2013年美国心力衰竭管理指南(心衰指南)-英文

5.3. Endocrine and Metabolic Causes of Cardiomyopathy

5.3.1. Obesity

Obesity cardiomyopathy is defined as cardiomyopathy due entirely or predominantly to obesity (Section

7.3.1.5). Although the precise mechanisms causing obesity-related HF are not known, excessive adipose accumulation results in an increase in circulating blood volume. A subsequent, persistent increase in cardiac output, cardiac work, and systemic blood pressure (124) along with lipotoxicity-induced cardiac myocyte injury and myocardial lipid accumulation have been implicated as potential mechanisms (125, 126). A study with

participants from the Framingham Heart Study reported that after adjustment for established risk factors, obesity was associated with significant future risk of development of HF (99). There are no large-scale studies of the safety or efficacy of weight loss with diet, exercise, or bariatric surgery in obese patients with HF.

5.3.2. Diabetic Cardiomyopathy

Diabetes mellitus is now well recognized as a risk factor for the development of HF independent of age,

hypertension, obesity, hypercholesterolemia, or CAD. The association between mortality and hemoglobin A1c (HbA1c) in patients with diabetes mellitus and HF appears U-shaped, with the lowest risk of death in those

patients with modest glucose control (7.1% <HbA1c ≤7.8%) and with increased risk with extremely high or low HbA1c levels (127). The optimal treatment strategy in patients with diabetes and HF is controversial; some studies have suggested potential harm with several glucose-lowering medications (127, 128). The safety and efficacy of diabetes therapies in HF, including metformin, sulfonylureas, insulin, and glucagon-like peptide analogues await further data from prospective clinical trials (129-131). Treatment with thiazolidinediones (e.g., rosiglitazone) is associated with fluid retention in patients with HF (129, 132) and should be avoided in patients with NYHA class II through IV HF.

Hyperthyroidism has been implicated in causing DCM but most commonly occurs with persistent sinus tachycardia or AF and may be related to tachycardia (133). Abnormalities in cardiac systolic and diastolic

performance have been reported in hypothyroidism. However, the classic findings of myxedema do not usually indicate cardiomyopathy. The low cardiac output results from bradycardia, decreased ventricular filling, reduced cardiac contractility, and diminished myocardial work (133, 134). 5.3.3. Thyroid Disease

5.3.4. Acromegaly and Growth Hormone Deficiency

Impaired cardiovascular function has been associated with reduced life expectancy in patients with growth hormone deficiency and excess. Experimental and clinical studies implicate growth hormone and insulin-like growth factor I in cardiac development (135). Cardiomyopathy associated with acromegaly is characterized by