Heparin-induced thrombocytopenia: recent experience in a large teaching hospital.

BACKGROUND: Heparin-induced thrombocytopenia (HIT) is a potentially serious adverse reaction caused by platelet-activating antibodies. AIM: To describe experience with HIT. METHODS: Twenty-two patients identified by laboratory records of heparin-associated antibodies with a 50% or greater decrease in platelet count were reviewed in our 600-bed metropolitan teaching hospital from 1999 to April 2005. RESULTS: There was an increase in the frequency of HIT diagnosed during the review period, which was associated with a rise in the number of requests for HIT antibodies. Thrombotic complications were identified in 14 of 22 patients with HIT. Mean age was 65 years, and 11 patients were men. Seven patients died and HIT was considered contributory in four. One patient required mid-forearm amputation. Unfractionated heparin was used in all cases and five patients also received enoxaparin. Mean time to HIT screen, reflecting when the diagnosis was first suspected, was 14 days. Platelet nadir ranged from 6 x 10(9)/L to 88 x 10(9)/L, with a percentage drop in platelet count of 67-96%. Alternative anticoagulation (danaparoid) was not used in three patients, two of whom died. CONCLUSIONS: HIT is a potentially life-threatening complication of heparin therapy, associated with a fall in platelet count and a high incidence of thromboembolic complications. It is most frequently seen using unfractionated heparin therapy. The increase in frequency of HIT diagnosed in our hospital appears to be associated with a greater awareness of the entity, although detection is often delayed. Platelet count should be monitored in patients on heparin and the presence of antiplatelet antibodies determined if HIT is suspected. Treatment involves both discontinuation of heparin and the use of an alternative anticoagulant such as danaparoid because of the persisting risk of thrombosis.

Carotid endarterectomy relieves pulsatile tinnitus associated with severe ipsilateral carotid stenosis.

OBJECTIVES: Pulsatile tinnitus is a rare and often disabling condition. Pulsatile tinnitus sometimes occurs in patients with severe atherosclerotic carotid stenosis. It is uncertain whether carotid endarterectomy (CEA) relieves pulsatile tinnitus in patients with severe carotid stenosis. DESIGN, MATERIALS AND METHODS: This is a retrospective study of 14 patients with pulsatile tinnitus who underwent CEA. Demographic and clinical features and pre-operative duplex results were recorded. Operative results in this group were assessed. RESULTS: CEA relieved symptoms of pulsatile tinnitus in 10 out of 14 cases (70%). Of 10 patients that had lateralisable tinnitus and ipsilateral surgery, 9 (90%) reported symptomatic improvement. CONCLUSIONS: CEA is effective in improving pulsatile tinnitus in patients with unilateral symptoms and severe ipsilateral carotid stenosis.

A multicenter randomized trial comparing a percutaneous collagen hemostasis device with conventional manual compression after diagnostic angiography and angioplasty.

OBJECTIVES: A new percutaneous collagen hemostasis device was compared with conventional compression techniques after diagnostic catheterization and angioplasty. Background. Peripheral vascular complications after diagnostic catheterization or more complex interventional procedures, as well as the discomfort of manual compression and prolonged bed rest, represent significant morbidity for invasive cardiac procedures. METHODS: A prospective, multicenter, randomized trial was designed to compare the hemostasis time in minutes and the incidence of vascular complications in patients receiving a vascular hemostasis device with those undergoing conventional compression techniques. RESULTS: After diagnostic catheterization, hemostasis time was significantly less with the vascular hemostasis device than with conventional manual compression (4.1 +/- 2.8 min [n=90 patients] vs. 17.6 +/- 9.2 min [n= 75], p < 0.0001). This difference was greater in patients undergoing angioplasty and was unrelated to the anticoagulation status (4.3 +/- 3.7 min [n = 71 not receiving the heparin], 7.6 +/- 11.6 min [n= 85 receiving heparin], 33.6 +/- 24.2 min [n= 134 control patients not receiving heparin], p < 0.0001 vs. control patients). The time from the start of the procedure to ambulation was slightly less after diagnostic catheterization in patients treated with the device (13.3 +/- 12.1 hours vs. 19.2 +/- 17.8 hours, p < 0.05). It was also less in patients who underwent angioplasty when the device was used after discontinuation of anticoagulation (23.0 +/- 11.1 hours, without heparin), as compared with control compression techniques (32.7 +/- 18.8 hours, p < 0.0001). Time to ambulation was even shorter (16.1 +/- 11.1 h, p < 0.0001) in patients in whom the device was placed immediately after angioplasty while they were still fully anticoagulated with a prolonged activated clotting time (336 +/- 85 s). There were no major complications (surgery or transfusion) after diagnostic catheterization and a low incidence of major complications in patients who underwent angioplasty (0.7% in control patients, 1.4% with the device without heparin, 1.2% with the device and heparin, p = NS). After angioplasty, there was a trend toward fewer hematomas when the device was used in the absence of heparin (4.2% vs. 9.7% in control patients, p = 0.14). CONCLUSION: A new vascular hemostasis device can significantly reduce the puncture site hemostasis time and the time to ambulation without significantly increasing the risk of peripheral vascular complications The role of this technology in reducing complications, length of hospital stay and cost remains to be determined.

