Culprit Site Research Articles

Front cover: 2D‐DIGE‐based proteomic analysis of intracoronary versus peripheral arterial blood platelets from acute myocardial infarction patients: Upregulation of platelet activation biomarkers at the culprit site

Front cover: 2D‐DIGE‐based proteomic analysis of intracoronary versus peripheral arterial blood platelets from acute myocardial infarction patients: Upregulation of platelet activation biomarkers at the culprit site

Abstract 13930: Culprit Lesion in Patients With ST-elevation Myocardial Infarction is Severely Narrowed With Large Plaque Burden: A Combined Intravascular Ultrasound and Optical Coherence Tomography Study

Background: There have been controversies on the degree of stenosis of the culprit lesion in patients with ST-elevation myocardial infarction (STEMI). In the past it was thought the culprit lesion for STEMI had only mild to moderate stenosis. However, recent studies suggested that in fact the degree of the luminal narrowing might be severe at the culprit site. Aim: The aim of the current study was to investigate the severity and the detailed morphologic characteristics of the culprit lesion in patients with STEMI using intravascular ultrasound (IVUS) and optical coherence tomography (OCT). Methods and Results: A total of 111 STEMI patients (67.8±11.2 years, 89 male) who underwent percutaneous coronary intervention within 12 hours from symptom onset were included. TIMI flow grade 2 or 3 was achieved in 108 (97%) patients after thrombectomy. Both OCT and IVUS were performed. Minimum lumen cross-sectional area (MLA) and plaque burden (PB) were 3.14±1.45 mm 2 and 83.0±7.24% by IVUS. Patients were divided into 2 groups on the basis of MLA by IVUS: Group A (MLA <4 mm 2 , n=104) and Group B (MLA >4 mm 2 , n=7). Group A had a higher incidence of PB >70% compared to Group B (99.0% vs 28.6%, p<0.001). OCT revealed that lipid plaque, microchannel and macrophage were more frequent in Group A than in Group B. The incidence of plaque rupture tended to be higher in Group A than in Group B (Figure). Conclusions: Among STEMI patients, more than 90% of culprit lesions have a small MLA (<4.0 mm 2 ) with large plaque burden. Severely narrowed culprit lesion had more features of vulnerability.

Abstract 16001: Relationship Between Serum n-3 to n-6 Poly-unsaturated Fatty Acid Ratios and Coronary Plaque Components Identified by iMap-Intravascular Ultrasound in Patients With Stable Angina Pectoris

Background: Residual risk of cardiovascular disease exists even in patients achieving low-density lipoprotein cholesterol (LDL-C) goals. A low value of serum eicosapentaenoic acid to arachidonic acid (EPA/AA) ratio is well known to be associated with cardiovascular events. However, the association between serum EPA/AA ratio and coronary plaque components has not been fully investigated. Purpose: We evaluated the relationships between serum EPA/AA ratio and coronary plaque morphology on iMap-intravascular ultrasound (IVUS) which is a 40 MHz IVUS tissue characteristic system. Methods: We investigated 80 consecutive coronary culprit lesions with stable angina pectoris (SAP) patients, who underwent pre-intervention iMap-IVUS. All patients were divided into two groups; groups with higher values of the median EPA/AA ratio and lower values of the median EPA/AA ratio. We assessed the relationship between the two groups. Results: Median values of EPA, AA and EPA/AA ratio were 67.5 (44.3-100.3) μg/ml, 174.2 (145.5-202.9) μg/ml, and 0.38 (0.23-0.60). Patients in lower EPA/AA ratio group (<0.38) showed younger age (65±11 vs 70±6, p=0.02), more OMI patients (40 vs 18%, p=0.03), higher value of LDL-C (94.5±29.3 vs 80.9±26.5 mg/dl, p=0.03), lower ejection fraction (61.4±8.8 vs 65.4±7.2%, p=0.04), greater lesion plaque area (11.5±4.4 vs 9.6±4.4 mm2, p<0.05), compared with higher EPA/AA ratio group. In multivariate analysis, LDL-C value was an independent predictor of lower EPA/AA ratio (odds ratio 1.02, 95% confidence interval 1.00-1.04, p= 0.04). In lower LDL-C group (<70 mg/dl), EPA/AA inversely correlated with %-necrotic area and volume (r=-0.56, p=0.004, and r=-0.54, p=0.01), and positively correlated with %-fibrotic area and volume (r=0.57, p=0.003, and r=0.54, p=0.01), although EPA/AA ratio did not correlate with plaque components in higher LDL-C groups. In lower LDL-C group, for prediction of the highest %-necrotic volume tertile (>42.1%), cut-off value of EPA/AA ratio was 0.20 (sensitivity 50%, specificity 94%, area under the curve 0.77, p=0.02). Conclusion: serum EPA/AA ratio may be related to plaque components at the culprit site in SAP patients with low LDL-C values.

