Indium-111 antimyosin scintigraphy before and after coronary bypass surgery: unexpected preoperative myocardial uptakes.

The present study was designed to evaluate 111In-antimyosin scintigraphy in detecting pre- and post-operative myocardial infarction in patients undergoing coronary artery bypass surgery. Fab antimyosin scintigraphy has been shown to be sensitive and specific in detecting myocardial necrosis and to be potentially valuable in situations where other criteria are not reliable. In a previous study, postoperative antimyosin uptakes occurred in 82% of the studied patients. Sixteen consecutive patients with an indication of coronary artery surgery were assessed by preoperative coronary angiography, serial electrocardiograms, and myocardial scanning with 111Indium-labeled antimyosin antibodies performed before and after operation. In four patients, a recent myocardial infarction (1 to 3 months) was detected with an accurate localization when compared to the classic criteria of myocardial infarction. One more patient with a 21-year old myocardial infarction showed an intense uptake whereas there was no recent acute coronary event. Four other patients had an unexpected preoperative uptake, since there were no acute coronary events in their medical history. All preoperative scintigraphic uptakes were still present on the second scan performed postoperatively in these nine patients. Only one patient showed a new postoperative uptake when compared to the preoperative scan which was normal; this postoperative septal infarct was confirmed by a postoperative coronary angiography. Extracardiac uptakes (sternum and ribs) were frequently observed after operation and might hamper the interpretation of postoperative scintigrams. Unexpected preoperative uptakes may be related to non diagnosed small necrosis. A preoperative reference scan is required for an accurate interpretation of a postoperative 111In-antimyosin uptake. Moreover, extracardiac uptakes may limit the interpretation of perioperative cardiac damage.

[Hyperhomocysteinemia in coronary artery diseases. Apropos of a study on 102 patients]. / Hyperhomocystéinémie chez des patients coronariens. A propos d'une étude portant sur 102 sujets.

Homocystein is at the crossroads of the metabolic pathways of sulphuric amino acids. Homocystinuria is a congenital autosomal recessive disease, usually related to cystathionine beta-synthetase deficiency. Children with homozygotic forms of the disease have early vascular complications which represent the main cause of death. Moderately elevated serum homocystein levels are related to two major genetic factors (heterozygotic cystathionine beta-synthetase deficiency and mutation of the 5-10 methylene tetrahydrofolate reductase) and several minor, genetic and non-genetic factors (folic acid, vitamins B6 and B12 and betain deficiencies). Previous studies have suggested that hyperhomocysteinaemia could be a cardiovascular risk factor. This study was based on 222 subjects including 102 consecutive patients with angiographically documented coronary artery disease and 120 control subjects without vascular disease. No relationship was observed between serum homocystein concentrations and the classical cardiovascular risk factors. Coronary patients had higher average homocystein concentrations than control subjects (11.27 +/- 0.52 vs 8.77 +/- 0.31 mumol/l); p < 0.0001): moreover, the prevalence of hyperhomocysteinaemia (> 15.67 mumol/l) was higher in the coronary group (15.7%) than in the controls (2.5%). A significant relationship was also observed between homocystein concentrations and the severity of the coronary disease (defined by a coronary score) and the number of diseased vascular territories. These results underline the relationship between homocystein and vascular risk, especially that of coronary artery disease. The treatment of hyperhomocysteinaemia by folic acid supplements is effective in correcting plasma levels, without side effects and at a relatively low cost.

[Indium III monoclonal antimyosin antibody scintigraphy for the detection of chronic myocardial infarction apart from the acute phase]. / Scintigraphie aux anticorps monoclonaux antimyosine marqués à l'indium 111 pour la détection de l'infarctus du myocarde en dehors de la phase aiguë.

Fab antimyosin scintigraphy has been shown to be sensitive and specific in detecting acute myocardial necrosis. This study was designed to evaluate the preoperative frequency of Indium-111 (In-111) antimyosin myocardial uptake in patients scheduled for coronary artery bypass surgery. The scintigraphic results were compared with other criteria of myocardial infarction (MI). Sixteen consecutive patients were included. Recent MI (1 to 3 months) were detected in four patients, with an accurate localization in three cases when compared to the classic criteria for MI. Two more patients had old Q wave MI: one did not show any uptake in the territory of MI whereas the second patient with a 21 year old infarct without recent acute coronary events showed an intense uptake consistent with the ECG and angiographic localization. Four other patients with stable angina showed limited uptakes that were unexpected, since there were no acute coronary events in their medical history, and ECG. Their left ventricle angiography were considered as normal. In these four cases, the scintigraphic location corresponded to a territory supplied by an occluded coronary artery (n = 2) or by a coronary artery with a tight stenosis requiring a bypass graft (n = 2). These antimyosin uptakes are probably related to small necroses which did not modify the ECG and did not alter the ventricular segmental wall motion. We conclude: 1) recent MI are detected by In-111 antimyosin scintigraphy; 2) In-111 antimyosin uptake may occur in patients without a diagnosis of recent myocardial infarction and correspond to older MI or limited necroses without detectable changes of the ECG and left ventricle angiography.

