Occlusion of the common femoral artery complicating total hip arthroplasty.

Vascular injuries after total hip arthroplasty are occasionally reported, but we have found only two cases of major arterial occlusion, and none at all involving the common femoral artery. We report two cases of occlusion of the common femoral artery after Charnley arthroplasties, one of which resulted in a below-knee amputation.

Platelet survival, atherosclerotic intermittent claudication and ticlopidine.

Platelet survival times were measured twice within 6 months using autologous 111-Indium-labelled platelets in 13 male patients diagnosed as stable intermittent claudicants. Linear, exponential, weighted mean and gamma function (multiple-hit) analyses were carried out on the data. Of these methods, exact mathematical models such as linear and exponential are unsuitable for the comparison of curves which may alter with treatment or disease progression. Weighted mean platelet survival correlated (r = 0.96) with platelet survival calculated by the precision reference method of analysis, gamma function. Statistics were expressed from gamma function analyses unless otherwise stated. Severity of claudication was measured by doppler; the ratio of brachial to mean ankle pressures was directly related to platelet survival (r = 0.84). In 7 patients, where duration of claudication was greater than 5 years, platelet survival was significantly reduced (P less than 0.02) compared with 6 newly diagnosed claudicants of less than 18 months duration. Six randomly selected patients were treated with 250 mg b.d. ticlopidine during one of the study periods. Ticlopidine significantly increased platelet survival (P less than 0.02) in all patients irrespective of disease duration or severity. The involvement of platelets in atherosclerosis observed in these claudicants, can be reduced by therapy with ticlopidine, however, the lack of clinical improvement following long-term drug treatment only confirms the platelet's secondary role in this disabling disease.

111-Indium platelet imaging, Doppler spectral analysis and angiography compared in patients with transient cerebral ischaemia.

We have evaluated carotid gamma imaging using 111Indium-labelled platelets in the diagnosis of carotid artery disease and measured the accumulation of labelled platelets on endarterectomy specimens. Autologous 111In labelled platelets were injected in 25 patients with TIA. Gamma images were then taken daily and independently interpreted by two observers. Carotid endarterectomy was performed in 11 patients allowing measurement of the radioactivity on the operative specimen. These results were compared to the findings on angiography and Doppler spectral analysis. All endarterectomy specimens accumulated platelets with the most active equivalent to platelets from 1.8 ml blood. Atheromatous ulcers were more active than stenoses with mean (+/- SEM) activities of 1.12 +/- 0.37 and 0.38 +/- 0.10 respectively. These radioactivity levels were at the threshold of gamma camera resolution in a theoretical model. Both observers agreed that 22 of the 50 carotid bifurcations showed platelet accumulation on gamma imaging. Of the 12 atheromatous ulcers demonstrated by angiography 11 were visualized, but only five of ten stenoses greater than 80% were detected. As Doppler identified all stenoses only one angiographically diseased carotid was not detected by combining ultrasound with platelet scanning. Atherosclerotic arteries accumulate 111In platelets and the more thrombogenic ulcerated plaques are identified more frequently than stenoses. Long-term follow-up is required to establish the clinical relevance of platelet deposition.

Platelet inhibition with Ticlopidine in atherosclerotic intermittent claudication.

Fifty-one men with atherosclerotic intermittent claudication and haemorheological abnormalities completed a double-blind, one-year randomised trial of Ticlopidine (500 mg/day), a new antiplatelet agent. Ticlopidine caused significant inhibition of platelet aggregation but did not fully correct abnormalities of coagulation, viscosity, and fibrinolysis. There was no significant improvement in walking ability, Doppler ankle-pressure indices, or calf blood flow. Sustained platelet inhibition for 12 months was insufficient to correct the prothrombotic abnormality of extensive atherosclerosis.

Studies of the haemodynamic effects of creatine phosphate in man.

1 The haemodynamic effects of intravenous creatine phosphate 1000 mg have been studied. 2 During the first 60 min following drug administration heart rate and blood pressure did not change but cardiac output fell significantly by approximately 18%. Calculated total peripheral resistance showed a corresponding significant rise, the maximum increase being approximately 24%. All these changes were beginning to diminish within 90 min after the injection. 3 Total limb blood flow measured in both arm and leg (using venous occlusion strain-gauge plethysmography) showed no appreciable changes following injection of creatine phosphate. 4 There was a progressive reduction in leg muscle blood flow (Xe133 clearance method) following injection which was statistically significant with respect to the initial level and reached a minimum (46% reduction) 50 min after the injection. 5 Skin blood flow, estimated by infra-red photoplethysmography, showed changes complementary to those seen with muscle flow. There was a progressive and significant rise to a peak (73% increase) 30 min after the injection. 6 No adverse reactions to the injections were noted. 7 Reduced cardiac output in the absence of altered total limb blood flow presumably reflects a reduction in visceral blood flow, which was not measured in this study. Within the limbs, creatine phosphate appears to result in a redistribution of blood flow from muscle to skin. Thus, these preliminary results suggest that intravenous creatine phosphate could be clinically useful in situations where short term improvement in skin blood flow would be advantageous and that further controlled studies would be justified.

Carotid artery occlusion following endarterectomy: evaluation by spectral analysis of Doppler ultrasound signals.

The clinical results of carotid endarterectomy are well documented, but there is little objective information on the incidence of postoperative occlusion. We have studied the postoperative patency of the internal and external carotid arteries using continuous wave Doppler ultrasound with spectral analysis (Spectrascribe BOC--Medishield). Seventy-nine patients who had had 89 endarterectomies during the past 5 years entered the study. The mean follow-up was 21 months. Fourteen patients had an occluded internal carotid artery of whom 4 had suffered an immediate postoperative stroke and 1 a delayed stroke: transient ischaemic attacks occurred in another 4 patients. Of the 60 patients with a patent internal carotid artery one suffered an immediate postoperative stroke and 2 a delayed stroke; 6 patients had recurrent transient ischaemic attacks. None of the 5 patients who had an external carotid endarterectomy developed postoperative symptoms, although there was occlusion in 2. The carotid artery was occluded in 4 of 43 completely asymptomatic patients. Thus, 18 per cent of all carotid endarterectomies and 9 per cent of asymptomatic patients in this series had postoperative occlusion of the carotid artery.

Haematological stress syndrome in atherosclerosis.

Forty patients with atherosclerotic peripheral vascular disease, as compared to 29 healthy controls, showed a significant increase in platelet number and activity, a neutrophil leucocytosis, and a raised level of several acute-phase reactant proteins (fibrinogen, antithrombin III, factor VIII, and serum globulin). The hyperproteinaemia was associated with increases in plasma-, serum-, and blood-viscosity and is the likely cause of the hyperviscosity of vascular disease. These multiple haemostatic abnormalities closely resemble the non-specific, haematological stress-syndrome response to acute and chronic inflammatory disorders. In atherosclerosis also they may represent a non-specific, secondary response and neither be of aetiological significance nor reflect continuing low-grade intravascular coagulation.