Circulatory Effects of Chronic Hypervolemia in Polycythemia Vera*

Cobb, Leonard A.; Kramer, Robert J.; Finch, Clement A.

doi:10.1172/jci104194

Cited by 30 publications

(14 citation statements)

References 18 publications

(15 reference statements)

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“…The normal cardiac output, however, implies that other regions yet to be measured undergo a flow increment. A similar discrepancy seems to exist in polycythemia vera where certain regions have reduced blood flow (1,18), but total blood flow has been found to be elevated (22).…”

Section: Discussionmentioning

confidence: 83%

Myocardial Oxygen Consumption During Exercise in Fasting and Lipemic Subjects*

Regan¹,

Timmis²,

Gray³

et al. 1961

J. Clin. Invest.

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Section: Discussionmentioning

confidence: 83%

Myocardial Oxygen Consumption During Exercise in Fasting and Lipemic Subjects*

Regan¹,

Timmis²,

Gray³

et al. 1961

J. Clin. Invest.

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“…Therefore, hypothetical human red cell curves can be plotted on the same graph ( Figure 6 curves A and C). Figure 6 curve C represents a hypothetical patient with PCV and an elevated blood and, hence, stroke volume and CO. As derived from the studies of Cobb et al, 72 the curve is shifted upward and to the right, but with a much steeper negative slope above the peak Hct because, at such very high viscosity and peripheral resistance, stroke volume and CO drop precipitously despite the high blood volume. The curve demonstrates that increments in blood volume can compensate in part for high viscosity.…”

Section: The Viscosity Paradoxmentioning

confidence: 88%

“…72 The influence of Hct on oxygen transport was carefully analyzed by Richardson and Guyton, 73 who demonstrated in an isovolumic canine model that the effect of Hct on oxygen transport describes a parabolic curve with a somewhat steeper negative slope above the peak Hct of 40% (Figure 6 curve B). That steeper negative slope is caused by a reduced cardiac output (CO) secondary to progressively increased peripheral resistance, the latter resulting from elevated blood viscosity.…”

Section: The Viscosity Paradoxmentioning

confidence: 99%

Sickle cell disease and stroke

Verduzco

Nathan

2009

Blood

163

121

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Twenty-four percent of sickle cell disease (SCD) patients have a stroke by the age of 45 years. Blood transfusions decrease stroke risk in patients deemed high risk by transcranial Doppler. However, transcranial Doppler has poor specificity, and transfusions are limited by alloimmunization and iron overload. Transfusion withdrawal may be associated with an increased rebound stroke risk. Extended blood typing decreases alloimmunization in SCD but is not universally adopted. Transfusions for thalassemia begun in early childhood are associated with lower rates of alloimmunization than are seen in SCD, suggesting immune tolerance. Optimal oxygen transport efficiency occurs at a relatively low hematocrit for SCD patients because of hyperviscosity. Consequently, exchange rather than simple transfusions are more effective in improving oxygen transport efficiency, but the former are technically more demanding and require more blood units. IntroductionSickle cell disease (SCD) is a protean disorder caused by elevations of intraerythrocyte and total blood viscosity. Hypoxiainduced gelation of hemoglobin S (HbS) deforms the erythrocyte and its membrane and causes massive cation loss as well as increased erythrocyte surface expression of adhesion molecule receptors. The concomitant lack of deformability and enhanced stickiness lead to obstructive adhesion of sickle cells to each other and to vascular endothelium. 1 The result is ischemia reperfusion injury and endothelial cell damage with leakage of von Willebrand factor, platelet clumping, cytokine release, and attraction of granulocytes, macrophages, T cells, and invariant natural killer T (iNKT) cells to areas that become both infarcted and inflamed. 2,3 The obstruction and inflammation in turn cause further hypoxia and acidosis and, consequently, further sickling, the so-called vicious cycle of SCD.Of the many severe consequences of SCD, acute stroke and chronic cerebral ischemia are among the most disabling. 4 The fragile cerebral vessels of young children are particularly vulnerable: crippling strokes may blight a child's life even before the age of 2 years. The terrible consequences of SCD-induced stroke have prompted multiple approaches to prevention of this pernicious complication.Stroke in SCD was initially noted in 1923, 5 13 years after the first description of the disease. 6 A landmark angiographic case study in 1972 demonstrated the particular vulnerability of the internal carotid artery and circle of Willis 7 with consequent formation of fragile collaterals. This can lead to Moyamoya syndrome, a characteristic finding on cerebral angiograms consisting of multiple small collateral vessels around the circle of Willis that give a "puff of smoke" appearance.In this review, we offer a brief discussion of the natural history and prevention of stroke in SCD. We first discuss secondary prevention studies because they have led to landmark trials of primary prevention strategies. The review then highlights the potential pitfalls of nonspecific imaging modalities to sc...

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“…262 Brown and Giffin added to that description in 1923 with their study of nail-fold capillaries, which were elongated and engorged to capacity due to the formation of red cell aggregates, leading to diminution of blood flow that was most marked in the venous limb. 263 Since cardiac output was either normal or increased in polycythemia vera patients due to an increased stroke volume, 264,265 the diminution in capillary flow appeared to represent the influence of both peripheral vasodilatation and increased blood viscosity. In this regard, it needs to be emphasized that major vessel venous thrombosis in polycythemia vera most likely represents the end stage of a process beginning in very small vessels.…”

Section: Whole Blood Viscositymentioning

confidence: 99%