Culprit Coronary Lesion Research Articles

Identifying False-positive ST-elevation Myocardial Infarction in Emergency Department Patients

BackgroundIn a push to treat ST-elevation myocardial infarction (STEMI) patients with primary percutaneous coronary intervention (PCI) within 90min of door-to-balloon time, emergency cardiac catheterization laboratory activation protocols bypass routine clinical assessments, raising the possibility of more frequent catheterizations in patients with no culprit coronary lesion. ObjectiveTo determine the incidence, predictors, and prognosis of false-positive STEMI. MethodsWe followed a prospective cohort of patients diagnosed with STEMI by usual criteria receiving emergency cardiac catheterization with intention of primary PCI between January 2005 and December 2007 at a tertiary care center. False-positive STEMI was defined as absence of a clear culprit lesion on coronary angiography. ResultsOf 489 patients who received emergency cardiac catheterization indicated for STEMI, 54 (11.0%, 95% confidence interval [CI] 8.3–13.8) had no culprit lesion on coronary angiography. Independent predictors of false-positive STEMI were absence of chest pain (odds ratio [OR] 18.2, 95% CI 3.7–90.1), no reciprocal ST-segment changes (OR 11.8, 95% CI 5.14–27.3), fewer than three cardiovascular risk factors (OR 9.79, 95% CI 4.0–23.8), and symptom duration longer than 6h (OR 9.2, 95% CI 3.6–23.7); all p<0.001. Using predictors, we modeled a risk score that achieved 88% (95% CI 81–94%) accuracy in identifying patients with negative coronary angiography. Among the false-positive STEMI patients, 48.1% had other serious diagnoses related to their electrocardiographic findings. ConclusionWhen the diagnosis of STEMI is in doubt, clinicians may use predictors to quickly reassess the likelihood of an alternative diagnosis.

Positive Vascular Remodeling in Culprit Coronary Lesion is Associated With Plaque Composition: An Intravascular Ultrasound-Virtual Histology Study.

Background and ObjectivesThe relationship between the positive remodeling (PR) of a coronary artery and plaque composition has been studied only in a relatively small number of study population or non-culprit lesion. We evaluated the association between coronary plaque composition and coronary artery remodeling in a relatively large number of culprit lesions.Subjects and MethodsThe study population consisted of 325 consecutive patients with coronary artery disease that underwent intravascular ultrasound-virtual histology examination in a culprit lesion. The remodeling index (RI) was calculated as the lesion external elastic membrane (EEM) area divided by the average reference EEM area.ResultsThe lesions with PR (RI>1.05, n=97, mean RI=1.19±0.12) had a higher fibrous volume/lesion length (3.85±2.12 mm3/mm vs. 3.04±1.79 mm3/mm, p=0.003) and necrotic core volume/lesion length (1.26±0.89 mm3/mm vs. 0.90±0.66 mm3/mm, p=0.001) than those with negative remodeling (NR) (RI<0.95, n=132, mean RI=0.82±0.09). At the minimal luminal area site, the lesions with PR had a higher fibrous area (5.81±3.17 mm2 vs. 3.61±2.30 mm2, p<0.001), dense calcified area (0.73±0.69 mm2 vs. 0.46±0.43 mm2, p=0.001), and necrotic core area (1.93±1.33 mm2 vs. 1.06±0.91 mm2, p<0.001) than those with NR. RI showed significant positive correlation with fibrous volume/lesion length (r=0.173, p=0.002), necrotic core volume/lesion length (r=0.188, p=0.001), fibrous area (r=0.347, p<0.001), fibrofatty area (r=0.111, p=0.036), dense calcified area (r=0.239, p<0.001), and necrotic core area (r=0.334, p<0.001). Multivariate analysis showed that the independent factor for PR was the necrotic core volume/lesion length (beta=0.130, 95% confidence interval; 0.002-0.056, p=0.037) over the entire lesion.ConclusionThis study suggests that PR in a culprit lesion is associated with the necrotic core volume in the entire lesion, which is a characteristic of vulnerable plaque.

