Timely topics in medicine. Cardiovascular diseases最新文献

Fabry disease is an inherited enzyme deficiency of galactosidase A that results in various phenotypes: classic, cardiac or renal. It can present variably and may represent an important cause of occult neurological and cardiac syndromes and renal failure. Preclinical and clinical studies demonstrate effectiveness of enzyme infusion in controlling and preventing these manifestations of the disease.

Cerebrovascular disease and dementia are extremely prevalent and disabling disorders affecting older people. Results of previous pathological investigations and later epidemiological studies have raised the possibility that the two disorders may be causally related. The study of such causal associations may provide insights that could lead to the development of strategies intended to prevent or treat dementia more effectively. Cerebrovascular disease has many manifestations, some of which are strong causal factors in the development of a future dementia. However, uncertainty and controversy exist regarding the presence and nature of the causal contribution of others. Potential therapeutic strategies for dementia are hindered by the lack of understanding of such relationships and the consequent difficulty in identifying a clear phenotype of dementia occurring predominantly due to cerebrovascular disease. The field is ripe for further examination of the associations between vascular factors and dementia, and the mechanisms underlying such associations. The interface between basic and clinical science has much to offer in clarifying the relationships between aging, vascular factors and cognitive decline in older people. In this review, we will attempt to synthesize data available from epidemiological, clinical and basic science research in the field of dementia related to cerebrovascular disease, highlighting potential avenues for further research.

Molecular and cellular immune activities have a fundamental role in all stages of the atherosclerotic process and in the pathogenesis of cerebrovascular and cardiovascular diseases. Recent studies have demonstrated how chronic infections can support a local and systemic chronic inflammation, leading to the atherosclerotic process. The pathogenic link between infection and cardiovascular and cerebrovascular disease is not completely defined. Some therapeutic strategies, able to influence the persistence of the infections or to modify the inflammatory process, could be useful in primary and secondary vascular disease prevention and in modifying the acute event outcome.

Recent developments highlighted from the First International Conference in Vascular Medicine, held in Melbourne, Australia, August 26-28, 2005, are in nitric oxide signaling, oxidative stress, homeostasis, the angiotensin-aldosterone system, diabetes, new vessel formation and P-selectin.

From the World Congress on Inflammation, held August 20-24, 2005 in Melbourne, Australia, new targets and new drugs for inflammation of the respiratory system (asthma, allergic rhinitis, chronic obstructive pulmonary disease and cystic fibrosis), inflammatory bowel disease (ulcerative colitis and Crohn's disease), arthritis (rheumatoid and osteoarthritis), atherosclerosis and cancer are discussed.

Cardiovascular disease and major depression are highly prevalent disorders in our society. Evidence has been found that confirms a reciprocal relationship between mechanisms of depression and those of cardiovascular pathology. This possible feedback between both pathologies is a subject of great concern. In recent years some studies suggest that platelets and serotonergic mechanisms could be involved in both conditions. The present review seeks a better understanding of the mechanisms that could link depression with an enhanced cardiovascular risk.

Leptin is a recently isolated circulating peptide hormone that is primarily synthesized and secreted by adipocytes. One of the major functions of this hormone is the control of energy balance by binding to receptors in the hypothalamus, leading to reduction in food intake, elevation in temperature and energy expenditure. In addition, increasing evidence suggests that leptin, through both direct and indirect actions, may play an important role in cardiovascular and renal functions. While the relevance of endogenous leptin needs further clarification, it appears to be a potential pressure- and volume-regulating factor, and may function pathophysiologically as a common link to obesity and hypertension.

Atherosclerosis is acknowledged as an active inflammatory and thrombotic disease, as opposed to simple degeneration. Infection with microorganisms may contribute to this inflammation and hence the atherosclerotic process. The "infective" hypothesis - first proposed more than a century ago by Virchow - has been revisited in recent years and has implicated numerous microorganisms as potential stimuli. The greatest body of evidence points to Chlamydia pneumoniae, a respiratory pathogen, as the "culprit" microorganism. Consistent finding of bacterial antigens, DNA and occasionally live "viable" organisms within human atherosclerotic plaque support the evidence for the concept linking C. pneumoniae to atherosclerosis. Although original seroepidemiological studies indicated an association, more recent prospective and larger studies suggest that there may be only a weak link between elevated antibodies and immune complexes to C. pneumoniae and coronary heart disease (CHD). Animal models have shown how atherogenesis can be induced by endovascular infection with C. pneumoniae; in vitro studies have explored various immunological and inflammatory pathways linking infection and atherothrombosis. On the basis of this, antibiotic trials have been explored to assess whether there is any role for antichlamydial agents in the treatment of cardiovascular events. Here, we focus on the main antibiotic studies and explores patient criteria and choice, duration of therapy, and whether effects on clinical events could be reduced.