A multicenter randomized trial comparing a percutaneous collagen hemostasis device with conventional manual compression after diagnostic angiography and angioplasty.

OBJECTIVES: A new percutaneous collagen hemostasis device was compared with conventional compression techniques after diagnostic catheterization and angioplasty. BACKGROUND: Peripheral vascular complications after diagnostic catheterization or more complex interventional procedures, as well as the discomfort of manual compression and prolonged bed rest, represent significant morbidity for invasive cardiac procedures. METHODS: A prospective, multicenter, randomized trial was designed to compare the hemostasis time in minutes and the incidence of vascular complications in patients receiving a vascular hemostasis device with those undergoing conventional compression techniques. RESULTS: After diagnostic catheterization, hemostasis time was significantly less with the vascular hemostasis device than with conventional manual compression (4.1 +/- 2.8 min [n = 90 patients] vs. 17.6 +/- 9.2 min [n = 75], p < 0.0001). This difference was greater in patients undergoing angioplasty and was unrelated to the anticoagulation status (4.3 +/- 3.7 min [n = 71 not receiving heparin], 7.6 +/- 11.6 min [n = 85 receiving heparin], 33.6 +/- 24.2 min [n = 134 control patients not receiving heparin], p < 0.0001 vs. control patients). The time from the start of the procedure to ambulation was slightly less after diagnostic catheterization in patients treated with the device (13.3 +/- 12.1 h vs. 19.2 +/- 17.8 h, p < 0.05). It was also less in patients who underwent angioplasty when the device was used after discontinuation of anticoagulation (23.0 +/- 11.1 h, without heparin), as compared with control compression techniques (32.7 +/- 18.8 h, p < 0.0001). Time to ambulation was even shorter (16.1 +/- 11.1 h, p < 0.0001) in patients in whom the device was placed immediately after angioplasty while they were still fully anticoagulated with a prolonged activated clotting time (336 +/- 85 s). There were no major complications (surgery or transfusion) after diagnostic catheterization and a low incidence of major complications in patients who underwent angioplasty (0.7% in control patients, 1.4% with the device without heparin, 1.2% with the device and heparin, p = NS). After angioplasty, there was a trend toward fewer hematomas when the device was used in the absence of heparin (4.2% vs. 9.7% in control patients, p = 0.14). CONCLUSIONS: A new vascular hemostasis device can significantly reduce the puncture site hemostasis time and the time to ambulation without significantly increasing the risk of peripheral vascular complications. The role of this technology in reducing complications, length of hospital stay and cost remains to be determined.

Percutaneous transluminal coronary angioplasty of a right coronary artery arising from the left main coronary artery.

Angioplasty of anomalous coronary arteries presents unique technical challenges. Correct guiding catheter selection is important to ensure adequate access to the anomalous vessel and to provide support to cross the lesion. A case of successful PTCA of a lesion in an anomalous right coronary artery arising from the left main coronary artery is presented.

Nitroglycerin has more favourable effects on left ventricular afterload than apparent from measurement of pressure in a peripheral artery.

Nitroglycerin (0.3 mg) was administered sublingually to 14 patients undergoing cardiac catheterization, and pressure waves compared in the ascending aorta and brachial artery. After nitroglycerin, ascending aortic systolic pressure fell in all cases (by 6-44, average 22 mmHg) whereas brachial systolic pressure remained unchanged (in three) or fell to a lesser degree (4-33, average 12 mmHg). Diastolic pressure did not change significantly. Alterations in pressure and in wave contour were explained on the basis of arterial dilation, with reduction in wave reflection. Nitroglycerin reduces left ventricular afterload through arterial dilation as well as preload through venous dilation. This effect on afterload is not apparent from measurement of pressure in the brachial artery.