Clinical value of coronary culprit lesion score determined by 64-slice spiral CT scanning in diagnosing acute coronary syndrome

Clinical value of coronary culprit lesion score determined by 64-slice spiral CT scanning in diagnosing acute coronary syndrome

Comparison of drug-eluting versus bare-metal stents after rotational atherectomy for the treatment of calcified coronary lesions

Calcified coronary lesions are a well-known risk factor for short and long-term failure after both bare metal stent (BMS) [ 1 Tan K. Sulke N. Taub N. Sowton E. Clinical and lesion morphologic determinants of coronary angioplasty success and complications: current experience. J Am Coll Cardiol. 1995; 25: 855-865 Google Scholar , 2 Hoffmann R. Mintz G.S. Popma J.J. et al. Treatment of calcified coronary lesions with Palmaz–Schatz stents. An intravascular ultrasound study. Eur Heart J. 1998; 19: 1224-1231 Google Scholar ] and drug eluting stent (DES) implantation [ 3 Moussa I. Ellis S.G. Jones M. et al. Impact of coronary culprit lesion calcium in patients undergoing paclitaxel-eluting stent implantation (a TAXUS-IV sub study). Am J Cardiol. 2005; 96: 1242-1247 Google Scholar , 4 Berenguer A. Mainar V. Bordes P. Valencia J. Gomez S. Lozano T. Incidence and predictors of restenosis after sirolimus-eluting stent implantation in high-risk patients. Am Heart J. 2005; 150: 536-542 Google Scholar , 5 Migliorini A. Shehu M. Carrabba N. et al. Predictors of outcome after sirolimus-eluting stent implantation for complex in-stent restenosis. Am J Cardiol. 2005; 96: 1110-1112 Google Scholar ]. Rotational atherectomy facilitates the delivery of stents in severely calcified coronary lesions by modifying plaque anatomy and smoothing inner vascular lumen. Recent reports suggest that the use of rotational atherectomy in combination with DES implantation for the treatment of severely calcified lesions might result in high procedural success and acceptable restenosis rate [ 6 Clavijo L.C. Steinberg D.H. Torguson R. et al. Sirolimus-eluting stents and calcified coronary lesions: clinical outcomes of patients treated with and without rotational atherectomy. Catheter Cardiovasc Interv. 2006; 68: 873-878 Google Scholar , 7 Garcia de Lara J. Pinar E. Ramon Gimeno J. et al. Percutaneous coronary intervention in heavily calcified lesions using rotational atherectomy and paclitaxel-eluting stents: outcomes at one year. Rev Esp Cardiol. 2010; 63: 107-110 Google Scholar , 8 Furuichi S. Sangiorgi G.M. Godino C. et al. Rotational atherectomy followed by drug-eluting stent implantation in calcified coronary lesions. EuroIntervention. 2009; 5: 370-374 Google Scholar , 9 Mezilis N. Dardas P. Ninios V. Tsikaderis D. Rotablation in the drug eluting era: immediate and long-term results from a single center experience. J Interv Cardiol. 2010; 23: 249-253 Google Scholar , 10 Benezet J. de la Llera LS Diaz Cubero J.M. Villa M. Fernandez-Quero M. Sanchez-Gonzalez A. Drug-eluting stents following rotational atherectomy for heavily calcified coronary lesions: long-term clinical outcomes. J Invasive Cardiol. 2011; 23: 28-32 Google Scholar ]. However, the long-term efficacy and safety of DES compared to BMS, in combination with rotational atherectomy in patients with calcified coronary lesions is limited.

Abstract 9934: Levels of Plasma Pentraxin 3 Predict Presence of Thin-cap Fibroatheroma in Patients with Stable Angina Pectoris: Assessment by Optical Coherence Tomography