Abstract 12944: Patients With Acute Coronary Syndrome, Compared to Those With Stable Angina Pectoris, Have Increased Bright Spots at the Culprit Site by Optical Coherence Tomography

Background: Recent studies reported that bright spots detected by optical coherence tomography (OCT) represent more complex plaques including macrophages and cholesterol crystals. We hypothesized that the density and area of bright spots would be greater at the culprit lesion in patients with acute coronary syndrome (ACS) compared to those with stable angina pectoris (SAP). Aim: To compare the density and extent of bright spots in the culprit lesion between patients with ACS and with SAP. Methods: We identified 14 ACS and 17 SAP patients who underwent pre-PCI OCT imaging of the culprit lesion. Cases with poor image quality or left main disease were excluded. Bright spots within superficial 125μm of the vessel wall were identified in a 5mm length segment at the culprit site. The density was calculated as the number of bright pixels identified by the algorithm divided by the number of pixels in each frame (total 25 frames in one case). The area of bright spots was also calculated. Results: There were no significant differences in the baseline characteristics including mean age (65.9 ± 10.2 vs 65.2 ± 9.32 yrs, P=0.83) and the prevalence of coronary risk factors between ACS and SAP. Mean and maximum density of bright spots was significantly greater in ACS than in SAP (Table). The area of bright spots was also significantly larger in ACS. Among ACS patients, a subgroup with plaque rupture (n=11) had much greater mean density and area compared with SAP (1.20 [0.41-1.73] vs 0.44 [0.21-0.58], P=0.01, 5.32 [1.88-8.07] vs 2.06 [0.97-2.64], P=0.01). Conclusions: Using the novel algorithm, we demonstrate that the density and area of bright spots are significantly greater in ACS than in SAP. This result suggests that the measurement of bright spots can be useful to determine plaque vulnerability.

Abstract 15573: Impact of Coronary Calcification on Different Culprit Lesion Morphology in Acute Coronary Syndrome

Background: Previous studies have reported plaque rupture and erosion were the most common causes of acute coronary syndrome (ACS) and spotty calcifications was identified as a marker of plaque rupture. Optical coherence tomography (OCT) offers a high-resolution imaging to assess the plaque morphology and coronary calcification. Purpose: The aim of this study was to evaluate the relationship between the distribution of coronary calcification and the culprit lesion morphology in patients with ACS. Methods: We enrolled consecutive 183 patients with ACS (mean age: 68 ± 11 years, 148 males). Culprit lesion was assessed by OCT and patients were divided into the rupture and non-rupture group according to the OCT findings. Maximum radial thickness, cross-sectional area of calcification and radial depth from the lumen and longitudinal length of calcification were compared between 2 groups. Results: Plaque rupture was detected at culprit site in 105 patients and coronary calcification was identified in 58 patients. There were no significant differences in age and gender between 2 groups. Maximum thickness, area and longitudinal length of calcification were smaller in rupture group (457.4 ± 284.9 μm vs. 722.1 ± 384.1 μm, p < 0.01, 0.7 ± 0.4 mm 2 vs. 1.8 ± 1.4 mm 2 , p < 0.01, 2.2 ± 1.1 mm vs. 5.6 ± 5.3 mm, p[[Unsupported Character - Codename ­]] < 0.01, respectively). Radial depth of calcification from the lumen was significantly geater in rupture group (150.0 ± 65.3 μm vs. 83.1 ± 63.3 μm, p<0.001). Conclusions: Distribution of coronary calcification could be associated with morphological etiology of ACS.

