The site of plaque rupture in native coronary arteries: a three-vessel intravascular ultrasound analysis

OBJECTIVES: We evaluated the axial location of plaque ruptures in native coronary arteries. BACKGROUND: It is clinically important to understand the potential sites of plaque rupture. METHODS: We performed three-vessel intravascular ultrasound (IVUS) examination in 392 patients; 231 had acute coronary syndrome (ACS) and 161 had stable angina pectoris (SAP). The IVUS detected plaque ruptures in 206 patients: 158 ACS patients and 48 SAP patients. The distance between each coronary plaque rupture segment and the respective coronary ostium was measured with motorized IVUS transducer pullback in all three coronary arteries. RESULTS: There were a total of 273 plaque ruptures in these 206 patients; 143 in the left anterior descending artery (LAD), 40 in the left circumflex artery (LCX), and 90 in the right coronary artery (RCA). There were 67 plaque ruptures in SAP patients and 206 in ACS patients; there were 197 culprit/target lesion plaque ruptures and 76 non-culprit/non-target lesion plaque ruptures. The LAD plaque ruptures were predominantly located between 10 and 40 mm from the LAD ostium (83%, 119 of 143). The LCX plaque ruptures were evenly distributed in the entire LCX tree. Most RCA plaque ruptures were located in segments between 10 and 40 mm (48%, 43 of 90) and in segments >70 mm from the ostium (32%, 29 of 90). CONCLUSIONS: Three-vessel IVUS imaging showed that plaque ruptures occurred mainly in proximal segments of the LAD (83% of LAD plaque rupture), the proximal and distal segments of the RCA (48% and 32% of RCA plaque ruptures, respectively), and the entire LCX.     

Graphical comparison of coronary arterial culprit lesions in acute myocardial infarction and unstable angina pectoris

OBJECTIVE: The culprit lesion morphology at acute myocardial infarction (AMI) and unstable angina pectoris (UAP) was investigated by observing the responsible vessels through intravascular ultrasound (IVUS) during the acute stage. METHODS: As the subjects of study, 54 lesions of 54 ACS patients (26 in AMI patients, 28 in UAP patients) were enrolled prospectively from June 1994 to June 1998. The appearance of plaque in the lesion, the distal and proximal sites, extent of calcification, eccentricity, remodeling and shrinkage were observed through IVUS before the intervention. RESULTS: At lesion and distal site, significantly more soft plaques were observed in AMI than UAP. As to the extent of calcification in the former, mild calcification was noted significantly more in distal site as well as a tendency of more mild calcification in the lesion and proximal site. CONCLUSION: These results suggested that the condition of responsible coronary artery is involved in the onset mechanism of AMI and UAP.     

Value of the electrocardiogram in localizing the occlusion site in the left anterior descending coronary artery in acute anterior myocardial infarction.

OBJECTIVES: The study assessed the value of the electrocardiogram (ECG) as predictor of the left anterior descending coronary artery (LAD) occlusion site in relation to the first septal perforator (S1) and/or the first diagonal branch (D1) in patients with acute anterior myocardial infarction (AMI). BACKGROUND: In anterior AMI, determination of the exact site of LAD occlusion is important because the more proximal the occlusion the less favorable the prognosis. METHODS: One hundred patients with a first anterior AMI were included. The ECG showing the most pronounced ST-segment deviation before initiation of reperfusion therapy was evaluated and correlated with the exact LAD occlusion site as determined by coronary angiography. RESULTS: ST-elevation in lead aVR (ST elevation(aVR)), complete right bundle branch block, ST-depression in lead V5 (ST depression(V5)) and ST elevation(V1) > 2.5 mm strongly predicted LAD occlusion proximal to S1, whereas abnormal Q-waves in V4-6 were associated with occlusion distal to S1 (p = 0.000, p = 0.004, p = 0.009, p = 0.011 and p = 0.031 to 0.005, respectively). Abnormal Q-wave in lead aVL was associated with occlusion proximal to D1, whereas ST depression(aVL) was suggestive of occlusion distal to D1 (p = 0.002 and p = 0.022, respectively). For both the S1 and D1, inferior ST depression > or = 1.0 mm strongly predicted proximal LAD occlusion, whereas absence of inferior ST depression predicted distal occlusion (p < or = 0.002 and p < or = 0.020, respectively). CONCLUSIONS: In anterior AMI, the ECG is useful to predict the LAD occlusion site in relation to its major side branches.     