Background: Thin-cap fibroatheroma (TCFA) is the primary type of rupture prone plaque, but biomarkers predicting it are not established. Recently, pentraxin 3 (PTX3) has been shown to be a novel biomarker specific to vascular inflammation. The aim of this study was to clarify the association between plasma PTX3 level and TCFA as determined by optical coherence tomography (OCT) in patients with stable angina pectoris (SAP). Methods: Thirty-four patients with SAP who underwent OCT at de novo culprit lesions before percutaneous coronary intervention were evaluated. TCFA was defined as a plaque with lipid contents in &gt;90°and with thinnest part of the fibrous cap measuring &lt;70μ m. Plasma PTX3 and serum high sensitive C-reactive protein (hsCRP) were measured among these patients. Plasma PTX3 level was categorized into low (&lt; 25th percentile), intermediate (25th to 75th percentiles), and high (&gt; 75th percentile) groups. Results: Fourteen patients with TCFA and 20 patients without TCFA were identified. Levels of PTX3 (median [interquartile range]) were significantly greater in patients with TCFA than without TCFA (4.66 [2.44 - 6.80]) vs. 2.60 [1.79 - 3.18] ng/mL; p = 0.009). Levels of hsCRP were comparable between the two groups. PTX3 level significantly inversely correlated with fibrous cap thickness (r = -0.53, p = 0.009), but hsCRP did not. The frequency of TCFA was 22, 29, and 88% in low, intermediate, and high PTX3 group, respectively (p = 0.009). Univariate analysis revealed that hypercholesterolemia, statin use, and level of PTX3 were related to the presence of TCFA. Multivariate logistic regression analysis in these factors showed that plasma PTX3 level was the significant independent factor associated with TCFA existence (OR, 1.99; 95%CI, 1.10 - 3.58; p = 0.023). The area under the receiver-operating characteristics curve for PTX3 level for prediction of TCFA was 0.766 (p = 0.009). The optimal cut-off value of PTX3 for predicting TCFA was 2.88 ng/mL (sensitivity 71%, specificity 70%). Conclusions: Plasma PTX3 level was associated with the presence of TCFA and thinner fibrous cap thickness at coronary culprit lesions in patients with SAP. These findings suggest that plasma PTX3 might be a useful marker reflecting the plaque vulnerability.

Seizure-associated Takotsubo cardiomyopathy

Takotsubo cardiomyopathy is characterized by chest pain, dyspnea, electrocardiographic changes resembling an acute coronary syndrome, and transient wall-motion abnormalities without identifiable coronary culprit lesion explaining the wall-motion abnormality. Takotsubo cardiomyopathy occurs frequently after emotional or physical stress. Seizures have been reported as triggers of takotsubo cardiomyopathy. It is unknown if seizure-associated takotsubo cardiomyopathy differs from takotsubo cardiomyopathy associated with other triggers. Seizure-associated takotsubo cardiomyopathy cases from the literature were compared with takotsubo cardiomyopathy series comprising 30 or more patients. Thirty-six seizure-associated takotsubo cardiomyopathy cases (6 male, mean-age 61.5 years) were found. Seizure-type were tonic-clonic (n = 13), generalized (n = 5), status epilepticus (n = 6), grand mal (n = 2), or not reported (n = 13). Twelve patients had a history of epilepsy, in 15 patients takotsubo cardiomyopathy-associated seizure was the first or the information was not given (n = 9). In 17 patients takotsubo cardiomyopathy occurred immediately after the seizure, in 9 patients 1-72 h postictally, and in 10 patients, the interval was not reported. In 20 patients neurologic disorders were reported and in 14 psychiatric disorders were reported. There were medical comorbidities in 17 patients, arterial hypertension (n = 11), hyponatremia (n = 2), and cancer (n = 2). Compared with 974 patients reported in takotsubo cardiomyopathy -series, patients with seizure-associated takotsubo cardiomyopathy were younger (61.5 vs. 68.5 years, p < 0.0001), more frequently males (17 vs. 9%, p = 0.004), had less frequent chest pain (6 vs.76%, p < 0.005), more frequent cardiogenic shock (25 vs. 8%, p = 0.003), and more frequent recurrency (14 vs. 3%, p = 0.004). Seizure-associated takotsubo cardiomyopathy manifests frequently as sudden hemodynamic deterioration, which could result in death in the absence of adequate help. Probably some cases of sudden unexpected death in epilepsy are attributable to takotsubo cardiomyopathy.

