Search

Resting heart rate is a very accessible clinical parameter in medical practice. Several observational studies have described the link between resting heart rate and the risk of cardiovascular events. An elevated resting heart rate was associated with an increased risk of heart failure and cardiovascular mortality, independently of cardiovascular risk factors. By contrast, interventional studies have shown that reducing heart rate with drugs was beneficial only in patients with pre-existing heart failure or those with coronary heart disease. We aim to review the role and implications of resting heart rate for cardiovascular prevention.

Psoriasis is a common genetic disorder that may be initiated (drug-induced psoriasis) or exacerbated (drug-triggered psoriasis) by some drug intakes. Beta-blockers, lithium, some antimelarial drugs, non steroidal anti-inflammatory agents and tetracyclines are recognized to influence the clinical course of psoriasis. Other drugs are likely or possibly involved in this process.

Several studies suggest that the beta(3)-adrenergic stimulation could be a new therapeutic target for the treatment of cardiovascular diseases. The vascular effects induced by beta(3)-adrenergic stimulation are able to decrease the left ventricular strain allowing to reduce after-load. In addition, the increased coronary blood flow due to vasorelaxation increases the myocardial oxygene delivery. The hypothesis about the beneficial role of beta(3)-adrenoceptors is supported by recent data about a beta-blocker of third generation, nebivolol, currently used in the treatment of heart failure and hypertension. The present review presents the beta(3)-adrenoceptors characteristics as well as its involvement in the cardiovascular effects of nebivolol.

Cardiovascular involvement in polymyositis constitutes a major cause of death. However, the cardiac location is rarely symptomatic and does not usually represent the principle clinical feature at the time of the initial presentation. We present here an unusual case of polymyositis with severe and polymorph cardiac disturbances that predominant the muscular signs.

There is strong evidence that reduced sympathetic nervous system (SNS) activity is involved in the etiology of obesity in several animal models of obesity. In humans the situation is more complex but humans with low SNS activity, reduced beta-adrenergic sensitivity, reduced lipid mobilizing efficacy of catecholamines have lowered energy expenditure and are at greater risk of obesity. The SNS with its effect on food intake, lipid mobilization and energy expenditure has a major potential as a target for novel pharmacotherapies in weight reducing strategies. Extended cellular and molecular knowledge about the nature, the distribution and the role of the adrenergic receptors (beta(1)-, beta(2)-, beta(3)-, alpha(2)- and alpha(1)-) existing in tissue effectors involved in the control of lipid mobilization (adipose tissue) and energy expenditure (brown adipose tissue, skeletal muscle) has opened new pathways for pharmacological strategies. In this manuscript, after a summary of current knowledge on the regulation of lipid mobilization and energy expenditure in humans, we briefly review the putative targets and the most recent attempts to develop agents acting at various adrenergic receptor types in SNS effectors or on SNS activity. These include major questions about putative utilization of beta(3)-agonists, alpha(2)-antagonists and beta-antagonists in pharmacotherapy and/or prevention of obesity in humans.