The decrease of plaque volume during percutaneous coronary intervention has a negative impact on coronary flow in acute myocardial infarction: a major role of percutaneous coronary intervention-induced embolization

OBJECTIVES: The aim of this study was to evaluate how decreased plaque volume during percutaneous coronary intervention (PCI) affects coronary flow in patients with acute myocardial infarction (AMI). BACKGROUND: Coronary flow after reperfusion therapy is a major determinant of clinical outcomes in patients with AMI. However, little is still known about the changes in coronary flow that appear after PCI in response to the decreased plaque during the procedure. METHODS: The study group comprised 60 patients with AMI who underwent pre- and post-PCI intravascular ultrasound (IVUS). Qualitative and quantitative analyses were performed on all IVUS procedures. External elastic membrane volume (EEMV), lumen volume (LV), and plaque volume (PV) were measured every 1.0 mm to include the lesion and reference segments 3.0 mm proximal and distal to the lesion. The difference between pre- and post-PCI PV was defined as the index of the decrease in plaque volume (DeltaPV). The corrected TIMI frame count (CTFC) was used to evaluate coronary flow after PCI. RESULTS: Plaque volume was decreased at post-PCI IVUS in all 60 patients. Inadequate reflow (CTFC >40) was observed in 13 patients (21.7%). The decrease in PV was significantly larger in patients with inadequate reflow than in those with reflow (49.4 +/- 18.9 vs. 31.7 +/- 15.5 mm(3), p = 0.0010). Also, DeltaPV was significantly correlated with CTFC after PCI (r = 0.415, p = 0.0012). CONCLUSIONS: The decrease in PV during PCI has a negative impact on coronary flow after PCI in patients with AMI. Embolization induced by PCI may occur in all patients with AMI.     

Impact of plaque rupture on infarct size in ST-segment elevation anterior acute myocardial infarction.

OBJECTIVES: We sought to assess whether coronary plaque rupture at culprit lesions is associated with infarct size in patients with anterior acute myocardial infarction (AMI). BACKGROUND: Some patients with AMI have large infarcts despite early reperfusion. Whether culprit plaque morphology impacts infarct size or not remains unknown. METHODS: Patients who had a first anterior AMI with reperfusion within 6 hours after onset were enrolled and divided into 2 groups according to the presence or absence of plaque rupture at the culprit lesion as defined by preintervention intravascular ultrasound (IVUS): patients with rupture (n = 54) and without rupture (n = 37). RESULTS: Patients with plaque rupture had a higher incidence of no-reflow phenomenon (15% vs. 3%; p = 0.08) and a lower myocardial blush grade (1.5 vs. 2.3; p < 0.05) after percutaneous coronary intervention. The IVUS analysis showed that patients with plaque rupture had a higher incidence of soft plaque and positive remodeling. Peak creatine kinase levels were higher (4,707 vs. 2,309 IU/l; p < 0.0001) and left ventricular ejection fraction in the chronic phase was lower (54% vs. 63%; p < 0.01) in patients with plaque rupture. A multivariate logistic regression analysis revealed that plaque rupture and the proximal lesion site correlated with a left ventricular ejection fraction of <50% in the chronic phase (odds ratios 6.5 and 17.5, respectively; p < 0.05). CONCLUSIONS: Plaque rupture is associated with morphologic characteristics of vulnerable lesions, as well as with larger infarcts and a higher incidence of no-reflow phenomenon, suggesting that plaque embolism contributes to the progression of myocardial damage in patients with anterior AMI.     