13 Neutrophil activation at the culprit lesion in acute ST-segment elevation myocardial infarction with multiple complex coronary plaques

<h3>Introduction</h3> The activation of neutrophils at the culprit coronary lesion following acute plaque disruption has not been reported. We hypothesised that neutrophil activation occurs in ST elevation myocardial infarction (STEMI) prior to percutaneous intervention (PCI), and that differences in activation may be detectable locally at the culprit lesion, particularly in patients with multiple complex coronary plaques. <h3>Methods</h3> Forty STEMI patients having primary PCI were compared to 10 controls with chronic stable angina (CSA) undergoing elective PCI. The clinical, demographic and angiographic characteristics of patients and controls are shown in Abstract 13 table 1. The culprit lesion was sampled after passage of a guide wire across the lesion and use of a low profile sampling catheter (Multifunctional probing catheter, Boston Scientific Corporation, Natick, Massachusetts, USA) at the site of occlusion, prior to further mechanical intervention. Neutrophil activation was measured by flow cytometry using neutrophil intracellular myeloperoxidase content (MPO Index) and the expression of the β2- integrin CD11b, a leukocyte adhesion and activation marker at the culprit coronary lesion (CA), the aorta at the coronary ostium (Ao), the coronary sinus (CS), and femoral artery (FA) prior to primary PCI. A lower MPO content indicates the depletion of intracellular MPO and cell activation. <h3>Results</h3> A marked decrease in MPO content occurred at the CA, Ao and FA in STEMI compared to elective controls (p&lt;0.01). Furthermore, MPO content was lower at the CA (−23.1, (−25.6 to −17.1), n=37) compared to Ao (−22.0, (−24.7 to −16.2), n=37), CS (−20.6, (−24.8 to −16.9), n=30) and FA (−20.4, (−24.4 to −13.1), n=40), all p&lt;0.001 (Abstract 13 figure 1). Neutrophil MPO content was correlated with CD11b expression only at the culprit CA in STEMI (r=−0.4, p=0.03, n=31) (Abstract 13 figure 2). Neutrophil MPO content at the CA in patients with multiple complex plaques was similar to those with a single culprit however only in those with multiple complex plaques was a correlation between MPO content and CD11b (r=−0.7, p=0.02) shown. Conclusion: In acute STEMI, neutrophils are activated systemically, regionally and locally at the culprit coronary lesion. In patients with multiple complex plaques, there may be an extended local role for the activated neutrophil following acute plaque destabilisation.

Assessment of Echo-Attenuated Plaque by Optical Coherence Tomography and its Impact on Post-Procedural Creatine Kinase-Myocardial Band Elevation in Elective Stent Implantation

This study examined morphological characteristics of echo-attenuated plaques by optical coherence tomography (OCT) and evaluated their influence on creatine kinase-myocardial band (CK-MB) elevation after percutaneous coronary intervention (PCI) in patients with elective stent implantation. Recent intravascular ultrasound studies have described atherosclerotic plaques with echo attenuation (EA) without associated bright echoes that are correlated with no-reflow phenomenon after PCI. We studied 135 native de novo culprit coronary lesions in 135 patients with normal pre-PCI CK-MB levels (28 with unstable angina; 107 with stable angina) who underwent intravascular ultrasound and OCT examinations before elective stent implantation. The lesions were divided into 2 groups based on the presence or absence of EA, and OCT findings were compared. We then determined predictors of post-PCI CK-MB elevation. EA was found in 47 (34.8%) lesions and was associated with the presence of OCT-derived thin-capped fibroatheroma, ruptured plaques, greater lipid content, intravascular ultrasound-derived large reference and plaque area, lesion eccentricity, and microcalcification. Elevated CK-MB levels were observed in 36 (26.7%) lesions, and significantly more frequently in lesions with EA than without. In multivariable analysis, EA (odds ratio [OR]: 3.49; 95% confidence interval [CI]: 1.53 to 7.93; p = 0.003) and OCT-derived ruptured plaque (OR: 2.92; 95% CI: 1.21 to 7.06; p = 0.017) were independent predictors of post-PCI CK-MB elevation. Atherosclerotic plaques with EA were associated with characteristics considered to be high risk or unstable. OCT examination showed an additive predictive value to the presence of EA for post-PCI CK-MB elevation.

