Affiliations: [a] Herz-Kreislaufklinik, Bad Wörishofen, Federal Republic of Germany | [b] Medizinische Klinik, Technische Universität München, Federal Republic of Germany
Note: [1] Supported bei Deutsche Forschungsgesellschaft
Note: [] Accepted by: Guest Editor S. Forconi
Abstract: The fluidity of blood in patients with coronary heart disease (CHD) is impaired. Earlier studies revealed an increased plasma viscosity, intensified red cell aggregation (RCA) and a reduced red cell filtrability (RCF) in CHD patients in comparison to healthy subjects. To clarify the causes of these changes the influences of physical activity, extent of coronary artery stenoses and rheological effect of the common therapy with nitrates and/or betablockers was been studied. In 105 patients with proven CHD (89 male, 16 female) and in 114 control subjects (69 male, 45 female) matched for age and risk factors blood viscosity, several of its determinants (haematocrit, plasma fibrinogen, serum protein concentration, plasma viscosity), RCA and RCF have been measured. Following stress testing patients with CHD exhibited a more pronounced increase in fibrinogen, RCA and a significantly reduced RCF, despite their lower working capacity. In patients with stable CHD the degree of coronary stenoses is hardly related to altered blood fluidity but correlates significantly with the number of stenosed coronary arteries. A daily dose of 120 mg Isosorbitdinitrate was effective in a small group of 7 patients to improve their impaired RCF. In another small placebo controlled study in patients under nitrates an additional positive effect of 150 mg Metoprolol per day on RCF could be observed. To investigate the direct influence of myocardial ischaemia blood samples have been taken from the coronary sinus during right heart cathetrisation in 6 CHD patients and 4 control subjects. Whereas in the normal circulation arterial and venous blood behave rheologically identical, this does not seem to apply to coronary circulation. The fluidity of coronary venous blood turned out to be lower than that of the arterial control both in CHD and control patients.