Abstract 13746: Relationships between Neointimal Tissue Characteristics and Occurrence of Periprocedural Myocardial Infarction in Lesions with In-Stent Restenosis

Background: Recent studies have reported several types of neointimal tissues including neoatherosclerotic progression in stent restenosis. However, the influence of neointimal tissue characteristics on outcomes after percutaneous coronary intervention (PCI) for in-stent restenosis (ISR) remains unclear. Periprocedural myocardial infarction (PMI) is related to poor outcomes after PCI. We assessed relationships neointimal tissue characteristics and occurrence of PMI after PCI in ISR lesions. Methods: We investigated 45 ISR lesions in 45 stable angina pectoris (SAP) patients who underwent pre- and post-PCI coronary angioscopy (CAS) and optical coherence tomography (OCT) examination. We excluded patients with hemodialysis. All lesions were divided into lesions with PMI, defined as high-sensitivity cardiac troponin-T (hs-cTnT) values after PCI ≥5 times of the upper reference limit in patients with normal baseline values or ≥5 times of baseline values if hs-cTnT values were elevated before PCI, and those without. Clinical and lesion characteristics including intrastent neointimal tissues were compared between two groups. Results: PMI was observed in 15 (33.3%) lesions. Clinical characteristics including stent types and terms after stenting were similar between lesions with and without PMI. CAS analysis showed higher frequency of white neointimal proliferation with irregular surface or yellow neointima at the culprit site before PCI (86.7% vs. 43.3%, p=0.009) and atheromatous appearance (CAS-AP), defined as yellow plaque including complex thrombi underneath disrupted neointimal coverage after ballooning (66.7% vs. 16.7%, p=0.003) in lesions with PMI than those without. OCT analysis demonstrated higher frequency of heterogeneous neointima or neointimal thin-cap fibroatheroma in lesions with PMI (73.3% vs. 33.3%, p=0.02). Multivariate analysis including clinical and lesion characteristics and procedural results showed CAS-AP as an independent predictor for occurrence of PMI (odds ratio:6.90, 95% CI:1.68-28.41, p=0.008). Conclusions: In ISR lesions with SAP patients, the assessment of neointimal tissue characteristics by using CAS and OCT images may be useful for the prediction of occurrence of PMI.

Coronary liposuction during percutaneous coronary intervention: evidence by near-infrared spectroscopy that aspiration reduces culprit lesion lipid content prior to stent placement.

Intracoronary near-infrared spectroscopy (NIRS) in ST-segment elevation myocardial infarction (STEMI) has demonstrated substantial lipid in STEMI culprit plaques. Thrombus aspiration during primary PCI reduces distal embolization and improves reperfusion. This study was performed to examine if aspiration thrombectomy reduces the lipid content of acute coronary syndrome (ACS) culprit plaques. NIRS-IVUS imaging was performed in patients with an ACS at two hospitals in the US and Sweden. After establishment of TIMI 3 flow with an undersized balloon, NIRS was performed, followed by aspiration thrombectomy, followed by repeated NIRS. The same culprit segment was identified on the post-aspiration chemogram. The culprit lipid content was quantified before and after thrombectomy as the lipid core burden index (LCBI). Aspirates were examined by histological staining for lipids, calcium, and macrophages. In 18 ACS patients (age 65 ± 11, 61% male), culprit lesions were characterized by high lipid content prior to aspiration thrombectomy. Thrombectomy resulted in a 28% reduction in culprit lesion lipid content (pre-aspiration LCBI 466 ± 141 vs. post-aspiration 335 ± 117, P = 0.0001). In addition to thrombus, histological analysis of aspirates demonstrated the presence of lipids, calcium, and macrophages, indicating that fragments of atherosclerotic plaques had been aspirated. Thrombectomy aspirates both thrombus and lipid-rich fragments of the culprit atherosclerotic plaques, thereby reducing material that may embolize during stenting. Reduction of lipid content before stenting might contribute to the beneficial effects of thrombectomy and may be particularly useful if a large lipid core is present at the culprit site.