Diastolic Dysfunction as Assessed with Grid-Tagged Cardiac MRI Correlates with Microvascular Dysfunction and Markers of Left Ventricular Remodelling Following ST-Segment Elevation Myocardial Infarction

Purpose: Troponin positive acute coronary syndromes (ACS) are usually related to disruption of an atherosclerotic coronary plaque. However, a subgroup of these patients do not have an identifiable culprit lesion at angiography. Establishing a diagnosis in these patients is vital to ensure they receive appropriate treatment. We examine the diagnostic value of cardiac magnetic resonance (CMR) in these patients. Methods: CMR (1.5 T) was performed in consecutive patients presenting with a troponin positive ACS, without obvious culprit coronary lesions at angiography. All patients underwent CMR with cine-SSFP, T2-weighted, and late gadolinium enhancement imaging. Clinical demographics, peak Troponin I (TnI) and imaging data were collected.

129 Detection of coronary in-stent restenosis by 64-slice Computed Tomography in asymptomatic patients after acute myocardial infarction treated by primary angioplasty using stents with thin struts

The occurrence of instent restenosis (ISR) after myocardial infarction (MI) treated by primary angioplasty is considered as a factor of poor prognosis. The methods to detect ISR are still debated in asymptomatic patients in whom functional scintigraphic or ultrasound investigations are usually proposed. Our study sought to evaluate the effectiveness of anatomic diagnosis of ISR by 64-slice Multidetector Computed Tomography (MDCT) in patients (pts) treated with one or more stents whose thickness of strut is less than 100 μm. The diagnosis of ISR by MDCT was controlled by coronary angiography, pts without ISR at MDCT were followed clinically by physicians according to their practice. We included from January 2007 to June 2009 54 pts (50 men and 4 women) of 53.0 ± 10.8 years old. The culprit coronary lesion of MI was treated with 1.4 ± 0.6 stents (3.1 ± 0.4 mm diameter and 19.9 ± 9.7 mm length). Seventy four stents with strut of 84.6 ± 8.1 μm thickness were implanted on culprit lesions. The treated artery was LAD in 19 pts (35.2%), circumflex in 8 pts (14.8%) and RCA in 27 pts (50%). MDCT was performed 206 ± 136 days after MI. Seventeen pts (31.4%) received beta-blocker before acquisition, heart rate was 58.7 ± 7.2 bpm and effective radiation dose was 16.3 ± 1.5 msv. Two stents (2.7%) were considered nonassessable in 2 pts (3.7%). MDCT showed ISR in 14 pts (26.9%). Coronary angiography performed in 12 pts confirmed ISR in 9 pts 55 ± 50 days after MDCT. The positive predictive value of angiographic ISR after MDTC was 75%. Thirty eight pts without ISR were followed during 392 ± 200 days. No patient died, 2 pts experienced MI in relation to a definite late stent thrombosis, no patient had revascularization for ISR. Thus 64-slice MDCT could be a useful tool in systematic detection of ISR after MI in asymptomatic patient treated with thin strut stents. An evaluation of MDCT in addition to conventional functional methods should be discussed on a larger population.

Calcium scoring and chest pain: Is it dead on arrival?

Coronary artery calcium (CAC) scoring has been shown to be a measure of overall coronary artery disease (CAD) burden and is a well-validated screening test that significantly improves cardiovascular risk prediction in asymptomatic adults beyond that provided with standard risk factors. The absence of coronary artery calcification identifies persons at very low cardiovascular risk. Among symptomatic patients, calcium scans have been shown to have high sensitivity for the presence of obstructive CAD among stable, low-intermediate risk middle-aged adults. This has prompted many to advocate for the expanded use of calcium scanning as a diagnostic test in symptomatic patients to rapidly identify patients without CAD, serving as a filter for invasive coronary angiography or hospital admission or both. However, recent studies suggest that the negative predictive value of CAC scoring to exclude obstructive CAD may be significantly decreased among patients at higher pretest likelihood for obstructive CAD, consistent with Bayesian reasoning. In a point-counterpoint format, this article discusses several considerations and potential limitations to the widespread use of CAC to exclude obstructive CAD in symptomatic patients which include (1) the effect of pretest disease prevalence on test accuracy, (2) limited clinical efficiency due to low specificity for obstructive CAD and myocardial ischemia and high background prevalence of CAC in adults, (3) occurrence of CAC relatively late in the atherosclerotic process, (4) lack of association of CAC with vulnerable and culprit coronary artery lesions, and (5) interindividual and racial heterogeneity in the process of atherosclerosis calcification.

