Yeh S J, Kou H C, Lin F C, Hung J S, Wu D
Am J Cardiol. 1983 Aug;52(3):271-8. doi: 10.1016/0002-9149(83)90121-2.
Electrophysiologic studies were performed before and 2 hours after the oral administration of 270 mg of diltiazem in 3 divided doses at 8-hour intervals in 36 patients with paroxysmal supraventricular tachycardia (SVT). Before diltiazem, all 36 patients had induction of sustained SVT: 24 with atrioventricular (AV) reentrance incorporating an accessory pathway (Group 1) and 12 with AV nodal reentrance (Group 2). After diltiazem, 20 patients in Group 1 lost the ability to induce or sustain SVT because of increased anterograde normal pathway refractoriness in 19 patients and increased retrograde accessory pathway refractoriness in 1. Eight patients in Group 2 could no longer induce or sustain SVT because of increased anterograde slow pathway refractoriness in 2 patients and increased retrograde fast pathway refractoriness in 6. Diltiazem concentration in the blood, measured in 29 patients, was 156 +/- 75 ng/ml (mean +/- standard deviation). Fifteen patients, 2 with and 13 without induction of sustained SVT after diltiazem, were discharged on the same dosage of diltiazem and followed up 5 +/- 3 months. The former 2 patients had attacks of sustained SVT, whereas the latter 13 have been free of sustained SVT. In conclusion, oral diltiazem prevents induction and sustenance of paroxysmal SVT in most patients and may be used as an alternative agent for the prophylaxis of SVT.
对36例阵发性室上性心动过速（SVT）患者进行了电生理研究。在口服270mg地尔硫䓬（分3次给药，间隔8小时）之前及之后2小时进行研究。在服用地尔硫䓬之前，所有36例患者均诱发出持续性SVT：24例为房室（AV）折返合并旁路（第1组），12例为房室结折返（第2组）。服用地尔硫䓬后，第1组20例患者因19例患者前向正常路径不应期增加和1例患者逆向旁路不应期增加而失去诱发或维持SVT的能力。第2组8例患者因2例患者前向慢径路不应期增加和6例患者逆向快径路不应期增加而不再能诱发或维持SVT。对29例患者测量的血液中地尔硫䓬浓度为156±75ng/ml（平均值±标准差）。15例患者，2例在服用地尔硫䓬后诱发了持续性SVT，13例未诱发，以相同剂量的地尔硫䓬出院并随访5±3个月。前2例患者发生了持续性SVT发作，而后13例未发生持续性SVT。总之，口服地尔硫䓬可预防大多数患者阵发性SVT的诱发和维持，可作为预防SVT的替代药物。
