The influence of thyroid hormones on cardiovascular system is well established. Thyroid diseases can effectively enhance the alteration on cardiovascular system by influencing chronotropic and inotropic actions of the heart; altering the strength and the speed of contraction, the speed of relaxation, the duration of the potential of action, and the duration of the refractory period and atrio-ventricular conduction time; modulating circulation and peripheral vascular beds. One of the more intriguing insights in the connection between thyroid diseases and cardiovascular alterations is related to the evaluation of the influence of thyroid hormones on pulmonary vascular beds. Literature reported several studies regarding the association between both hypothyroidism and hyperthyroidism and the occurrence of increased vascular pulmonary arterial pressure. Nevertheless, the pathogenetic mechanisms able to explain such relationship are not fully understood. Many doubts still persist in the comprehension of the mechanisms of pulmonary hypertension in thyroid diseases. The aim of this review was to provide possible explanation about the possible interaction between pulmonary vascular beds and thyroid function in order to evaluate the possibility of novel perspectives in the general management of patients suffering from thyroid and cardiovascular diseases.

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Nonbacterial thrombotic endocarditis (NBTE) is a rare clinical condition characterized by the presence of sterile vegetations on valvular leaflets Gross and Friedberg (1936). The most frequent cause of NBTE is antiphospholipid syndrome Hughson and et al. (1993); malignancy, through an intrinsic condition of hypercoagulability, is the second most common cause Thomas (2001). Systemic thromboembolic complications are frequently associated with this condition, but coronary embolism is not common. We report the case of a patient with NBTE secondary to gastric adenocarcinoma with clinical symptoms of coronary and systemic emboli.