Viscosity of Blood in Myocardial Infarction

Kellogg, Frederick; Goodman, Joshua

doi:10.1161/01.res.8.5.972

Cited by 22 publications

(11 citation statements)

References 7 publications

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“…Its lowering (afibrinogenaemia) leads to the recovery of newtonian properties and the lack of yield stress (MERRILL, 1969). Its increasing leads to enhanced viscosity, as in heart failure (KELLOG and GOODMAN, 1960). Similar effects can be expected to result from the presence of abnormal proteins, as macroglobulins (Waldenstrom 1 s disease) or IgG1 myeloma (LINDSLEY et al, 1973).…”

Section: B)mentioning

confidence: 87%

Blood Rheology and Its Implication in Flow of Blood

Quemada¹

1983

Arteries and Arterial Blood Flow

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Section: B)mentioning

confidence: 87%

Blood Rheology and Its Implication in Flow of Blood

Quemada¹

1983

Arteries and Arterial Blood Flow

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“…Previous works (Hatschek, 1918(Hatschek, , 1928 demonstrated that the increase of hematocrit had a direct relation to the increase of red cells (this was once thought to be the only cause). In recent years it has become necessary to add to the high globular concentration other pathogenic causes, independent of the number of red cells, but also to their greater or smaller deformability talent, and to a reduction of the normal elasticity of its membrane, since the maintenance of those qualities allows the normal flow (Braasch, 1963;Erdi et al, 1976;Faraesm and Lindquist, 1931;Harkness, 1980;Hatschek, 1918Hatschek, , 1928Kellog and Goodman 1960;LaCelle, 1969).…”

Section: Discussionmentioning

confidence: 99%

“…In myocardial infarction the plasma viscosity increases significantly and the increase is correlated with the severity of the infarction (Kellog and Goodman, 1960). It is important from all points of view to know whether or not heparin decreases blood viscosity.…”

Section: Introductionmentioning

confidence: 99%

Heparin effect on blood viscosity

Ruggiero

Castellanos

Caprissi

et al. 1982

Clinical Cardiology

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~um~ary: ~he effect of heparin on blood viscosity was ~nvestl~ated In a group of patients with acute myocardial mfarctlon (AMI) and preinfarction angina (PA), whose blood viscosity was elevated. Viscosity was measured with Cannon, Fenske, and Routine viscometers. Kinematic viscosity, bath and whole blood, plasma, and serum viscosity were determined as well as dependent parameters (fibrinogen, serum proteins, number of platelets, and hematocrit). All of them were found to increase, and it was significantly proved that intravenous heparin immediately decreased plasma viscosity, but has a lesser effect on serum and whole blood viscosity. A dose of 1 cc = 50 mg = 5000 IU intravenous heparin, will maintain this decrease for' a month. In our four-week study, I cc Lv. heparin was administered at 6-hour intervals for the first 2 weeks, and 2 cc heparin subcutaneous injections were administered at 12-hour intervals for the next 2 weeks. We found that heparin also decreased fibrinogen, hematocrit, serum alpha2 globulin, and number of platelets. Hyperviscosity, hypercoagulability, and the mcrease of platelet' adhesiveness are some of the most important physiopathological alterations of AMI and PA. The decrease of blood viscosity due to heparin is one of the most important and beneficial effects of it in this pathology.

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“…Other authors (Erdi et al, 1976;Kellog and Goodman, 1960), have found blood hyperviscosity in patients with myocardial infarction, and one of them studied the effect of low doses of heparin administered subcutaneously on the whole blood viscosity.…”

Section: Mechanism Of Actionmentioning

confidence: 99%

Heparin effect on plasma fibrinogen in the thrombophilic syndrome

Ruggiero

Castellanos

Caprissi

et al. 1983

Clinical Cardiology

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Summary: The effects of heparin were studied in a group of 42 patients with preinfarction angina (PA) and acute myocardial infarction (AMI) whose plasma fibrinogen was increased. Plasma fibrinogen was measured by the turbidimetric method in timol turbidimetric units. Statistically significant results proved that heparin reduces the plasma fibrinogen progressively over a treatment period of 6 weeks. During the first three weeks a dose of I cc (50 mg or 5000 IU) was given by intravenous injection at 6-h intervals, this was followed by a dose of 2 cc (100 mg or 10,000 IU) given by subcutaneous injection at 12-h intervals for a further three weeks. Hyperfibrinogenemia is perhaps one of the most important factors in the thrombophilic syndrome, and at the same time it is one of the fundamental physiopathological alterations observed in AMI and PA. Because heparin reduces hyperfibrinogenemia it has a beneficial effect in these diseases.

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Viscosity of Blood in Myocardial Infarction

Cited by 22 publications

References 7 publications

Blood Rheology and Its Implication in Flow of Blood

Blood Rheology and Its Implication in Flow of Blood

Heparin effect on blood viscosity

Heparin effect on plasma fibrinogen in the thrombophilic syndrome

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