The chemical structure of lipoprotein (a) is similar to that of LDL, from which it differs due to the presence of apolipoprotein (a) bound to apo B100 via one disulfide bridge. Lipoprotein (a) is synthesized in the liver and its plasma concentration, which can be determined by use of monoclonal antibody-based methods, ranges from < 1 mg to > 1,000 mg/dL. Lipoprotein (a) levels over 20-30 mg/dL are associated with a two-fold risk of developing coronary artery disease. Usually, black subjects have higher lipoprotein (a) levels that, differently from Caucasians and Orientals, are not related to coronary artery disease. However, the risk of black subjects must be considered. Sex and age have little influence on lipoprotein (a) levels. Lipoprotein (a) homology with plasminogen might lead to interference with the fibrinolytic cascade, accounting for an atherogenic mechanism of that lipoprotein. Nevertheless, direct deposition of lipoprotein (a) on arterial wall is also a possible mechanism, lipoprotein (a) being more prone to oxidation than LDL. Most prospective studies have confirmed lipoprotein (a) as a predisposing factor to atherosclerosis. Statin treatment does not lower lipoprotein (a) levels, differently from niacin and ezetimibe, which tend to reduce lipoprotein (a), although confirmation of ezetimibe effects is pending. The reduction in lipoprotein (a) concentrations has not been demonstrated to reduce the risk for coronary artery disease. Whenever higher lipoprotein (a) concentrations are found, and in the absence of more effective and well-tolerated drugs, a more strict and vigorous control of the other coronary artery disease risk factors should be sought.

Background: The effect of home-based exercise training on neurovascular control in heart failure patients is unknown. Aims: To test the hypothesis that home-based training would maintain the reduction in muscle sympathetic nerve activity (MSNA) and forearm vascular resistance (FVR) acquired after supervised training. Methods and results: Twenty-nine patients (54±1.9 years, EF<40%) were randomised into two groups: untrained control (n=12) and exercise trained (n=17). Both groups underwent assessment of Quality of Life (QoL), MSNA, and forearm blood flow. The exercise group underwent a 4-month supervised training program followed by 4 months of home-based training. After the initial 4 months of training, patients in the exercise group showed a significant increase in peak VO2 and reduction in MSNA, compared to the untrained group, but this was not maintained during 4 months of home-based training. In contrast, the decrease in FVR (56±3 vs. 46±4 vs. 40±2 U, p=0.008) and the improvement in QOL that were achieved during supervised training were maintained during home-based training. Conclusions: Home-based training following supervised training is a safe strategy to maintain improvements in QoL and reduction in FVR in chronic heart failure patients, but is an inadequate strategy to maintain fitness as estimated by peak VO2 or reduction in neurohumoral activation.