Diuretics, serum and intracellular electrolyte levels, and ventricular arrhythmias in hypertensive men.
Diuretics, serum and intracellular electrolyte levels, and ventricular arrhythmias in hypertensive men.
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DOI：
10.1001/jama.1992.03480080053026
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发表时间：
1992-02
期刊：
影响因子：
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通讯作者：
D. Siegel;S. Hulley;D. Black;M. Cheitlin;A. Sebastian;D. Seeley;N. Hearst;R. H. Fine
中科院分区：
文献类型：
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作者：
D. Siegel;S. Hulley;D. Black;M. Cheitlin;A. Sebastian;D. Seeley;N. Hearst;R. H. Fine
目的探讨噻嗪类药物引起的电解质异常的模式及其是否引起室性心律失常，并帮助解决临床医生是否应常规对所有噻嗪类药物治疗的患者进行保钾治疗的争议。设计：随机双盲对照试验。对象233例男性高血压患者，年龄35 ~ 70岁。干预参与者退出先前的利尿剂治疗，并补充口服氯化钾和氧化镁。然后将他们随机分配至2个月的治疗组：（1）氢氯噻嗪;（2）氢氯噻嗪+口服钾;（3）氢氯噻嗪+口服钾和镁;（4）氢氯噻嗪+氨苯蝶啶;（5）氯噻酮;或（6）安慰剂。主要观察指标：24小时动态霍尔特监测室性心律失常及血清和细胞内钾镁水平。结果在233名参与者中，212人（91%）完成了研究。氢氯噻嗪组的血清钾水平比安慰剂组低0.4 mmol/L（P <0.01），这种平均差异不受补充钾、钾和镁或氨苯蝶啶的影响。然而，补充剂确实防止了偶尔发生的明显低钾血症;所有12名血清钾水平为3.0 mmol/L或更低的男性都在90名接受利尿剂而不补充的男性中（P <0.01）。同样，随机治疗对室性心律失常男性患者的总体比例没有影响，但在血清钾水平为3.0 mmol/L或更低的12名男性患者中，心律失常的比例增加了两倍（P = .02）。氢氯噻嗪未降低血清镁和细胞内钾和镁水平，也与室性心律失常无关。结论：在大多数高血压患者中，50 mg/d氢氯噻嗪治疗不会引起明显的低钾血症或室性心律失常。然而，由于有些人在开始利尿剂治疗后会出现低钾血症，因此应监测血清钾水平，并在有指征时使用保钾策略。
OBJECTIVE To investigate the patterns of electrolyte abnormalities resulting from thiazide administration and whether they cause ventricular arrhythmias, and to help resolve the controversy over whether clinicians should routinely prescribe potassium-conserving therapy to all patients treated with thiazides. DESIGN Double-blind, randomized controlled trial. PARTICIPANTS A total of 233 hypertensive men aged 35 to 70 years. INTERVENTIONS Participants were withdrawn from prior diuretic treatment and were replenished with oral potassium chloride and magnesium oxide. They were then randomized to 2 months of treatment with (1) hydrochlorothiazide; (2) hydrochlorothiazide with oral potassium; (3) hydrochlorothiazide with oral potassium and magnesium; (4) hydrochlorothiazide and triamterene; (5) chlorthalidone; or (6) placebo. MAIN OUTCOME MEASURES Ventricular arrhythmias on 24-hour Holter monitoring and serum and intracellular potassium and magnesium levels. RESULTS Of the 233 participants, 212 (91%) completed the study. Serum potassium levels were 0.4 mmol/L lower in the hydrochlorothiazide group than in the placebo group (P less than 0.01), and this mean difference was not affected by supplementation with potassium, with potassium and magnesium, or with triamterene. However, the supplements did prevent the occasional occurrence of marked hypokalemia; all 12 of the men who developed serum potassium levels of 3.0 mmol/L or less were among the 90 who received diuretics without supplementation (P less than 0.01). Similarly, the overall proportion of men with ventricular arrhythmias was not affected by randomized treatment, but there was a twofold increase in the proportion with arrhythmias among the 12 men with serum potassium levels of 3.0 mmol/L or less (P = .02). Serum magnesium and intracellular potassium and magnesium levels were not reduced by hydrochlorothiazide, nor were they related to ventricular arrhythmias. CONCLUSIONS In the majority of hypertensive patients, treatment with 50 mg/d of hydrochlorothiazide does not cause marked hypokalemia or ventricular arrhythmias. However, because some individuals will develop hypokalemia after starting diuretic therapy, serum potassium levels should be monitored and potassium-sparing strategies should be used when indicated.