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Heparin-induced thrombocytopenia (HIT) is the most common drug-related thrombocytopenia. Thromboembolic complications occur in approximately 50% of patients with HIT and result in limb amputation and death in up to 20% and 30% respectively. Because patients with a history of HIT may require future intravenous anticoagulation but have a high-risk of thromboembolism if re-challenged with heparin, alternative therapies are necessary when further anticoagulation is indicated. The use of direct thrombin inhibitors in HIT patients who also require thrombolytic therapy offers unique challenges to anticoagulant monitoring and safety. We present a case of progressive ileofemoral deep venous thrombosis in a patient with a history of HIT in order to review the combined use of hirudin and thrombolysis in this setting.

Because the extent of myocardial bulging after acute coronary occlusion is primarily dependent on wall tension, this study examined whether the decrease in systolic bulging with postextrasystolic potentiation was due to contractile reserve or to changes in loading conditions. Seven dogs were atrially paced at 100 beats/min after the sinus node was crushed and atrial extrasystoles were generated. The left ventricular minor axis diameter and segment lengths in the ischemic and nonischemic zones were measured with sonomicrometers. Wall tension was estimated using Laplace's law, and regional tension-length loops were determined.

In a study to test the hypothesis that vascular reserve is exhausted in the setting of a resting blood flow deficit, the left anterior descending or circumflex artery was cannulated and perfused from the left carotid artery. After reactive hyperaemia had been assessed a stenosis was produced with a screw clamp. In the first experiment a moderate stenosis (diastolic perfusion pressure 40 mmHg) was produced in the left anterior descending artery (three dogs) or left circumflex artery (three dogs). Blood pressure was held constant with aortic constriction during intracoronary adenosine infusion (6 µmol·min–1). The stenosis was then adjusted to the preadenosine perfusion pressure. In the second experiment the anterior interventricular coronary vein was also isolated and segment length crystals were placed in the ischaemic and non-ischaemic zones. Severe stenosis (flow reduction of at least 50% and evidence of decreased segmental shortening) was produced in the cannulated left anterior descending artery (eight dogs). Intracoronary adenosine was given with aortic pressure held constant by transfusion and coronary venous drainage. In the first experiment resting coronary flow (ml·min–1) decreased from 41(3) to 29(6) (p<0.05) with stenosis. Coronary flow increased from 29(6) to 34(7) (p<0.05) with adenosine and to 50(10) (p<0.05) with stenosis adjustment. Subendocardial flow (ml·g–1·min–1) decreased from 0.89(0.26) to 0.78(0.23) (p<0.05) with adenosine and then increased from 0.94(0.49) with perfusion pressure adjustment. Subepicardial flow tended to increase with adenosine, and increased further with stenosis adjustment. In the second experiment subendocardial, subepicardial, and coronary flow did not change with adenosine. Thus there was no demonstrable vascular reserve in any layer of myocardium with a resting flow deficit.

Objective: The aim of the study was to assess the contraction of myocardium stunned by repetitive brief coronary occlusions by examining the response to alterations in loading and inotropy of systolic contraction on isovolumetric and ejection phase shortening. Methods: Fourteen open chest anaesthetised dogs were used for the studies. After destruction of the sinus node, the heart was atrially paced and atrial extrasystoles were introduced followed by a short (400 ms) or long (700 ms) postextrasystole. The left anterior descending coronary artery was occluded for 5 min and reperfused for 10 min a total of eight times to produce stunned myocardium, followed by a final 60 min of reflow. Regional function was assessed with segment length sonomicrometers. Results: With successive periods of occlusion there was an increase in the end diastolic segment length and a progressive decrease in total percent systolic shortening (baseline 22.3%, 1st reflow 14.5%, 8th reflow 7.9%) with some recovery after 60 min of reflow (12.0%). This was predominantly due to the development of bulging during isovolumetric systole (4.5%, -4.9%, and -8.3%, respectively) which diminished during 60 min recovery to -3.1%. Ejection shortening was relatively constant (17.8%, 19.4%, 16.3%, and 15.1%, respectively). Postextrasystolic potentiation resulted in an increase in total percent systolic shortening, but not to the baseline value, as slight isovolumetric bulging persisted. Similar changes were seen with the short and long postextrasystoles although the latter had a greater increase in ejection shortening. Conclusions: The decrease in function after repetitive occlusion and reflow is predominantly due to bulging during isovolumetric systole which persists after postextrasystolic potentiation in our model of stunned myocardium.

The hypothesis that there is a lateral border zone with function intermediate to adjacent ischaemic and non-ischaemic tissue was tested in 10 open chest anaesthetised dogs. Four pairs of segment length crystals were placed in parallel so as to span the ischaemic and non-ischaemic zones. Graded occlusion was produced with a screw clamp applied to a carotid to left anterior descending artery cannulation system. Contractile reserve was assessed using postextrasystolic potentiation. A balloon perfusion labelling system was used to label negatively the potentially ischaemic zone and quantify the admixture of ischaemic and non-ischaemic tissue in the lateral border zone, defined by the fraction of normal zone tissue. When the 40 crystal pairs from the 10 dogs were grouped according to fraction of normal zone tissue (FNZT), 13 were in the central ischaemic zone(FNZT<0.1), seven were in the border ischaemic zone (FNZT 0.1–0.5), five were in the border non-ischaemic zone (FNZT 0.5–1.0), and 15 were in the non-ischaemic zone (FNZT 1.0). When the lateral border zone is predominantly non-ischaemic tissue, the tissue behaves as though it is non-ischaemic. Segmental shortening before and after postextrasystolic potentiation in the border non-ischaemic zone and non-ischaemic zone did not change with ischaemia. When tissue in the lateral border zone is predominantly ischaemic, it behaves as though it is ischaemic. Segmental shortening decreased in parallel with progressive ischaemia in the border ischaemic zone and ischaemic zone. At total occlusion, segmental shortening in the border ischaemic zone was –2.3(5.9)% and in the ischaemic zone –3.5(3.6)% (NS). Segmental shortening after postextrasystolic potentiation also decreased in parallel with ischaemia in the border ischaemic zone and ischaemic zone and was 7.0(3.9)% and 8.4(4.5)% respectively at total occlusion (NS). Thus in the heterogeneously perfused lateral border zone function was not intermediate but was determined by the proportions of ischaemic and non-ischaemic tissue.