Plasma levels of active Von Willebrand factor are increased in patients with first ST-segment elevation myocardial infarction: a multicenter and multiethnic study.

AIMS: Von Willebrand factor (VWF), a key player in hemostasis and thrombosis, is released from endothelial cells during inflammation. Upon release, VWF is processed by ADAMTS13 into an inactive conformation. The aim of our study was to investigate whether plasma levels of active VWF, total VWF, ADAMTS13, osteoprotegerin (OPG) and the ratios between VWF and ADAMTS13 are risk factors for first ST-segment elevation myocardial infarction (STEMI). METHODS AND RESULTS: We assessed 1026 patients with confirmed first STEMI and 652 control subjects from China, Italy and Scotland, within six hours after their cardiovascular event. Median plasma levels of total VWF, active VWF, OPG and ratios VWF/ADAMTS13 were increased, while plasma levels of ADAMTS13 were decreased in patients compared to controls. The odds ratio (OR) of STEMI in patients with high plasma levels of active VWF was 2.3 (interquartile range (IQR): 1.8-2.9), total VWF was 1.8 (1.4-2.3), ADAMTS13 was 0.6 (05-0.8), OPG was 1.6 (1.2-2.0) and high VWF/ADAMTS13 ratios was 1.5 (1.2-2.0). The OR for total VWF, active VWF and ratios VWF/ADAMTS13 remained significant after adjustment for established risk factors, medical treatment, C-reactive protein, total VWF, ADAMTS13 and OPG. When we adjusted for levels of active VWF, the significance of the OR for VWF and ratios VWF/ADAMTS13 disappeared while the OR for active VWF remained significant. CONCLUSIONS: We found evidence that plasma levels of active VWF are an independent risk factor for first STEMI in patients from three different ethnic groups. Our findings confirm the presence of VWF abnormalities in patients with STEMI and may be used to develop new therapeutic approaches.

Cardiometabolic and immune factors associated with increased common carotid artery intima-media thickness and cardiovascular disease in patients with systemic lupus erythematosus.

BACKGROUND AND AIM: Patients with systemic lupus erythematosus (SLE) have a higher prevalence of subclinical atherosclerosis and higher risk of cardiovascular (CV) events compared to the general population. The relative contribution of CV-, immune- and disease-related risk factors to accelerated atherogenesis in SLE is unclear. METHODS AND RESULTS: Fifty SLE patients with long-lasting disease (mean age 44 ± 10 years, 86% female) and 50 sex- and age-matched control subjects were studied. Common carotid artery intima-media thickness (CCA-IMT) was used as a surrogate marker of atherosclerosis. We evaluated traditional and immune- and disease-related factors, assessed multiple T-cell subsets by 10-parameter-eight-colour polychromatic flow cytometry and addressed the effect of pharmacological therapies on CCA-IMT. In SLE patients, among several cardiometabolic risk factors, only high-density lipoprotein levels (HDL) and their adenosine triphosphate-binding cassette transporter 1 (ABCA-1)-dependent cholesterol efflux capacity were markedly reduced (p < 0.01), whereas the CCA-IMT was significantly increased (p = 0.03) compared to controls. CCA-IMT correlated with systolic blood pressure, low-density lipoprotein (LDL) cholesterol and body mass index (BMI), but not with disease activity and duration. The activated CD4(+)HLA-DR(+) and CCR5(+) T-cell subsets were expanded in SLE patients. Patients under hydroxychloroquine (HCQ) therapy showed lower CCA-IMT (0.62 ± 0.08 vs. 0.68 ± 0.10 mm; p = 0.03) and better risk-factor profile and presented reduced circulating pro-atherogenic effector memory T-cell subsets and a parallel increased percentage of naïve T-cell subsets. CONCLUSION: HDL represents the main metabolic parameter altered in SLE patients. The increased CCA-IMT in SLE patients may represent the net result of a process in which 'classic' CV risk factors give a continuous contribution, together with immunological factors (CD4(+)HLA-DR(+) T cells) which, on the contrary, could contribute through flares of activity of various degrees over time. Patients under HCQ therapy present a modified metabolic profile, a reduced T-cell activation associated with decreased subclinical atherosclerosis.

Remote health monitoring with wearable non-invasive mobile system: The HealthWear project.

