Non-culprit Coronary Artery Research Articles

Results of Fractional Flow Reserve Measurement to Evaluate Nonculprit Coronary Artery Stenoses in Patients With Acute Coronary Syndrome

Introduction and objectives Multivessel disease is usually present in almost half of patients with acute coronary syndromes. Angiography is insufficiently accurate to decide on coronary revascularization in moderate nonculprit lesions. There is some debate about the usefulness of fractional flow reserve assessed by intracoronary pressure wire in acute coronary syndromes. We studied the results of using fractional flow reserve values to decide whether to perform coronary revascularization of nonculprit angiographically moderate lesions in patients with acute coronary syndrome and multivesel disease. Methods The fractional flow reserve was used to decide whether to revascularize angiographically moderate nonculprit lesions in a cohort of consecutive patients with acute coronary syndromes recruited in 2 centers. Results One hundred and seven patients were included. Based on fractional flow reserve values, 81 patients (75.7%) were not revascularized. All lesions studied were revascularized in 26 patients (24.3%). Patient characteristics of the nontreated group and treated group were, respectively, diseased vessels, 1.3 (0.7) vs 1.4 (0.6) ( P<.4); fractional flow reserve-studied lesions, 1.2 (0.5) vs 1.1 (0.4) ( P=.3); stenosis, 46.1 (8.3)% vs 47.9 (10.3)% ( P=.4); fractional flow reserve, 0.86 (0.1) vs 0.70 (0.1) ( P<.005). After 1 year of follow-up, no significant differences in major cardiovascular events were observed between groups. There no deaths or nonfatal myocardial infarctions attributable to fractional flow reserve -deferred lesions. Coronary revascularization of the studied lesions was performed in 3 nontreated group patients (3.7%) due to disease progression. Conclusions Fractional flow reserve assessed by intracoronary pressure wire is useful in deciding whether to revascularize angiographically moderate nonculprit lesions in patients with acute coronary syndrome and multivessel disease.

Frequency and Healing of Nonculprit Coronary Artery Plaque Disruptions in Patients With Acute Myocardial Infarction

The pathophysiology of plaque disruption and healing in nonculprit segments has not been clarified. Therefore, we investigated the frequency of plaque disruptions in nonculprit segments and whether those plaques are stabilized during follow-ups in patients with acute myocardial infarction (AMI) by serial angioscopic observations. Analyzed were 13 consecutive patients with AMI in whom infarct-related arteries were serially observed by angioscopy immediately after reperfusion and at 1- and 6-month follow-ups. Color of plaques was graded as 0 (white), 1 (slight yellow), 2 (yellow), or 3 (intensive yellow). Plaques with thrombus were defined as disrupted. Although number of nonculprit yellow plaques did not change from immediately after reperfusion to 6 months, the maximum color grade of those plaques and incidence of disrupted plaques in nonculprit segments (immediate vs 1 month vs 6 months 31% vs 8% vs 0%) decreased significantly by 6 months. Plaque stabilization as shown by disappearance of thrombus was significantly associated with plaque regression as shown by a decrease of maximum yellow color grade in nonculprit segments. In conclusion, patients with AMI frequently had disrupted and actively thrombogenic yellow plaques in nonculprit segments of the culprit vessel, and those plaques healed with decreases of yellow color grade and thrombogenicity during 6-months follow-up. Plaque disruption and healing occur not only at the culprit lesion but may be a pan-coronary process in patients with AMI.

Embolisation of a non-culprit coronary artery complicating thrombus aspiration in acute myocardial infarction: The “drag and drop” effect of the thrombus aspiration catheter

A fifty seven year-old male presented with acute central chest pain waking him up from sleep. He reported exertional chest pain in the weeks preceding and had a background of hypertension, hypercholesterolemia and was an ex-smoker. His examination on arrival was unremarkable and remained haemodynamically stable. His ECG on arrival showed inferior-lateral ST elevation with reciprocal ST depression in anterior leads and Q waves in leads III, aVF. He was treated for aspirin, clopidogrel, low molecular weight heparin and nitrates. He proceeded to have an urgent coronary angiogram with a view to primary angioplasty for acute ST-elevation myocardial infarction.

