Chlamydia pneumoniae antibodies and markers of inflammation in patients with cardiovascular diseases.

BACKGROUND: Chlamydia pneumoniae is suggested to be associated with cardiovascular diseases. OBJECTIVES: To study the presence of IgG, IgA anti-C. pneumoniae antibodies, interleukin-6 (IL-6), and C-reactive protein (CRP) as markers of previous C. pneumoniae infection and inflammation, in sera of patients with acute myocardial infarction (AIM), hypertension (HT), and coronary heart disease (CHD). METHODS: Determination of these markers by ELISA method. RESULTS: Proportion of samples containing both IgG and IgA antibodies as well as IL-6 was significantly higher in all groups of patients than in a control group. The CRP was significantly higher in patients with AIM and HT, however, in other patients, the proportion of positive samples depended on the chosen cut-off value. CONCLUSIONS: The results obtained indicate the feasibility of following chlamydial antibodies on higher number of serum samples extended to direct detection of C. pneumoniae in blood and vascular tissue (Tab. 2, Ref. 24).

Serum ex vivo lipoprotein oxidizability in patients with ischemic heart disease supplemented with vitamin E.

The decreased oxidizability of plasma lipoproteins is related to the increased vitamin E intake and its association with a relatively lower incidence of coronary heart disease has been proposed. We investigated the effect of the in vivo vitamin E supplementation on the oxidizability of serum lipids in patients with ischemic heart disease and a moderate hypercholesterolemia. Thirty-two patients (16 males and 16 postmenopausal women) participated in this placebo-controlled, randomized trial. They were treated with 400 mg vitamin E/day for 6 weeks. The copper-induced serum lipid oxidizability ex vivo was assessed by measuring conjugated diene formation at 245 nm. We also measured vitamin E, malondialdehyde (MDA) and uric acid concentrations in the plasma. Because of observed significant differences in parameters of serum lipid oxidizability (lag time and maximal rate of oxidation), plasma alpha-tocopherol and MDA levels between male patients and postmenopausal women supplemented with vitamin E, the results were compared between both genders. Six weeks of vitamin E supplementation significantly increased plasma vitamin E levels (by 87 %) in male patients but in postmenopausal women only by 34 %. Concomitantly with increased plasma levels of vitamin E the decrease in plasma MDA levels was observed in male patients (decrease by 20 %; p=0.008), but in postmenopausal women the decrease did not attain statistical significance. Plasma uric acid levels were not apparently changed in placebo or vitamin E supplemented groups of patients. The changes in ex vivo serum lipid oxidizability after vitamin E, supplementation have shown a significantly prolonged lag time (by 11 %; p=0.048) and lowered rate of lipid oxidation (by 21 %; p=0.004) in male patients in comparison with postmenopausal women. Linear regression analysis revealed a significant correlation between plasma vitamin E levels and the lag time (r=0.77; p=0.03) and the maximal rate of serum lipid oxidation (r=-0.70; p=0.05) in male patients. However, in postmenopausal women the correlations were not significant. We conclude that 400 mg vitamin E/day supplementation in patients with ischemic heart disease and a moderate hypercholesterolemia influenced favorably ex vivo serum lipid oxidation of male patients when compared with postmenopausal women. The observed differences between both genders could be useful in the selection of the effective vitamin E doses in the prevention of coronary heart disease.

Ciprofibrate increases plasma concentration of platelet-derived growth factor AB in patients with advanced atherosclerosis and hyperlipidemia independently of its hypolipidemic effects.

Fibrates, besides their hypolipidemic action, share alternative effects, such as decreased plasma fibrinogen and uric acid levels. Because of their complex action, additional effects have been investigated. A group of 23 patients with clinical signs of atherosclerosis and hyperlipoproteinemia was randomly allocated after a 1-month washout period and treated with either 100 mg/d of ciprofibrate or 100 mg/d of aspirin for 2 months. Patients were then treated with a combination of these two agents for the next 2 months. Ciprofibrate decreased plasma concentrations of triglycerides (-29%) and very-low-density lipoprotein cholesterol (-27%) in monotherapy and a larger reduction was observed if ciprofibrate was added to the aspirin therapy: triglycerides (-39%), very-low-density lipoprotein cholesterol (-33%), total cholesterol (-18%), low-density lipoprotein cholesterol (-17%), and increased high-density lipoprotein cholesterol (+36%). Ciprofibrate increased plasma levels of platelet-derived growth factor (PDGF) AB in both monotherapy patients (+162.9 pg/ml, +297%) and in aspirin-pretreated patients (+129.8 pg/ml, +134%); the increase of PDGF AB platelet store was significant only in aspirin-pretreated patients (+11.1 ng/ml, +51%). Aspirin in monotherapy did not modulate either plasma or platelet store of PDGF AB. Ciprofibrate did not inhibit thromboxane B 2 synthesis in platelets. Aspirin did not influence plasma thromboxane B 2 concentration at all, whereas it decreased thromboxane B 2 platelet production markedly in monotherapy (-85%) and in combination with ciprofibrate (-91%). Ciprofibrate increases PDGF AB content, which is amplified by aspirin pretreatment without correlation with its hypolipidemic action. The increase of PDGF production is suggested to participate in plaque stabilization.

[The effect of monotherapy with ciprofibrate and in combination with acetylsalicylic acid on the spectrum of lipids, thromboxane and fibrinogen in patients with atherosclerosis and hyperlipoproteinemia]. / Vplyv ciprofibrátu v monoterapii a v kombinácii s acetylosalicylovou kyselinou na spektrum lipidov, tromboxán a fibrinogén u pacientov s manifestnou aterosklerózou a hyperlipoproteinémiou.