Fibrinogen after coronary angioplasty as a risk factor for restenosis.

BACKGROUND: Fibrinogen is a risk factor for cardiovascular disease and is related to the severity of coronary atherosclerosis. Its role in restenosis after coronary angioplasty remains unknown. Although platelets and thrombosis contribute to the pathogenesis of restenosis, few clinical data are available concerning the relations between restenosis and proteins of the coagulation and fibrinolytic systems. METHODS AND RESULTS: In 107 consecutive patients undergoing coronary angioplasty, we measured plasma levels of tissue-type plasminogen activator (t-PA), plasminogen activator inhibitor-1 (PAI-1), von Willebrand factor, and fibrinogen before and immediately after angioplasty and at a 6-month follow-up. The individual changes of intraluminal diameter were measured by quantitative coronary angiography, and patients were classified according to four definitions of restenosis: (1) a final stenosis > 50%, (2) a loss of minimal luminal diameter during the follow-up period greater than the measurement variability in our laboratory (> 0.52 mm), (3) a loss of at least 50% of the gain in luminal diameter achieved by angioplasty, and (4) the combination of definitions 1 and 2. The relations between coagulation variables and each definition of restenosis were assessed univariately; then with the clinical variables included, the relations were analyzed multivariately. Angiographic follow-up was obtained in 92% of patients with a primary success of angioplasty. Global restenosis rates were 38%, 43%, 48%, and 30% for definitions 1 through 4, respectively. Plasma levels of t-PA antigen and PAI-1 antigen were not associated with any of the four definitions of restenosis. Multivariate analysis demonstrated that von Willebrand factor measured immediately after angioplasty predicted restenosis according to definitions 2 and 3. Fibrinogen measured within 6 months of follow-up was significantly increased in all restenosis groups of the four definitions. Patients with a fibrinogen concentration > 3.5 g/L at follow-up had higher restenosis rates than patients with a concentration < 3.5 g/L: 55% versus 22% (P = .001), 68% versus 31% (P = .002), 63% versus 37% (P = .01), and 74% versus 26% (P = .002) for definitions 1 through 4, respectively. The loss index was lower (P = .003) and the net gain higher (P = .03) in patients with a fibrinogen level < 3.5 g/L. There was a significant correlation between fibrinogen level and angiographic loss index (r = .41; P < .0001). Multivariate analysis confirmed that the fibrinogen level predicted restenosis with all definitions. CONCLUSIONS: An independent relation exists between von Willebrand factor measured immediately after angioplasty and restenosis defined by the degree of intraluminal renarrowing. An elevated fibrinogen level during follow-up is a strong biochemical predictor of restenosis. Therefore, fibrinogen should be considered at least as an independent marker of restenosis and perhaps as a common risk factor for both spontaneous coronary atherosclerosis and postangioplasty restenosis, which is an accelerated form of atherosclerosis.

[Coronary restenosis: the cardiologist facing problems of definitions]. / Resténose coronaire: le cardiologue face aux problèmes de définitions.

Many angiographic definitions have been proposed to define restenosis after coronary angioplasty. The utility of each remains poorly defined. The aims of this study were: a) to analyse groups of patients defined by each of three criteria: > 50% stenosis (definition 1), loss > or = 50% of initial gain in diameter (definition 2), loss > or = 0.52 mm of minimal luminal diameter based on the variability of the angiographic measurement (definition 3) and, b) to compare the immediate attitude of the interventional cardiologist with the deferred quantitative angiographic analysis. The angiographic follow-up included 89 patients. The angiographic restenosis rate was 37% (definition 1), 48% (definition 2) and 43% (definition 3). Restenosis as defined by criterion 1 was associated with the greatest degree of postangioplasty residual stenosis (p = 0.02) whereas, with criteria 2 and 3, it was associated with less severe residual stenosis (p = 0.03 and p = 0.007). Definition 2 and 3 are the most similar and definitions 1 and 3 the most complementary. The sensitivity, specificity positive and negative predictive values for recurrence of angina with respect to angiographic restenosis (definition 1) were respectively 63.6%, 77.8%, 63.6%, and 77.8% and are not significantly improved by associated analysis of exercise testing. Discordances between the decision of the interventional cardiologist and the results of quantitative angiography (definition 1) were noted in 12.4% of the stenosis studied, there measuring 44 to 64%. The judgement of the cathetiser of these intermediary stenoses was essentially influenced by the recurrence of angina during follow-up.(ABSTRACT TRUNCATED AT 250 WORDS)