Fractional Flow Reserve for the Assessment of Nonculprit Coronary Artery Stenoses in Patients With Acute Myocardial Infarction

We investigated the reliability of fractional flow reserve (FFR) of nonculprit coronary stenoses during percutaneous coronary intervention (PCI) in acute myocardial infarction. Assessing the hemodynamic severity of the nonculprit coronary artery stenoses at the acute phase of a myocardial infarction could improve risk stratification and shorten the diagnostic work-up. One hundred one patients undergoing PCI for an acute myocardial infarction (n = 75 with ST-segment elevation myocardial infarction [STEMI], and n = 26 with non-ST-segment elevation myocardial infarction) were prospectively recruited. The FFR measurements in 112 nonculprit stenoses were obtained immediately after PCI of the culprit stenosis and were repeated 35 ± 4 days later. In addition, left ventricular ejection fraction, quantitative coronary angiographic measurements of the nonculprit stenoses, Thrombolysis In Myocardial Infarction (TIMI) flow, corrected TIMI frame count (cTFC), and the index of microcirculatory resistance (n = 14) of the nonculprit vessels were assessed in the acute phase and at control angiogram. The FFR value of the nonculprit stenoses did not change between the acute and follow-up (0.77 ± 0.13 vs. 0.77 ± 0.13, respectively, p = NS). In only 2 patients, the FFR value was higher than 0.8 at the acute phase and lower than 0.75 at follow-up. The TIMI flow, cTFC, percentage diameter stenosis, minimum lumen diameter, and index of microcirculatory resistance did not change. Left ventricular ejection fraction increased significantly in patients with STEMI (from 54 ± 13% to 57 ± 13%, p = 0.03). During the acute phase of acute coronary syndromes, the severity of nonculprit coronary artery stenoses can reliably be assessed by FFR. This allows a decision about the need for additional revascularization and might contribute to a better risk stratification.

E0536 Comparative effects of percutaneous coronary intervention for culprit coronary artery or together with non-culprit coronary artery in patients with multi-vessel coronary artery disease

BackgroundRapid recanalisation of the culprit lesion is the main goal of primary angioplasty for acute ST-segment elevation myocardial infarction (STEMI), but strategy for treatment of culprit and non-culprit lesions in...

Non-culprit coronary artery percutaneous coronary intervention during acute ST-segment elevation myocardial infarction: insights from the APEX-AMI trial

To examine the incidence of and propensity for non-culprit interventions performed at the time of the primary percutaneous coronary intervention (PCI) and its association with 90-day outcomes. We examined the incidence, propensity for, and associated 90-day outcomes following non-culprit interventions performed at the time of primary PCI among ST-elevation myocardial infarction patients with multi-vessel coronary artery disease (MVD). Of the 5373 patients who underwent primary PCI in the APEX-AMI trial, 2201 had MVD. Of those, 217 (9.9%) underwent non-infarct-related arteries (IRA) PCI, whereas 1984 (90.1%) underwent PCI of the IRA alone. Ninety-day death and death/CHF/shock were higher in the non-IRA group compared with the IRA-only PCI group (12.5 vs. 5.6%, P (log-rank) < 0.001 and 17.4 vs. 12.0%, P (log-rank) = 0.020, respectively). After adjusting for patient and procedural characteristics as well as propensity for performing non-IRA PCI, this procedure remained independently associated with an increased hazard of 90-day mortality [adjusted hazard ratio 2.44, 95% CI (1.55-3.83), P < 0.001]. Non-culprit coronary interventions were performed at the time of primary PCI in 10% of MVD patients and were significantly associated with increased mortality. Our data support current guideline recommendations discouraging the performance of such procedures in stable primary PCI patients. Prospective randomized study of this issue may be warranted.

Correlation between circulating adiponectin levels and coronary plaque regression during aggressive lipid-lowering therapy in patients with acute coronary syndrome: Subgroup analysis of JAPAN-ACS study

ObjectiveThe Japan assessment of pitavastatin and atorvastatin in acute coronary syndrome (JAPAN-ACS) study demonstrated that aggressive lipid-lowering therapy with a statin resulted in a significant regression of coronary atherosclerotic plaques in patients with ACS. Adiponectin is an adipocyte-derived protein with anti-atherogenic properties. Here, we investigated the association between adiponectin levels and the change in the plaque volume in ACS patients. MethodsIntravascular ultrasound (IVUS)-guided percutaneous coronary intervention (PCI) was undertaken, followed by the initiation of statin treatment, in 238 patients with ACS. Follow-up IVUS was performed between 8 and 12 months after the PCI. The percent change in the plaque volume (%PV) in a non-culprit coronary artery segment was evaluated. The serum adiponectin and lipid parameters were measured both at baseline and at the follow-up. ResultsAt baseline, adiponectin was correlated positively with HDL-cholesterol and negatively correlated with triglyceride, but no correlation was observed with the PV. Adiponectin levels increased significantly from 7.8±4.6μg/mL at baseline to 10.3±6.9μg/mL at the 8–12 months follow-up. The increase in adiponectin was also associated with an increase of HDL-cholesterol and decrease of triglyceride, however, no significant correlation was observed with the %PV. A significantly higher incidence of major adverse cardiac events (MACE) was observed in patients with hypo-adiponectinemia at baseline. A multiple logistic regression analysis identified adiponectin as a significant independent predictor of MACE. ConclusionAdiponectin levels measured after PCI could serve as a marker of MACE in patients with ACS.

