Pharmacologic effects on coronary microvessels during myocardial ischaemia.
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Animals↗
Biomedical subjects
F J Neumann
Publications and source records attributed to F J Neumann.
Activation and decreased deformability of neutrophils after intermittent claudication.
This study investigated local alterations in neutrophil activation and deformability after intermittent claudication. In 17 patients with one-sided peripheral arterial occlusive disease, neutrophil count, proportion of activated neutrophils (by nitro blue tetrazolium test), and neutrophil filterability as a measure of passive deformability were assessed in the femoral arterial and venous blood of the diseased leg and in the femoral venous blood of the healthy leg (n = 10). The values were obtained at rest, immediately after claudication, and 10 minutes after claudication induced by repetitive toe stands. Immediately after exercise, the arterial and venous blood differences in the diseased leg were 1) neutrophil count, 9% (95% confidence interval [CI], 5-14%; relative increase in the venous blood compared with arterial blood); 2) the proportion of activated neutrophils, 26% (CI, 10-42%); and 3) the neutrophil filterability, -10% (CI, -4% to -15%). At rest and 10 minutes after exercise, neutrophil parameters did not differ significantly between the femoral arterial and venous blood. Furthermore, no arterial and venous blood differences in the neutrophil parameters were found in the healthy leg. In addition to local changes, systemic changes occurred immediately after exercise. In the femoral arterial blood, the total neutrophil count had risen by 13% (CI, 8-18%), the proportion of activated neutrophils had risen by 41% (CI, 25-58%), and average neutrophil rigidity had risen 17% (CI, 11-22%) compared with the values obtained before exercise. At 10 minutes after exercise, all neutrophil parameters were still elevated. We conclude that even short periods of ischemia, as in intermittent claudication, cause local alterations in neutrophil function and distribution.
Arteries↗
Microcirculation in the hypertrophic and ischemic heart.
1. Myocardial hypertrophy, for instance in patients with hypertensive heart disease, is characterized by a reduction of coronary vascular reserve, even in the presence of normal coronary arteries. In hypertensive animals, on the microcirculatory level functional changes can be observed before the onset of any structural rarefications. In 10 rats with renal hypertension and pressure-induced left ventricular hypertrophy (LVH), the microcirculation of the left ventricular myocardium was studied using in vivo fluorescence microscopy and morphometric analysis. Renal hypertension was provoked by clipping of the left renal artery. After 8 weeks, systolic blood pressure in LVH rats averaged 172 +/- 8 mm Hg, compared to 91 +/- 2 mm Hg in 10 normotensive (NT) rats. In LVH rats, distances of plasma-perfused capillaries were significantly increased (NT = 17.7; LVH = 20 microns; p less than 0.001). Volume density, surface density, and length density of capillaries in LVH rats were reduced by 20% compared to NT rats. Capillary red cell content as measured by the ratio of capillaries filled with red cells to those containing plasma alone (Q) in LVH animals exceeded that in NT rats (LVH: Q = 0.83 +/- 0.04; NT: Q = 0.77 +/- 0.04; p less than 0.025). During hypoxia (H, 5% O2) capillary red cell recruitment in LVH rats (Q: control c = 0.83; H = 0.95) was diminished by 33% as compared to NT rats (Q: c = 0.77; H = 0.95). Thus, in addition to the decreased capillary density, the reduction of capillary red cell recruitment may be responsible for chest pain in patients with LVH and normal coronary arteries.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Haemorheologic studies in patients with reduced coronary vasodilator capacity but normal coronary angiogram (syndrome X).