The culprit lesion score on multi-detector computed tomography can detect vulnerable coronary artery plaque

Vulnerable plaques are characterized by large lipid cores, positive remodeling and small coronary calcium deposits. Multi-detector computed tomography (MDCT) has recently been shown to be able to characterize coronary artery plaques. The aim of this study was to evaluate culprit coronary lesions for differentiating acute coronary syndrome (ACS) from stable angina pectoris (SAP) using MDCT. 64-slice MDCT was conducted on 71 patients (ACS: 35, SAP: 36). The culprit coronary lesions were assessed according to the type and plaque attenuation (PA) of the plaque and the remodeling index (RI) as the ratio of the lesion and the reference area. The culprit lesion score (CLS) was defined as the sum of every score as 1.2 for a PA≤60 Hounsfield units (HU), 1.1 for a RI≥1.05 and 1.2 for a non-calcified or spotty calcification. More spotty calcification (95.0% vs. 23.1%, P<0.001), a lower PA (40.17±20.08 HU vs. 96.96±58.19 HU, respectively, P<0.001) and a higher RI (1.44±0.43 vs. 0.90±0.44, respectively, P<0.001) were observed in the ACS patients. Also, the CLS of the ACS patients was significantly higher than that of the SAP patients (3.07±0.63 vs. 1.18±1.12, respectively, P<0.001). A CLS more than 2.0 helped us to differentiate ACS from SAP with a sensitivity of 97.1% and a specificity of 67.6%. The CLS might be a useful tool for differentiating ACS from SAP.

Location of Coronary Culprit Lesions at Autopsy in 41 Nondiabetic Patients With Acute Myocardial Infarction

Coronary artery disease and myocardial infarction (MI) are major causes of patient morbidity, hospital mortality, and out-of-hospital sudden death. The precise location of culprit lesions in acute MI at autopsy has not been reported. The purpose of this retrospective histopathologic autopsy study was to determine the distribution of coronary culprit lesions in acute fatal MI. Cross-sections of epicardial coronary arteries were evaluated microscopically. For each culprit lesion, its distance from the coronary ostium and its grade of luminal stenosis were recorded. The study group included 41 nondiabetic patients (mean age of 65 years, 66% males) who underwent autopsy at Mayo Clinic Rochester (1994-2005). Culprit lesions occurred within the proximal 3.0 cm of the left anterior descending artery in 86% and the left circumflex artery in 100%. In contrast, culprit plaques within the right coronary artery (RCA) were distributed evenly throughout its length. Among nondiabetic patients with acute fatal MI, culprit lesions exhibited proximal clustering in the left anterior descending artery and left circumflex artery, in contrast to more uniform distribution in the RCA. Thus, for the autopsy investigation of sudden death, evaluation for culprit lesions in the entire length of the RCA, not just its proximal region, is recommended.

FC2 Activating transcription factor 1 co-regulates iron, lipid and anti-inflammatory target genes to direct a novel atheroprotective human plaque macrophage subset

RationaleMonocytes entering tissues, including advanced atherosclerotic plaques, rapidly mature and adapt to their new microenvironment. Intraplaque haemorrhage promotes human atherosclerosis progression and destabilisation via a dual metabolic challenge: cholesterol-enriched erythrocyte...