Serum adipocyte fatty acid-binding protein is independently associated with coronary atherosclerotic burden measured by intravascular ultrasound

ObjectivesAdipocyte fatty acid-binding protein (A-FABP) has been shown to have an effect on insulin resistance, lipid metabolism, and atherosclerosis in animals. We therefore investigated the association between the serum A-FABP level and coronary atherosclerosis. MethodsOne hundred twenty-five consecutive patients with coronary artery disease (CAD) were enrolled after coronary angiography. Plaque volume in non-culprit coronary arteries was determined using intravascular ultrasound and expressed as percent plaque volume (%PV). Voluntary blood donors (n=120), matched for age and gender, served as controls. Serum levels of A-FABP, adiponectin, and inflammatory markers were measured by enzyme-linked immunosorbent assay. ResultsThe serum A-FABP level in CAD patients was significantly higher than in control subjects (median [25th–75th percentiles], 27.2 [20.5–37.1]ng/mL vs. 18.9 [14.6–24.5]ng/mL) (p<0.01). Serum A-FABP showed 0.74 of the area under the curve in the receiver operating characteristic curve for the detection of CAD, with 76% specificity and 65% sensitivity with a cut-off value of 20.1ng/mL. Further, in CAD patients, serum A-FABP had a significant correlation with %PV in all subjects (r=0.33, p<0.01). Serum A-FABP was positively correlated with the body mass index, serum interleukin-6 and high-sensitive CRP, and negatively correlated with HDL-cholesterol and serum adiponectin in CAD patients. Stepwise regression analysis revealed that serum A-FABP was independently associated with %PV. ConclusionIncreased serum A-FABP was significantly associated with a greater coronary plaque burden. Our findings revealed that the measurement of serum A-FABP could be utilized for the evaluation of the extent of coronary atherosclerosis.

Diagnostic accuracy of dual-source computed tomography in the characterization of coronary atherosclerotic plaques: Comparison with intravascular optical coherence tomography

Background Dual-source computed tomography (DSCT) has enabled us to non-invasively visualize coronary artery stenosis, but its ability to characterize coronary atherosclerotic plaques (ASPs) has not been evaluated. Intravascular optical coherence tomography (OCT) provides tissue images of coronary artery wall that are validated by pathohistological studies. We studied the diagnostic accuracy of DSCT in the characterization of coronary ASPs, especially lipid-rich ASP with thin fibrous cap (TCFA), in comparison with OCT. Methods DSCT and OCT were used to image non-stenotic ASPs in non-culprit coronary arteries of 17 acute coronary syndrome (ACS) patients, and 162 coronary regions were enrolled. Results The mean CT values of fibrous ASP, ASP with lipid core, and ASP with calcium deposit were 77.5, 28.9, and 515.9 HU, respectively ( P < 0.0001). ASP with calcium deposit was detected with a sensitivity of 88.9% and a specificity of 98.6%, while ASP with lipid core was detected by DSCT with a relatively low sensitivity of 73.1% and a high specificity of 94.0%. In TCFA, cross-sectional areas of both ASP and lipid core were significantly larger, mean CT value of ASP was significantly lower, and concomitant calcification was more frequently observed compared with lipid-rich ASP with thick fibrous cap (ThCFA). The combination of these CT parameters seems to be a useful index for the differentiation of TCFA from ThCFA. Conclusion DSCT is useful for non-invasive evaluation of calcified and fibro-fatty tissue characters in coronary artery plaque, but it is still not able to differentiate TCFA, one of the features of vulnerable plaque.

