Black H R
Department of Internal Medicine, Yale University School of Medicine, New Haven, CT 06510.
Am Heart J. 1991 Feb;121(2 Pt 2):707-15. doi: 10.1016/0002-8703(91)90451-m.
The objective of treating patients with hypertension is not simply to reduce blood pressure but rather to prevent the associated morbidity and mortality. Recent assessments of clinical trials have shown that while the risk of stroke is consistently lower with antihypertensive therapy, the same degree of success has not been demonstrated for coronary artery disease (CAD). Although there are many explanations of why we have not done as well in preventing CAD, one possibility is that the therapy used in clinical trials, primarily thiazide diuretics and beta-adrenoreceptor blockers, has increased the patient's risk of developing coronary atherosclerosis or lethal arrhythmias. Four classes of antihypertensive agents are recommended for initial therapy--thiazide diuretics, beta-adrenoreceptor blockers, angiotensin-converting enzyme (ACE) inhibitors, and calcium entry blockers. The metabolic effects of thiazide diuretics include electrolyte disturbances (hypokalemia, hypomagnesemia, and hyponatremia), dyslipidemia (increased triglycerides), abnormalities of glucose metabolism (hyperglycemia, hyperinsulinemia, and peripheral insulin resistance), and hyperuricemia. beta-Adrenoreceptor blockers have many of the same metabolic adverse reactions. beta-Adrenoreceptor blockers without intrinsic sympathomimetic activity (ISA) also cause dyslipidemias (lowered high-density lipoprotein cholesterol and increased triglycerides) and abnormalities of glucose metabolism (hyperglycemia, hyperinsulinemia, and peripheral insulin resistance). beta-Adrenoreceptor blockers with ISA and third-generation beta-blockers with selective partial agonist activity (celiprolol and dilevalol) do not cause dyslipidemia and to date do not appear to induce abnormalities in glucose metabolism. ACE inhibitors may decrease triglycerides and increase high-density lipoprotein cholesterol, and captopril may improve insulin sensitivity. Calcium entry blockers are metabolically neutral.(ABSTRACT TRUNCATED AT 250 WORDS)
治疗高血压患者的目标不仅仅是降低血压，更重要的是预防相关的发病率和死亡率。近期对临床试验的评估表明，虽然抗高血压治疗能持续降低中风风险，但在预防冠状动脉疾病（CAD）方面尚未取得同样程度的成功。尽管对于为何在预防CAD方面效果不佳有多种解释，但一种可能性是临床试验中使用的治疗方法，主要是噻嗪类利尿剂和β-肾上腺素能受体阻滞剂，增加了患者发生冠状动脉粥样硬化或致命性心律失常的风险。推荐四类抗高血压药物用于初始治疗——噻嗪类利尿剂、β-肾上腺素能受体阻滞剂、血管紧张素转换酶（ACE）抑制剂和钙通道阻滞剂。噻嗪类利尿剂的代谢作用包括电解质紊乱（低钾血症、低镁血症和低钠血症）、血脂异常（甘油三酯升高）、糖代谢异常（高血糖、高胰岛素血症和外周胰岛素抵抗）以及高尿酸血症。β-肾上腺素能受体阻滞剂有许多相同的代谢不良反应。无内在拟交感活性（ISA）的β-肾上腺素能受体阻滞剂也会导致血脂异常（高密度脂蛋白胆固醇降低和甘油三酯升高）和糖代谢异常（高血糖、高胰岛素血症和外周胰岛素抵抗）。具有ISA的β-肾上腺素能受体阻滞剂和具有选择性部分激动剂活性的第三代β-阻滞剂（塞利洛尔和地来洛尔）不会引起血脂异常，且迄今为止似乎不会诱发糖代谢异常。ACE抑制剂可能会降低甘油三酯并增加高密度脂蛋白胆固醇，卡托普利可能会改善胰岛素敏感性。钙通道阻滞剂在代谢方面是中性的。（摘要截选至250词）
