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[Blood viscosity in ischemic heart disease]

C Malkun Paz, M Alvarado Molina, R Hurtado Figueroa

Archivos Del Instituto De Cardiologia De Mexico

|March 1, 1987

Insights

Blood viscosity (BV) is elevated in patients with ischemic heart disease (IHD), including unstable angina (UA) and acute myocardial infarction (MI). This elevation occurs independently of hematocrit, suggesting other factors contribute to increased BV in IHD patients.

Area of Science:

Cardiovascular Medicine
Hematology
Biophysics

Context:

Ischemic heart disease (IHD) is a significant health concern.
Blood viscosity (BV) is a critical hemorheological parameter.
Understanding factors influencing BV in IHD is crucial for patient management.

Purpose:

To measure and compare venous and arterial blood viscosity in patients with IHD.
To correlate blood viscosity with coronary risk factors and clinical parameters.
To investigate the independence of elevated BV from hematocrit in IHD.

Summary:

Venous and arterial blood viscosity were measured in 25 IHD patients (10 UA, 15 MI) and 100 controls.
Elevated BV was observed in both UA (4.03 cP) and MI (3.65 cP) groups compared to controls (2.70 cP).
BV remained elevated independently of hematocrit, suggesting roles for plasmatic viscosity and platelet aggregation.

Impact:

Highlights elevated blood viscosity as a potential biomarker in IHD.
Suggests further investigation into non-hematocrit related factors affecting BV in IHD.
Provides insights into hemorheological alterations in cardiovascular disease.

Read full analysis

Abstract:

Through a capillary viscometer we measured venous and arterial blood viscosity (BV) in 25 patients with the diagnosis of ischemic heart disease (IHD); 10 of them with unstable angor pectoris (UA) and 15 with acute myocardial infarction (MI). The control group consisted of 100 normal individuals in whom the normal values were 2.70 +/- 0.10 centipoises, where as in patients with AU the values were 4.03 +/- 1.40 centipoises and in the group with MI was 3.65 +/- 1.20 centipoises. Statistically, we correlated the BV obtained in both groups with the following parameters: coronary risk factors, cell blood count; serum glucose, cholesterol and triglycerides as well as the number of coronary arteries involved. The levels of venous and arterial BV were elevated in both groups of patients in comparison with the control group. We concluded that arterial and venous BV is elevated in patients with IHD independently of the hematocrit. This suggest the probability of some other factors such as plasmatic viscosity and platelets aggregation could play a role in the BV elevation of this group of patients.

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