Aspirin. Aspirin does not alter native blood viscosity.
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Aspirin↗
Biomedical subjects
R S Rosenson
Publications and source records attributed to R S Rosenson.
Metastatic tumor infiltration of the pericardium masquerading as pericardial tamponade.
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Cardiac Tamponade↗
Hypertriglyceridemia and other factors associated with plasma viscosity.
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Analysis of Variance↗
Oral 17beta-estradiol and medroxyprogesterone acetate therapy in postmenopausal women increases HDL particle size.
Menopause is accompanied by changes in lipoprotein particles that include an increase in density of low density lipoproteins (LDL) and high density lipoproteins (HDL) particles. The effect of 3 months of oral hormone replacement therapy (HRT) on lipoprotein particle size in postmenopausal women who were randomized to (1) estrogen replacement therapy (ERT) alone (either 17beta-estradiol (1 mg) or conjugated equine estrogens (CEE) (0.625 mg); (2) combination therapy (17beta-estradiol plus medroxyprogesterone acetate (MPA) or CEE plus MPA); and (3) placebo were examined. Lipoprotein subclass concentrations and particle size were quantified by nuclear magnetic resonance spectroscopy (NMR). Combination HRT resulted in significant (P=0.002) increases in HDL particle size as compared with those on placebo formulations or ERT alone. Women assigned to combined HRT had lower concentrations of smaller HDL particles after 3 months (P=0.005) and higher concentrations of larger HDL particles (P=0.02), whereas women assigned to ERT or placebo experienced non-significant changes. In summary, combined HRT increases HDL particle size by altering concentrations of the smallest and largest HDL subspecies.
Administration, Oral↗
Comparative study of HMG-CoA reductase inhibitors on fibrinogen.
Statins have a variable response on fibrinogen, and these changes may have implications on cardiovascular events. In this randomized placebo-controlled crossover study, we evaluated whether changes in fibrinogen levels were different between atorvastatin and other statin-treated patients. Adult coronary heart disease (CHD) patients aged 39-83 years with LDL cholesterol levels > or = 130 mg/dl were randomized to atorvastatin 80 mg (n = 84) and one of the following statins: fluvastatin 80 mg (n = 23), lovastatin 80 mg (n = 20), pravastatin 40 mg (n = 22) or simvastatin 40 mg (n = 20) each for 12 weeks in either order. Fibrinogen was analyzed by an automated method of Clauss. Three independently acquired samples were obtained within 1 min of tourniquet application, and each specimen was measured in duplicate. Statistical analyses were performed using a mixed model repeated measures analysis of variance procedure with SAS version 6.12. There were no significant changes in fibrinogen between treatment groups. This study evaluated changes in fibrinogen with established pre-analytical and analytical procedures known to minimize variability in fibrinogen measurement, and we did not observe any differences in fibrinogen levels in the treatment groups.
Adult↗
Variability in fibrinogen measurements: an obstacle to cardiovascular risk stratification.
The clinical utility of fibrinogen measurement has been limited by large intraindividual variability. Several approaches that have been shown to improve the repeatability of fibrinogen include acquisition of samples at the same time of day, standardized sample procurement techniques, and multiple replicate sampling. This study employed established pre-analytical and analytical techniques known to reduce fibrinogen variability, including the acquisition of three replicate samples, each analyzed in duplicate, to evaluate the impact of intraindividual variability in fibrinogen measurement at baseline and 3 months on cardiovascular risk in 60 healthy subjects. Classification accuracy was evaluated by the ability to categorize subjects into tertiles of fibrinogen. Only 55% (33/60) of the subjects were correctly assigned to the appropriate fibrinogen tertile. Fibrinogen measurements varied by more than 10% in 45% of subjects and by 5% in 80% of subjects. Intraindividual variability in fibrinogen measurement with a functional assay limits cardiovascular risk assessment even when three replicates are averaged.
Adult↗
Elevated blood viscosity in systemic lupus erythematosus.