This paper focuses on the technical solutions enabling the monitoring of health conditions by means of ECG, HR, oxygen saturation, impedance pneumography and activity patterns. The Healthwear service is based on the Wealthy prototype system. A new design has been made to increase comfort in wearing of the system during daily patient activities. The cloth is connected to a patient portable electronic unit (PPU) that acquires and elaborates the signals from the sensors. The PPU transmits the signal to a central processing site through the use of GPRS wireless technology. This service is applied to three distinct clinical contexts: rehabilitation of cardiac patients, following an acute event; early discharge program in chronic respiration patients; promotion of physical activity in ambulatory stable cardio-respiratory patients.

Prognostic value of ventricular arrhythmias and heart rate variability in patients with unstable angina.

OBJECTIVES: To assess the prognostic value of ventricular arrhythmias (VA) and heart rate variability (HRV) in patients with unstable angina. DESIGN: Multicentre prospective study. SETTING: 17 cardiological centres in Italy. PATIENTS: 543 consecutive patients with unstable angina and preserved left ventricular function (ejection fraction >or=40%) enrolled in the SPAI (Stratificazione Prognostica dell'Angina Instabile) study. METHODS: Patients underwent 24 h ECG Holter monitoring within 24 h of hospital admission. Tested variables were frequent ventricular extrasystoles (>or=10/h), complex (that is, frequent or repetitive) VA, and bottom quartile values of time-domain and frequency-domain HRV variables. Primary end points were in-hospital and six-month total and cardiac deaths. RESULTS: Eight patients died in hospital (1.5%) and 32 (5.9%, 29 cardiac) during follow up. Both complex VA and frequent extrasystoles were strongly predictive of death in hospital and at follow up, even after adjustment for clinical (age, sex, cardiac risk factors and history of myocardial infarction) and laboratory (troponin I, C reactive protein and transient myocardial ischaemia on Holter monitoring) variables. At univariate analysis bottom quartile values of three HRV variables (standard deviation of RR intervals index, low-frequency amplitude and low to high frequency ratio) were associated with in-hospital death, and bottom quartile values of most HRV variables predicted six-month fatal events. At multivariate Cox survival analysis reduced low-frequency amplitude was consistently found to be independently associated with fatal end points. CONCLUSION: In patients with unstable angina with preserved myocardial function, both VA and HRV are independent predictors of in-hospital and medium-term mortality, suggesting that these factors should be taken into account in the risk stratification of these patients.

Temporal evolution and functional outcome of no reflow: sustained and spontaneously reversible patterns following successful coronary recanalisation.

OBJECTIVE: To identify in humans the temporal patterns of no reflow and their functional implications. METHODS: 24 patients with first acute myocardial infarction and successful coronary recanalisation by recombinant tissue-type plasminogen activator (n = 15) or primary percutaneous transluminal coronary angioplasty (n = 9) were studied by myocardial contrast echocardiography within 24 hours of recanalisation and at one month's follow up. Myocardial contrast echocardiography was performed by intermittent harmonic power Doppler and intravenous Levovist. The regional contrast score index (CSI) was calculated within dysfunctioning myocardium. Videointensity was measured (dB) within risk and control areas and their ratio was calculated. RESULTS: In 8 patients reflow was observed at 24 hours and persisted at one month. Conversely in 16 patients areas of no reflow were detectable at 24 hours. At one month, no reflow was spontaneously reversible in 9 patients (mean (SD) CSI and videointensity ratio improved from 2.5 (0.5) to 1.4 (0.6) and from 0.6 (0.1) to 0.7 (0.1), respectively; p < 0.05) and was sustained in the remaining 7 patients (CSI and videointensity ratio remained unchanged from 2.6 (0.6) to 2.6 (0.5) and from 0.5 (0.2) to 0.5 (0.2), respectively; NS). Left ventricular function improved significantly in patients with reflow and reversible no reflow. Volumes were enlarged only in patients with sustained no reflow. CONCLUSIONS: No reflow detected at 24 hours may be sustained or spontaneously reversible at one month. Such reversibility of the phenomenon is associated with preserved left ventricular volumes and function. Clarification of the mechanisms of delayed reversibility may lead to tailored treatment of no reflow even in the subacute phase of myocardial infarction.

Autoantibodies against oxidized low density lipoproteins in patients with stable angina, unstable angina or peripheral vascular disease; pathophysiological implications.

