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Lipoprotein (a) (Lp (a)) is one risk factor for the development of cardiovascular diseases. Several studies have shown that Lp (a) hyperlipoproteinaemia has a particular influence on the development of coronary heart disease (CHD). A retrospective single-centre observation study was performed to evaluate the effectiveness of lipid apheresis on the basis of consecutively performed percutaneous coronary interventions (PCI) in patients with high Lp (a) values and angiographically documented CHD.In 23 pts (male 18, age 60.04 ± 0.58 years) with angiographically documented CHD (first manifestation 48.00 ± 9.41 years), elevated LDL cholesterol (144.39 ± 92.01 mg/dl) and Lp (a) (133.04 ± 39.68 mg/dl), 49 PCI and 3 coronary artery bypass grafting (CABG) procedures had been performed prior to the initiation of lipid apheresis. Following the initiation of weekly lipid apheresis, LDL cholesterol was 99.43 ± 36.53 mg/dl and Lp (a) 91.13 ± 33.02 mg/dl. In a time interval of 59.87 ± 49.49 months (median 51.00, range 1-153 months) 15 pts did not require an additional PCI. In 8 pts (7 pts 3‑vessel disease, 1 pt 2‑vessel disease) 14 PCI - no CABG - were performed after 69.38 ± 71.67 months (median: 32.50, range 17-232 months). The incidence of PCI could thus be reduced by 71.43%.

Background: To date, there have been no studies evaluating the effect of isolated lipoprotein(a) (Lp(a)) lowering therapy on carotid atherosclerosis progression., Methods: We enrolled 30 patients who had coronary heart disease (CHD) verified by angiography, Lp(a) level ≥50 mg/dL, and low density lipoprotein cholesterol (LDL-C) level ≤2.6 mmol/L (100 mg/dL) on chronic statin therapy. Subjects were allocated in a 1:1 ratio to receive apheresis treatment on a weekly basis with immunoadsorption columns ("Lp(a) Lipopak"(®), POCARD Ltd., Russia) added to atorvastatin, or atorvastatin monotherapy. The primary efficacy end-point was the change from baseline in the mean intima-media thickness (IMT) of the common carotid arteries., Results: After one month run-in period with stable atorvastatin dose, LDL-C level was 2.3 ± 0.3 mmol/L and Lp(a) - 105 ± 37 mg/dL. As a result of acute effect of specific Lp(a) apheresis procedures, Lp(a) level decreased by an average of 73 ± 12% to a mean of 29 ± 16 mg/dL, and mean LDL-C decreased by 17 ± 3% to a mean of 1.8 ± 0.2 mmol/L. In the apheresis group, changes in carotid IMT at 9 and 18 months from baseline were -0.03 ± 0.09 mm (p = 0.05) and -0.07 ± 0.15 mm (p = 0.01), respectively. In the atorvastatin group no significant changes in lipid and lipoprotein parameters as well as in carotid IMT were received over 18-month period. Two years after study termination carotid IMT increased by an average of 0.02 ± 0.08 mm in apheresis group and by 0.06 ± 0.10 mm in the control group (p = 0.033)., Conclusion: Isolated extracorporeal Lp(a) elimination over an 18 months period produced regression of carotid intima-media thickness in stable CHD patients with high Lp(a) levels. This effect was maintained for two years after the end of study., Trial Registration: Clinicaltrials.gov (NCT02133807)., (Copyright © 2015 Elsevier Ireland Ltd. All rights reserved.)

The standard lipid profile has an enormous scientific evidence base and has provided simple clinical lipid-altering goals focused on low-density lipoprotein (LDL) cholesterol that have been shown to reduce coronary heart disease. Its limitations in estimating LDL cholesterol are well known: increasing inaccuracies in the nonfasting state, in individuals with triglycerides greater than 200 to 400 mg/dL, and as an accurate measure of LDL particle risk in size and concentration. Until studies are done comparing the benefit of targeting LDL particle concentration and size versus ever lower LDL cholesterol concentration, widespread clinical use of continuing revisions of the standard lipid profile goals will continue to remain one of the giant clinical and public health achievements of the last 50 years.

Epidemiologic studies and in vitro experiments indicate that low density lipoprotein (LDL) subtypes differ concerning their atherogenic potential. Small, dense LDL are more atherogenic than large, buoyant LDL. LDL apheresis is a potent therapeutic modality to lower elevated LDL-cholesterol. It is unknown whether such therapy induces a shift in the LDL subtype distribution. In this study we evaluated the influence of LDL apheresis on the LDL subtype distribution in patients with CHD and familial hypercholesterolemia (FH, n = 22), combined hyperlipidemia (CHLP, n = 6), or Lp[a]-hyperlipoproteinemia (Lp[a]-HLP, n = 4) regularly treated by LDL apheresis (immunoadsorption (n = 14), HELP apheresis (n = 8), dextran sulfate adsorption (n = 7), cascade filtration (n = 3)). On the basis of 6 LDL subfractions (d 1.020;-1.057 g/mL) isolated by density gradient ultracentrifugation the LDL-density profile was determined in each patient before and after apheresis. There was a relative increase of LDL-subfractions 1, 2, and 3 (P < 0.01, P < 0. 05, and P < 0.01, respectively) and a concomitant decrease of LDL subfractions 5 and 6 (P < 0.05) after apheresis. Subgroup analysis indicates that the degree of the small, dense LDL reduction was much more prominent in patients with CHLP compared to patients with FH or Lp[a]-HLP, whereas the type of apheresis technique had no effect. The extent of small, dense LDL reduction correlated with the preapheresis concentrations of small, dense LDL and triglycerides but not with the extent of triglyceride reduction.We conclude that LDL apheresis not only decreases LDL mass, but also improves LDL-density profile, particularly in patients with CHLP.