Anatomic characteristics of culprit sites in acute coronary syndromes

BACKGROUND: A detailed analysis of the anatomic relationships of the site of culprit lesions that have resulted in acute coronary syndromes (ACS) has not been reported. METHODS: Coronary angiograms of consecutive patients who presented with ACS were analyzed according to multiple anatomic criteria. RESULTS: In left anterior descending artery (LAD) (n = 85), 85% of culprit lesions were located in the first 40 mm from the ostium. The presence of angulation on the lesion increased the risk of an ACS 1.92 times (95% confidence interval [CI] 1.9-3.07), and the presence of bifurcation after the lesion increased the risk 1.65 times (95% CI 1.04-2.62). Angulated lesions located within the first 40 mm from the ostium and before a bifurcation presented an 11-fold increased risk for an ACS. In right coronary artery (RCA) (n = 58), the risk of plaque rupture was almost 2.5 times higher in lesions located between 10 and 50 mm from the ostium compared to those located in 90-130 mm (relative risk [RR] 2.38, 95% CI 1.25-4.56). In left circumflex (LCx) (n = 40), the risk of plaque rupture was almost 4.5 and 5 times higher in the first 20 mm, and between 20 and 40 mm from the ostium, respectively, compared to 60 and 80 mm (relative risk [RR] 4.58, 95% CI 1.01-20.68 for 0-20 mm, and RR 4.95, 95% CI 1.14-21.47 for 20-40 mm) after adjustment for the presence of curve on the lesion. The presence of lesion angulation increased the risk of plaque rupture almost three times (RR 3.22, 95% CI 1.49-6.93). CONCLUSION: Specific anatomic features of the coronary arteries predispose to development and/or subsequent rupture of vulnerable plaques.     

Electrocardiographic criteria for predicting total occlusion of the proximal left anterior descending coronary artery in anterior wall acute myocardial infarction

BACKGROUND: Patients with occlusion of the left anterior descending coronary artery (LAD) proximal to both the first septal branch and the first diagonal branch may benefit most from early reperfusion therapy due to extensive area at risk. HYPOTHESIS: The aim of the study was to examine whether 12-lead electrocardiograms (ECGs) in the acute phase of acute myocardial infarction (AMI) could identify total occlusion of the LAD proximal to both the first septal and the first diagonal branch. METHODS: A 12-lead electrocardiogram was recorded on admission in 128 patients with anterior AMI within 12 h from symptom onset. Patients were divided into three groups according to the culprit lesion: 33 patients had total occlusion of the LAD proximal to both the first septal perforator and the first diagonal branch (Group P), in 51 it was proximal to either the first septal perforator or the first diagonal branch (Group D-a), and in 44 it was distal to both the first septal perforator and the first diagonal branch (Group D-b). RESULTS: Sensitivity and specificity of a greater degree of ST-segment depression in lead III than that of ST-segment elevation in lead aVL were 85 and 95%, respectively, which was better than the results derived by all other ECG criteria (p< 0.001). CONCLUSIONS: We conclude that a greater degree of ST-segment depression in lead III than that of ST-segment elevation in lead aVL is a useful predictor of proximal LAD occlusion in patients with anterior AMI.     

Evaluation of the association of proximal coronary culprit artery lesion location with clinical outcomes in acute myocardial infarction