OBJECTIVES: It has been proposed that elevated blood viscosity contributes to atherothrombotic and thromboembolic processes. We evaluated whether there is increased blood viscosity in systemic lupus erythematosus (SLE) that might contribute to cardiovascular complications and reduced tissue perfusion. METHODS: Blood viscosity profiles were evaluated in SLE patients to determine whether rheologic disturbances contribute to the cardiovascular risk profile. Blood viscosity profiles were evaluated in 27 patients with SLE and 46 age- and gender-matched controls. Blood viscosity was measured at 37 degrees C and shear rates of 1 s(-1) and 100 s(-1), then corrected to the average hematocrit of the SLE patients. RESULTS: Corrected blood viscosity values were higher in SLE patients than in controls at 100 s(-1) (P =.002). Positive correlations were found between the Systemic Lupus International Collaborating Clinics/American College of Rheumatology Damage Index for SLE, which quantifies damage to 12 organ systems and fibrinogen (rho =.39; P =.042) and plasma viscosity (rho =.38; P =.049). CONCLUSIONS: Our data indicate that blood viscosity values at a standard hematocrit are elevated in SLE patients. Further investigations are needed to evaluate whether the increased blood viscosity values in SLE patients contribute to cardiovascular complications and tissue ischemia. CLINICAL RELEVANCE: Because blood viscosity values correlate with the clinical severity of SLE, blood viscosity may contribute to the cardiovascular complications and reduced tissue perfusion in SLE patients. Semin Arthritis Rheum 31:52-57.
Adult↗
Asessing coronary heart disease risk and managing lipids.
Elevated low-density lipoprotein (LDL) and below normal high-density lipoprotein (HDL) cholesterol are risk factors for coronary heart disease (CHD). According to clinical guidelines, LDL cholesterol is the primary target for lipid-altering therapy. Many patients who develop CHD have LDL and HDL cholesterol levels that fall within the desirable or low-risk category; consequently, conventional measurements of plasma lipids may not accurately detect high-risk patients. This article discusses the clinical significance of lipoprotein subclasses and methods of measurement. Assessing lipoprotein subclasses provides a more comprehensive and efficacious therapeutic approach compared with the standard lipid profile.
Anticholesteremic Agents↗
The accumulative effects of physical activity in hypertensive post-menopausal women.
BACKGROUND: Lifestyle modifications, such as physical activity, are recommended as first-line or adjunctive therapy for hypertension. However, controversy exists regarding the type, amount, and intensity of physical activity for optimal blood pressure lowering. DESIGN AND METHODS: This study evaluated the blood pressure changes in 18 post-menopausal, sedentary, untreated hypertensive women randomized to an individualized 8-week programme of intermittent moderate-intensity physical activity versus no change in physical activity. The physical activity group was asked to select activities (such as walking) to engage in physical activity for 10 min, three times a day, 5 days per week at an intensity of 50-60% heart rate reserve. RESULTS: Independent T-tests were used to compare the difference in resting blood pressure between groups. After 8 weeks, resting blood pressure was 8/5 mmHg lower in the physical activity group (systolic blood pressure, P= 0.006 and diastolic blood pressure, P = 0.059). The between group differences remained significant after adjustment for age, baseline blood pressure and previous use of antihypertensive drug therapy. CONCLUSION: These data show that hypertensive, post-menopausal women who engage in intermittent, moderate-intensity physical activity experience a reduction in blood pressure.
Aged↗
Pluripotential mechanisms of cardioprotection with HMG-CoA reductase inhibitor therapy.
