[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.]

[Nonsteroidal antiinflammatory drugs (NSAIDs) are among the most frequently used medicines all over the world. In the year 2012 in the LAM, we summarized data on cardiovascular (CV) safety of these drugs. We emphasized that all NSAIDs may potentially be harmful on the CV system, as they can increase the blood pressure, the risk of coronary events (angina, myocardial infarction), and that of stroke, as well as they may deteriorate renal functions. We also outlined that in this respect there are substantial differences between different compounds, and the CV risk does not depend on the ratio of COX- 1/COX-2 selectivity. The newly available data of original papers and metaanalyses shed light on further details. Even naproxen which drug was previously considered the less harmful on CV system can increase the risk of blood pressure, stroke, and gastrointestinal (GI) complications. We have to emphasize that the most important risk of NSAIDs is still the GI bleeding. This adverse effect is significantly less for drugs which are more selective for COX-2 than COX-1 enzyme, but other, pleiotropic effects can also beneficially modify the GI as well as the CV risk. E.g. the aceclofenac was found to be among NSAIDs with the less adverse effects on GI system and is also among those having the less CV risk.]

[Chronic kidney disease (CKD) is endemic affecting 850 million people worldwide. Adequate antihypertensive treatment slows the progression of the kidney disease and also decreases the mortality of this population. Because of the comorbidities and the high cardiovascular risk beta-blockers have to be administered frequently in these patients. Carvedilol is a 3rd generation non-selective beta-blocker with alpha- 1 receptor blocking and antioxidant properties. It is metabolically neutral, it does not increase the risk of new onset diabetes and it does not increase the patients’ body weight. In some animal models of CKD and in several human CKD studies carvedilol has shown to have nephroprotective properties and it also decreased the cardiovascular risk in combination therapies.]

[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.]

[Sarcopenia, or the age-related involution of muscle strength and muscle mass, is a serious public health concern, due to the growing number of elderly population caused by nowadays demographic changes i.e. prolonged life expectancy. By ageing, the muscle tissue is shrinking gradually, leading to the loss of muscle strength and masses. This condition is called sarcopenia. Sar­co­penia is the simultaneous decrease of muscle mass, muscle strength and functional independence. In parallel the physical performance deteriorates (weakness, slowness and poor physical balancing). Fatigue, el­derly behaviour and weight loss are the consequences of these accumulating deficits, which associate with cognitive decline and result in increasing social isolation. The primary form of sarcopenia is the decrease of the energy production of muscle cells and then the death of muscle cells. Se­con­dary, endocrine dysfunctions, diseases of the nervous system, decreased physical activity, malnutrition or malabsorption, chronic infection accelerate the process and aggravate the patient’s condition. Complex genetic, biochemical and endocrine mechanisms take part in the development of sarcopenia. This involution is due to the impaired balance of restoring and depleting processes of muscles. A questionnaire and algorithm have been developed to recognize, screen and diagnose the risks of sarcopenic condition; these separate the sarcopenic and non-sarcopenic patients with specific cut-off values. Sar­co­penia can be diagnosed based on walking speed, decreased handgrip strength and measured or calculated muscle mass in persons over 65. Sarcopenia can be considered as a phenomenon of “physiological” aging, however, it becomes a disease when diagnostic cut-offs are exceeded and the patient experiences functional disability and declining quality of life. Prevention and treatment of sarcopenia and reducing the risk of falling are based on regular active resistance and coordination exercises. Options for pharmaceutical treatments are limited since despite of identified molecular targets there are no convincingly effective innovative therapy on the horizon. Nevertheless, there are some weak evidence for efficacy of the application of amino acids stimulating muscle cell differentiation, such as leucine or the analogue of beta-hydoxy-methylbutyrate beside exercise therapy.]