Impaired coronary artery blood flow and left anterior descending (LAD) artery culprit location are angiographic variables that have been associated with poorer outcomes after fibrinolytic administration in patients with acute myocardial infarction (AMI). We hypothesized that culprit lesion location in the proximal portion of the culprit artery would also be associated with poorer clinical outcomes compared with a mid or distal location. Lesion location and clinical outcomes were evaluated in 2,488 patients from the Thrombolysis In Myocardial Infarction (TIMI) 4, 10A, 10B, and 14 trials. Proximal lesions were located before or at the first major branch of the parent artery, mid lesions were between the first and the second major branches, and all other lesions were classified as distal. Proximal lesions were associated with a higher incidence of in-hospital death or recurrent AMI compared with mid or distal lesions (10.5% [n = 478] vs 6.1% [n = 1,498] vs 3.7% [n = 511], p <0.001), and they were associated with a higher rate of in-hospital death (6.7% [n = 478] vs 3.2% [n = 1,498] vs 2.5% [n = 511], p = 0.001). In a multiple logistic regression model adjusting for TIMI flow grade, age, gender, and pulse, the planimetered distance from the ostium to the LAD culprit lesion was associated with 30-day death or recurrent AMI (odds ratio 0.79 per centimeter increase in distance down the artery, p = 0.01). Proximal culprit lesion location is associated with an increased risk of adverse outcomes after fibrinolytic administration, which is likely due to a larger area of subtended myocardium. In patients with a LAD culprit lesion, proximal lesion location is a multivariate correlate of adverse outcomes even after adjustment for coronary blood flow and other covariates.     

Usefulness of the electrocardiogram in predicting the occlusion site in acute anterior myocardial infarction with isolated disease of the left anterior descending coronary artery

INTRODUCTION AND OBJECTIVES: In acute anterior myocardial infarction (AMI), the site of occlusion in the left anterior descending coronary artery (LAD) is related to the extension of myocardial necrosis and the prognosis. The aim of this study was to assess the value of the electrocardiogram (ECG) as a predictor of the LAD occlusion site in patients with anterior AMI. METHODS: Forty-five consecutive patients with a first anterior AMI and isolated disease of the LAD were included. We evaluated retrospectively the ECG with the most pronounced ST-segment changes before fibrinolysis and correlated the findings with the site of LAD occlusion in angiography before hospital discharge in relation to the first dominant septal and first diagonal branch: first septal affected (S), first diagonal affected (D), both affected (S + D), or neither affected were considered. RESULTS: ST depression in leads II, III, or aVF strongly predicted proximal LAD occlusion in S + D, S, and D (p = 0,003, p = 0,04, and p = 0,02, respectively). ST elevation in leads II, III, or aVF was observed only in the presence of wrap-around LAD and was related with occlusion distal to the first diagonal branch. ST elevation > or = 3 mm in lead V1 was a specific predictor of occlusion proximal to first septal (S, p = 0,01). ST elevation in aVR was associated with proximal LAD occlusion in S + D and S (p = 0,03 and p = 0,03, respectively) and absence of coronary collateral circulation. CONCLUSIONS: In anterior AMI and isolated LAD disease, the ECG can be useful in predicting the LAD occlusion site in relation to its major side branches.     

Relationship between coronary artery remodeling and plaque composition in culprit lesions: an intravascular ultrasound radiofrequency analysis.

BACKGROUND: The relationship between coronary artery remodeling and culprit plaque composition in vivo has not been fully evaluated by spectral analysis of intravascular ultrasound (IVUS) radiofrequency (RF) data. METHODS AND RESULTS: IVUS RF analyses were performed for 56 consecutive de novo culprit lesions of 52 patients undergoing percutaneous coronary intervention. Remodeling of culprit lesions was determined using the remodeling index (RI), calculated as the external elastic membrane area of the minimum lumen area (MLA) site divided by that of the proximal reference site. Positive remodeling was defined as RI >1.05, intermediate remodeling as 0.95< or = RI < or =1.05 and negative remodeling as RI <0.95. Among the 56 lesions, positive remodeling was detected in 24, intermediate remodeling in 16, and negative remodeling in 16. At MLA sites, positive remodeling lesions had a larger percentage of the fibrofatty component than negative remodeling lesions (22.5+/-10.3% vs 10.4+/-6.6%, p=0.0001), whereas the latter contained a larger percentage of the dense calcium component than the former (2.8+/-2.9% vs 8.4+/-7.0%, p=0.016). CONCLUSIONS: Culprit plaques with positive remodeling have a large lipid burden, whereas those with negative remodeling contain a large amount of calcium.     