Endothelin-1 in patients with coronary heart disease undergoing cardiac catheterization.

OBJECTIVES: This study examined the possible association between endothelin and coronary atherosclerosis and evaluated the synthesis and release of endothelin in the presence of various stimuli that occur during cardiac catheterization. BACKGROUND: Circulating endothelin has been reported to be increased in diffuse atherosclerosis and acute myocardial infarction. However, the relation between coronary artery disease and endothelin release remains unclear. METHODS: We measured the plasma and urinary concentrations of endothelin immunoreactivity in 45 patients and 10 healthy control subjects. RESULTS: In group IA (n = 9), simultaneous blood sampling in the coronary sinus and femoral artery during coronary angioplasty of the left anterior descending coronary artery demonstrated no immediate changes in plasma immunoreactive endothelin-1 (ir-ET-1) levels. In 11 patients in group IB undergoing coronary angioplasty of a major artery, we did not detect changes in peripheral plasma concentrations of ir-ET-1 within 24 h, but urinary ir-ET-1 levels increased from 9.2 +/- 2.3 to 18.6 +/- 4.9 pg/mg of creatinine a few hours after coronary angioplasty (mean +/- SEM, p < 0.05). This increase in urinary endothelin excretion persisted 24 h later. Group II patients (n = 12) had coronary angiography without coronary angioplasty. Levels of both plasma and urinary ir-ET-1 did not change during the 24-h follow-up period. There was no relation between the severity of coronary atherosclerosis and the plasma or urinary concentrations of ir-ET-1. Systolic aortic pressure correlated with basal urinary excretion of endothelin (r = 0.54, p = 0.03, n = 15). In group III (n = 13), levels of ir-ET-1 in patients undergoing right heart catheterization without angiography did not differ from those in the control group. CONCLUSIONS: The presence or the severity, or both, of coronary atherosclerosis is not associated with a detectable increase in endothelin release. The diagnostic procedures of catheterization do not modify endothelin concentrations in plasma and urine. Vascular stretch or injury, or both, during coronary angioplasty increases urinary ir-ET-1 levels a few hours after the procedure. This increase persists for at least 24 h but is not detectable by brief sampling of peripheral or coronary sinus blood.

Eicosanoid biosynthesis in patients with stable angina: beneficial effects of very low dose aspirin.

OBJECTIVE: We assessed the production of eicosanoids and the effects of very low dose aspirin in patients with stable angina under basal conditions and during rapid atrial pacing. BACKGROUND: Platelet activation occurs in acute ischemic syndromes but is still controversial in stable angina. Very low dose aspirin is known to be platelet selective and can be used to test the hypothesis of the platelet origin of increased thromboxane production in stable angina. METHODS: Urinary excretion of eicosanoids was measured in 42 patients, including 24 patients with and 18 patients without coronary artery disease. The effects of 50 mg/day of aspirin were measured at rest and during pacing-induced ischemia in 10 patients with stable angina and were compared with a similar group of patients not treated by aspirin. RESULTS: Excretion of 11-dehydro-thromboxane B2 was 2.6 times higher in patients with stable angina than in healthy subjects (mean [+/- SEM] 74.8 +/- 13.0 [24 patients] vs. 29.0 +/- 5.4 [18 patients] ng/mmol of creatinine, p < 0.01). Urinary prostacyclin metabolite levels did not differ between the two groups. Treatment for 8 days with 50 mg/day of aspirin inhibited platelet cyclooxygenase, as reflected by the 97% reduction of in vitro serum thromboxane production. This aspirin regimen normalized the level of urinary thromboxane metabolites in patients with angina (17.3 +/- 3.4 ng/mmol of creatinine [10 patients], p < 0.001 from baseline level before treatment) and did not change prostacyclin metabolite levels. Atrial pacing in patients with angina not treated with aspirin caused lactate and thromboxane release into the coronary sinus. In patients with very low dose aspirin therapy, pacing did not cause thromboxane release despite inducing myocardial ischemia. However, fractional lactate extraction decreased less sharply in patients with than without aspirin therapy. CONCLUSIONS: Thromboxane production is greatly increased in patients with stable angina. Very low dose aspirin administered to these patients reduces thromboxane synthesis to normal levels, preserves prostacyclin biosynthesis and prevents acute thromboxane release into the coronary circulation during pacing-induced ischemia. Our data suggest that platelets (not monocytes/macrophages) are activated in stable angina to produce thromboxane.