Influence of Second- and Third-Degree Heart Block on 30-Day Outcome Following Acute Myocardial Infarction in the Drug-Eluting Stent Era

This study was conducted to investigate the prognostic value of heart block among patients with acute myocardial infarction (AMI) treated with drug-eluting stents. A total of 13,862 patients with AMI, registered in the nation-wide AMI database from January 2005 to June 2013, were analyzed. Second- (Mobitz type I or II) and third-degree atrioventricular block were considered as heart block in this study. Thirty-day major adverse cardiac events (MACE) including all causes of death, recurrent myocardial infarction, and revascularization were evaluated. Percutaneous coronary intervention with implantation of drug-eluting stent was performed in 89.8% of the patients. Heart block occurred in 378 patients (2.7%). Thirty-day MACE occurred in 1,144 patients (8.2%). Patients with heart block showed worse clinical parameters at initial admission, and the presence of heart block was associated with 30-day MACE in univariate analyses. However, the prognostic impact of heart block was not significant after adjustment of potential confounders (p = 0.489). Among patients with heart block, patients with a culprit in the left anterior descending (LAD) coronary artery had worse clinical outcomes than those of patients with a culprit in the left circumflex or right coronary artery. LAD culprit was a significant risk factor for 30-day MACE even after controlling for confounders (odds ratio 5.28, 95% confidence interval 1.22 to 22.81, p = 0.026). In conclusion, despite differences in clinical parameters at the initial admission, heart block was not an independent risk factor for 30-day MACE in adjusted analyses. However, a LAD culprit was an independent risk factor for 30-day MACE among patients with heart block.

Prognostic value of culprit site neutrophils in acute coronary syndrome

Recent data suggest that acute coronary syndromes (ACS) and acute myocardial infarction (AMI) are characterized by an inflammatory subset of thrombosis. We have previously described the accumulation of neutrophils at the coronary culprit lesion site. In this work, we assessed the prognostic value of culprit site (CS) neutrophil accumulation on long-term mortality in patients with AMI. In this prospective study, 417 AMI patients were enrolled after thrombectomy during primary percutaneous coronary intervention. The optimal cut-off for CS neutrophil accumulation for predicting 4-year all-cause mortality was calculated using time-dependent receiver operator characteristic curve analyses. The median follow-up time was 39months interquartile range (IQR 21·4-54·6months) corresponding to 1217 patient years of follow-up. The cut-off for CS neutrophil accumulation (difference between culprit neutrophil counts and systemic neutrophil counts) was 0·25 Giga/l. CS neutrophil accumulation occurred in 195 patients (47%) and was independently associated with mortality (hazard ratio 1·88 (95%CI 1·02-3·41, P=0·043)). In patients with CS neutrophil accumulation, 1-year mortality (10·8% vs. 7·2%) and 4-year mortality (19·8% vs. 10·4%) were markedly increased compared with patients without local neutrophil accumulation. Concordance index for CS neutrophil accumulation and mortality was 0·64 (95% CI 0·51-0·77; P=0·035). Patients with CS neutrophil accumulation had significantly more often nonobstructive lesions compared with patients without neutrophil accumulation (32·6% vs. 22·4%; P=0·024). Neutrophil accumulation at the coronary culprit lesion site is a strong and independent predictor of mortality in patients with ACS/AMI.

Local Intracoronary Eptifibatide versus Mechanical Aspiration in Patients with Acute ST-Elevation Myocardial Infarction.

Objectives. We compared local delivery of intracoronary eptifibatide via perfusion catheter to thrombus aspiration in primary PCI. Background. Perfusion catheter increases local concentration of the drugs at the culprit site and prolongs their residency time. Methods. 75 patients with acute STEMI were randomized to three groups: 25 received local intracoronary eptifibatide and verapamil via perfusion catheter; 25 patients were managed by Diver CE thrombectomy device and 25 patients by primary PCI without thrombus aspiration. Primary end point was assessment of postprocedural TIMI flow, MPG, and corrected TIMI frame count (cTFC) in the culprit vessel. Results. Perfusion catheter was superior to thrombus aspiration and conventional PCI as regards MBG (68% versus 36% in Diver CE and 20% in the control arm; P value = 0.002), with shorter cTFC rates than thrombectomy and control groups (20.76 ± 4.44 versus 26.68 ± 8.40 and 28.16 ± 5.96, resp.; P = 0.001). TIMI flow was not different between the 3 groups. Eptifibatide led to less time to peak CK (13.12 hours versus 16.5 and 19.5 hours, respectively, P value = 0.001). Conclusion. Local intracoronary eptifibatide by perfusion catheter reduces thrombus burden with better results in microvascular perfusion assessed by cTFC and MBG compared to aspiration device or conventional PCI.