Out-of-hospital ventricular fibrillation in patients with acute myocardial infarction: coronary angiographic determinants

OBJECTIVES: The study intended to compare the acute coronary anatomy of patients with acute myocardial infarction (AMI) complicated by out-of-hospital ventricular fibrillation (VF) versus patients with AMI without this complication. BACKGROUND: More than half of the deaths associated with AMI occur out of the hospital and within 1 h of symptom onset. The angiographic determinants of out-of-hospital VF in patients with AMI have not been investigated in detail. METHODS: Acute coronary angiographic findings of 72 consecutive patients with AMI complicated by out-of-hospital VF were compared with findings from 144 matched patients with AMI without this complication. RESULTS: Patients with an acute occlusion of the left anterior descending coronary artery (LAD) or left circumflex coronary artery (LCx) had a higher risk for out-of-hospital VF compared with patients with an acute occlusion of the right coronary artery (RCA) (odds ratio and 95% confidence interval, respectively, 4.82 [2.35 to 9.92] and 4.92 [2.34 to 10.39]). With regard to extent of coronary artery disease (CAD), the location of the culprit lesion in the coronary arteries (proximal vs. mid or distal), the flow in the infarct related artery (IRA), the presence or absence of collaterals to the IRA and chronic occlusions, there were no differences between the two groups. CONCLUSIONS: Acute myocardial infarction due to occlusion in the left coronary artery (LCA) is associated with greater risk for out-of-hospital VF compared to the RCA. The location of occlusion within LCA (LAD, LCx, proximal or distal), amount of myocardium at risk for necrosis and extent of CAD are not related to out-of-hospital VF.     

Angiographic morphology impacts outcomes in STEMI patients with LAD occlusion

Objectives and background: Acute proximal occlusion of the left anterior descendent coronary artery (LAD) is a critical medical condition often leading to heart failure and death. Our objective was to investigate how additional angiographic findings might influence prognosis. Methods: In a single center setting by using consecutive data from the Swedish angiography and angioplasty registry (SCAAR), we identified all patients with acute myocardial infarction (AMI) related to the proximal LAD referred for primary coronary angioplasty. Clinical and angiographic data were collected from January 2004 to December 2008. Results: In the study period, 359 patients (mean age 67.9 ± 12.3 years, 111 women) were identified as having proximal LAD‐related culprit lesion. Follow‐up was up to 5.5 years. Compared to patients with LAD occlusion only, having both a small conus branch (<0.5 mm in diameter) and an occluded first septal perforator was associated with increased risk of death after adjustment for age, diabetes mellitus and prior AMI (hazard ratio 4.5, 95% CI; 1.1–18, P = 0.033). A small conus branch in itself was not important. Multivessel coronary artery disease in addition to occlusion of the first septal perforator branch and having a small conus branch was also associated with increased risk of death (hazard ratio 5.2, 95% CI; 1.3–20), P = 0.018). Conclusions: In patients with STEMI because of a proximal LAD lesion treated by primary PCI, the combination of a small conus branch and an occluded first septal perforator branch is associated with a poorer outcome. Additional presence of multivessel coronary artery disease further aggravates outcome. © 2010 Wiley‐Liss, Inc.     

