Spöttl F, Pimmingstorfer E, Froschauer J
Wien Klin Wochenschr. 1978 Nov 24;90(22):792-6.
Therapeutic defibrination by Arwin was induced in a group of nine patients suffering from unstable angina combined with hyperfibrinogenaemia and in a further six patients who developed hyperfibrinogenaemia accompanied by angina pectoris after thrombolytic therapy with streptokinase for recent myocardial infarction. In patients of the former group with unstable angina a mean pretreatment plasma fibrinogen concentration of 4.9 g/1 was lowered to 1.4 g/l over a period of four weeks, whilst in the latter group, the plasma fibrinogen was lowered from 5.7 g/l to 2.0 g/l over 10 days. In all cases a remarkable improvement in the severe anginal symptoms was achieved already at fibrinogen levels within the lower range of normal. This improvement outlasted the period of therapy in most patients. Two patients died following acute myocardial infarction; one of the patients with unstable angina died 15 months after Arwin therapy and the second patient discontinued therapy after one week and died three weeks later.
在一组9例患有不稳定型心绞痛合并高纤维蛋白原血症的患者以及另外6例近期心肌梗死接受链激酶溶栓治疗后出现伴有心绞痛的高纤维蛋白原血症的患者中，进行了阿尔文（Arwin）的治疗性去纤维蛋白治疗。在前一组患有不稳定型心绞痛的患者中，平均治疗前血浆纤维蛋白原浓度4.9g/L在四周内降至1.4g/L，而在后一组中，血浆纤维蛋白原在10天内从5.7g/L降至2.0g/L。在所有病例中，在纤维蛋白原水平处于正常较低范围时，严重心绞痛症状就已取得显著改善。这种改善在大多数患者中持续超过治疗期。两名患者死于急性心肌梗死；一名不稳定型心绞痛患者在接受阿尔文治疗15个月后死亡，第二名患者在治疗一周后停止治疗，三周后死亡。
