Elastase-type enzymes and their relation to blood lipids in atherosclerotic patients.

Serum elastase-type activity, elastase inhibitory capacity and their relation to lipids were examined in 140 male patients with ischemic vascular disease (coronary, cerebral, peripheral) and in 60 control subjects. In a further 24 patients with acute myocardial infarction elastase activity, inhibitory capacity and lipids during the course of the illness have also been investigated. Serum elastase-type activity was found to be significantly lower and inhibitory capacity significantly higher in the groups of patients than in the controls. HDL- and HDL2-cholesterol as well as apo A concentration showed significant negative correlation with elastase inhibitory capacity both in atherosclerotic and in control subjects. During the course of myocardial infarction a significant elevation of serum elastase-type activity could be observed at the end of the first week; serum triglyceride levels increased, HDL- and HDL2-concentrations decreased significantly in the first 3 weeks, than gradually approached the initial values. In the patients with an elevation of serum elastase-like activity by more than 30% in the first week, there was a significantly higher elevation of serum GOT and LDH1 and a greater occurrence of transmural (Q) infarction than in those with a smaller variation of elastase-like activity.

The effect of some drugs on in vitro cellular immune reactions and on circulating immune complexes in patients with myocardial infarction.

The immunomodulatory effect of the lipid-reducing etofibrate, the calcium antagonist nifedipine and the immunosuppressive cyclosporine A was studied on in vitro cellular immune response in the presence of human aortic extract and of human LDL in 56 patients with acute myocardial infarction. 50 sex- and age-matched healthy persons were used as controls. Leukocyte migration test, level of C1q and of immune complexes and serum lipid parameters were measured. Leukocyte migration inhibition was observed against aorta in 68%, against LDL in only 23% of patients, which were significantly reduced by etofibrate and nifedipine and a similar, but not significant tendency was found using cyclosporine A against aorta. Leukocyte migration stimulation was observed in 9.0% and in 27% of patients against aorta and LDL, respectively. They were also considerably decreased by etofibrate and nifedipine. A high level of circulating immune complexes was found in hyperlipemic younger patients together with lower migration inhibition against LDL, which may be explained by authors' hypothesis: LDL is a component of circulating immune complexes, so there are few free LDL for lymphokines in the circulation. A correlation between specific (anti-aorta, anti-LDL) and nonspecific (PHA) immune responses was also detected in patients. The use of these drugs may be useful in the therapy of patients with myocardial infarction in order to modulate cellular immune reactions against vascular wall and LDL.

[Serum elastinolytic activity and blood lipids in various clinical forms of arteriosclerosis and in acute myocardial infarct]. / Szérum elasztinolitikus aktivitás és vérlipidek az arteriosclerosis különbözö klinikai formáiban és acut myocardialis infarctusban.

Serum elastase-type activity, elastase inhibitory capacity and their relation to lipids were examined in 140 male patients with ischemic vascular disease (coronary, cerebral, peripheral) and in 60 control subjects. In further 24 patients with acute myocardial infarction dynamics of elastase activity, inhibitory capacity and of lipids during the course of the illness have also been investigated. Serum elastase-type activity was found to be significantly lower, inhibitory capacity significantly higher in the groups of patients than in the controls. HDL- and HDL2 cholesterol and apo-A concentrations showed significant negative correlations with elastase inhibitory capacity both in atherosclerotic and in control subjects. During the course of myocardial infarction a significant elevation of serum elastase-type activity could be observed at the end of the first week; serum triglyceride levels increased, HDL- and HDL2 concentrations decreased significantly in the first 3 weeks, then gradually approached the initial values. In the subgroup of patients with an elevation of serum elastase-like activity by more than 30% in the first week, there was a significantly higher elevation of serum GOT and LDH1 and a greater occurrence of transmural (Q) infarction than in those with a smaller variation of elastase-like activity.

Occurrence of anti-low density lipoprotein antibodies and circulating immune complexes in aged subjects.

The incidence of circulating immune complexes, anti-low density lipoprotein (LDL) autoantibodies and the anti-LDL activity of immune complexes was studied in healthy young and aged controls and in patients with vascular diseases. Circulating immune complexes (CIC) frequently occurred both in the young or old patient groups and in the aged healthy control groups, whereas they could not be found in the young controls. Marked differences were found in the incidence of anti-LDL antibodies between the groups tested. In both young and aged control groups such antibodies were very rarely observed (4-5%). In contrast anti-LDL antibodies were present in 35-45% in the aged, or young patients. Similarly, no anti-LDL activity was found in CIC of the controls, whereas in the patients with vascular diseases a significant CIC-associated anti-LDL activity was detected. These results suggest that the presence of anti-LDL antibodies are associated with the arteriosclerotic manifestations, while that of circulating immune complexes is connected by the ageing process itself.

Free and complexed anti-lipoprotein antibodies in vascular diseases.

The cell-mediated immune response against low density lipoproteins (LDL) was demonstrated by the migration inhibition test in patients with various vascular diseases. Anti-high density lipoprotein2 (HDL2) cellular immune response was found only in a few patients. LDL and HDL2 binding factors were detected in about 50% of coronary patients. No significant difference in their occurrence was found between the normolipidemic and hyperlipidemic patients nor between patients with hyperlipidemia type II/b and type IV. On the assumption that lipoproteins may act as auto-antigens by forming immune complexes, the presence of anti-LDL and anti-HDL2 activity was investigated in circulating immune complexes obtained by polyethylene glycol (PEG) precipitation from the sera of coronary patients and controls. Using an ELISA technique, PEG-precipitable anti-LDL activity was detected in 23, 11 and 18% of cases with myocardial infarction, angina pectoris and healthy old subjects, respectively. In the immune complexes obtained from the sera of the healthy young donors no anti-LDL activity was found. Anti-HDL2 activity in the immune complexes was demonstrated only in a few cases from among the patients and elderly persons we investigated.

Serial measurement of circulating immune complexes in myocardial infarction.

To study the changes in the quantity of circulating immune complexes in myocardial infarction two serial investigations were performed in 45 and 63 patients, respectively. For the detection of circulating immune complexes in the first series, two methods, a complement consumption test and a Clq-solubility test were used. In the second series, a polyethylene glycol (PEG)-precipitation assay was added to these methods. The incidence of circulating immune complexes was studied on the first, third, seventh, 14th, and 21st day. On the first day the complexes were detected in 59% of the patients. Their occurrence increased in the further samplings to 77%, but from the seventh day their concentration decreased and on the 21st day they were detected in 63%. Three types of changes in the level of circulating immune complexes could be shown. In type I immune complexes were detected in the first days after the onset of the infarction, then, after a gradual decrease, the results became negative. In type II immune complexes appeared in the second to third week and their quantity did not alter during the entire observation period. In type III the circulating immune complexes could be detected throughout the whole period of the study. These changes in their concentration were frequently associated with the clinical course of the disease.