BACKGROUND: Antibody antioxidized low density lipoproteins (oxLDL) might play a role both in atherogenesis and in the pathogenesis of acute coronary syndromes. METHODS AND RESULTS: Antibody titres to oxLDL and levels of C-reactive protein were compared in unstable angina, stable angina or peripheral artery disease. Antibody titres to LDL oxidated by CuSO(4)for 2, 4 and 18 h (Cu-oxLDL-Ab(2-4-18)) or by peroxidase (HRP-oxLDL-Ab) were assessed by ELISA. Cu-oxLDL-Ab(2-4-18)were consistently higher in peripheral artery disease than in unstable angina (P<0.001, P<0.001, P=0.01, respectively) or in stable angina (P<0.001, P=0.01, P=ns) but similar in unstable and stable angina. Accordingly, HRP-oxLDL-Ab were higher in peripheral artery disease than in unstable angina (P<0.001) or stable angina (P=0.04) but similar in unstable and stable angina. The number of arterial stenoses was higher in peripheral artery disease than unstable and stable angina (P<0.01). Cu-oxLDL-Ab and HRP-oxLDL-Ab correlated with the severity of atherosclerosis (P<0.01, R=0.4;P=0.02, R=0.3 respectively). Conversely, C-reactive protein levels were higher in unstable than in stable angina (P<0.001) or in peripheral artery disease (P<0.03) but similar in stable angina and peripheral artery disease and did not correlate with the severity of atherosclerosis. CONCLUSION: The autoimmune response to oxLDL is likely to play an important role in atherogenesis but not in precipitating acute coronary syndromes.

[Reporting echocardiography exams with the G8-Cardio ANMCO software]. / Refertazione dell'esame ecocardiografico con il software G8-Cardio ANMCO.

BACKGROUND: The availability of a common computerized program for echocardiographic study archiving and reporting at national and/or international level could make it possible to standardize the echo reports of different echocardiographic laboratories, and to use the wealth of data thus obtainable with echocardiography, and to exploit its capillary territorial distribution, with the aim of collecting echocardiographic data in a standard format for epidemiological, scientific and administrative purposes. METHODS: To develop such a software, an ad hoc joint National Association of Hospital Cardiologists and Italian Society of Echocardiography task force worked in conjunction with the Italian Branch of Agilent Technologies to standardize the phraseology of accepted echocardiographic terms and of the quantitative parameters derived from transthoracic and transesophageal echocardiographic examination at rest as well as during exercise and pharmacological stress, and to develop an ad hoc software. This echocardiographic study archiving and reporting program is part of the whole G8-Cardio ANMCO software developed to computerize the whole cardiological chart. The software has been developed by Agilent Technologies to provide a fast, easy-access and easy to use report generator for the non-computer specialist using DBMS Oracle 7.3 database and Power Builder 5.0 to develop a user-friendly interface. RESULTS: The number of qualitative and quantitative variables contained in the program is 733 for echocardiography at rest, while it depends on the stressor and on the length of the examination for the stress echo (dipyridamole 214-384, dobutamine 236-406, exercise 198-392). The program was tested and refined in our laboratory between November 1999 and May 2000. During this time period, 291 resting and 56 stress echocardiographic studies were reported and recorded in a database. On average, each resting echocardiographic study lasting 10 +/- 4 (range 5-17) min was recorded using 50 +/- 11 (range 33-67) variables and 41,566 bytes of hard-disk memory space. Stress echocardiographic studies, each lasting 7 +/- 5 (range 5-21) min, were recorded using 143 +/- 74 (range 38-194) variables and 38,531 bytes of hard-disk memory space. CONCLUSIONS: To our knowledge this software represents the first experience of a common computerized program for echo archiving and reporting carried out at national level.

Coronary risk factors: new perspectives.

The predisposing and precipitating causes of acute myocardial infarction (MI) are multiple; furthermore, different individuals may have different susceptibility, to a large extent genetically determined, to each of them. In spite of the complex aetiology of MI and of our limited knowledge of the causes responsible for the formation of persistent occlusive thrombosis in epicardial coronary arteries, the achievements obtained by controlling traditional risk factors are remarkable. Traditional risk factors, however, have a limited sensitivity among subjects with low/moderate levels of risk. Furthermore, in particular among subjects at medium risk, current preventive strategies are limited by the low incidence of preventable events which makes it necessary to also treat the vast majority of subjects who would not develop cardiac events even without any treatment. An improvement in preventive strategies for IHD can be achieved with the identification of: (1) new risk factors; (2) genotypes enhancing the susceptibility to specific risk factors; (3) phenotypes and genotypes making patients susceptible to specific preventive strategies; (4) genotypes protecting from risk factors. Although a word of caution is necessary as a number of recent studies on genetic markers, on new risk factors and on the interaction between genetic markers and environment have failed to withstand the rigour of population-based studies, the early findings available to date suggest that cost-effective preventive strategies based on individual susceptibility to specific predisposing and precipitating causes of MI may become a reality in the foreseeable future.

