A case-control comparison within the framework of the prospective, multidisciplinary PLAT Study was performed to assess whether altered baseline fibrinolytic variables were associated with an elevated risk of ischemic thrombotic events in patients with documented coronary, cerebral, and/or peripheral atherosclerotic disease. Fibrinogen, D-dimer, tissue plasminogen activator (t-PA) antigen, and fibrinolytic activity before and after venous stasis (A=difference between the two values), t-PA inhibitor, and lipid levels in 60 atherosclerotic patients with a thrombotic event during the first year of follow-up were compared with those in 94 atherosclerotic patients without such events, who were matched for age, sex, and diagnosis at enrollment. Events were associated with a higher release of A t-PA antigen (P=.O47), higher D-dimer (P=.O24), and higher t-PA inhibitor (P=.001) levels. A Fibrinolytic activity was correlated inversely with t-PA inhibitor (P<.01) and triglycerides (J*<.05). D-Dimer was also correlated with systolic blood pressure (P<.01). Atherosclerotic patients at higher risk of thrombotic ischemic events are characterized by increased fibrin turnover and impaired fibrinolytic activity due to high t-PA inhibitor levels. This hemostatic disequilibrium may participate with conventional risk factors such as elevated triglyceride levels and systolic blood pressure in the multifactorial mechanism of ischemic sequelae in patients with preexisting vascular atherothrombotic disease. (ArUrioscler Thromb. 1993;13:1412-1417.) KEY WORDS • atherothrombosis • ischemic events • fibrinolytic variables • plasminogen activator inhibitor • D-dimerR ecent clinical studies have reported decreases in fibrinolytic activity in patients with coronary artery disease. 15 The major mechanisms involved in the type of fibrinolytic impairment seen in these patients are an increase in plasma tissue-type plasminogen activator (t-PA) inhibitor, particularly in subjects with hypertriglyceridemia, and a selective depression of t-PA activity in euglobulins. The t-PA inhibitor (PAI-1) has also been shown to be an independent risk factor for reinfarction in young survivors of myocardial infarction (MI). 6The prospective, multidisciplinary PLAT Study, which was performed to investigate the associations between hemostatic variables and ischemic events in 953 patients with documented atherosclerotic disease, 79 afforded the opportunity of carrying out a nested casecontrol study, with the aim of assessing whether altered baseline fibrinolytic variables characterize subjects at a higher risk of ischemic sequelae, and we now report the results. Fibrinogen, fibrinolytic activity, and t-PA anti-

, and the PLAT Study Group* The Progetto Lombardo Atero-Trombosi (PLAT) Study was a prospective, multicenter, multidisciplinary study of the association among hemostatic variables, conventional risk factors, and atherothrombotic events in four groups of patients with preexisting vascular ischemic disease (335 myocardial infarction survivors, 123 patients with stable angina pectoris, 160 with transient ischemic attacks, and 335 with peripheral vascular disease). In the myocardial infarction group, univariate analysis showed that atherothrombotic events were associated with high fibrinogen (p=0.001), factor VIII C (p<0.001), and von Willebrand factor antigen (vWF:Ag) (p=0.004) levels and with low high density lipoprotein cholesterol (p=0.043), factor VII (p=0.019), and protein C (p=0.044) levels; multivariate analysis produced associations with high fibrinogen and factor VIII: C levels and low protein C levels. By both univariate and multivariate analysis, events in the angina pectoris group were associated with high vWF:Ag (i=0.026) and leukocyte (p=0.033) levels and the presence of carotid arterial stenosis (p=0.063); associations with high leukocyte (p=0.037) and factor VIII :C (p=0.186) levels, family history (p=0.031), and diabetes (p=0.061) were also found in the group with transient ischemic attacks. In those with peripheral vascular disease, events were associated with Fontaine stage allB (p =0.024), high factor Vm:C levels (p=0.073), and low protein C (p=0.028), fibrinogen (p=0.030), antithrombin m (p=0.054), and factor VII (p=0.057) levels by univariate analysis and with Fontaine stage and low fibrinogen levels by multivariate analysis. In conclusion, the different associations observed in the four groups of patients may reflect a different hemostatic system involvement in the development of atherosclerosis and/or its clinical sequelae. (

Comparison was made between platelet concentrates prepared from pools of buffy coats removed from standard blood donations and stored in a glucose-free, commercially available crystalloid solution (BC-PCs) and standard platelet concentrates prepared from platelet-rich plasma (PRP-PCs). Platelet yield in BC-PCs and PRP-PCs was 59 and 75 percent of donated platelets, respectively. The number of total white cells in 1 BC-PC unit, prepared from a pool of 7 buffy coats, was 21 x 10(6), i.e., 50 times lower than that of 7 units of PRP-PCs. The in vitro values of adequate platelet quality were maintained for 10 days in BC-PCs stored in 1000-mL polyolefin bags. Prolonged bleeding times were reduced or corrected in three of three thrombocytopenic leukemic patients evaluated before and after transfusion of stored BC-PCs. Pretransfusion and 1- and 24-hour posttransfusion median platelet counts in 57 leukemic recipients during 4 months of routine transfusion of BC-PCs (n = 93) were 14, 35, and 27 x 10(9) per L, while those of PRP-PCs (n = 246) were 13, 37, and 31 x 10(9) per L, respectively. No reactions to BC-PCs were reported, but a 1.3 percent rate of reaction to PRP-PC transfusions was reported. This study indicates that BC-PCs are a good alternative to PRP-PCs for platelet support of thrombocytopenic patients.

No abstract

I n the recent Lescol Intervention Prevention Study (LIPS), long-term therapy with fluvastatin decreased the incidence of cardiac events in patients who underwent percutaneous coronary intervention. 1 The present study analyzed the results of LIPS to investigate (1) the effect of baseline renal function on occurrence of long-term adverse events, (2) whether therapy with fluvastatin decreased the expected hazardous effect of renal impairment, (3) the effect of fluvastatin on renal function during follow-up, and (4) the relation between changes in renal function over time and the occurrence of adverse events. METHODS Study design and patient population:The study design and primary results of LIPS have been described elsewhere. 1 Briefly, after a first successful percutaneous coronary intervention (residual stenosis Ͻ50%, absence of postprocedural in-hospital myocardial necrosis, repeat revascularization, or death), patients were randomized to receive fluvastatin therapy (Lescol, Novartis Pharma AG, Basel, Switzerland; 40 mg 2 times daily) or placebo for 3 to 4 years.At enrollment, patients had to fulfill Ն1 of the following lipid profile criteria: (1) total cholesterol level of 135 to 270 mg/dl with a fasting triglyceride level Ͻ400 mg/dl, (2) total cholesterol level Ͻ212 mg/dl for patients whose lipids levels were measured 24 hours to 4 weeks after an episode of myocardial infarction, or (3) total cholesterol level Ͻ232 mg/dl for patients who had diabetes mellitus. Exclusion criteria included a baseline serum creatinine value Ͼ1.8 mg/dl. The study protocol was approved by the local ethics committees, and all patients gave informed written consent.Lipoproteins and evaluation of renal function: Each patient was clinically evaluated Ն8 times after randomization. Blood lipid levels were measured at all visits, and serum creatinine was measured at baseline