Diabetes Mellitus, Microalbuminuria, and Subclinical Cardiac Disease: Identification and Monitoring of Individuals at Risk of Heart Failure.

Diabetes Mellitus, Microalbuminuria, and Subclinical Cardiac Disease: Identification and Monitoring of Individuals at Risk of Heart Failure.
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DOI:
10.1161/jaha.117.005539
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发表时间:
2017-07-17
影响因子:
5.4
通讯作者:
Plein S
Plein S
中科院分区:
医学2区
文献类型:
--
作者:
Swoboda PP;McDiarmid AK;Erhayiem B;Ripley DP;Dobson LE;Garg P;Musa TA;Witte KK;Kearney MT;Barth JH;Ajjan R;Greenwood JP;Plein S

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2型糖尿病合并尿白蛋白:肌酐比值(ACR)升高的患者发生心力衰竭的风险增加。我们推测这是因为心脏组织的改变而不是无声的冠状动脉疾病。在一项病例对照观察性研究中,130名受试者(包括50名ACR+ve糖尿病合并持续性微量白蛋白尿患者(男性ACR+ b1 2.5 mg/mol,女性>3.5 mg/mol),≥2次测量,既往未接受肾素-血管紧张素-醛固酮治疗,50名ACR+ve糖尿病患者和30名对照)接受了心血管磁共振检查,以调查心肌纤维化、缺血和梗死,并进行了超声心动图检查。30例ACR+ve患者在接受肾素-血管紧张素-醛固酮阻断治疗1年后接受进一步检测。糖尿病患者的心脏细胞外体积分数(弥漫性纤维化的衡量指标)高于对照组(26.1±3.4%和23.3±3.0% P=0.0002), ACR+ve患者的心脏细胞外体积分数高于ACR - ve患者(27.2±4.1%对25.1±2.9%,P=0.004)。ACR+ve患者超声心动图测得的E′也较低(8.2±1.9 cm/s vs 8.9±1.9 cm/s, P=0.04),高敏感心肌肌钙蛋白T升高18% vs 4%≥14 ng/L (P=0.05)。无症状心肌缺血或梗死发生率不受ACR状态的影响。肾素-血管紧张素-醛固酮阻断与左心室射血分数升高(59.3±7.8至61.5±8.7%,P=0.03)和细胞外体积分数降低(26.5±3.6至25.2±3.1,P=0.01)相关,但未改变舒张功能或高敏感性心肌肌钙蛋白T水平。无症状糖尿病伴持续性微量白蛋白尿的患者有弥漫性心脏纤维化的标志物,包括细胞外体积分数升高、高敏感性心肌肌钙蛋白T和舒张功能障碍,这些可能部分通过肾素-血管紧张素-醛固酮阻断可逆转。这些患者的风险增加可能是由组织结构和功能的亚临床变化介导的。URL: http://www.clinicaltrials.gov。唯一标识符:NCT01970319。
Patients with type 2 diabetes mellitus and elevated urinary albumin:creatinine ratio (ACR) have increased risk of heart failure. We hypothesized this was because of cardiac tissue changes rather than silent coronary artery disease. In a case‐controlled observational study 130 subjects including 50 ACR+ve diabetes mellitus patients with persistent microalbuminuria (ACR >2.5 mg/mol in males and >3.5 mg/mol in females, ≥2 measurements, no previous renin–angiotensin–aldosterone therapy, 50 ACR−ve diabetes mellitus patients and 30 controls underwent cardiovascular magnetic resonance for investigation of myocardial fibrosis, ischemia and infarction, and echocardiography. Thirty ACR+ve patients underwent further testing after 1‐year treatment with renin–angiotensin–aldosterone blockade. Cardiac extracellular volume fraction, a measure of diffuse fibrosis, was higher in diabetes mellitus patients than controls (26.1±3.4% and 23.3±3.0% P=0.0002) and in ACR+ve than ACR−ve diabetes mellitus patients (27.2±4.1% versus 25.1±2.9%, P=0.004). ACR+ve patients also had lower E′ measured by echocardiography (8.2±1.9 cm/s versus 8.9±1.9 cm/s, P=0.04) and elevated high‐sensitivity cardiac troponin T 18% versus 4% ≥14 ng/L (P=0.05). Rate of silent myocardial ischemia or infarction were not influenced by ACR status. Renin–angiotensin–aldosterone blockade was associated with increased left ventricular ejection fraction (59.3±7.8 to 61.5±8.7%, P=0.03) and decreased extracellular volume fraction (26.5±3.6 to 25.2±3.1, P=0.01) but no changes in diastolic function or high‐sensitivity cardiac troponin T levels. Asymptomatic diabetes mellitus patients with persistent microalbuminuria have markers of diffuse cardiac fibrosis including elevated extracellular volume fraction, high‐sensitivity cardiac troponin T, and diastolic dysfunction, which may in part be reversible by renin–angiotensin–aldosterone blockade. Increased risk in these patients may be mediated by subclinical changes in tissue structure and function. URL: http://www.clinicaltrials.gov. Unique identifier: NCT01970319.