UNEXPECTED EFFECTS OF TREATING HYPERTENSION IN MEN WITH ELECTROCARDIOGRAPHIC ABNORMALITIES - A CRITICAL ANALYSIS
UNEXPECTED EFFECTS OF TREATING HYPERTENSION IN MEN WITH ELECTROCARDIOGRAPHIC ABNORMALITIES - A CRITICAL ANALYSIS
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DOI：
10.1161/01.cir.73.1.114
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发表时间：
1986-01-01
期刊：
影响因子：
37.8
通讯作者：
NEATON, J
中科院分区：
文献类型：
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作者：
KULLER, LH;HULLEY, SB;NEATON, J
利尿剂治疗与可能增加的冠心病（CHD）风险，尤其是猝死之间的关系存在争议。多危险因素干预试验（MRFIT）的初步报告提出了这样一种可能性，即在一组高血压和基线检查时某些心电图异常的特殊干预男性中观察到的CHD死亡率增加可能是利尿剂治疗的意外不良反应。来自MRFIT的后续报告显示，CHD死亡率与氢氯噻嗪的相关性强于与氯噻酮的相关性。冠心病死亡率与两种药物的剂量、最近的血清钾水平或室性早搏的存在没有一致的关系。在高血压检测和随访项目和奥斯陆高血压试验中，相似的白色男性也出现了同样程度的不利趋势，尽管这两项研究的样本量太小，无法得出明确的结论。临床研究表明，男性高血压伴左室肥厚者冠心病死亡风险增加。这类男性即使在没有利尿剂治疗的情况下，也有较高的室性早搏频率。其他研究表明，利尿剂引起的低钾血症在肾上腺素存在下加重，低钾水平降低了心室颤动的阈值。因此，尽管证据还不完全，但MRFIT特殊干预的心电图异常男性中CHD死亡率过高可能是由冠状动脉粥样硬化时左心室质量增加和利尿剂治疗依从性好引起的低钾血症以及应激诱导的循环儿茶酚胺升高共同引起的。考虑到接受利尿剂治疗的患者人群非常大，进一步评估这种可能性很重要。
The relationship between diuretic therapy and possible increased risk of coronary heart disease (CHD), especially sudded death, is controversial. The initial report from the Multiple Risk Factor Intervention Trial (MRFIT) raised the possibility that the increased CHD mortality observed in a subset of special intervention men with hypertension and certain electrocardiographic abnormalities on their baseline examination might be an unexpected adverse effect of diuretic therapy. Subsequent reports from the MRFIT Have revealed a stronger association of CHD mortality to hydrochlorothiazide than to chlorthalidone. There was no consistent relationship of CHD mortality to the dose of either drug, to the most recent serum potassium level, or to the presence of ventricular premature beats. Unfavorable trends of the same magnitude were also seen among similar white men in the Hypertension Detection and Follow-up Program and in the Oslo hypertension trial, although the sample sizes in these two studies were too small to yield clearcut conclusions. Clinical studies have shown an increased risk of CHD death among hypertensive men with left ventiruclar hypertrophy. Such men are also noted to have a higher frequency of ventricular premature beats, even in the absence of diutretic therapy. Other studies have shown that diuretic-induced hypokalemia is accentuated in the presence of epinephrine and that low potassium levels decrease the threshold for ventricular fibrillation. Thus, although the evidence is still incomplete, it is possible that the excess CHD mortality among MRFIT special intervention men with electrocardiographic abnormalities may have been caused by a combination of increase left ventricular mass in the presence of coronary atherosclerosis, and hypokalemia caused by goodcompliance with diuretic therapy and accentuated by stress-induced increases in circulating catecholamines. Given the very large population of patients receiving diuretic therapy, further evaluation of this possibility is important.