Treatment with hydroxymethylglutaryl coenzyme A (HMG-CoA) reductase inhibitors has been accompanied by a reduced risk of cardiovascular events. Rapid onset of clinical benefit and weak correlations between plasma low density lipoprotein-cholesterol levels and coronary lumen change or cardiovascular events indicates that nonlipid mechanisms are involved in this beneficial effects with HMG-CoA reductase inhibitors. Furthermore, more rapid onset of clinical benefit with HMG-CoA reductase inhibitors in patients with acute coronary syndromes or acute myocardial infarction than in those with stable coronary heart disease suggest that HMG-CoA reductase inhibitors facilitate repair of ruptured or ulcerated atherosclerotic plaque, facilitate plaque stabilization and/or reduce thrombus formation on ruptured plaques. Treatment with HMG-CoA reductase inhibitors improved endothelial dysfunction in patients with hypercholesterolemia and this improvement in endothelial function was not correlated with reduction in total serum cholesterol levels. Similarly, reduction in endothelial pre-proendothelin mRNA expression and endothelin synthesis and blood pressure lowering with HMG-CoA reductase inhibitors occurred independent of lipid-lowering. Finally, HMG-CoA reductase inhibitors increased endothelial nitric oxide levels i.e. upregulated endothelial nitric oxide synthetase expression via post-transcriptional mechanisms and prevented its down-regulation by oxidized LDL-C. HMG-CoA reductase inhibitors have been shown to modulate the immune response by inhibiting activation of immune-competent cells such as macrophages, and antigen presentation to macrophages by T cells. Treatment with HMG-CoA reductase inhibitors can reduce expression, production and circulating levels of chemokines (monocyte chemoattractant protein-1) and proinflammatory cytokines [tumor necrosis factoralpha, interleukin (IL)-6 and IL-1beta]. HMG-CoA reductase inhibitors reduced inflammation in human atheroma: significantly fewer macrophages and T cells, less oxidized LDL-C and higher collagen content. In addition, treatment with HMG-CoA reductase inhibitor led to decreased cell death within the atheroma. Treatment with these agents also reduced expression of inducible cellular adhesion molecules, decreased secretion of metalloproteinases by macrophages, reduced vascular smooth muscle cell apoptosis. Lastly, HMG-CoA reductase inhibitors appear to have important effects on the thrombogenesis: reduced expression of tissue factor production and activity; increased production of tissue factor package inhibitor; decreased platelet thrombus formation and improved fibrinolysis as a result of lowered plasminogen activator inhibitor-1 levels. As the pluripotential cardioprotective mechanisms of HMG-CoA reductase inhibitors are further elucidated, it is envisaged that treatment with HMG-CoA reductase inhibitors will be initiated earlier and more frequently in patients with hypercholesterolemia.
Angina, Unstable↗
Basic mechanisms of stroke prevention with lipid-lowering therapy.
Cholesterol-lowering therapy has not been considered an important risk factor for stroke; however, lipid-lowering therapies reduce cerebrovascular events in patients with coronary heart disease (CHD). The basic mechanisms of cerebrovascular protection have emphasized reduced atheroemboli from the left ventricle and aortic arch, delayed carotid artery disease progression, stabilization of vulnerable carotid atherosclerotic plaque, and improvement in cerebral blood flow.
Carotid Artery Diseases↗
Biological basis for statin therapy in stroke prevention.
Hypercholesterolemia has not been considered an important risk factor for stroke; however, statin therapy reduces stroke in coronary heart disease patients. Statins may provide cerebrovascular protection through various mechanisms that include a reduction in the incidence of embolic stroke from cardiac, aortic and carotid sites, stabilization of vulnerable carotid atherosclerotic plaque, and improvement in cerebral blood flow.
Animals↗
Inhibition of proinflammatory cytokine production by pravastatin.
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Aged↗
Long-term safety of pravastatin-gemfibrozil therapy in mixed hyperlipidemia.
BACKGROUND: Combined HMG-CoA reductase inhibitor and fibric acid derivative therapy is often necessary for the effective reduction of concentrations of low-density lipoprotein (LDL) cholesterol and triglycerides in patients with mixed hyperlipidemia; however, the potential risk of myopathy has limited the use of these agents. HYPOTHESIS: This study evaluated long-term safety and efficacy of combined pravastatin and gemfibrozil therapy. METHODS: Eighty-three patients with hyperlipidemia were treated with combined pravastatin and gemfibrozil therapy for a median of 44 months (range 9-78 months). Plasma lipids, serum liver function tests, creatinine, and creatinine kinase (CK) levels were measured every 3 to 4 months. RESULTS: One patient developed myalgia with a normal CK level after 4 months of combination therapy. Three patients had transient elevations in CK levels that ranged from 3 to 5 times the upper limits of "normal" and that returned to normal upon repeat testing. Liver function tests did not change significantly from baseline. In a subset of 26 previously untreated patients, combined pravastatin (mean daily dose 22 mg) and gemfibrozil (mean daily dose 1,154 mg) therapy lowered total cholesterol by 25% (p < 0.001), triglycerides by 53% (p = 0.0001), LDL cholesterol by 14% (p = 0.24), and increased high-density lipoprotein (HDL) cholesterol by 20% (p = 0.012). CONCLUSION: Pravastatin and gemfibrozil therapy is safe and efficacious in patients with mixed hyperlipidemia. The long-term safety results are consistent with other reports on follow-up of shorter duration.
Cholesterol, HDL↗
Non-lipid-lowering effects of statins on atherosclerosis.