Plaque characterization of non-culprit lesions by virtual histology intravascular ultrasound in diabetic patients: Impact of renal function

The aim of this study was to characterize coronary plaque composition of non-target lesions in diabetic patients using virtual histology intravascular ultrasound (VH-IVUS). In 134 stable angina pectoris patients, plaque components of non-culprit (< 50% in diameter stenosis) lesions in de novo target vessels were analyzed by VH-IVUS. Plaque characterization was compared between diabetic (n=65) and non-diabetic groups (n=69). Diabetic patients were further divided into four groups according to estimated glomerular filtration rate (eGFR, ml/min): eGFR > or = 70 (n=20), 50 < or = eGFR < 70 (n=19), GFR < 50 (n=18), and end stage renal disease (ESRD) on hemodialysis (HD) (n=11). There was no significant difference in plaque composition between the diabetic and the non-diabetic patients except for the percentage of dense calcium (8.9% vs. 6.2%; p<0.05). In the diabetic patients, the percent volume of necrotic core was 9.6%, 11.4%, 14.8%, and 20.8% in the eGFR > or = 70, 50 < or = eGFR < 70, eGFR < 50, and the ESRD on HD groups, respectively, showing significantly higher percentage in eGFR < 50 (p<0.05 vs. eGFR > or = 70) and ESRD on HD group (p<0.001). Diabetic patients have significantly larger amount of dense calcium than non-diabetic patients in non-culprit coronary artery segments, and the plaque components of non-culprit lesions in diabetes are significantly different according to the decline in renal function.

Multiple channel appearance with low-echoic divisions detected by intravascular ultrasound image in acute myocardial infarction with antiphospholipid syndrome

“Arteries within the artery” is a particular image suggesting spontaneous recanalization after coronary thrombotic events in Kawasaki disease and it appears as multiple channels with highly echoic, thick divisions on intravascular ultrasound (IVUS) images. On the other hand, antiphospholipid syndrome (APS) can clinically manifest as arterial thrombosis, including coronary thrombotic events. We describe a 32-year-old male patient who presented with anteroseptal acute myocardial infarction (AMI) due to APS. Examination by IVUS revealed a multiple channel appearance similar to that of “arteries within the artery” associated with Kawasaki disease but low-echoic division in the non-culprit right coronary artery. We speculated that the multiple channel appearance was due to spontaneous recanalization after thrombotic events due to APS.

Obstructive Sleep Apnea Leads to Transient Uncoupling of Coronary Blood Flow and Myocardial Work in Humans

Obstructive Sleep Apnea (OSA) is associated with a poor prognosis in patients with coronary artery disease. We hypothesized that abnormalities of coronary blood flow (CBF) associated with obstructive apneas may predispose patients to ischemia. We aimed to determine CBF during respiratory events in patients with OSA. University Hospital. Ten subjects undergoing elective percutaneous coronary intervention We measured CBF and myocardial work (rate-pressure product [RPP]) in a non-culprit coronary artery in patients sleeping in the cardiac catheterization laboratory. Hemodynamic responses were matched to spontaneously occurring respiratory events. Events comprised a mixture of obstructive apneas, central apneas and hypopneas. RPP increased at the termination of each type of respiratory event. Following the rise in RPP, there was a delay, identified with breakpoint analysis, before CBF began to increase (P<0.001) that differed in duration with event type: 8 sec for obstructive apnea, 5 sec for central apnea, and 4 sec for hypopnea. The delay in CBF with obstructive apnea was associated with an increase in coronary vascular resistance of 16% +/- 4% (P < 0.05). Stepwise multilinear regression analysis showed the increase in CBF was predicted by the rise in RPP (R=0.52, P<0.001) and presence of arousal from sleep (R=0.30, P<0.05), but not the degree of O2 desaturation. Following obstructive apneas there is a transient uncoupling of CBF from myocardial work and an increase in CVR. This disturbed flow-metabolic coupling may lead to nocturnal myocardial ischemia in patients with both OSA and coronary artery disease.

Predictive factors for in-stent late loss and coronary lesion progression in patients with type 2 diabetes mellitus randomized to rosiglitazone or placebo

