[Affective temperaments (cyclothymic, hypertymic, depressive, anxious, irritable) are stable parts of personality and after adolescent only their minor changes are detectable. Their connections with psychopathology is well-described; depressive temperament plays role in major depression, cyclothymic temperament in bipolar II disorder, while hyperthymic temperament in bipolar I disorder. Moreover, scientific data of the last decade suggest, that affective temperaments are also associated with somatic diseases. Cyclothymic temperament is supposed to have the closest connection with hypertension. The prevalence of hypertension is higher parallel with the presence of dominant cyclothymic affective temperament and in this condition the frequency of cardiovascular complications in hypertensive patients was also described to be higher. In chronic hypertensive patients cyclothymic temperament score is positively associated with systolic blood pressure and in women with the earlier development of hypertension. The background of these associations is probably based on the more prevalent presence of common risk factors (smoking, obesity, alcoholism) with more pronounced cyclothymic temperament. The scientific importance of the research of the associations of personality traits including affective temperaments with somatic disorders can help in the identification of higher risk patient subgroups.]

[The world population in both industrialized and developing countries is aging. The clinical and economic implications of this demographic shift are staggering because age is the most powerful risk factor for cardiovascular diseases. The incidence and prevalence of hypertension, coronary artery disease, congestive heart failure, and stroke increase steeply with advancing age. Although epidemiologic studies have discovered that some aspects of lifestyle and genetics are risk factors for these diseases, age, per se, confers the major risk. There is a continuum of age-related alterations of cardiovascular structure and function in healthy humans, however these alterations are not synonymous with diseases processes. Old age is not a disease. Although cardiovascular aging changes are considered “normative”, they lower the threshold for development of cardiovascular disease, and appear to influence the steep increases in hypertension, atherosclerosis, stroke, left ventricular hypertrophy, chronic heart failure, and atrial fibrillation with increasing age. Specific pathophysiologic mechanisms that underlie these diseases become superimposed on cardiac and vascular substrates that have been modified by an “aging process”, and the latter modulates disease occurrence and severity. Age-associated changes in cardiovascular structure and function become “partners” with pathophysiologic disease mechanisms, lifestyle, genetics, and other presently unknown factors in determining the threshold, severity, prognosis, and therapeutic response of cardiovascular disease in older persons. However, the role of specific age-associated changes in cardiovascular structure and function in such age-disease interactions has not been considered in most epidemiologic and clinical studies of cardiovascular disease. Quantitative information on age-associated alterations in cardiovascular structure and function in health is essential to unravel age-disease interactions and to target the specific characteristics of cardiovascular aging that render it such a major risk factor for cardiovascular diseases. Such information is also of practical value to differentiate between the limitations of an older person that relate to disease and those that might be expected, within limits, to accompany advancing age or a sedentary lifestyle.]

[Prevalence of renal anaemia due to insufficient production of erythropoietin increases progressively in the course of renal function deterioration. Renal anaemia is treated by erythropoesis stimulating agents (ESA). Outcomes of randomized clinical trials have taught us to avoid the strategy of normalization of hemoglobin (HGB) levels by ESA therapy as it may increase the risk of cardiovascular events and mortality. The Kidney Disease: Improving Global Outcomes (KDIGO) Clinical Practice Guideline for Anaemia published in 2012 recommends to start ESA therapy in the 90-100 g/l HGB range and suggests to keep HGB concentrations below 115 g/l. It is an inappropriate strategy to aim at normalizing hemoglobin (HGB) levels by ESA therapy because it may lead to progressive escalation of ESA doses even in the presence of diminished ESA responsiveness. High ESA doses and diseases causing ESA hyporesponsiveness eg. infections, chronic inflammation, malnutrition, insufficient dose of dialysis, severe hyperparathyroidism, iron deficiency are related to increased risk of mortality. KDIGO Clinical Practice Guideline for Anaemia emphasizes the importance of assessing and treating causes of ESA hyporesponsiveness, limits ESA dose escalation and recommends gradually changing ESA doses to avoid high amplitude HGB oscillation.]

[Reading the title most of us (but not everyone) can recall from our memories the classic heroes of the movie of Sergio Leone and we can almost hear (or not?) the melody of Ennio Morricone. This sentence is full of strangeness, isn’t it? However it’s hardly at all sure that everyone had seen the movie (indeed certainly not) and the catching music is maybe elusive. Like or not we are related to classics of lipidology, as well. Most of the readers of this review of the three clinicians know much (but not everything!) of these topics but probably for some of them this paper will arise their further interest. We are going to separate the “inseparable”, only together functioning whole thing in order to build a model in our thinking regarding its operation. This is what we do with the scientific cognition. We are making models, simplifying indeed… (sometimes erroneously) proclaiming. Let’s throw out our (or at least try to do it) the stereotypes living inside us. Let’s talk about the “always” good HDL-cholesterol, the bad LDL-cholesterol and the ugly (or cruel) triglyceride, actually (and now the analogy is lost of the three key players of the classic western movie) about the other faces of the together ugly and bad lipoprotein(a) according to a lot of opinions! As everything is connected with everything in the human body and nothing is accidental - nothing can be only good, bad or ugly nor the Good, the Bad and the Ugly yet.]

[Administration of the alpha-glucosidase enzyme inhibitor acarbose leads to a prolonged absorption of carbohydrates, which has a smoothing effect on blood glucose excursions, and results in a more even daily blood glucose profile. The glucose lowering effect is mainly due to the reduction of postprandial blood glucose levels. Non-glycaemic effects of acarbose, including those on blood pressure, lipids and the coagulation system are also clearly beneficial. According to the available data, the preparation also reduces cardiovascular risk. If used as a monotherapy, acarbose does not cause hypoglycaemia. Flatulence and diaorrhea represent the main side effects. From a professional point of view, acarbose should be given if postprandial blood glucose excursions exceed 2.2 mmol/l.]