Impact of glucose fluctuation and monocyte subsets on coronary plaque rupture

Background and aimsIt remains unclear whether glycemic fluctuation can affect plaque rupture in acute myocardial infarction (AMI). Here we investigate the impact of glucose fluctuation on plaque rupture, as observed by optical coherence tomography (OCT), and monocyte subsets in patients with AMI. Methods and resultsWe studied 37 consecutive patients with AMI. All patients underwent OCT examination, which revealed 24 patients with plaque rupture and 13 patients without plaque rupture at the culprit site. Peripheral blood sampling was performed on admission. Three monocyte subsets (CD14+CD16−, CD14brightCD16+, and CD14dimCD16+) were assessed by flow cytometry. Glycemic variability, expressed as the mean amplitude of glycemic excursion (MAGE), was determined by a continuous glucose monitoring system 7 days after the onset of AMI. MAGE was significantly higher in the rupture patients than in the non-rupture patients (P=0.036). Levels of CD14brightCD16+ monocytes from the rupture patients were significantly higher than those from the non-rupture patients (P=0.042). Of interest, levels of CD14brightCD16+ monocytes correlated positively and significantly with MAGE (r=0.39, P=0.02). ConclusionDynamic glucose fluctuation may be associated with coronary plaque rupture, possibly through the preferential increase in CD14brightCD16+ monocyte levels.

Manifestations of coronary arterial injury during catheter ablation of atrial fibrillation and related arrhythmias

The prevalence and clinical consequences of coronary arterial injury in a large series of patients undergoing radiofrequency ablation (RFA) of atrial fibrillation (AF) are unknown. The purpose of this study was to describe the frequency and clinical consequences of coronary arterial injury in a large series of patients undergoing catheter ablation of AF and postablation atrial tachycardia. The medical records of 5,709 consecutive patients undergoing RFA of AF were reviewed. Heart specimens were also dissected to analyze the course of the coronary arteries. Arterial injury occurred in 8 patients (0.14%). Three patients developed ventricular fibrillation (VF) due to occlusion of the distal or proximal circumflex (Cx) artery related to RFA in the distal coronary sinus (CS) or base of the LA appendage, respectively. Two VF patients underwent stenting. Five patients developed acute sinus node (SN) dysfunction. In 4/5 patients, the culprit site was subjacent to the SN artery (per computed tomography) coursing over the anterior LA (n = 3) or the septal RA (n = 1). Two patients required a permanent pacemaker. In the heart specimens, the SN artery, after its origin from the proximal Cx artery, coursed along the anterior LA. Also, the proximal Cx artery was found in the atrioventricular groove underneath the base of the LA appendage. Clinically apparent injury to the coronary arteries during LA ablation for AF is rare. However, it may be associated with potentially life-threatening ventricular arrhythmias and acute SN dysfunction requiring permanent pacing. The culprit sites seem to be in the distal coronary sinus and the anterior LA, and correlate well with the course of the coronary arteries in pathologic specimens. Vigilance and low-power settings are important in minimizing the risk of arterial injury.

Impact of glucose fluctuation and monocyte subsets on coronary plaque rupture

Background: It remains unclear whether glycemic fluctuation can affect plaque rupture in acute myocardial infarction (AMI). Here we investigate the impact of glucose fluctuation on plaque rupture, as observed by optical coherence tomography (OCT), and monocyte subsets in patients with AMI. Methods: We studied 26 consecutive patients with AMI. All patients underwent OCT examination, which revealed 16 patients with plaque rupture and 10 patients without plaque rupture at the culprit site. Peripheral blood sampling was performed on admission. Three monocyte subsets (CD14+CD16-, CD14brightCD16+, and CD14dimCD16+) were assessed by flow cytometry. Glycemic variability, expressed as the mean amplitude of glycemic excursion (MAGE), was determined by a continuous glucose monitoring system 7 days after the onset of AMI. Results: MAGE was significantly higher in the rupture patients than in the non-rupture patients (P=0.01). Levels of CD14brightCD16+ monocytes from the rupture patients were significantly higher than those from the non-rupture patients (P=0.03). Of interest, levels of CD14brightCD16+ monocytes correlated positively and significantly with MAGE (r=0.45, P=0.02). Conclusions: Dynamic glucose fluctuation may be associated with coronary plaque rupture, possibly through the preferential increase in CD14brightCD16+ monocyte levels.