The cause of syndrome X, i.e. typical angina, positive exercise test, normal coronary angiogram, normal resting cardiac function, but reduced coronary vasodilator capacity is still unknown. The purpose of the study was to investigate blood fluidity as a possible cause of syndrome X. Haematocrit, plasma viscosity, erythrocyte aggregation, and erythrocyte deformability were examined in 14 patients with syndrome X (group 1), 24 patients with typical angina, positive exercise test, but normal coronary vasodilator capacity (group 2), and 37 patients with atypical chest pain and normal coronary arteries (control group). Coronary vasodilator capacity was determined by the argon method. Compared with normals, patients with syndrome X showed an elevated plasma viscosity (1.31 +/- 0.05 mPas vs 1.26 +/- 0.04 mPas, 2P less than 0.01), an elevated erythrocyte photometric aggregation index (141 +/- 27% vs 100 +/- 23%, 2P less than 0.01) and a reduced erythrocyte filterability (0.51 +/- 0.12 vs 0.66 +/- 0.09, 2P less than 0.01). Significant differences in the haemorheologic parameters between group 1, group 2 and the control group, however, were not detected. Multiple regression analysis did not reveal a significant relationship between coronary vasodilator capacity and the haemorheologic parameters tested. The data suggest that the reduction in coronary vasodilator capacity in patients with syndrome X cannot be attributed to haemorheologic alterations.
Adult↗
Haemorrheological abnormalities in unstable angina pectoris: a relation independent of risk factor profile and angiographic severity.
Plasma viscosity, photometric erythrocyte aggregation index, and erythrocyte filterability were measured in 194 patients with coronary artery disease. Patients with unstable angina (n = 64) had a higher plasma viscosity and photometric erythrocyte aggregation index than patients with stable angina (95% confidence intervals for the mean difference: 0.052-0.100 mPa.s for plasma viscosity, and 43%-72% for the photometric erythrocyte aggregation index). Multiple regression with fibrinogen, cholesterol, high density lipoprotein cholesterol, triglycerides, blood pressure, smoking habits, coronary artery score, and left ventricular ejection fraction as independent variables showed a significant partial correlation between fibrinogen and the photometric erythrocyte aggregation index (r2 = 0.20) and plasma viscosity (r2 = 0.09), between triglycerides and plasma viscosity (r2 = 0.05), and between aortic pressure and erythrocyte filterability (r2 = 0.03). Logistic regression for unstable/stable angina with the haemorrheological variables as independent variables correctly identified 72% of the patients with stable angina and 78% of those with unstable angina. Inclusion of all the variables investigated did not substantially improve the discriminative potential of the logistic regression model. Unstable angina is associated with an impairment of blood fluidity that is essentially independent of risk factor profile and angiographic data.
Angina Pectoris↗
[Effect of prostaglandin E1 on function and deformability of neutrophilic granulocytes in patients with stage IV peripheral arterial occlusive disease].
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Alprostadil↗
[Effects of gallopamil on iodine-123-phenyl-pentadecanoic acid and thallium 201 uptake in patients with coronary heart disease].
Numerous experimental and clinical studies indicated that in the presence of coronary artery stenoses, myocardial thallium-201 and free fatty acid uptake in poststenotic regions is reduced during exercise. The aim of this study was to investigate the effect of the calcium antagonist gallopamil on myocardial thallium-201 and free fatty acid uptake in patients suffering from coronary artery disease. In 6 patients with angiographically proven coronary artery disease--2 patients with 1-vessel, 2 patients with 2-vessel and 2 patients with 3-vessel disease--as well as good left ventricular performance and stable, exerciseinduced angina, quantitative double-tracer scintigraphy was performed. Patients were investigated after a placebo period of 1 week, after oral gallopamil medication for 4 weeks (3 X 50 mg gallopamil daily), and after a double-blind period of 1 week. During symptom-limited exercise, 2 mCi thallium-201 and 5 mCi iodine-123 phenyl-pentadecanoic acid (IPPA) were simultaneously injected intravenously. Immediately after exercise, as well as 1 and 4 hours later, planar images were obtained in ap, 30 degrees LAO and 60 degrees LAO projections. By means of a newly developed computer algorithm, global and regional myocardial tracer uptake as well as IPPA clearance were evaluated. - Gallopamil provoked a decrease of global myocardial thallium-201 and IPPA uptake due to a reduction of myocardial oxygen consumption. Regional thallium-201 and IPPA uptake as well as myocardial IPPA clearance in poststenotic areas tended to rise following gallopamil medication. Thus, in the presence of coronary artery disease, gallopamil provokes an improvement of regional perfusion (dilatation of larger coronary arterioles) as well as an enhanced free fatty acid utilization in reversibly ischemic myocardial regions.
