in 25%, and ABI in 26% of our population. If ABI was present, CAD was also present in 53% and PAD in 33% of our population. If PAD was present, CAD was also present in 58% and ABI in 34% of our pop- ulation. If CAD was present, ABI was also present in 32% and PAD in 33% of our population. 1. Hertzer NR, Beven EG, Young JR, O’Hara PJ, Ruschhaupt WF III, Graor RA, dewolfe VG, Maljovec LC. Coronary artery disease in peripheral vascular patients: a classification of 1,000 coronary angiograms and results of surgical management. Ann Surg 1984;199:223-233. 2. Smith GD, Shipley h4J, Rose G. Intermittent claudication, heart disease risk fac- tors, and mortality: the Whitehall study. Circulation 1990;82:1925-1931. 3. Aronow WS, Ahn C, Mercando AD, Epstein S. Prognostic significance of silent ischemia in elderly patients with peripheral arterial disease with and without pre- vious myocardial infarction. Am .I Cardiol 1992;69:137-139. 4. Hertzer NR, Young JR, Beven EG, Graor RA, O’Hara PJ, Ruschhaupt WF III, deWolfe VG, Maljovec LC. Coronary angiography in SO6 patients with extracra- nial cerebrovascular disease. Arch Intern Med 1985;145:849-852. 1. Cbimowitz MI, Man&i GBJ. Asymptomatic coronary artery disease in patients with stroke. Prevalence, prognosis, diagnosis, and treatment. Srroke 199223: 4331136. 6. Aronow WS, Ahn C, Schoenfeld MR. Mercando AD, Epstein S. Prognostic sig- nificance of silent myocardird ischemia in patients >61 years of age with extracra- nial internal or common carotid arterial disease with and without previous myo- cardial infarction. Am J Cardiol 1993;71: 115-l 17. 7. Aronow WS, Schoenfeld MR. Prevalence of atherothrombotic brain infarction and extracranial carotid arterial disease, and their association in elderly blacks, His- panics and whites. Am .I Cardiol 1993;71:999-lOCHI, 8. Mautner GC, Maumer SL, Roberts WC. Amounts of coronary arterial narrow- ing by atherosclerotic plaque at necropsy in patients with lower extremity amputa- tion. Am .I Cordial 199270: 1147-l 15 1. Low Formation of Nitric Oxide in Polymorphonuclear Cells in Unstable An@na Pectoris Vincenzo Mollace, MD, Francesco Romeo, MD, Eugenio Martuscelli, MD, Giuseppe M.C. Rosano, MD, Giorgio Federici, MD, Giuseppe Nistic6, MD, and Benedetto Marino, MD T he development of unstable angina pectoris and acute myocardial infarction is a process that is as- sociated with an increased platelet aggregation and thrombus formation combined with local coronary vaso- constriction.’ In such diseases, an altered releaseof an- tithrombotic substances by vascular endothelium or cir- culating blood cells has been suggestedto play a role. Nitric oxide (NO) is a nitrogen-free radical generated by endothelial cells, circulating white blood cells and many other cell types through bioconversion of L-arginine into citrulline.2 The release of NO produces vasodilatation and inhibition of platelet aggregation, thereby partici- pating in the regulation of general as well as regional hemodynamics.2In particular, NO formation seemsto mediate the coronary vasodilating activity of agents (e.g., acetylcholine) that, under normal conditions, affect the coronary tone. 3,4In addition, the microinfusion of selective inhibitors of NO synthase, such as the NG- monomethyl-L-arginine (L-NMMA) or NW-nitro-L-argi- nine methyl ester (L-NAME), strongly reducesmyocar- dial blood flo~.~ The present experiments were performed in order to study the L-arginine-NO pathway in polymorphonuclear cells obtained from the blood of patients with unstable angina. This was achieved using platelet aggregation as a bioassay for NO or by mea- suring nitrite (the breakdown product of NO) in the su- pematant of polymorphonuclear cells. The rate of cit- rulline generated from L-arginine by polymorphonuclear cell homogenates was measured to evaluateNO synthase activity. From the Department of Biology, University of Rome, Tor Vergata, Rome: the University of Catania, Catania; the Department of Clinical and Experimental Medicine, University of Reggio, Calabria; and Isti- tuto di Chirurgia de1 Cuoree dei GrossiVasi, University “La Sapienza,” Rome, Italy. Dr. Nistici6’s address is: Department of Biology, Uni- versity of Rome, Tor Vergata, Via della Ricerca Scientifica, 00173 Rome, Italy. Manuscript received July 21, 1993; revised manuscript received November 22, 1993, and acceptedNovember 23. We studied 20 patients (12 men and 8 women, 38 !I 5 years old) with primary characterized unstable angina pectoris. No changes in the creatine kinase-MB fiaction were found on admission to the intensive care unit. A group of 20 apparently healthy volunteers (10 men and 10 women, 35 + 5 years old) was used as a control. Healthy subjects had an equivalent age and lifestyle to patients with unstable angina, had no history of chest pain or hemorrheologic diseases, and had a normal elec- trocardiographic pattern. Both patients and healthy vol- unteers were taking no drugs that could inter$ere with platelet aggregation or blood coagulation for 215 days before blood sampling and did not have diabetes, dys- lipidemia or alterations in hemocoagulative parameters and fibrinogen blood levels. Smoking was documented in only 2 of the patients with unstable angina; 7 were moderately hypertensive and only 3 received treatment with nitroglycerin and calcium antagonists before ad- mission to the intensive care unit. Blood for polymorphonuclear cell separations was collected on admission to the intensive care unit (within 24 hours of onset of angina pectoris) in plastic flasks containing 3.15% sodium citrate. Coronary angiogra- phy was per$ormed the day after blood sampling and showed signi@ant coronary artery stenoses 270% in all patients who entered the study. All patients gave their informed consent to use blood samples for the study. Human washed platelets were prepared as described by Radomski and Moncada.6 Indomethacin (10 pM) was added to the jnal platelet suspension to prevent the for- mation of cyclooxygenase products. The platelet count was adjusted to approximately 1.5-2 X I@ ml-‘. For platelet aggregation studies, a suspension of washed platelets was incubated at 37°C for 4 minutes in a Payton dual-channel aggregometer with continuous stirring at 1,000 rpm, and then stimulated with throm- bin (40 mU ml-‘) to give a submaximal aggregation (80% to 9OYo).Polymorphonuclear cells (l-4 X 106) alone or in the presence of oxyhemoglobin were added to platelet BRIEF REPORTS 65