Diagnosis of ventricular tachycardia using a pacemaker Holter function.

The diagnosis of ventricular tachycardia (VT) using the Holter function of an implanted pacemaker has not yet been reported. We present the case of a patient with episodes of slow VT, hemodynamically stable, but in whom long lasting attacks were not identified by the patient as VT recurrences, finally leading to progressive heart failure. Prospective analysis of the 24-hour ECG and comparison with the pacemaker Holter data allowed us to determine diagnostic criteria to recognize VT using the pacemaker Holter function. Using these criteria it was possible to retrospectively diagnose VT occurrence during the weeks when the patient was out-of-hospital.

[Transcatheter ablation of atrioventricular accessory pathways. Immediate results and long-term follow-up]. / Ablación trans-cáteter de vías accesorias atrioventriculares. Resultados inmediatos y seguimiento a largo plazo.

We present the immediate results and follow-up, from our initial serie of patients, where radiofrequency was attempted to ablate atrio-ventricular accessory pathways. Initiation policy included direct current-shocks following every unsuccessful radiofrequency session. Initial ablation success rate with radiofrequency solely was 75% (17/22), same as when direct current-shocks were associated 80% (8/10); but accessory pathway conduction recurrence was present only in this latter (6/10). During follow-up period of 18 to 25 months, from the recurrence group, one patient had spontaneous delta-wave disappearance, and four more required two to three ablation sessions. Permanent elimination with both methods was attained in 91% (20/22 pathways), and all patients remain asymptomatic, and drug free. There were one acute major complication, but no deaths. Because of its superior initial success rate, minor technical requirements, and their economical implications, radiofrequency catheter ablation of accessory pathways is the first choice of treatment. At our institution, direct current-shock remain an alternative method whenever a serious tachycardia prevents radiofrequency treatment.

Oxidative stress in patients with unstable angina.

The aim of this study was to determine whether oxidative stress occurs in unstable angina. Thirty patients with unstable angina class B (Braunwald classification) were prospectively studied. Control groups consisted of 23 patients presenting with stable angina and of 21 age-matched healthy volunteers. Upon admission and every 8 h for 24 h, blood samples were drawn for the determination of plasma malondialdehyde (MDA) levels, Se-glutathione peroxidase (GPX) activity, erythrocyte reduced glutathione (GSH) concentrations, erythrocyte GPX and superoxide dismutase (SOD) activities. Coronary angiograms were performed within 4 days of admission in 26 out of the 30 patients included in the study. Nine of these 30 patients were subsequently identified as presenting a non-Q wave myocardial infarction and were separately examined. On admission, only plasma MDA levels and erythrocyte GSH concentrations differed among groups. Plasma MDA levels of patients presenting with unstable angina (P < 0.01) and acute myocardial infarction (P < 0.05) were higher than those of patients with stable angina and of normal volunteers, whereas there was no difference in these parameters between unstable angina and non-Q wave myocardial infarction groups. Erythrocyte GSH concentration was lower in all patient groups as compared to normal subjects. ANOVA for repeated measures showed no difference between admission and subsequent levels for all parameters. Finally, no difference was observed for any of the parameters when anti-ischaemic or anti-aggregant treatment before admission, or the number of affected vessels on coronary angiograms, were considered. We conclude that an oxidative stress can be evidenced in patients with unstable angina or acute myocardial infarction.

[Postinfarction hibernating myocardium]. / Myocarde hibernant postinfarctus.