Angina Pectoris↗
Regional myocardial nitrogen-13 glutamate uptake in patients with coronary artery disease: inverse post-stress relation to thallium-201 uptake in ischemia.
The purpose of the present study was to evaluate the clinical significance of myocardial scintigraphy with nitrogen-13 (N-13) glutamate as a marker of myocardial metabolism. Within 2 weeks after cardiac catheterization, 25 patients with single vessel left anterior descending coronary artery disease underwent thallium-201 imaging (5 min and 3 h after injection) and N-13 glutamate scintigraphy (10 min after injection). Radionuclide studies were performed in the 30 degrees left anterior oblique projection after symptom-limited bicycle exercise, and regional tracer uptake was quantified by computer-assisted placement of regions of interest within the regions of myocardial activity. Poststenotic tracer uptake in the perfusion bed of the left anterior descending coronary artery (septum) was then normalized to the tracer uptake in the nondiseased left circumflex territory (posterolateral segments = 100%). In 14 patients with a history of previous myocardial infarction (Subgroup A), deficient poststenotic N-13 uptake correlated closely with thallium-201 uptake in both initial (r = 0.82, p less than 0.001) and redistribution (r = 0.74, p less than 0.01) scintigrams. By contrast, in 11 patients with no previous myocardial infarction and normal left ventricular function at rest (Subgroup B), initial uptake of both tracers was inverse: poststenotic N-13 glutamate uptake increased with decreasing thallium-201 uptake during exercise-induced ischemia (r = -0.64, p less than 0.05) and was closely correlated with the percent thallium-201 redistribution (r = 0.74, p less than 0.01). Thus, augmented accumulation of N-13 glutamate in reversibly ischemic (that is, viable) myocardium, and decreased uptake in myocardial scar tissue suggest the clinical usefulness of this metabolic tracer in the differentiation between viable (metabolically active) and irreversibly damaged myocardium.
Coronary Disease↗
Noninvasive assessment of coronary artery bypass patency: determination of myocardial thallium-201 washout rates.
This prospective study was undertaken to investigate the response of thallium-201 washout rates to coronary artery bypass surgery. Thirty-four patients with coronary heart disease were studied before and after coronary artery bypass grafting, 27 patients with normal coronary arteries serving as controls. All patients underwent cardiac catheterization and thallium-201 serial imaging, including assessment of myocardial washout rates. Pre-operatively, thallium-201 washout rates yielded a considerably higher sensitivity in detection of coronary artery disease, without significant loss of specificity compared to qualitative evaluation of serial static thallium-201 scintigrams. Post-operatively, 50 of 57 segments supplied by a patent graft showed normal washout rates, while in 9 out of 11 segments an occlusion of the graft was indicated by decreased washout rates. Compared to pre- and post-operative qualitative interpretation of static thallium-201 images, the post-operative assessment of washout rates increased both sensitivity (82% vs. 64%) and specificity (88% vs. 77%) for the evaluation of bypass graft patency. Thus, quantitative assessment of thallium-201 washout rates improves the diagnostic reliability of noninvasive detection of myocardial ischaemia with regard to the evaluation of coronary artery bypass graft patency.
Coronary Artery Bypass↗
Temperature-dependence of red cell aggregation.
To investigate the temperature-dependence of red cell aggregation 20 blood samples of normal donors and 20 blood samples of patients with venous ulcers of the leg were examined by photometric aggregometry at 3 degrees C, 10 degrees C, 20 degrees C, 30 degrees C and 37 degrees C. With decreasing temperature red cell aggregates become more resistant to hydrodynamic dispersion and they become more prone to growing under low shear stress. It is concluded that a decrease in temperature causes an increase in adsorptive energy of red cell aggregation, which is most likely due to an increase in molecular adsorption stress. Red cell aggregate formation as an overall process is retarded by a decrease in temperature, which is primarily due to an increase in plasma viscosity causing increased damping of aggregate formation. Accordingly the rate constant of aggregate formation corrected for plasma viscosity increases with decreasing temperature. The temperature-dependence of the kinetic parameters can be explained by a theoretical model that suggests the increase in contact area between aggregating red blood cells as the rate-limiting step of red cell aggregation. As a whole red cell aggregation is favoured by lowering of temperature.