Type 2 diabetics (DM2) are at increased risk for restenosis as well as nonculprit coronary artery lesion (NCCL) progression. Rosiglitazone (RSG) favorably modifies many of the altered biologic processes in DM2, although recent reports have questioned its safety. We conducted a double-blind randomized trial to assess the effects of RSG versus placebo on in-stent late lumen loss (LL) and angiographic progression of NCCL. A total of 65 DM2 were randomized to RSG (4 mg/d) (n = 32) or placebo (n = 33) at the time of stenting and underwent clinical and laboratory analysis at 1 and 4 months and 8-month angiography (n = 46 patients). Rapid angiographic progression (RAP) was defined as > or =20% diameter reduction of preexisting NCCL by quantitative coronary angiography, or a new narrowing > or =30%. Mean LL in RSG (n = 33 lesions) was not different from that of placebo (0.62 +/- 0.59 vs 0.70 +/- 0.67, P = NS). Seven (13.5%) of 52 NCCLs have RAP in RSG versus 9 (16.1%) of 56 in placebo (P = NS). High-sensitivity C-reactive protein (hs-CRP) was the only predictor of RAP. Patients with a 120-day hs-CRP > or =75th percentile had an OR of 7.35 (95% CI 2.35-23) for RAP versus those below. Although RSG treatment also lowered log (hs-CRP) at 4 months (RSG 0.10 +/- 0.37 vs placebo 0.26 +/- 0.49, P = .06), it did not decrease the likelihood of plaque progression while also raising LDL and N-terminal brain naturetic peptide. Rosiglitazone appears not to lower LL or reduce angiographic progression of NCCL in DM2 and had complex effects on markers of cardiac risk.

Vulnerable plaque intervention: State of the art

Progressive atherosclerotic disease is responsible for many of the late adverse clinical events that detract from the high procedural and clinical success of percutaneous coronary intervention. Despite recent advances in catheter based technology for the treatment of obstructive coronary artery disease, the greater risk to the patient over time may in fact come from the significant rate of acute coronary events triggered by nonculprit and/or nonobstructive coronary artery lesions. These areas of vulnerability within the epicardial coronary tree have generated a great deal of interest surrounding the concepts of vulnerable plaque (VP), vulnerable blood and the vulnerable patient. This 'state of the art' review discusses the limitations of coronary angiography alone in providing risk assessment; reviews the underlying biological concepts of VP; discusses evolving noninvasive and invasive imaging technologies for the detection of VP; and finally provides a futuristic look at how the field of interventional cardiology may transcend the traditional angiogram and move toward a more comprehensive treatment approach that benefits the patients' overall coronary health.

Progression of Non-Culprit Coronary Artery Atherosclerosis After Acute Myocardial Infarction in Comparison with Stable Angina Pectoris

We previously found, using a mouse model, that activation of proinflammatory cytokines after acute myocardial infarction (AMI) augments neointimal hyperplasia of a remote artery. The present study assessed the progression of luminal narrowing of non-culprit coronary arteries (NCCA) in patients following AMI. The study group comprised 21 AMI patients successfully treated with bare-metal stents and 16 stable angina (SA) patients treated with sirolimus-eluting stents. Clinical backgrounds were similar for both groups. Quantitative coronary angiography was performed before and after stent implantation and at 6-months of follow-up. We evaluated 126 non-culprit coronary segments (73 in AMI and 53 in SA). The minimum lumen diameter (MLD) (mm) of NCCA decreased significantly from 2.61+/-0.79 to 2.44+/-0.71 in the AMI group, but changed only slightly from 2.02+/-0.56 to 2.02+/-0.50 in the SA group. The absolute change in the MLD of NCCA was significantly greater (0.17+/-0.53) in the AMI, than in the SA (0.0070+/-0.261) group. luminal narrowing of non-culprit coronary segments progressed in AMI patients within 6 months of stent implantation, but progressed only slightly in SA patients.

Myocardial infarction associated with thrombus formation in non-culprit coronary arteries

Acute coronary syndromes may be associated with a systemic acute pro-thrombotic condition, possibly involving inflammatory mechanisms as well, which are not confined to a single spot in the coronary circulation. Multivessel coronary thrombosis appears to be an exceptionally rare clinical finding. Here we present a case of anterior MI complicated by thrombi in circumflex and right coronary arteries.

Intravascular Ultrasound-Guided Coronary Artery Stenting for Spontaneous Coronary Artery Dissection in a Case of Acute Myocardial Infarction Associated with Vasospasm in a Non-Culprit Coronary Artery during the Hospitalization

We report a case of spontaneous coronary artery dissection (SCAD) causing acute myocardial infarction, which was complicated by vasospastic angina (VA). The patient received intravenous administration of t-PA. Emergency coronary angiography demonstrated narrowing of the left anterior descending artery (LAD) due to SCAD. During hospitalization, the patient suffered chest pain, and ECG showed ST elevation in the inferior leads. Sublingual administration of nitroglycerin provided temporary remission. Coronary stent implantation was performed electively using intravascular ultrasound imaging. This is the first reported case of SCAD associated with vasospasm in a non-culprit coronary artery during the hospitalization.