Primary percutaneous coronary intervention and intravascular ultrasound imaging for coronary thrombosis after cisplatin-based chemotherapy

Although cisplatin is indispensable for the chemotherapy treatment of many malignancies, cisplatin-associated thrombosis is attracting increasing attention. However, experience of primary percutaneous coronary intervention (PCI) and intravascular ultrasound imaging (IVUS) for coronary thrombosis, possibly due to cisplatin-based chemotherapy, has been limited. Case 1 with postoperative gastric cancer developed acute myocardial infarction (AMI) on the sixth day of the second chemotherapy course with conventional doses of cisplatin and tegafur gimeracil oteracil potassium. Emergency coronary angiography (CAG) showed a filling defect in the proximal left anterior descending coronary artery (LAD) concomitant with no reflow in the distal LAD. Case 2 with advanced lung cancer and brain metastasis suffered AMI on the fifth day of the first chemotherapy course with conventional doses of cisplatin and gemcitabine. Emergency CAG delineated a total occlusion in the proximal right coronary artery. In both cases, thrombectomy using aspiration catheter alone obtained optimal angiographic results and subsequent IVUS revealed no definite atherosclerotic plaque, while slow flow still remained even after selective intra-coronary infusion of vasodilator in the case 1. These cases suggest that primary PCI using thrombus-aspiration catheter might be safe and effective for coronary thrombosis due to cisplatin-based chemotherapy.     

Intravascular ultrasound assessment of remodelling and reference segment plaque burden in type-2 diabetic patients.

AIMS: Intravascular ultrasound (IVUS) assesses arterial remodelling by comparing the lesion external elastic membrane (EEM) with the reference segments; however, reference segments are rarely disease-free. The aim was to assess lesion and reference segment remodelling and plaque burden in patients with type-2 diabetes mellitus. METHODS AND RESULTS: We used pre-intervention IVUS to study 62 de novo lesions in 43 patients with type-2 diabetes mellitus. The lesion site was the image slice with the smallest lumen cross-sectional area (CSA). The proximal and distal reference segments were the most normal-looking segments within 5 mm proximal and distal to the lesion. Plaque burden was measured as plaque CSA/EEM CSA. The remodelling index was defined as lesion EEM CSA/mean reference EEM CSA. Reference segment plaque burden measured 0.54 +/- 0.09. The majority of lesions (83.9%) had negative remodelling (lesion EEM < reference). Similarly, the slope of the regression line relating EEM to plaque CSA within the lesion was less than the reference substantiating negative remodelling. The reference segment plaque burden correlated inversely with the difference between IVUS lumen and quantitative coronary angiographic artery size [slope = -0.12 (95% CI -0.17 to -0.07); P < 0.001] in all patients with type-2 diabetes mellitus. CONCLUSION: Lesions in type-2 diabetic patients are different from previous reports in non-diabetics. Lesions in type-2 diabetics are characterized by a large reference segment plaque burden and negative lesion site remodelling. These IVUS findings may explain the angiographic appearance of small arteries in diabetic patients.     

Primary percutaneous coronary intervention for acute myocardial infarction due to possible sequelae of Kawasaki disease in young adults: a case series

Experience of primary percutaneous coronary intervention (PCI) for young adults with acute myocardial infarction (AMI) due to sequelae of Kawasaki disease (KD) has been extremely limited. In the present report on three young adults (two males and one female; age 20-35 years) with AMI, we performed primary PCI and intravascular ultrasound imaging (IVUS). Case 1 underwent thrombectomy alone in the proximal left circumflex coronary artery, and subsequent IVUS depicted a large aneurysm with an asymmetrically intimal thickening and a residual thrombus in the culprit. Case 2 underwent balloon dilation with adjunctive intracoronary thrombolysis in the proximal left anterior descending coronary artery (LAD), and IVUS during follow-up coronary angiography (CAG) delineated a regressed giant aneurysm with a markedly intimal thickening in the culprit. Case 3, with past history highly suggesting KD, underwent balloon dilation in the proximal LAD, and follow-up CAG as well as IVUS revealed a neoaneurysmal formation in the culprit. In all of the patients, PCI was angiographically effective at the acute phase without complication. Follow-up CAG performed 3-6 months after the procedure revealed no restenosis in all three cases, but a new coronary aneurysm still remained in case 3. Although case 1 and case 2 had no obvious history of KD, the vessel wall morphology from IVUS closely resembled the coronary sequelae after KD, suggesting that they might have antecedent incomplete KD. These cases suggest that primary PCI against coronary sequelae of KD in young AMI patients might be safe and effective in the short term.     