Transient microvascular vasoconstriction: a possible cause of unstable angina.

We report the case of a 65-year-old woman who developed unstable angina 2 months after successful coronary angioplasty of the left anterior descending coronary artery. Coronary angiography failed to show angiographic restenosis, but intracoronary ergonovine caused ST segment elevation and her habitual chest pain in the absence of epicardial coronary spasm and important pressure changes in the distal left anterior descending coronary artery assessed by a pressure wire, thus suggesting that distal vessel constriction was responsible for unstable angina.

Major racial differences in coronary constrictor response between japanese and caucasians with recent myocardial infarction.

BACKGROUND: Enhanced coronary vasomotion may contribute to acute coronary occlusion during the acute phase of myocardial infarction (AMI). Japanese have a higher incidence of variant angina than Caucasian patients, but racial differences in vasomotor reactivity early after AMI are controversial. METHODS AND RESULTS: The same team studied 15 Japanese and 19 Caucasian patients within 14 days of AMI by acetylcholine injection into non-infarct-related (NIRA) and infarct-related (IRA) coronary arteries followed by nitroglycerin. Incidence of vasodilation, vasoconstriction, spasm, and basal tone were assessed in proximal, middle, and distal segments after each drug bolus by quantitative angiography. Japanese patients had much lower cholesterol levels than Caucasians (183+/-59 versus 247+/-53 mg/dL, P<0.006) but showed a lower incidence of vasodilation (2% versus 9% of coronary segments) and a greater incidence of spasm after acetylcholine (47% versus 15% of arteries, P<0.00001). Incidence of spasm was higher in IRAs than in NIRAs in both populations (67% versus 39% and 23% versus 11%, respectively). Multivessel spasm was more common (64% versus 17%, P<0.02) and vasoconstriction of nonspastic segments was greater in Japanese patients (-23.4+/-14.9% versus -20.1+/-15.7%, P<0.02) in the presence of similar average basal coronary tone with respect to post-nitroglycerin dilation and of nonsignificant differences of coronary atherosclerotic score. CONCLUSIONS: Soon after AMI, Japanese patients exhibited a 3-fold-greater incidence of spasm and greater vasoconstriction of nonspastic segments after acetylcholine than Caucasians. The causes of such differences warrant further investigation because they may have relevant pathophysiological and therapeutic implications.

Incremental prognostic value of serum levels of troponin T and C-reactive protein on admission in patients with unstable angina pectoris.

Management of unstable angina is largely determined by symptoms, yet some symptomatic patients stabilize, whereas others develop myocardial infarction after waning of symptoms. Therefore, markers of short-term risk, available on admission, are needed. The value of 4 prognostic indicators available on admission (pain in the last 24 hours, electrocardiogram [ECG], troponin T, and C-reactive protein [CRP]), and of Holter monitoring available during the subsequent 24 hours was analyzed in 102 patients with Braunwald class IIIB unstable angina hospitalized in 4 centers. The patients were divided into 3 groups: group 1, 27 with pain during the last 24 hours and ischemic electrocardiographic changes; group 2, 45 with pain or electrocardiographic changes; group 3, 30 with neither pain nor electrocardiographic changes. Troponin T, CRP, ECG on admission, and Holter monitoring were analyzed blindly in the core laboratory. Fifteen patients developed myocardial infarction: 22% in group 1, 13% in group 2, and 10% in group 3. Twenty-eight patients underwent revascularization: 37% in group 1, 35% in group 2, and 7% in group 2 (p <0.01 between groups 1 or 2 vs group 3). Myocardial infarction was more frequent in patients with elevated troponin T (50% vs 9%, p=0.001) and elevated CRP (24% vs 4%, p= 0.01). Positive troponin T or CRP identified all myocardial infarctions in group 3. Only 1 of 46 patients with negative troponin T and CRP developed myocardial infarction. Among the indicators available on admission, multivariate analysis showed that troponin T (p=0.02) and CRP (p=0.04) were independently associated with myocardial infarction. Troponin T had the highest specificity (92%), and CRP the highest sensitivity (87%). Positive results on Holter monitoring were also associated with myocardial infarction (p=0.003), but when added to troponin T and CRP, increased specificity and positive predictive value by only 3%. Thus, in patients with class IIIB unstable angina, among data potentially available on admission, serum levels of troponin T and CRP have a significantly greater prognostic accuracy than symptoms and ECGs. Holter monitoring, available 24 hours later, adds no significant information.

