Search

Adipose tissue, besides being an important energetic storage, is also a source of cytokines and hormones which act in a paracrine, autocrine and especially endocrine manner, influencing the cardiometabolic axis. Adipokines are a group of mediators with pleiotropic function, that are involved in many physiological processes, so that a disregulation in their secretion can lead to multiple pathological conditions. In this review our aim was to clarify the role of adipokines in the pathogenesis of atherosclerosis, especially in coronary artery disease, and based on current scientific evidence, to analyze the therapeutic and behavioral strategies that are so far available.

Peripheral arterial disease is a common clinical condition and represents a manifestation of systemic atherosclerosis. It has been demonstrated that peripheral arterial disease impairs significantly quality of life, and thus its improvement has become an important goal of therapy, particularly in symptomatic patients. In addition, the impact of this disease on quality of life is not adequately described by physical examination findings and common clinical data, such as the ankle-brachial index. Thus, to properly understand the clinical evolution of peripheral arterial disease and its treatment, it is useful to integrate clinical outcome measures with data derived from the patient's point of view in order to avoid that procedural success is evaluated only in terms of appropriate use of the available technical tools and of a good angiographic result without taking into account its consequences on daily future life of patients. It would therefore be necessary that the caregivers involved in the evaluation and treatment of patients with peripheral arterial disease are able to use and interpret the validated instruments for quality of life assessment. Among therapeutic strategies, percutaneous transluminal angioplasty is emerging as a suitable option to improve both clinical outcome and quality of life, even though it cannot contrast the progression of atherosclerotic disease. In this article we review major generic and specific instruments to assess patient-reported quality of life. Moreover, we describe the impact of peripheral arterial disease and its endovascular treatment on quality of life.

Beta-adrenergic vasodilation plays a key role in the regulation of coronary blood flow, in particular during sympathetic nervous system activation. Beta1-adrenergic receptors are mostly represented in epicardial coronary vessel, while beta2 receptors are located in microvasculature. Coronary atherosclerosis is associated with a significant impairment of beta-adrenergic receptor response. This might contribute to precipitate myocardial ischemia.

During liver cirrhosis many important changes occur in the cardiovascular system and these abnormalities appear more evident as portal hypertension and liver dysfunction progress. The cirrhotic heart develops a series of structural and functional abnormalities consisting in diastolic dysfunction and reduced myocardial reactivity during exercise, likely due to a diminished myocardial beta-adrenergic receptor function. Nevertheless, the peculiarity of the cardiovascular involvement during liver cirrhosis is represented by a progressive development of a hyperdynamic circulation that seems to be due to portal hypertension rather than to liver insufficiency. In fact, it has been hypothesized that this syndrome raise from the venous portal bed and is primarily determined by an increase in blood volume that leads to an enhanced cardiac output. Later, as liver cirrhosis progresses, new important pathogenetic elements occur and lead to a reduction in peripheral vascular resistances and to the full clinical expression of hyperdynamic circulation. The pathogenesis of hyperdynamic circulation is very interesting for scientific research because of the complex and still in part unknown origin. In addition, this syndrome has an important clinical meaning for its severely adverse prognostic value and it represents the pathogenetic background for a number of severe complications of advanced liver cirrhosis.