Cohen Natan, Golik Ahuva
Department of Internal Medicine F, Assaf Harofeh Medical Center, Zerifin, Israel.
Heart Fail Rev. 2006 Mar;11(1):19-24. doi: 10.1007/s10741-006-9189-1.
Heart failure (HF) is a prevalent syndrome resulting in a high mortality rate. HF may be associated with zinc deficiency through a reduction in dietary intake, decreased absorption due to gastrointestinal edema, impaired motility or intestinal zinc losses. Diseases concomitant with HF such as diabetes mellitus (DM) and hypertension may enhance zinc deficiency. Medications given for HF may affect zinc metabolism in different ways. It was shown that thiazides may cause zincuria and a decrease in tissue zinc concentration. There is conflicting evidence about furosemide, even though patients with chronic furosemide treatment showed low tissue zinc levels in autopsies. Treatment with angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs) resulted in zincuria and zinc deficiency, but this outcome was not consistent in all studies. Beta-blockers did not alter plasma zinc concentration. Matrix metalloproteinases (MMPs) and ACE are zinc-containing enzymes, which play a role in the process of remodeling in HF. It was shown that ACE inhibitors may inhibit the activity of different MMPs. The exact interrelationship between HF, zinc-containing enzymes, zinc deficiency and the clinical manifestation of HF has to be investigated.
心力衰竭(HF)是一种普遍存在的综合征,死亡率很高。HF可能通过饮食摄入减少、胃肠道水肿导致吸收减少、运动功能受损或肠道锌流失而与锌缺乏有关。与HF并发的疾病,如糖尿病(DM)和高血压,可能会加重锌缺乏。用于治疗HF的药物可能以不同方式影响锌代谢。研究表明,噻嗪类药物可能导致锌尿症和组织锌浓度降低。关于呋塞米存在相互矛盾的证据,尽管接受慢性呋塞米治疗的患者在尸检中显示组织锌水平较低。使用血管紧张素转换酶(ACE)抑制剂和血管紧张素受体阻滞剂(ARB)进行治疗会导致锌尿症和锌缺乏,但并非所有研究都得出了一致的结果。β受体阻滞剂不会改变血浆锌浓度。基质金属蛋白酶(MMPs)和ACE是含锌酶,在HF的重塑过程中发挥作用。研究表明,ACE抑制剂可能会抑制不同MMPs的活性。HF、含锌酶、锌缺乏与HF临床表现之间的确切相互关系有待研究。