Lipid and nonlipid mechanisms contribute to the beneficial effects of some statins on endothelial function, plaque stability and thrombus formation. The nonlipid effects of statins may contribute to alleviation of tissue ischemia and prevention of acute cardiovascular syndromes. Endothelial dysfunction is reversed by a statin and this beneficial property results, in part, from direct actions on the endothelial vasoactive factors, nitric oxide and endothelin-1. Some statins have been shown to inhibit production of proinflammatory cytokines that regulate many key functions of the vascular wall including monocyte adhesion, chemotaxis, and metalloproteinase secretion. Vascular smooth muscle cell synthetic capacity and viability is inhibited by lipophilic agents, whereas a hydrophilic agent does not interfere with this reparative response. Some statins may impede thrombogenesis by reduced activation of the extrinsic coagulation pathway, inhibition of platelet adhesion and aggregation, and improvement in the rheologic profile.
Anticholesteremic Agents↗
Low high density lipoprotein levels are associated with an elevated blood viscosity.
Low levels of high density lipoprotein (HDL) have been inversely correlated with blood viscosity and plasma viscosity; however, the contribution of concomitant hypertriglyceridemia may confound this association. This study evaluated the relationship between blood viscosity and HDL cholesterol in 70 subjects with fasting levels of total cholesterol <5.2 mmol/l (200 mg/dl) and triglycerides <2.3 mmol/l (200 mg/dl). Viscosity (mPa x s) was measured at 37 degrees C with a coaxial cylinder microviscometer. HDL cholesterol was inversely associated with corrected blood viscosity at 100 s(-1) (beta = -0.49, P<0.00005) and 20 s(-1) (beta = -0.38, P = 0.001) but not at 1 s(-1) (beta = -0.05, P = 0.69) using stepwise multivariate analyses. Low HDL levels are associated with an elevated blood viscosity, and this rheological abnormality may contribute to cardiovascular risk in subjects with isolated low HDL levels.
Adult↗
Antiatherothrombotic properties of statins: implications for cardiovascular event reduction.
Clinical trials of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors or statin therapy have demonstrated that baseline or treated low-density lipoprotein (LDL) cholesterol levels are only weakly associated with net coronary angiographic change or cardiovascular events. The beneficial effects of statins on clinical events may involve nonlipid mechanisms that modify endothelial function, inflammatory responses, plaque stability, and thrombus formation. Experimental animal models suggest that statins may foster stability through a reduction in macrophages and cholesterol ester content and an increase in volume of collagen and smooth muscle cells. The thrombotic sequelae caused by plaque disruption is mitigated by statins through inhibition of platelet aggregation and maintenance of a favorable balance between prothrombotic and fibrinolytic mechanisms. These nonlipid properties of statins may help to explain the early and significant cardiovascular event reduction reported in several clinical trials of statin therapy.
Animals↗
Treatment of severe hypertriglyceridemia lowers plasma viscosity.
Elevated plasma viscosity is a predictor of atherosclerotic vascular disease and is a potential mechanism by which hypertriglyceridemia increases cardiovascular risk. Previous studies of plasma viscosity reduction in hypertriglyceridemic patients used medications that lowered both triglyceride and fibrinogen levels. Because fibrinogen is a major determinant of viscosity, it is unclear whether triglyceride reduction alone is sufficient to reduce plasma viscosity. The purpose of this study was to determine whether triglyceride-lowering therapy reduces plasma viscosity. This was a prospective study of 24 adult patients with severe hypertriglyceridemia (> or = 5.67 mmol/l). Fasting lipid, total serum protein, fibrinogen, plasma viscosity and serum viscosity levels were measured before and after therapy with 1200 mg/d of gemfibrozil. Triglyceride levels decreased by 70% (P < 0.001). Mean plasma and serum viscosity levels decreased by 0.082 mPa/s (P = 0.003) and 0.086 mPa/s (P = 0.013), respectively. Fibrinogen levels did not change significantly. Triglyceride-lowering therapy reduced plasma and serum viscosity without changes in fibrinogen levels. Since serum samples are deplete of fibrinogen, the serum viscosity reduction observed is corroborative evidence for an independent effect of triglyceride-lowering therapy on plasma viscosity. This observation provides a physiological rationale for triglyceride-lowering therapy in patients at risk for atherosclerotic vascular disease, the chylomicronemia syndrome and pancreatitis.
Adult↗