Three-Month Therapy with Calcium-Heparin in Comparison with Ticlopidine in Patients with Peripheral Arterial Occlusive Disease at Leriche-Fontaine IIb Class

Abstract

Forty patients with a mean age of 62.6 ± 6 years, 36 men and 4 women, with peripheral arterial occlusive disease (PAOD) at Leriche-Fontaine IIb class, were randomly allocated to one of two treatment groups, receiving either 12,500 IU/ day of subcutaneous (sc) calcium-heparin (CAE) or 250 mg/day of oral ticlopi dine, each given for ninety days. The following parameters were evaluated be fore the start of the active treatment period and after thirty and ninety days of treatment: pain-free walking distance (PWD), maximum walking distance (WDmax), systolic and diastolic blood pressure (BP), posterior tibial arterial pressure and Winsor index at rest and after exercise (treadmill), transcutaneous oxygen and carbon dioxide pressures at rest (TcPO₂ and TcPCO₂ respectively), and time to 50% TcPo₂ recovery after three-minute ischemia. Both treatments induced an improvement in PWD/WDmax, which, at the end of the study, were increased by 50.7/58.7% and 31.7/36.2%, respectively, for CAE and ticlopidine treatments, respectively.

Statistical analysis did not show any difference between treatments, al though a statistically significant difference was found in comparison with basal measurements for both CAE and ticlopidine treatments (p < 0.01). Neverthe less, the effects determined by ticlopidine were, on the whole, less impressive than those of CAE.

In fact, interestingly, although not in a statistically significant way, the CAE group walked longer in comparison with the ticlopidine group irrespective of the more critical baseline clinical conditions.

Moreover, TcPo₂ was favorably modified by CAE (p < 0.01) but not by ticlopidine treatment while the other parameters remained unchanged.

In conclusion, CAE, given at the daily dose of 12,500 IU in patients with PAOD at the Leriche-Fontaine IIb class, showed beneficial clinical effects, which, in turn, could be due both to the removal of the thrombophilic im balance and to the restoration of the fibrinolytic-coagulatory hemostasis in the involved microvascular circulation.

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