Clinical communicationPotential significance of plasma viscosity and hematocrit variations in myocardial ischemia☆
References (43)
- et al.
Hematocrit, viscosity, and coronary blood flow
Dis. Chest
(1965) - et al.
Experimental polycythemia and hemodilution
J. Thorac. Cardiovasc. Surg.
(1970) Microcirculation and coronary blood flow
Am. J. Cardiol.
(1972)- et al.
Plasma fibrinogen levels in coronary artery disease
Lancet
(1963) - et al.
Acute ischemia of inner layers of ventricular wall
Am. Heart J.
(1963) - et al.
The Fahraeus effect
Microvasc. Res.
(1971) - et al.
The effects of fibrination on the in vivo rheology of dog blood
Microvasc. Res.
(1972) - et al.
oxygen transport in man
N. Engl. J. Med.
(1972) Rheology of blood
Physiol. Rev.
(1969)Circulatory physiology: Cardiac output and its regulation
Determinant of the optimal hematocrit
J. Appl. Physiol.
Influence of hematocrit ratio on survival of unacclimatized dogs at simulated high altitude
Am. J. Physiol.
Oxygen transport in hemorrhagic shock as a function of the hematocrit ratio
Am. J. Physiol.
The viscosity of human blood plasma: Its change in disease and on the exhibition of drugs
Rheol. Acta
The viscosity of human blood plasma: Its measurement in health and disease
Biorheology
Rheology of the circulation
Blood microrheology—viscosity factors in blood flow, ischaemia and thrombosis
Fibrinogen concentration in various clinical conditions
Am. J. Med. Sci.
The hematocrit in patients with myocardial infarction
J.A.M.A.
Hematocrit and prognosis in patients with acute myocardial infarction
J.A.M.A.
Transmural distribution of blood flow, oxygen tension, and metabolism in myocardium: Mechanism and adaptations
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The impact of preoperative fibrinogen-albumin ratio on mortality in patients with acute ST-segment elevation myocardial infarction undergoing primary percutaneous coronary intervention
2019, Clinica Chimica ActaCitation Excerpt :In addition, inflammation is positively associated with myocardial ischemia-reperfusion injury, suggesting that a higher degree of inflammation leads to a larger infarct size [37]. In contrast, the tendency toward ischemia and thrombosis in vascular stenosis is because of the hemorheological alteration of slower blood flow and increased viscosity, which could have direct mechanical effects on either the vascular endothelium or an existing atheromatous plaque [38]. The magnitude of plasma viscosity is of major importance in determining blood flow in microcirculation and tissue perfusion.
Symptomatic thromboembolic events in patients treated with intravenous-immunoglobulins: Results from a retrospective cohort study
2014, Thrombosis ResearchCitation Excerpt :In healthy patients this increase is often insignificant, but in patients with other risk factors such as vascular disease and those with an already elevated plasma viscosity, (e.g. polycythemia, paraproteinemia, inflammation, hypercholesterolemia, leukocytosis, or dehydration thromboembolic events may be precipitated by this phenomenon) [18]. In addition, blood viscosity is one determinant of oxygen delivery to the tissues, and viscosity changes can lead to a decrease in cardiac perfusion [25]. A relationship between IVIg administration and cerebral vasospasm has also been suggested by Sztajzel et al. [26].
Treatments with immunoglobulin and thrombotic adverse events
2014, Revue de Medecine InterneHematologic toxicities associated with intravenous immunoglobulin therapy
2011, International ImmunopharmacologyCitation Excerpt :It has been repeatedly suggested that acute coronary syndromes associated with IVIG may be caused by the increased blood viscosity discussed previously [18,19,21]. Blood viscosity is one determinant of oxygen delivery to the tissues, and changes in viscosity can lead to a decrease in cardiac perfusion [29]. Acute myocardial infarction is more likely to occur in patients who are older, have pre-existing atherosclerotic disease or other cardiovascular risk factors, and who receive high-dose IVIG [18,19,21].
Arterial blood pressure and hyperviscosity in sickle cell disease
2005, Hematology/Oncology Clinics of North AmericaAntithrombotic treatment for the preservation and enhancement of myocardial perfusion in chronic coronary artery disease
1997, Fibrinolysis and Proteolysis
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This work was supported in part by a grant from the Palm Beach County Heart Association and National Institutes of Health Cardiovascular Graduate Training Grant No. 5 T01 HL05784-05 (Dr. G. K. Snyder and Dr. H. Tritel, Trainees).
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Department of Chemical Engineering, College of Engineering, University of Florida, Gainesville, Fla.
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Department of Medicine, College of Medicine, University of Florida, Gainesville, Fla.