This paper reports 2 years' experience with lipoprotein (a) (Lp[a]) immunapheresis which was successfully handled on a now 40-year-old patient with familial Lp(a) hyperlipoproteinemia inducing severe coronary heart disease with 2 myocardial infarctions and diffuse coronary sclerosis. Continued treatment by Lp(a) immunabsorption with specific sheep antibodies reduced stenosis in coronary vessels more than 50% and stopped the progression of coronary heart disease. A special apheresis technique and the results of continued absorption effects are described.

The rationale for the identification and aggressive treatment of lipid disorders in the patient with established vascular disease is thoroughly convincing. Elevated LDL cholesterol level is one of the few risk factors for which there is evidence of involvement in endothelial dysfunction, smooth-muscle proliferation, plaque destabilization, and thrombosis. Longitudinal studies have identified the role of elevated LDL cholesterol and low HDL cholesterol levels in the natural history of coronary artery disease. Clinical trials have successfully tested the feasibility of preventing coronary events using diet therapy or cholesterol-lowering drugs. These experiments have used a variety of end points, including myocardial infarction, cardiac death, total mortality rate, progression and regression of coronary artery stenoses, and progression of extracardiac atherosclerotic disease. The results are strikingly consistent. Economic analyses of the cost-benefit ratios also support these interventions in high-risk patients. These analyses also suggest that patients at high risk for coronary disease prior to its symptomatic presentation may be identified and treated to provide additional avenues for cost-effective primary prevention of this disease. The cardiologic community cannot ignore these results while embracing interventions such as angioplasty, coronary artery disease, antiarrhythmic therapy, and so forth. The scientific basis of cardiology demands the integration of techniques to control the atherosclerotic disease process itself, rather than merely the symptoms that it produces. Cardiology practices must reorganize to allow these proven interventions to become an integral part of comprehensive cardiologic care.

This paper focuses on the development and study of multiple population models for multivariate random length data, of the type often encountered in clinical trials. If experimental outcomes per subject consist of multiple measurements of a quantitative variable and the number of these measurements, then a multivariate random length vector is observed. For this type of data, the experimental treatment is likely to affect both the quantitative measurements and the number of these measurements. One example of such data is from the National Heart, Lung and Blood Institute Type II coronary intervention study (Brensike et al. (1982; Controlled Clinical Trials 3, 91-111; 1984, Circulation 69, 313-324)). The outcome data consist of vectors of lesion sizes with lengths determined by the number of underlying lesions assessed from the patients' angiograms, where both the numbers and the lesion sizes depend on patients' overall disease status. We propose models which can realistically describe the relationships between the quantitative variables and the number of responses. The asymptotic covariance of the maximum likelihood estimators is obtained. Data from the Type II study are analyzed using this multiple population model.

A total of 158 males with coronary risk factors and excessive (4 to 55% above normal) body weight were treated by diet and exercise for hyperlipoproteinemia in an out-patient clinic for 18 months. Blood cholesterol decreased significantly, by 14.4% (p less than 0.001), in 10% of the males who had lost at least 10% of excessive weight. Blood triglycerides decreased by 23% in 22% of the patients, who had lost 5.5% and more of excessive body weight (p less than 0.01). A two-month course of treatment with essential forte in combination with diet and regular exercise reduced blood cholesterol by 15.1% in 62%, and blood triglycerides, by 44.5% in 61.9% (p less than 0.001).

141 children and adolescents (7-21 years, mean age 14.2 years) showed values of blood pressure, total cholesterol and triglycerides greater than or equal to 90 percentile and HDL-cholesterol values less than or equal to 10 during an examination of 639 children of parents with distinct coronary risk factors or early percentile infarction. By randomization they were subdivided into two groups. (A and B) and underwent intervention measures of different intensity. While group B got only a unique recommendation concerning the preventive measures, in group A a regular, non medicamentous individual treatment was performed. After one year a decrease of blood pressure could be proved in the two groups. A significant decrease of total and HDL cholesterol was found only in group A. While the blood pressure was most clearly reduced in 7-13-year-old children, the most distinct lipid changes were shown in 14-17-year-old adolescents. An influence on body-weight and triglycerides could not be established. Our results confirm the possibilities and also the limits of preventive measures in childhood and adolescence. Apart from the intended decrease of blood pressure and total cholesterol the simultaneous decrease of HDL-cholesterol refers to open questions in the conception of the primary prevention, particularly in children.