Comparison of virtual histology to intravascular ultrasound of culprit coronary lesions in acute coronary syndrome and target coronary lesions in stable angina pectoris

Coronary plaque composition cannot be assessed accurately using gray-scale intravascular ultrasound (IVUS). Using virtual histology IVUS (VH-IVUS), a comparison of coronary plaque composition between acute coronary syndromes (ACS) and stable angina pectoris (SAP) was performed. Preintervention IVUS of de novo culprit and target lesions was performed in 318 patients (123 with ACS and 195 with SAP). Using VH-IVUS, plaque was characterized as fibrotic, fibrofatty, dense calcium, and necrotic core. VH-IVUS-derived thin-cap fibroatheroma (VH-TCFA) was defined as necrotic core>or=10% of plaque area without overlying fibrous tissue in a plaque burden>or=40%. Lesions were classified into 3 groups: ruptured, VH-TCFA, and non-VH-TCFA plaque. Unstable lesions were defined as either VH-TCFA or ruptured plaque. Compared with patients with SAP, those with ACS had significantly more unstable lesions (89% vs 62%, p<0.001). Planar VH-IVUS analysis at the minimum luminal site and at the largest necrotic core site and volumetric analysis over a 10-mm-long segment centered at the minimum luminal site showed that the percentage of necrotic core was significantly greater and that the percentage of fibrofatty plaque was significantly smaller in patients with ACS. The percentages of fibrotic and fibrofatty plaque areas and volumes were smaller, and the percentages of necrotic core areas and volumes were larger in VH-TCFAs compared with non-TCFAs. Ruptured plaques in VH-IVUS analyses showed intermediate findings between VH-TCFAs and non-VH-TCFAs. In conclusion, culprit lesions in patients with ACS were more unstable and had greater amounts of necrotic core and smaller amounts of fibrofatty plaque compared with target lesions in patients with SAP.     

A case report of late coronary stent thrombosis manifested as acute myocardial infarction 19 months after stenting

A 63-year-old Japanese man was readmitted to our hospital due to acute broad-anterior myocardial infarction (AMI). The proximal left anterior descending artery (LAD) at the prior stent, which was implanted 19 months earlier and in which no angiographic restenosis was recognized 13 months before the second study, was totally occluded. After crossing a guide wire and balloon angioplasty, angiographic radiolucency was observed at the prior stent, suggesting that AMI was induced by late coronary stent thrombosis. Intravascular ultrasound performed 19 days after the onset of AMI revealed superficial calcification without significant stenosis and an atherosclerotic plaque distal to the stent that was not significantly changed compared to 19 months previously, consistent with the culprit lesion being an intrastent site. AMI may thus be induced by late coronary stent thrombosis during long-term clinical follow-up without clinical symptoms or angiographic restenosis at the second study.     

aVR导联对前壁心肌梗死相关血管定位的作用

目的通过与冠状动脉造影（CAG）对比，研究aVR导联ST段改变的特征。对急性前壁心肌梗死（AAMI）的梗死相关动脉（IRA）阻塞部位的定位。方法对比89例急性前壁心肌梗死病人．其中左前降支近段（PS）闭塞43例、左前降支远段（DS）闭塞46例，胸痛发作12h内的心电图。结果两组胸导联的ST段抬高无明显差异，PS组aVR导联ST段抬高较明显（0．94±0．48mmvs0．30±0．56mm．p=0．021）：PS组Ⅱ、Ⅲ、aVF导联ST段压低较显著（分别为-1．21±0．72mm vs S-0．64±0．53mm。p=0．010；-1．63±0．92mmvs-0．98＋0．39mm．／9=0．016；-1．40±0．66mm vs -0．85±0．32mm，／9=0．000）。在胸导联ST段抬高的同时．aVR导联ST段抬高预测左前降支（LAD）近段闭塞的敏感性（Se）、特异性（Sp）、符合率（CR）、阳性预测值（PPV）、阴性预测值（NPV）分别为60．47％、93．48％、77．53％、89．66％、71．67％。结论在胸导联ST段抬高的同时合并aVR导联ST段抬高和／或下壁导联的ST段压低，可预测左前降支近段闭塞。     

