial dysfunction in the absence of significant stenosis or during recovery of ischaemic myocardium after successful angioplasty of stenosed or occluded coronary arteries. Diagnostic methods are morphologic/morphometric analyses, measurement of the global coronary reserve, measurement of the regional coronary microcirculation (scintigraphy, positron emission tomography) and laboratory analysis of haemorheological alterations (plasma, erythrocytes, leucocytes). After successful angioplasty, normalisation of glutamate extraction rate takes three to six months. In patients with unstable angina, changes in plasma viscosity, erythrocyte aggregation and neutrophil activation occur. Neutrophils are activated after successful angioplasty in acute myocardial infarction and even after elective angioplasty (when measured in the coronary sinus). Therapeutic improvements of disturbed microvascular flow can be obtained by increasing perfusion pressure (by revascularisation, nitrates, calcium antagonists, physical training), by improving the fluidity of the blood and by reducing the extravascular component of coronary vascular resistance (by antihypertensive treatment).