Ciprofibrate is one of the basic drugs used to lower risk values of lipid parameters and fibrinogen in atherosclerosis patients. Since antiaggregation treatment with acetylsalicylic acid is a complex part of obligatory therapy of these patients, the authors studied the influence of ciprofibrate on chosen lipid parameters, fibrinogen and thromboxane in monotherapy, and also in combination with acetylsalicylic acid (ASA) in patients with advanced atherosclerosis and hyperlipoproteinemia. In the first group of patients (A-C, n = 12) after one month of low-lipid diet acetylsalicylic acid in a dose of 100 mg was administered daily during a period of 2 months followed by addition of 100 mg of ciprofabrate daily during the next 2 months. In the second group of patients (C-A, n = 11) after one month of low-lipid diet the same drugs were administered but in opposite order. Ciprofibrate was most effective in lowering the levels of triacylglycerids (-41%) and VLDL-cholesterol (-34%), but effectively lowered also the values of total cholesterol and LDL-cholesterol. In both studied groups it led to mild increase of HDL-cholesterol levels. Simultaneous administration of ASA did not significantly influence its hypolipemic activity. Ciprofibrate also significantly lowered the level of fibrinogen (-17%). Increase of the total number of platelets by about 10% was not accompanied by changes of the values and production of thromboxane. Simultaneous administration of ASA caused more than 90% inhibition of thromboxane production in monotherapy and in combination with ciprofibrate. Ciprofibrate is an effective hypolipidemic agent, also lowering the level of fibrinogen. Its combination with ASA is adequate, safe and without negative interaction influencing treatment. (Tab. 6, Fig. 1, Ref. 16.)

Relationship between plasma fenofibric acid levels and the effect of micronized fenofibrate on cholesterol, low-density-lipoprotein cholesterol and apolipoprotein B in patients with primary hypercholesterolemia.

OBJECTIVE: We examined the relationship between plasma levels of fenofibric acid, the active metabolite of fenofibrate, and differences in concentrations of plasma lipids, in subjects with primary type IIA or IIB hyperlipoproteinemia (HLP). SUBJECTS AND METHODS: Twenty-nine patients (13 with type IIA and 16 with type IIB HLP) were treated with a single daily 200-mg dose of micronized fenofibrate for 3 months, after which the plasma levels of fenofibric acid were determined by HPLC after an overnight fast. RESULTS: In the type IIA HLP phenotype, statistically significant correlations were found between fenofibric acid levels and changes in total cholesterol, LDL-C and apo-B at all three control visits, with the highest correlation coefficients at V3 visit (total cholesterol r = 0.85. LDL-C r = 0.68, apo-B r = 0.85). In type IIB HLP, statistical significance was confirmed only when performing an analysis of pooled values for total cholesterol and LDL-C (r = 0.42, r = 0.34, respectively). The high correlation between plasma fenofibric acid levels and its effect on beta lipoprotein changes might reflect the effect of fenofibrate on the catabolism of plasma LDL by the LDL receptor, since that type of relationship is typical of drugs which directly influence the target compartment without an effect on intermediary steps of metabolism. An explanation for the different levels of correlations in type IIA and IIB patients might be found in their different metabolic defects. The fact that fenofibrate's impact on VLDLs is such an important part of its effect on lipoprotein metabolism supports the concept that the effect of circulating fenofibric acid is less pronounced on the LDL receptor in type IIB HLP.

[Diagnosis of primary hyperlipoproteinemia during a preventive examination]. / Diagnostika primárnej hyperlipoproteinémie pri preventívnej prehliadke.

The study analyses the occurrence and etiology of hyperlipoproteinemia (HLP) in healthy middle-aged probands who participated in a preventive examination. Frequency of HLP was 35%. After a 2-month low-cholesterol-diet, a control biochemical examination was done. The concentration of serum triglycerides decreased significantly (3.02 +/- 1.47, 2.02 +/- 1.14, p < 0.05, respectively). The occurrence of type IV HLP decreased from 51.6% to 24.4% (p < 0.003). For the analysis of etiology of HLP we divided the hyperlipemic probands on the basis of presence of normolipemy (I. group), or HLP (II. group) in the control, and compared the lipid levels between them. We found out that the cholesterol levels in the II. group were significantly higher than in the I. group already before the diet-period (7.0 +/- 0.87 mmol/l, 5.85 +/- 0.81 respectively, p < 0.001), although the both groups did not differ in the triglyceride levels. Genetic examination in families revealed familial combined HLP in 24.4%, primary hypercholesterolemia in 12%, familial hypertriglyceridemia in 2% polygenic hypertriglyceridemia in 18%. We found out not only very high incidence of HLP in a sample of Slovak population but also that the most cases have the genetic background. The most frequent type of HLP was type IV. Since the triglyceride levels give poor information about the coronary risk, we recommend to examine the HDL-cholesterol already in the screening preventive programs.

[Agreement analysis of the results of examinations performed by a physician and automated results in the preventive care system]. / Analýza zhodnosti záverov vysetrenia uzavretých lekárom a automatizovane v preventívnom systéme.

The authors elaborated an automated preventive system and examined by means of it 1000 probands with regard to the incidence of cardiovascular and bronchopulmonary diseases and analyzed the results. In the submitted paper they present the results of an analysis of agreement of conclusions of examination made in the traditional way by the doctor and those obtained in the automated diagnostic preventive system. Agreement in the sense of a positive statement (presence of disease) was recorded in 54.1%, agreement in the sense of a negative finding (disease not detected) was recorded in 28.7%. Falsely negative conclusions (the doctor detected the disease, the system did not) were found in 5.6% and falsely positive conclusions (the doctor did not detect the disease, the system did) were found in 11.6% of the patients. The calculated sensitivity of the system is 0.90 and the specificity 0.72.