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Thyroid hormones (THs) are synthesized in the thyroid gland, and they circulate in the blood to regulate cells, tissues, and organs in the body. In particular, they exert several effects on the cardiovascular system. It is well known that THs raise the heart rate and cardiac contractility, improve the systolic and diastolic function of the heart, and decrease systemic vascular resistance. In the past 30 years, some researchers have studied the molecular pathways that mediate the role of TH in the cardiovascular system, to better understand its mechanisms of action. Two types of mechanisms, which are genomic and non-genomic pathways, underlie the effects of THs on cardiomyocytes. In this review, we summarize the current knowledge of the action of THs in the cardiac function, the clinical manifestation and parameters of their hemodynamics, and treatment principles for patients with hyperthyroid- or hypothyroid-associated heart disease. We also describe the cardiovascular drugs that induce thyroid dysfunction and explain the mechanism underlying the thyroid toxicity of amiodarone, which is considered the most effective antiarrhythmic agent. Finally, we discuss the recent reports on the involvement of thyroid hormones in the regulation of myocardial regeneration and metabolism in the adult heart.

Heart transplantation alone has been recognized to be contraindicated when pulmonary hypertension (PH) and elevated pulmonary vascular resistance (PVR) are irreversible, irrespective of any medical intervention by the use of inotropic agents or pulmonary vasodilators, because such patients are at an increased risk of post-transplantation right ventricular failure and mortality. Therefore, end-stage heart failure patients with concomitant fixed PH and irreversibly high PVR are considered to be heart–lung transplant candidates. Recently, left ventricular assist device (LVAD) therapy has been reported to normalize PVR through persistent unloading of the left ventricle, even in patients with medically refractory PH. Therefore, LVAD therapy could make such patients suitable for “heart-only” transplants, which contributes to appropriate donor lung allocation for lung-only candidates. We review the literature regarding LVAD use for secondary PH and present a case with end-stage heart failure that could avoid a heart–lung transplant owing to LVAD therapy.

Background: Intracerebral hemorrhage (ICH) is one of the most serious complications in patients supported by a left ventricular assist device (LVAD). We evaluate the efficacy of prothrombin complex concentrate (PCC) for rapid reversal of warfarin-induced anticoagulation in this population. Methods: A total of 38 consecutive ICH events in patients supported by an LVAD between 1996 and 2007 were retrospectively reviewed. Fourteen ICH events were treated with fresh frozen plasma (FFP) (Group FFP) and 24 ICH events were treated with PCC (Group PCC). The efficacy and outcome of PCC administration versus FFP were evaluated. Results: The proportion of patients surviving after an ICH event was significantly smaller in Group FFP than Group PCC (35.7% vs. 75.0%, p < 0.05). None of the patients in Group FFP were able to undergo heart transplantation, whereas 21.4% patients in Group PCC successfully underwent heart transplantation. Conclusion: Patients on LVAD are in need for intensified anticoagulation and are at high risk of ICH; therefore, adequate use of PCC in the event of ICH could be of importance for survival and allow subsequent heart transplantation.