Erythrocyte Aggregation↗
Effect of temperature dependent changes in mechanical stability of red cell aggregates on relative apparent whole blood viscosity.
As the temperature dependence of relative apparent whole blood viscosity eta rel is still controversial, the relation between the temperature dependence of red cell aggregation (RCA) and that of eta rel was examined in normal donors and in patients with venous ulcers of the leg. Apparent whole blood viscosity was measured in the DEER-rheometer (0.01 Pa less than tau less than 2.9 Pa) at 10 degrees C, 20 degrees C, 30 degrees C and 37 degrees C. The instrument was calibrated for each temperature to correct for changes in viscometer geometry. Simultaneously the minimal shear stress tau Tmin to keep RCA dispersed was determined by photometric aggregometry. eta rel was found to increase with decreasing temperature. By basing the relative cold induced increase in eta rel on the state of RCA as defined by the ratio of tau/tau Tmin the relation between both features is verified: With increasing RCA the cold induced increase in eta rel is progressively enhanced.
Blood Viscosity↗
[Effect of a different energy and crude protein supply on the conversion of feed energy in laying hens].
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Animals↗
The cardiovascular activity of a new antidepressant DIV 154 in comparison with imipramine.
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Animals↗
Role of activation-dependent platelet membrane glycoproteins in development of subacute occlusive coronary stent thrombosis.
BACKGROUND: Platelets have an important role in coronary thrombosis. METHODS: We studied 151 consecutive patients undergoing implantation of Palmaz-Schatz stents because of suboptimal results after coronary balloon angioplasty treated by intense anticoagulation. Surface exposure of the constitutively expressed glycoprotein complex IIb-IIIa (CD41), P-selectin (CD62P) and of the GPIIb-IIIa complex activated exposure (of ligand-induced binding site-1) were determined, in addition to platelet count and plasma fibrinogen, before and daily for 12 days after stenting in peripheral venous blood samples. RESULTS: Six of 151 patients (3.9%) developed subacute stent thrombosis within the first week after stenting. The relative risk of stent thrombosis was 18.5-fold for patients with enhanced GPIIb-IIIa surface expression (P < 0.003; 95% confidence interval 2.1 to 163.1) before stent placement. In the period after stenting, platelet activation occurred, with an increase in fibrinogen receptor activity and P-selectin degranulation above pre-stent values (P < 0.01). In logistic regression analysis, GPIIb-IIIa before stenting emerged as a risk factor for stent thrombosis, independent of the activational status of platelets, platelet count or fibrinogen levels (P < 0.02). However, after stenting, P-selectin surface expression acquired prognostic importance for stent thrombosis (P < 0.05). CONCLUSION: We conclude that changes in platelet membrane glycoproteins are of prognostic value in predicting subacute stent thrombosis.
Acute Disease↗
Previous cytomegalovirus infection and risk of coronary thrombotic events after stent placement.
BACKGROUND: Cytomegalovirus (CMV) infection induces upregulation of tissue factor and loss of anticoagulants, including thrombomodulin, prostacyclin, and tissue plasminogen activator. CMV infection may thereby increase the procoagulant properties of coronary artery plaques. This prospective study investigated the effect of previous CMV infection on the early hazard of coronary stent placement. METHODS AND RESULTS: In 551 consecutive patients with successful coronary stent placement, we determined CMV IgG titers. The end point was the composite rate of death, nonfatal Q-wave myocardial infarction, and urgent reintervention during 30-day follow-up. The study population represented the entire spectrum of coronary stenting; an acute coronary syndrome was present in 50% of the patients. A positive CMV IgG titer (>/=1/230) was found in 340 patients (62%). Of these, 10 reached the end point during 30-day follow-up (2 deaths, 4 infarctions, 4 urgent reinterventions). In the group with negative CMV titer, thrombotic events did not occur (P=0.014 versus group with positive CMV titers). After correction for pertinent covariables, a significant relation between positive CMV titer and the 30-day end point prevailed (P<0.001). CONCLUSIONS: Previous CMV infection may increase the risk of coronary thrombotic events after stent placement.
Aged↗