Cost-effective pharmacological prevention of acute coronary syndromes.

The growing size of trials on primary and secondary prevention of acute coronary syndromes characterised by very broad inclusion criteria may seem logical to 'trialists', who reason that the the broader the inclusion criteria, the easier it is to recruit large numbers of patients in a short period of time and the more widely applicable are the results of the study. However, large trials with very broad inclusion criteria raise two grounds for concern for physicians. The first is that the broader the inclusion criteria for enrollment in a trial in order to prove a statistically significant benefit, the greater the heterogeneity of the study population which is likely to include both susceptible and non-susceptible patients to the tested treatment. The second is that this method of assessment rapidly increases the number of treatments that produce a statistically-significant improvement in prognosis within the same broad group of patients. On the contrary, the identification of potential responders to a specific treatment can provide a personalised form of medical care suited to the needs of each individual patient with an optimal cost-benefit ratio. This approach, however, represents a major challenge as it can only be based on the identification of homogeneous subgroups of patients with common risk factors for the development of acute coronary syndromes or of their recurrence. This challenge can only be overcome by a strong commitment in funding studies on the multiple causes of acute coronary syndromes.

Role of inflammation in the pathogenesis of unstable coronary artery disease.

In this article, the clinical, angiographic, and postmortem features of unstable angina are reviewed and its pathogenesis is discussed. Coronary plaque inflammation may play a key role in the pathogenesis of unstable angina and the evidence for this assertion is examined. Finally, the therapeutic implications of the involvement of inflammation in acute coronary syndromes are outlined.

Ischemic-like ST-segment changes during Holter monitoring in patients with angina pectoris and normal coronary arteries but negative exercise testing.

To evaluate whether Holter electrocardiographic monitoring may improve the detection of ST-segment depression in patients with anginal chest pain and normal coronary arteries, we performed symptom-limited exercise testing and 24-hour Holter monitoring in a group of 38 such patients (27 women, age 54 +/- 8 years). Patients were divided into 2 groups:group X1 included 28 patients with and group X2 10 patients without significant ST-segment depression during exercise testing. There were no significant differences between the 2 groups in age, gender, characteristics of chest pain, exercise duration, heart rate (HR), and blood pressure at peak exercise, but anginal pain during exercise testing was reported by 10 patients of group X1 (36%) and 9 of group X2 (90%) (p <0.01). Episodes of ST-segment depression on Holter monitoring were found in 17 patients of group X1 (61%) and in 5 patients of group X2 (50%) (p = NS). There were no differences between the 2 groups in daily number of ST episodes (3.6 +/- 4 vs 2.8 +/- 5 episodes per patient), symptomatic episodes (8% vs 18%), and duration of the episodes. On average, HR increased significantly, in a similar way, from 15 minutes before ST-segment depression to 1-mm ST in both groups, and its value at the onset of ischemia was similar in the 2 groups (102 +/- 22 vs 109 +/- 18 beats/min, p = NS). Finally, HR at 1-mm ST during Holter monitoring was significantly lower than that observed at 1-mm ST during exercise testing (127 +/- 16 beats/min, p < or = 0.01) in group X1, and it was also lower than that observed at peak exercise (136 +/- 22 beats/min, p < or = 0.01) in group X2. In conclusion, Holter monitoring can significantly increase the detection of ST-segment depression in patients with anginal pain and normal coronary arteries, indicating a cardiac, although not necessarily ischemic, origin of the pain. Indeed, 50% of our patients with negative symptom-limited exercise testing showed spontaneous ST changes, compatible with transient myocardial ischemia, during daily activities. Differences in the response of coronary microvascular tone to exercise testing and to stimuli operating during daily life are likely to play a significant role in determining these findings.

The risk and cost-effective individual patient management: the challenge of a new generation of clinical trials.

