Fazio Serafino, Palmieri Emiliano A, Lombardi Gaetano, Biondi Bernadette
Department of Clinical Medicine and Cardiovascular Sciences, University of Naples "Federico II" School of Medicine, 80131, Naples, Italy.
Recent Prog Horm Res. 2004;59:31-50. doi: 10.1210/rp.59.1.31.
Increased or reduced action of thyroid hormone on certain molecular pathways in the heart and vasculature causes relevant cardiovascular derangements. It is well established that overt hyperthyroidism induces a hyperdynamic cardiovascular state (high cardiac output with low systemic vascular resistance), which is associated with a faster heart rate, enhanced left ventricular (LV) systolic and diastolic function, and increased prevalence of supraventricular tachyarrhythmias - namely, atrial fibrillation - whereas overt hypothyroidism is characterized by the opposite changes. However, whether changes in cardiac performance associated with overt thyroid dysfunction are due mainly to alterations of myocardial contractility or to loading conditions remains unclear. Extensive evidence indicates that the cardiovascular system responds to the minimal but persistent changes in circulating thyroid hormone levels, which are typical of individuals with subclinical thyroid dysfunction. Subclinical hyperthyroidism is associated with increased heart rate, atrial arrhythmias, increased LV mass, impaired ventricular relaxation, reduced exercise performance, and increased risk of cardiovascular mortality. Subclinical hypothyroidism is associated with impaired LV diastolic function and subtle systolic dysfunction and an enhanced risk for atherosclerosis and myocardial infarction. Because all cardiovascular abnormalities are reversed by restoration of euthyroidism ("subclinical hypothyroidism") or blunted by beta-blockade and L-thyroxine (L-T4) dose tailoring ("subclinical hyperthyroidism"), timely treatment is advisable in an attempt to avoid adverse cardiovascular effects. Interestingly, some data indicate that patients with acute and chronic cardiovascular disorders and those undergoing cardiac surgery may have altered peripheral thyroid hormone metabolism that, in turn, may contribute to altered cardiac function. Preliminary clinical investigations suggest that administration of thyroid hormone or its analogue 3,5-diiodothyropropionic acid greatly benefits these patients, highlighting the potential role of thyroid hormone treatment in patients with acute and chronic cardiovascular disease.
甲状腺激素对心脏和血管系统某些分子途径的作用增强或减弱会导致相关的心血管紊乱。众所周知，显性甲状腺功能亢进会诱发高动力心血管状态（高心输出量伴低全身血管阻力），这与心率加快、左心室（LV）收缩和舒张功能增强以及室上性快速心律失常（即心房颤动）的患病率增加有关，而显性甲状腺功能减退则表现为相反的变化。然而，与显性甲状腺功能障碍相关的心脏功能变化主要是由于心肌收缩性改变还是负荷条件改变尚不清楚。大量证据表明，心血管系统会对循环甲状腺激素水平的微小但持续的变化做出反应，这是亚临床甲状腺功能障碍患者的典型特征。亚临床甲状腺功能亢进与心率加快、房性心律失常、左心室质量增加、心室舒张功能受损、运动能力下降以及心血管死亡风险增加有关。亚临床甲状腺功能减退与左心室舒张功能受损和轻微的收缩功能障碍以及动脉粥样硬化和心肌梗死风险增加有关。由于所有心血管异常都可通过恢复正常甲状腺功能（“亚临床甲状腺功能减退”）而逆转，或通过β受体阻滞剂和左旋甲状腺素（L-T4）剂量调整而减轻（“亚临床甲状腺功能亢进”），因此建议及时治疗以避免不良心血管影响。有趣的是，一些数据表明，患有急性和慢性心血管疾病的患者以及接受心脏手术的患者可能存在外周甲状腺激素代谢改变，这反过来可能导致心脏功能改变。初步临床研究表明，给予甲状腺激素或其类似物3,5-二碘甲状腺丙酸对这些患者大有裨益，突出了甲状腺激素治疗在急性和慢性心血管疾病患者中的潜在作用。