Usefulness of Tissue Doppler Imaging in the Diagnosis and Prognosis of Acute Right Ventricular Infarction With Inferior Wall Acute Left Ventricular Infarction

Tissue Doppler (TD) imaging is a novel echocardiographic technique that measures myocardial velocities. However, there are sparse data on TD imaging of the right ventricular (RV) free wall in the diagnosis and prognosis of RV myocardial infarction (MI) in inferior wall left ventricular MI. Fifty patients who had left ventricular MI underwent TD echocardiography and angiography within 48 hours of MI. For diagnosis, the ability of RV TD imaging to detect RV MI was assessed using coronary angiography as the reference standard. For prognosis, the ability of TD detection of RV dysfunction to predict cardiac death or rehospitalization at 1 year was determined. For diagnosis, the univariate predictors of RV MI included RV diastolic dimension (p = 0.001), TD imaging of tricuspid annular systolic velocity (p = 0.001), and early diastolic velocity (p = 0.002). On multivariate analysis, systolic annular velocity (p = 0.04) and RV dimension (p = 0.05) predicted RV MI. For prognosis, nonculprit coronary artery disease (p = 0.003), TD imaging of RV systolic annular velocity (p = 0.005), and early diastolic velocity (p = 0.01) were among the univariate predictors of cardiac death or rehospitalization. On multivariate analysis, nonculprit coronary artery disease (p = 0.02) and TD imaging of systolic annular velocity (p = 0.04) were independent predictors of outcome. Decreased RV systolic annular velocity on TD images detects RV MI in first left ventricular acute inferior MI and predicts cardiac death or rehospitalization at 1 year.

Angiographic evaluation of the effect of intracoronary abciximab administration in patients undergoing urgent PCI

Background Recent data suggest that the intracoronary (IC) administration of a systemic bolus dose of abciximab during PCI may increase the efficacy of this antiplatelet drug. However, the effect of IC abciximab on coronary angiographic flow has been not clarified. Methods We studied 37 consecutive patients with acute coronary syndromes (ACS) who underwent successful urgent PCI on the target vessel and were treated by an IC abciximab bolus (0.25 mg/kg) prior to the first balloon inflation (Group IC), and 37 matched controls who were treated by intravenous (IV) abciximab bolus at the same dose (Group IV). Corrected TIMI frame count (CTFC) in the culprit and in a non-culprit coronary artery branch was assessed before treatment, immediately after intracoronary administration of abciximab bolus and at the end of the procedure. Results After administration of abciximab, CTFC significantly decreased from 48 + 37 to 33 + 30 ( P = 0.001) in the culprit vessel while in the non-culprit vessel it remained unchanged (16 + 7 pre-treatment and 16 + 7 post-treatment, P = 0.68). Final CTFC was 12 + 4 in Group IC and 14 + 5 in Group IV ( P = 0.069). Post-treatment mean peak of the cardiac enzymes showed a trend toward reduction in Group IC compared with Group IV. Conclusions The IC administration of abciximab bolus acutely decreases CTFC through culprit vessels of patients with ACS undergoing urgent PCI. Further studies evaluating the potential clinical benefits associated with IC abciximab administration are warranted.

High frequency of endothelial vasomotor dysfunction after acute coronary syndromes in non-culprit and angiographically normal coronary arteries: A reversible phenomenon

This study aimed to assess endothelium-dependent vasomotor function in non-culprit coronary vessels in patients with recent acute coronary syndrome (ACS). Endothelial dysfunction can also concern peripheral vessels during ACS, but the frequency of this phenomenon at coronary circulation level is unknown. Endothelial function was assessed by infusion of graded doses of acetylcholine (ACh) in a non-culprit coronary artery of normal appearance in 43 patients having recently suffered from non-ST ACS, and reassessed 6 months later. Endothelium-dependent vasoreactivity was impaired at baseline in 81% (35/43) of the patients, and only 19% (8/43) of patients showed a normal response to ACh. Among the 35 subjects with initial dysfunction, 77% showed a significant improvement 6 months later. All patients without initial endothelial dysfunction remained normal. C-reactive protein (CRP) level was elevated at month 0, and had declined at follow-up, tending towards normal levels. At that time, apolipoprotein A-I (apoA-I) levels were correlated with vasomotor improvement in univariate ( p < 0.02) and multivariate analysis ( p < 0.04). In conclusion, endothelium dysfunction is very frequently observed after recent ACS in non-culprit and angiographically normal coronary arteries, and an improvement occurs within 6 months in most cases. After resolution of the initial inflammation, apoA-I seems to play an important role in endothelial function.