IPhone ECG monitoring — the gateway to the new paradigm of STEMI therapy

iPhone ECG monitoring — the gateway to the new paradigm of STEMI therapy

Angiographic Lesion Severity and Subsequent Myocardial Infarction

We sought to determine the angiographic severity of coronary lesions leading to ST-segment elevation myocardial infarction (STEMI) and non-STEMI (NSTEMI) with a focus on determining the impact of interval from initial angiogram to subsequent clinical event. In the late 1980s angiographic data on lesion characteristics that culminated in STEMI and NSTEMI were obtained from angiograms obtained several months before MI. It is not clear whether the conclusions on lesion severity would be different if elapsed interval from baseline angiogram to clinical event was factored in the analysis. From 2003 through 2010, we identified 84 patients with NSTEMI and 41 patients with STEMI in vessels without previous intervention. These patients had ≥1 previous angiographic study at our center. Angiograms were reanalyzed with quantitative coronary angiography, and relevant clinical data were obtained from medical records. Similar to previous studies, 71% of patients with STEMI and 63% of patients with NSTEMI had <50% baseline stenosis at the culprit site when the interval from initial angiogram to MI was >3 months. Interestingly, lesions that led to STEMI ≤3 months after evaluation were more severe than those leading to STEMI in >3 months (59 ± 31% vs 36 ± 21%, p = 0.02) with 57% of lesions having >50% stenosis. Although most MIs occurred at sites that did not have significant obstruction when examined >3 months before MI, most baseline lesions showed significant luminal narrowing when examined ≤3 months before STEMI. In conclusion, high-grade coronary stenosis may be an important predictor of STEMI in subsequent months.

Proteomic profiling of acute coronary thrombosis reveals a local decrease in pigment epithelium-derived factor in acute myocardial infarction

Thrombotic occlusion of an epicardial coronary artery on the grounds of atherosclerotic plaque is considered the ultimate step in AMI (acute myocardial infarction). However, the precise pathophysiological mechanisms underlying acute coronary occlusion are not fully understood. We have analysed proteomic profiles of systemic plasma and plasma derived from the site of coronary plaque rupture of non-diabetic patients with STEMI (ST-segment elevation myocardial infarction). Label-free quantification of MS/MS (tandem MS) data revealed differential regulation of complement cascade components and a decrease in anti-thrombotic PEDF (pigment epithelium-derived factor) between CS (culprit site)-derived plasma and systemic plasma. PEDF, which is known to have a protective role in atherothrombosis, was relatively decreased at the CS, with a level of expression inverse to local MMP-9 (matrix metalloproteinase-9) activity. CS plasma displayed enhanced proteolytic activity towards PEDF. Proteomics of coronary thrombus aspirates indicate that PEDF processing is associated with coronary plaque rupture.

Differential expression of Toll-like receptor 4 and human monocyte subsets in acute myocardial infarction

ObjectiveTo investigate the involvement of Toll-like receptor 4 (TLR4) expression on two monocyte subsets in the pathologic processes related to acute coronary syndrome. How monocytes, which have recently been shown to comprise two distinct subsets, mediate the process of coronary plaque rupture remains to be fully elucidated. Recent studies have shown that TLR4 is involved in monocyte activation of patients with accelerated forms of atherosclerosis. MethodsWe enrolled 65 patients with acute myocardial infarction (AMI, n=22), unstable angina pectoris (UAP, n=16), and stable angina pectoris (SAP, n=27) who underwent coronary angiography and 15 healthy controls. The expression of TLR4 on two monocyte subsets (CD14+CD16− and CD14+CD16+) was measured by flow cytometry. ResultsIn patients with AMI, TLR4 was more expressed on circulating CD14+CD16+ monocytes than on CD14+CD16− monocytes (p<0.001). The expression levels of TLR4 on CD14+CD16+ monocytes were significantly elevated in patients with AMI compared with other 3 groups. TLR4 expression levels on CD14+CD16+ monocytes were significantly elevated at the culprit site compared with the systemic level (p=0.044). The up-regulation of TLR4 on admission was remarkably decreased 12 days after AMI (p<0.001). In addition, plasma levels of tumor necrosis factor-α were positively correlated with TLR4 expression levels on monocytes in patients with AMI (r=0.47, p=0.027). ConclusionTLR overexpression on CD14+CD16+ monocytes in AMI, as demonstrated both in the circulation and at the coronary culprit site, might be associated with the pathogenesis of AMI.

