7. Gill JB, Moore RH, Tamaki N, Miller D, Barkai-Kovach M, Yasuda T . Boucher CA, Strauss HW. Multi-gated blood-pool tomography: new method for the assessmerit of left ventricular function. .I Nucl Med 1986;12:19161924. 8. Faber TL. Stokely EM, Corbett JR. Surface detection in tomographic myocardial perfusion images by relaxation labelling. VIE 1988: 1001:297-301. 9. Faber 72, Stokely EM, Templeton GH, Akers MS, Parkey RW. Corbett JR. Quantification of three-dimensional left ventricular segmental wall motion and vol-
umes from g&d
tomographic
radionuclide
K. Kahn,
MD,
Usha
Kodali,
305:337-338.
MD, V ic k i S avas,
he of reperfusion therapy for acute myocardial T infarction (AMI) is well accepted and routinely considered in patients identified in the initial hours of their use
attack. The choice between thrombolysis and angioplasty is dependent on institutional factors, such as the ready availability of a catheterization laboratory, and on patient factors such as contraindications to thrombolytic drugs. Patients receiving chronic anticoagulation with warfarin have been considered to have relative or absolute contraindications for intravenous thrombolytic therapy because of a fear of excessive hemorrhage.‘+” The results and complications of emergency cardiac catheterization and coronary angioplasty in these patients have not been explored. We report on 5 such patients treated with coronary angioplasty for AMI. . . . Over a 9-month period, 257 patients presented with AMI and were taken to the catheterization laboratory. Of these, 5 (2%) were taking warfarin at presentation and formed the study group. All patients received chewable aspirin in the emergency department and intravenous heparin during and after the angioplasty procedure. Three patients were taking war-harm for atria1 fibrillation, I for recent venous thrombosis, and 1 for recent hip surgery. All patients had ST-segment elevation on the initial electrocardiogram, indicating inferior AM1 in 3, anterior AM1 in 1, and lateral AM1 in 1. The degree of warfarin anticoagulation was therapeutic or greater in all patients (international normalized ratio, 2 to 37). Catheterization identified a severely diseased artery corresponding to the electrocardiographic site of infarction in all patients. Angioplasty was successful in recanalizing the infarct vessel in all 5 patients within 6 hours of symptom onset. Residual thrombus was detected in 1 patient, and 500,000 U of intracoronary urokinase was given with a subsequent excellent angiographic result. Peak creatine kinase level ranged from 1,146 to 4,200 U/L. From the Diwon of Cordlolog William Beaumont Hospital, Royal Oak, Michlgon Dr. Kahn’s a cr dress IS: 222 1 Livernois, Suite 103, Troy, hlichlgun 48083. Manuscript received September 20, 1994: revised mawscript received and accepted December 12, 1994.
724
THE AMERICAN
JXJRNAL
OF CARDIOIOGP
‘VOL.
7.5
J Nucl Med 1989;30:
10. Faber TL, Akers MS, Rshock RM, Corbett JR. Three dimensional motion and perfusion quantification in g&d single-photon emission computed tomograms. .f Nucl Med 1991;32:231 l-2317. II. Bulkley BH. Site and squelae of myocardial infarction. N .!?n~/ J Med 19Rl;
Effmts of Chronic War&in Thsmpy Complications d Coronary An ioplssty Acute Myocadd 1antarctbn Joel
ventriculograms.
638649.
MD, and
Richard
on During Gordon,
DO
When the prothrombin time returned to normal, the vascular sheaths were removed on hospital day 2 in 2 patients, and on days 3,4, and 7 in the other 3, respectively. Routine compression was applied. Only 1 moderate hematoma developed in 1 patient at a site where an intraaortic balloon pump was removed. No transfusions or vascular repairs were required. In 1 patient, the hemoglobin level increased between the time of admission and discharge, and in the other 4 it decreased (from between 1.6 and 4.1 g/d]). There were no episodes of recurrent myocardial ischemia or infarction. Four of the 5 patients were discharged on warfarin and all were taking aspirin. The length of hospital stay ranged from 5 to 9 days. . . . The experience reported here with primary angioplasty therapy of AMI is similar to larger series in that the treatment had a high initial reperfusion rate and a low rate of recurrent ischemic events. However, this series was unique with regard to patient management issues related to bleeding complications and vascular access. No serious episodes of bleeding were noted. Vascular sheaths are usually removed after primary infarct angioplasty within 24 to 48 hours. In 3 of the 5 patients in this series, sheath removal was delayed beyond this range to permit the prothrombin time to return to normal. Vitamin K and plasma were not administered because of the fear of precipitating recurrent coronary thrombosis. Additional sedation was required to assist the patients in maintaining prolonged bedrest. The additional bedrest until sheath removal prolonged hospital length of stays, but patients were still discharged between days 5 and 9. In this small series, no transfusions or serious vascular complications developed. This preliminary experience suggests that primary angioplasty for AM1 is efficacious and safe in patients previously receiving chronic therapy with warfarin. I. Anderson
VH, WilIerson IT. Thrombolysls m acute myocardul Infarction. N 1994;329:703-7139. 2. ACUAHA Task Force Report. Guidelines for the early management of patlent& with acute myocardinl infarction. .I Anr Co/f Cat-dioi 199O;ih:24%-292.
Engl J Med
APRll 1, 1995