Ardissino D, De Servi S, Barberis P, Demicheli G, Falcone C, Ochan M, Specchia G, Montemartini C
Division of Cardiology IRCCS Policlinico S. Matteo, University of Pavia, Italy.
J Am Coll Cardiol. 1989 Mar 15;13(4):804-10. doi: 10.1016/0735-1097(89)90220-9.
To investigate the significance of hyperventilation-induced ST segment depression, 329 consecutive patients with angina and documented coronary artery disease who underwent hyperventilation and exercise tests during pharmacologic washout were studied. The hyperventilation test induced ST segment depression in 79 patients. In 36 of these 79 patients, the electrocardiographic changes occurred early during overbreathing (Group I), whereas in 26 they occurred late during recovery (Group II). Seventeen patients developed ST segment depression both during over-breathing and during recovery (Group III). Group I patients had a higher frequency of history of angina during exercise, multivessel disease and lower tolerance to exercise as compared with patients in Group II. In Group I, the rate-pressure product at the time to onset of ST depression during overbreathing was similar to that during exercise (152 +/- 24 versus 148 +/- 42; p = NS), whereas in Group II the rate-pressure product at the time to onset of ST depression during recovery was comparable with that under control conditions (104 +/- 30 versus 98 +/- 27; p = NS) and far less than that required to produce ischemia during exercise (104 +/- 30 versus 201 +/- 56; p less than 0.0011). In nine Group III patients, the acute administration of propranolol prevented the early hyperventilation-induced ST segment depression, whereas nifedipine abolished the delayed hyperventilation-induced ST segment depression. These findings suggest that early hyperventilation-induced ST segment depression is due to increased oxygen demand in patients with poor coronary reserve and may be prevented by beta-adrenergic blockers, which are useful for lowering oxygen consumption.(ABSTRACT TRUNCATED AT 250 WORDS)
为研究过度通气诱发ST段压低的意义，我们对329例连续性心绞痛且有冠状动脉疾病记录、在药物洗脱期接受过度通气和运动试验的患者进行了研究。过度通气试验使79例患者出现ST段压低。在这79例患者中，36例患者在过度呼吸早期出现心电图改变（I组），而26例在恢复后期出现改变（II组）。17例患者在过度呼吸期和恢复期均出现ST段压低（III组）。与II组患者相比，I组患者运动时心绞痛病史、多支血管病变的发生率更高，运动耐量更低。在I组中，过度呼吸时ST段压低开始时的心率血压乘积与运动时相似（152±24对148±42；p=无显著性差异），而在II组中，恢复时ST段压低开始时的心率血压乘积与对照条件下相当（104±30对98±27；p=无显著性差异），且远低于运动时产生心肌缺血所需的值（104±30对201±56；p<0.0011）。在9例III组患者中，急性给予普萘洛尔可预防早期过度通气诱发的ST段压低，而硝苯地平可消除延迟性过度通气诱发的ST段压低。这些发现提示，早期过度通气诱发的ST段压低是由于冠状动脉储备功能差的患者氧需求增加所致，且可被β-肾上腺素能阻滞剂预防，β-肾上腺素能阻滞剂有助于降低氧消耗。（摘要截短于250字）