The detection of hibernating myocardium after infarction is important because it justifies the discussion concerning the revascularisation of infarcted zones irrigated by occluded or severely stenosed vessels, but with an adequate collateral circulation to allow hibernation. The detection of hibernating myocardium is particularly important in patients without the classical indications for revascularisation, such as residual spontaneous ischaemia or ischaemia provoked by exercise or pharmacological stress testing. All techniques currently in use tend to overestimate the size of the necrosed, fibrous scar, compared with the amount of viable myocardium. Improved regional myocardial function after revascularisation is the most convincing proof of hibernating myocardium but it can only be obtained retrospectively. The detection of a reserve of contractility in the necrosed territory by an inotropic stimulus is well adapted to the demonstration of stunned myocardium but this method has not been proved in hibernating myocardium. Thallium scintigraphy is certainly useful in the prospective diagnosis of hibernating myocardium but the protocol of examination should be adapted to this specific problem. There is little available data concerning the evaluation of hibernating myocardium by positron emission tomography: the technical advantages of this method in assessing myocardial viability should enable a more accurate evaluation of post-infarction hibernating myocardium. Adequate revascularisation of necrosed territories depends on a deeper understanding and more precise prospective assessment of postinfarction hibernating myocardium.

[Changes in plasma endothelin during coronary spasm]. / Variations de l'endothéline plasmatique au cours du spasme coronaire.

The role of endothelin, a powerful vasoconstrictor, was studied in coronary spasm. A methylergonovine stress test was performed in patients with normal coronary angiography. Patients who developed spasm (Group I, n = 6) were compared with those who did not (Group II, n = 6). Plasma endothelin was measured at 8, 11 a.m., 2 p.m., 4, 7, 9, 11 p.m. and 1 a.m. The stress test was carried out at 17 hours and an additional endothelin measurement was performed during spasm in positive cases. The clinical characteristics of the two groups were comparable especially with regards to cardiovascular risk factors. Except for the value recorded during coronary spasm, the plasma endothelin levels were significantly higher in the group with coronary spasm. A time-dependent variation was observed in both groups with higher endothelin levels in the morning. In group I the plasma endothelin levels were higher under basal conditions and during spasm in patients with spastic angina.

[Course of unstable angina and therapeutic implications. Apropos of 74 cases]. / Evolution de l'angor instable et implications thérapeutiques. A propos de 74 cas.

The role of thrombosis in the pathogenesis of unstable angina has been demonstrated experimentally. This retrospective study was designed to identify the potential usefulness of fibrinolytic treatment in this situation. The following parameters were evaluated in 74 patients (62 men, 12 women; mean age: 60 +/- 10.2) with primary unstable angina: the course of unstable angina (Braunwald classification), risk factors, electrocardiographic changes, echocardiographic segmental kinetics, coronary arteriography findings, treatment used and outcome with a minimum follow-up of 3 months (mean: 6.3 months). Thirty nine per cent of class I patients and 18% of classes II and III were stabilised by medical treatment only. This accounted for 18 patients in our series (24%). The other patients (76%) required one or more reperfusion techniques (thrombolysis: 5 patients; angioplasty: 42; bypass: 19). Serious complications were seen in 3 patients: myocardial infarction: 2 postoperative (including one fatal) and 1 occurring 24 hours after angioplasty followed by cardiogenic shock and death. Five patients required thrombolytic treatment leading to clinical stabilisation enabling an additional procedure (angioplasty or bypass). No complications of thrombolytic treatment were seen. Thus thrombolytic treatment appears to be useful for the stabilisation of unstable angina and enables subsequent radical treatment under better conditions.

[Antioxidative treatment in myocardial reperfusion ischemia]. / Le traitement antioxydant dans l'ischémie reperfusion myocardique.

Perfusion-induced myocardial ischaemia is observed in several situations: chronic coronary insufficiency, unstable angina, myocardial infarction, and during coronary angioplasty or bypass surgery. Oxygen-derived free radicals are liberated in large quantities during myocardial reperfusion ischaemia. Though very toxic in experimental studies, the responsibility of these free radicals in myocardial injury remains to be demonstrated clinically. Oxidant stress, characterised by an imbalance between the free radical attack and insufficient cellular defense seems partially responsible for reperfusion arrhythmias and post-ischemic stunning. On the other hand, its role is less evident in prolonged myocardial ischaemia causing irreversible myocardial lesions such as infarction. Antioxidant therapy is under evaluation in clinical trials. There are several options: some prevent the formation of free radicals by inhibiting the biochemical reactions which may produce them or by limiting the intervention of the neutrophils--the "fulcrum" of free radicals formations. Other antioxidant therapies inactivate free radicals as they are formed by promoting their degradation or their neutralisation. Experimental data is profuse and discordant. The models are very different. The first clinical trials are under way using either specific antioxidant molecules or molecules having other beneficial effects: in the latter case, the benefit of the antioxidant action is more difficult to demonstrate. Antioxidant therapy could play a role in surgical myocardial protection, especially of transplant organs, in very early forms of ischaemia. It could also prevent the pejorative hemodynamic consequences of myocardial stunning of the border zones of infarction, so enabling patients to survive a difficult period. The results of on-going studies should clarify the role of antioxidant therapy in reperfusion-induced myocardial ischaemia.

