Obesity may be an independent risk factor for coronary artery disease and contribute to a chronic state of systemic inflammation leading to atherosclerosis and metabolic abnormalities, such as diabetes, insulin resistance, dyslipidemia and hypertension. Visceral fat, in fact, may act as an endocrine organ, synthesizing and releasing atherogenic inflammatory cytokines, whose circulating levels depend on the individual's nutritional state, and the extent and anatomical location of fat stores. Unsuspected viral infections might also be involved in enhancing autocrine/paracrine mechanisms of cytokine release from omental fat. Elevated levels of blood cytokines may interact with the neuroendocrine system, autonomic nerves and peripheral lymphatic organs. This may lead to local inflammatory reactions in many body compartments, in particular in the heart tissue, possibly affecting the process of circulatory recovery in obese subjects, and predisposing these patients to a greater risk of myocardial inflammatory disease than individuals with normal body mass index. Circulating levels of inflammatory cytokines might be considered to determine risk categories for development of cardiovascular complications in obese subjects. In addition, their reduction with pharmacological antagonists might prevent and/or control acute cardiovascular events and increase energy expenditure in obese patients, especially after surgical treatment, through reduction of cytokine inhibition of the hypothalamic-pituitary-thyroid axis.
Knowledge of anatomic variability of the superior (STA), inferior (ITA), and lowest accessory (IMA) thyroid arteries may be helpful in certain clinical conditions. However, details of this variability have not been thoroughly described. Specifically, whether the presence and site of origin of STA, ITA, and IMA are influenced by the anthropological group, to what extent their origin is symmetric or asymmetric, and the role played by this variability in visualizing each thyroid artery by nonselective thyroid angiography is not known. To clarify this we conducted a meta-analytical study on Caucasian and Asian subjects, the latter including only Japanese and Koreans. In Caucasians and Asians the presence of superior vessels compared to inferior vessels was more frequent and the probability of symmetric or asymmetric arterial origin for STA were equivalent. However, better recognition of inferior rather than superior vessels was achieved by nonselective angiography in Caucasians. Finally, different frequencies of presence and site of origin for each artery were identified in Caucasians compared to Asians. Our results suggest that the higher frequency of IMA in Asians than in Caucasians should result in a search for an IMA-dependent feeding artery of inferior parathyroid adenomas, primarily the mediastinal ones, especially in Asians both by imaging and transcatheter ablative approaches. In addition, we have found that a small percentage of Caucasian subjects lack an STA on the left side. Therefore, anatomic arterial compatibility should be carefully evaluated in the preoperative stage of laryngeal transplantation maintaining in situ the donor's thyroid by terminal anastomoses between donor and recipient STAs. Finally, the lack of any individual thyroid artery in either Caucasians or Asians might influence the distribution of autonomic supply that runs with thyroid vessels to the thyroid parenchyma. This appears functionally relevant in cases of traumatic or surgical lesions of the cervical sympathetic chain involving thyroid nerves. In fact, a restricted local autonomic control of thyroid activity might be related to individual rami of thyroid nerves.
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