Inflammatory and vasoactive factors in the aspirate from the culprit coronary artery of patients with acute myocardial infarction

BACKGROUND: Besides distal embolization of thrombus and plaque debris, locally increased inflammatory markers at the site of ruptured plaque in acute myocardial infarction (AMI) are thought to have an adverse impact on myocardial reperfusion during primary percutaneous coronary intervention (PCI). However, there is lack of data on such factors. Therefore, we investigated the presence of locally increased inflammatory and vasoactive factors in culprit coronary artery. METHODS: We performed primary PCI with PercuSurge GuideWire system in 18 AMI patients. We collected blood samples from the femoral artery before PCI and from culprit coronary artery after first predilation while inflating the distal protection balloon and after completing PCI. We determined concentrations of C-reactive protein, soluble CD40 ligand, Interleukin (IL-6), serotonin, tissue factor, and factor VIIa. RESULTS: While the concentrations of soluble CD40 ligand (2.84+/-3.74 vs 0.98+/-0.63 ng/mL, p=0.004), IL-6 (33.67+/-32.63 vs 17.08+/-21.41 pg/mL, p<0.001), serotonin (2.05+/-0.76 vs 0.92+/-0.60 ng/mL, p<0.001), tissue factor (257.17+/-84.34 vs 154.60+/-87.99 pg/mL, p<0.001) and factor VIIa (34.30+/-27.30 vs 24.19+/-28.00 ng/mL, p=0.016) were significantly higher in the culprit coronary artery than in the femoral artery, CRP levels did not differ. The locally elevated concentrations of various factors were successfully reduced after multiple aspirations of blood using the PercuSurge GuideWire system. CONCLUSIONS: We found increased levels of soluble CD40 ligand, IL-6, serotonin, tissue factor and factor VII in the culprit coronary artery compared to those in peripheral blood. The clinical impact of such locally increased soluble factors in the culprit coronary artery needs to be investigated in further studies.     

Relationship between longitudinal morphology of ruptured plaques and TIMI flow grade in acute coronary syndrome: a three-dimensional intravascular ultrasound imaging study.

AIMS: In this study, we investigated the relationship between longitudinal morphology reconstructed from pre-intervention intravascular ultrasound (IVUS) images and thrombolysis in myocardial infarction (TIMI) flow grade at initial angiograms in the acute phase of acute coronary syndrome (ACS). METHODS AND RESULTS: Our patient population comprised 72 ACS patients in whom we obtained successful reconstructed longitudinal images. On the basis of the site of the maximum aperture of rupture in the longitudinally reconstructed IVUS images, patients were divided into three groups: plaques with rupture in the proximal shoulder (proximal type; n = 28), mid-portion (mid-type; n = 18), and distal shoulder (distal type; n = 26) of the plaque. There were no differences in terms of coronary risk factors or the angiographic findings. The proximal-type group more frequently showed TIMI 0 on initial angiogram (proximal type, 86%; mid-type, 50%; and distal type, 31%; P = 0.002). A multivariable logistic regression model revealed that the presence of a proximal-type rupture correlated with the presentation of ST-elevation myocardial infarction (P = 0.019; odds ratio, 8.12; 95% CI, 1.404-49.996). CONCLUSIONS: Longitudinal morphological features in a ruptured plaque may affect the formation of obstructive thrombus in ACS. Our results suggest that longitudinal morphology may be an important determinant of coronary artery occlusion.