Christopoulou E C, Filippatos T D, Megapanou E, Elisaf M S, Liamis G
Department of Internal Medicine, School of Medicine, University of Ioannina, 451 10, Ioannina, Greece.
Heart Fail Rev. 2017 May;22(3):349-356. doi: 10.1007/s10741-017-9615-6.
Patients with heart failure often exhibit electrolyte abnormalities, such as hyponatremia or hypokalemia/hyperkalemia. Although not as common as the other electrolyte disturbances observed in patients with heart failure, phosphate imbalance is also of high importance in this population. The aim of this review is to present the mechanisms of low or high phosphate serum levels in patients with heart failure and its role in the pathogenesis and progression of heart dysfunction. Hypophosphatemia in patients with heart failure may be the result of co-existing electrolyte and acid-base abnormalities, pharmacological treatments, decreased intestinal absorption or secondary to sympathetic nervous system activation and co-morbidities, such as diabetes mellitus or heavy alcohol consumption. Hypophosphatemia can affect multiple organ systems including the cardiovascular system. Depletion of phosphate can lead to ventricular arrhythmias and elimination of ATP synthesis, resulting in reversible myocardial dysfunction. Hyperphosphatemia, observed mainly in patients with chronic kidney failure, is also associated with cardiac hypertrophy, which may worsen cardiac contractility and heart failure. Studies have also shown an association of high-normal serum phosphate levels with vascular and valvular calcification. Therefore, serum phosphate imbalances may exhibit a causal role in the pathogenesis and progression of heart failure.
心力衰竭患者常出现电解质异常，如低钠血症或低钾血症/高钾血症。尽管磷酸盐失衡在心力衰竭患者中不如其他电解质紊乱常见，但在这一人群中也非常重要。本综述的目的是阐述心力衰竭患者血清磷酸盐水平过低或过高的机制及其在心脏功能障碍的发病机制和进展中的作用。心力衰竭患者的低磷血症可能是并存的电解质和酸碱异常、药物治疗、肠道吸收减少或继发于交感神经系统激活以及合并症（如糖尿病或大量饮酒）的结果。低磷血症可影响包括心血管系统在内的多个器官系统。磷酸盐耗竭可导致室性心律失常并消除ATP合成，从而导致可逆性心肌功能障碍。高磷血症主要见于慢性肾衰竭患者，也与心脏肥大有关，这可能会使心脏收缩力和心力衰竭恶化。研究还表明，血清磷酸盐水平略高于正常与血管和瓣膜钙化有关。因此，血清磷酸盐失衡可能在心力衰竭的发病机制和进展中起因果作用。