The percentage reduction of risk demonstrated in several recent trials in quite remarkable. For example 1 out of 5, and even as many as 1 out of 3, fatal cardiovascular events can be prevented by some treatments. Further efforts aimed at producing a substantially greater percentage reduction of risk than demonstrated so far with thrombolytic agents in acute MI, aspirin in patients discharged from the hospital with a diagnosis of unstable angina, or statins in the secondary and primary prevention of ischemic heart disease would be quite difficult to achieve and would require greater patient compliance and more powerful drugs, possibly with greater side effects and costs. The growing size of trials with very broad inclusion criteria may seem logical to "trialists," who reason that the broader the inclusion criteria, the easier it is recruit very large numbers of patients in a short space of time and the more widely applicable the results of the study. The pharmaceutical industry also prefers broad inclusion criteria, which imply wider indications for use of their products. However, very large trials with broad inclusion criteria raise two grounds for concern for practicing physicians and for the economics of health care. The first is the fact that the larger the number of patients that have to be included in a trial in order to prove a statistically significant benefit, the greater the uncertainty about the reason why the beneficial effects of the treatment cannot be detected in a smaller trial. Secondly, this method of assessment is rapidly increasing the number of treatments that produce a statistically significant improvement in prognosis within the same broad group of patients. A large percentage reduction in mortality that reaches statistical significance only in very large trials suggests either a relatively low rate of preventable deaths in all individuals in the group or considerable heterogeneity in the patients enrolled, only a few of whom benefit from the treatment. This alternative is of considerable practical importance, first because a large heterogeneity of patients implies a "dilution effect" of those susceptible to the benefits of treatment by those who are not susceptible and are treated unnecessarily, and second, because uniformly low rates of potentially preventable death rise such issues as prolongation of life expectancy, surrogate endpoints, and the effects of treatment on the quality of life. Only a new generation of clinical trials that include only homogenous groups of potential responders can produce both results more readily applicable to personalized patient care in clinical practice (which is a desirable target for the practicing physician) and a large reduction in the number of events per patient treated (which is a desirable target for the economics of health care.

Low incidence of serotonin-induced occlusive coronary artery spasm in patients with recent myocardial infarction.

Intracoronary infusion of serotonin has been reported to induce varying degrees of coronary vasoconstriction in different coronary syndromes, but it has never been studied in patients after myocardial infarction. In patients with recent myocardial infarction, we found a low incidence (11%) of serotonin-induced occlusive spasm only in the infarct-related artery (IRA), and a significantly higher vasoconstriction in the distal segment of the IRA than in the same segment of the non-IRA.

Comparison of coronary angiographic narrowing in stable angina pectoris, unstable angina pectoris, and in acute myocardial infarction.

Coronary angiographic findings were compared in patients who presented with acute myocardial infarction (AMI, n = 75), unstable angina pectoris (UAP, n = 36), or stable angina pectoris (SAP, n = 36) for > or = 2 years without evidence of any previous acute event and with an angiogram within 2 years of the initial symptoms. Angiograms were evaluated blindly for severity, extent (depending on the percentage of each coronary segment showing atherosclerosis), and pattern (discrete, < 3 loci of narrowings involving < 50% of any segment; diffuse, anything exceeding this). Patients in the SAP group had more narrowed arteries (2.4 +/- 0.7 vs 1.3 +/- 0.6 [p < 0.02] and 1.4 +/- 0.6 [p < 0.02]), more stenoses (6.0 +/- 3.3 vs 2.1 +/- 1.5 [p < 0.01] and 2.6 +/- 1.7 [p < 0.05]) and occlusions (1.3 +/- 1.1 vs 0.7 +/- 0.6 [p = 0.05] and 0.3 +/- 0.5 [p < 0.02]), and a greater extent index (0.9 +/- 0.5 vs 0.5 +/- 0.3 [p < 0.02] and 0.5 +/- 0.3 [p < 0.02]) than those in the AMI and UAP groups. Furthermore, a discrete pattern was less prevalent in patients with UAP than in those with SAP or AMI (3% vs 40% [p < 0.02] and 25% [p < 0.05], respectively). In conclusion, patients who present with acute coronary syndromes have less extensive atherosclerosis than those who present with chronic stable angina. Therefore, in the former group, coronary atherosclerosis appears to be more susceptible to ischemic stimuli responsible for acute coronary syndromes.(ABSTRACT TRUNCATED AT 250 WORDS)