Abstract 9155: Intravenous Adenosine Reveals Arrhythmogenic Foci in Patients with Atrial Fibrillation Undergoing Radiofrequency Catheter Ablation

Background: Intravenous adenosine often induces atrial fibrillation (AF). However, the role of adenosine in patients with AF undergoing radiofrequency ablation is not determined. We tested the hypothesis that intravenous adenosine reveals culprit site for AF. Method: We included 75 consecutive patients (57 male, 62±10 years) with symptomatic AF undergoing pulmonary vein (PV) isolation for either paroxysmal (N=63) or persistent (N=12) AF in whom PV venography was performed during sinus rhythm. For PV venography, intravenous adenosine triphosphate (ATP) at a dose of 40mg was administered to produce transient asystole. We determined the incidence and origin of ectopic beats emerged after intravenous ATP utilizing simultaneous recording of the left and right superior PVs, left inferior PV, coronary sinus, right atrial free wall, septum and superior vena cava (Figure). For each PV, a straight 10-pole catheter was used to determine the longitudinal activation sequence. Results: Repetitive beats initiating AF (RBAF) or single to triplet of premature beats (SPB) were induced within 1 minute after administration of ATP in 29 patients (39%) and 57 patients (76%), respectively. In 22 patients with RBAF from the PVs, the AF-free rate after 1.3±0.5 sessions of PVI was 86%, whereas that in 7 patients with extra-PV RBAF was 57% (P= 0.15). A total of 111 SPB origin was identified in 57 patients. The origin of 37 SPBs was in the PV, and that of the remaining 74 SPB was outside the PV. The AF-free rate in patients with SPB restricted in the PVs was 88%, and that with extra-PV SPB was 78% (P= 0.52) after PVI. In 9 patients in whom neither RBAF nor SPB was induced by ATP, AF-free rate was 67%. Conclusion: In most patients, RBAF or SPB could be induced by intravenous ATP within 1 minute from the injection, revealing culprit site for AF. Induction of extra-PV RBAF or non-inducibility of either RBAF or SPB correlates with higher incidence of recurrence. However, extra-PV SPB is less significant.

External Side-Compression of Radial Artery: A Simple Technique for Successful Advancement of Guidewires through the Radial Approach

The transradial approach has several pitfalls that include problems regarding the radial puncture and difficulties with the catheter technique. We evaluated whether external side-compression of radial artery was helpful to yield the success rate for advancement of guidewires under the presence of side branches or arterial tortuosity. The study population consisted of 11 patients with unsuccessful advancement of guidewires into the brachial artery. In 7 patients, the J-tip hydrophilic guidewire was not advanced into the brachial artery because it always directed into the side branch. During external side-compression of radial artery at the culprit site with a finger of the second operator, the guidewire was successfully advanced into the brachial artery in all patients. In 4 patients, the guidewire was not advanced into the brachial artery because the radial artery was tortuous. During external side-compression of radial artery at the culprit site, the guidewire was successfully advanced into the brachial artery in 2 patients. In the remaining 2 patients in whom this attempt was unsuccessful, coronary angiography was performed through the right brachial artery. Overall success rate of this technique was 82%. External side-compression of radial artery is an easy and feasible technique for difficulties in the advancement of guidewires due to the presence of side branches or arterial tortuosity.

Prominent precordial T waves as a sign of acute anterior myocardial infarction: electrocardiographic and angiographic correlations

In clinical practice, one occasionally encounters patients with symptoms lasting for relatively long time showing prominent positive T waves combined with minor ST elevation, or ST depression in the precordial leads. This electrocardiographic pattern has been described as Sclarovsky-Birnbaum grade 1 ischemia. We present 3 cases of patients with predominantly grade 1 ischemia, in whom the culprit site was in the left anterior descending coronary artery. The electro/pathophysiologic mechanisms of these electrocardiographic patterns are discussed.