Fonarow Gregg C
Division of Cardiology, David Geffen School of Medicine at the University of California-Los Angeles, Los Angeles, California 90095-1679, USA.
Am J Med. 2004 Mar 8;116 Suppl 5A:76S-88S. doi: 10.1016/j.amjmed.2003.10.022.
Heart failure affects nearly 5 million Americans and is associated with high morbidity and mortality rates. It is now recognized that activation of multiple neurohormonal systems is intrinsic in the pathophysiology of heart failure. Patients with diabetes mellitus are at high risk for heart failure, and some of the complications of diabetes (e.g., insulin resistance) contribute to the development and progression of heart failure, partly because of their effects on neurohormonal systems. Pharmacologic intervention directed toward these systems (i.e., angiotensin-converting enzyme [ACE] inhibition, use of aldosterone antagonists, and beta-adrenergic blockade) has been shown to decrease the morbidity and mortality associated with heart failure. Despite this knowledge, ACE inhibitors, aldosterone antagonists, and beta-blockers are grossly underused, and deaths and hospitalizations due to heart failure have steadily increased. Guidelines for the management of heart failure recommend the use of ACE inhibitors and beta-blockers in patients with mild, moderate, or severe disease. Aldosterone antagonists are recommended in severe heart failure, and recent data also support their use in mild to moderate heart failure. Concerns about the increased incidence of hypoglycemia, worsening dyslipidemia, and decreased insulin sensitivity with beta-blocker use may be preventing physicians from prescribing these agents for patients with diabetes with heart failure. Although evidence from earlier clinical trials justifies some of these concerns, newer vasodilating beta-blockers (e.g., carvedilol) have been shown to have a neutral or positive effect on dyslipidemia and insulin resistance. beta-Blockade in conjunction with ACE inhibition should be standard therapy for all patients with diabetes who have heart failure. Furthermore, early in-hospital initiation of neurohormonal intervention can provide earlier benefit to these patients.
心力衰竭影响着近500万美国人,且与高发病率和死亡率相关。现在人们认识到,多种神经激素系统的激活在心力衰竭的病理生理学中是内在的。糖尿病患者发生心力衰竭的风险很高,糖尿病的一些并发症(如胰岛素抵抗)会导致心力衰竭的发生和进展,部分原因是它们对神经激素系统的影响。针对这些系统的药物干预(即血管紧张素转换酶[ACE]抑制、使用醛固酮拮抗剂和β-肾上腺素能阻滞剂)已被证明可降低与心力衰竭相关的发病率和死亡率。尽管有这些认识,但ACE抑制剂、醛固酮拮抗剂和β受体阻滞剂的使用严重不足,因心力衰竭导致的死亡和住院人数仍在稳步增加。心力衰竭管理指南建议在轻度、中度或重度疾病患者中使用ACE抑制剂和β受体阻滞剂。严重心力衰竭患者推荐使用醛固酮拮抗剂,最近的数据也支持在轻度至中度心力衰竭中使用。对使用β受体阻滞剂导致低血糖发生率增加、血脂异常恶化和胰岛素敏感性降低的担忧可能阻止医生为心力衰竭合并糖尿病患者开具这些药物。尽管早期临床试验的证据证明了其中一些担忧是合理的,但新型血管舒张性β受体阻滞剂(如卡维地洛)已被证明对血脂异常和胰岛素抵抗具有中性或积极作用。β受体阻滞剂与ACE抑制联合应用应作为所有心力衰竭合并糖尿病患者的标准治疗。此外,在住院早期开始神经激素干预可为这些患者提供更早的益处。