Foo K, Sekhri N, Deaner A, Knight C, Suliman A, Ranjadayalan K, Timmis A D
Department of Cardiology, Newham HealthCare NHS Trust, London, UK.
Heart. 2003 Jan;89(1):31-5. doi: 10.1136/heart.89.1.31.
To compare serum potassium concentrations in diabetic and non-diabetic patients in the early phase of acute coronary syndromes.
Acute phase hypokalaemia occurs in response to adrenergic activation, which stimulates membrane bound sodium-potassium-ATPase and drives potassium into the cells. It is not known whether the hypokalaemia is attenuated in patients with diabetes because of the high prevalence of sympathetic nerve dysfunction.
Prospective cohort study of 2428 patients presenting with acute coronary syndromes. Patients were stratified by duration of chest pain, diabetic status, and pretreatment with beta blockers.
The mean (SD) serum potassium concentration was significantly higher in diabetic than in non-diabetic patients (4.3 (0.5) v 4.1 (0.5) mmol/l, p < 0.0001). Multivariate analysis identified diabetes as an independent predictor of a serum potassium concentration in the upper half of the distribution (odds ratio 1.66, 95% confidence interval 1.38 to 2.00). In patients presenting within 6 hours of symptom onset, there was a progressive increase in plasma potassium concentrations from 4.08 (0.46) mmol/l in patients presenting within 2 hours, to 4.20 (0.47) mmol/l in patients presenting between 2-4 hours, to 4.24 (0.52) mmol/l in patients presenting between 4-6 hours (p = 0.0007). This pattern of increasing serum potassium concentration with duration of chest pain was attenuated in patients with diabetes, particularly those with unstable angina. Similar attenuation occurred in patients pretreated with beta blockers.
In acute coronary syndromes, patients with diabetes have significantly higher serum potassium concentrations and do not exhibit the early dip seen in non-diabetics. This may reflect sympathetic nerve dysfunction that commonly complicates diabetes.
比较急性冠脉综合征早期糖尿病患者与非糖尿病患者的血清钾浓度。
急性期低钾血症是由肾上腺素能激活引起的,它刺激膜结合的钠钾ATP酶,促使钾进入细胞内。由于交感神经功能障碍的高患病率,目前尚不清楚糖尿病患者的低钾血症是否会减轻。
对2428例急性冠脉综合征患者进行前瞻性队列研究。患者根据胸痛持续时间、糖尿病状态和β受体阻滞剂预处理情况进行分层。
糖尿病患者的平均(标准差)血清钾浓度显著高于非糖尿病患者(4.3(0.5)mmol/L对4.1(0.5)mmol/L,p<0.0001)。多变量分析确定糖尿病是血清钾浓度处于分布上半部分的独立预测因素(优势比1.66,95%置信区间1.38至2.00)。在症状发作6小时内就诊的患者中,血浆钾浓度逐渐升高,从2小时内就诊的患者的4.08(0.46)mmol/L,升至2 - 4小时内就诊的患者的4.20(0.47)mmol/L,再升至4 - 6小时内就诊的患者的4.24(0.52)mmol/L(p = 0.0007)。随着胸痛持续时间增加血清钾浓度的这种模式在糖尿病患者中减弱,尤其是不稳定型心绞痛患者。在接受β受体阻滞剂预处理的患者中也出现类似减弱情况。
在急性冠脉综合征中,糖尿病患者的血清钾浓度显著更高,且未表现出非糖尿病患者中出现的早期下降。这可能反映了糖尿病常见的交感神经功能障碍。