[Effects of ultrasonic energy on blood clots in vitro]. / Effets de l'énergie ultrasonore sur des caillots sanguins in vitro.

Ultrasound may be used to dissolve arterial and venous thrombi. Its effects depends on the mode of ultrasonic vibration and on the length of the guide wire. The authors studied the in vitro effects of an ultrasonic angioplasty device coupled with a 130 cm long titanium flexible guide wire. The system comprises an automatic scanning function to determine the optimal frequency of resonance and works in the continuous mode of emission. Sixteen thrombi were studied of which 8 were acellular and 8 whole blood. In each group, 4 were treated in association with streptokinase and 4 by ultrasound alone. The ages of the thrombi in each subgroup were 1, 3, 7 and 15 days. All the thrombi were dissolved in 6 minutes or less (3'15" +/- 1'35") at an average optimal frequency of resonance of 19,444 Hz. Ninety six per cent of the debris had a diameter less than 10 microns. Less than 1% of the debris had a diameter larger than 100 microns. These large particles were observed in cellular thrombi and were almost completely absent in dissolved acellular thrombi. They were very fragile. The dissolution of the thrombi was not accelerated by the association of streptokinase. The ultrasonic energy did not induce D-dimer production and its action was probably due to cavitation. Ultrasonic energy could provide an alternative treatment for thrombotic vascular occlusion provided that more flexible guide wires could be designed.

Variations in plasma endothelin concentrations during coronary spasm.

A provocation test using methylergometrine was carried out in patients with a normal coronary angiogram. Patients exhibiting spasm (Group 1, n = 6) were compared with non-spasm patients (Group II, n = 6). The endothelin concentration was determined in all cases at 0800, 1100, 1400, 1600, 1900, 2100, 2300 and 0100 h. The provocation test was carried out at 1700 h and an additional determination was made during spasm if the test was positive. The two groups had similar clinical characteristics and did not differ in terms of risk factors. Apart from the value recorded during spasm, the endothelin plasma level was significantly higher in Group I. A time x measurement interaction was noted in both groups, with a higher endothelin level in the morning. The endothelin level increased significantly during spasm in Group I patients. The plasma concentration of endothelin appeared to be higher in the basal state and during spasm in patients exhibiting spastic angina.

Effect of pravastatin, a HMG CoA reductase inhibitor, on blood lipids and aortic lipidosis in cholesterol-fed White Carneau pigeons.

The effect of pravastatin, an inhibitor of HMG CoA reductase, on blood lipids and aortic lipidosis was studied in young cholesterol-fed White Carneau pigeons. The birds were fed with normal ('N group', n = 20) or atherogenic diet (grains + 0.4% cholesterol + 4% lard) alone ('C group', n = 20) and in association with pravastatin ('P group', n = 20). Plasma lipids and aortic intima lipidosis were studied after 3-5 and 8-12 months of the diet. Compared to the N group, pigeons from C group exhibited hypercholesterolemia (TC = 1000 mg/dl) and hyperlipoproteinemia of which level was independent of the duration of the diet. Total VLDL (VLDL+LDL)-cholesterol and apolipoprotein-B levels rose significantly 15, 8 and 4 times, respectively, whereas HDL were increased two times (P < 0.01) in females only. Macroscopically visible intima lipidosis areas covered 40% and 80% of aortic surface after 3-5 and 8-12 months of the diet. In P group, the increase in plasma lipid values was significantly lower than in WC from C group: -40% for total cholesterol (600 mg/dl) (P < 0.01), -71% for VLDL (P < 0.001), -53% for (VLDL+LDL)-cholesterol (P < 0.01) and -54% for apo-B (P < 0.05). HDL remained as high as in C group. Consequently TC/HDL-C ratio was improved and atherogenic risk of cholesterol was reduced by 41% (P < 0.05). Intima lipidosis areas were lowered by 35% (P < 0.01). We conclude that pravastatin treatment involves (1) a decrease in hypercholesterolemia and hyperlipoproteinemia and (2) a lowering in extensiveness and severity of macroscopically visible aortic lipidosis in cholesterol-fed White Carneau pigeon.