Factors Influencing Local and Systemic Levels of Plasma Myeloperoxidase in ST-Segment Elevation Acute Myocardial Infarction

Myeloperoxidase (MPO) is associated with risk in acute coronary syndromes. However, the precise role it plays in ST-elevation myocardial infarction (STEMI) remains unclear. In this study we tested the hypothesis that levels of MPO in plasma after a myocardial infarction are affected by its ability to bind to the endothelium and there is local release of the enzyme at the culprit lesion. We measured plasma MPO in systemic circulation and throughout the coronary circulation in patients with STEMI undergoing primary percutaneous coronary intervention (PCI). MPO levels at the femoral artery were higher (p <0.001) in patients with STEMI (n = 67, median 45 ng/ml, interquartile range 34 to 83) compared to control patients (n = 12, 25 ng/ml, 19 to 30) with chronic stable angina undergoing elective PCI. After administration of the anticoagulant bivalirudin in 13 patients with STEMI, plasma MPO was increased only at the culprit coronary artery lesion before PCI (178 ng/ml, 91 to 245) versus all other sites (femoral artery 86 ng/ml, 54 to 139, p = 0.019). Administration of heparin caused a marked increase of plasma MPO. Even so, it was still possible to detect an increase of plasma MPO at culprit lesion in patients with STEMI (n = 54, 171 ng/ml, 122 to 230) versus controls (n = 12, 136 ng/ml, 109 to 151, p <0.05) after heparin and before PCI. MPO levels were higher at the culprit lesion in patients with STEMI who presented early and in those with restricted flow (p <0.05). In conclusion, our results demonstrate that, in addition to a systemic increase of MPO in patients presenting early with STEMI, levels of this leukocyte enzyme are increased at the culprit coronary lesion before PCI.

Resting Echocardiography for the Early Detection of Acute Coronary Syndromes in Chest Pain Unit Patients

The purpose of this study is to assess the ability of resting echocardiography to detect an acute coronary syndrome (ACS) before the occurrence of ischemic electrocardiogram (ECG) changes or troponin-T elevations. Four hundred and three patients who presented to the emergency room (ER) with chest pain, normal ECGs, and normal troponin-T levels were admitted to the cardiologist-run Chest Pain Unit (CPU) for further monitoring. They underwent serial resting echocardiography for monitoring of left ventricle wall motion (LVWM), ECG telemetry monitoring, and serial troponin-T measurements. An ACS was detected in 49 patients (12.1%). These 49 patients were then subdivided into three different groups based on the initial mode of detection of their ACS. In group A, 16 of 49 (32.6%) patients had ACS shown by echocardiographic detection of LVWM abnormalities. In group B, 24 of 49 (48.9%) patients had an ACS detected by ischemic ECG changes. In group C, 9 of 49 (18.3%) patients had an ACS detected by troponin-T elevations. The shortest time interval between CPU-admission and ACS-detection occurred in group A (A vs. B, P < 0.003; A vs. C, P < 0.0001). In group A, cardiac angiogram showed that the culprit coronary lesion was more frequent in the circumflex artery (11 out of 16; 68.7%) (LCx vs. LAD, P < 0.02; LCx vs. RCA, P < 0.001) and of these 11 patients with circumflex lesions, the ECG was normal in eight (72.7%) patients. This study demonstrates the utility of LVWM monitoring by serial echocardiography as part of a diagnostic protocol that can be implemented in a CPU. Furthermore, echocardiography could become an essential tool used in the diagnosis of ACS secondary to circumflex lesions.

Culprit Coronary Lesions Requiring Percutaneous Coronary Intervention After Vascular Surgery Often Arise From In-Stent Restenosis of Bare Metal Stents

The natural history of coronary artery disease (CAD) after vascular surgery is poorly defined. The aim of this study was to determine the temporal change of coronary artery lesions requiring revascularization with a percutaneous coronary intervention (PCI) after elective vascular surgery and to determine the utility of preoperative biomarkers on predicting those patients at risk for new coronary lesions. The Coronary Artery Revascularization Prophylaxis Trial tested the long-term survival benefit of coronary artery revascularization before elective vascular surgery. Among randomized patients who subsequently required PCI after surgery, the stenosis of the culprit lesion from the follow-up angiogram was compared with the preoperative vessel stenosis at the identical site on the baseline angiogram. A total of 30 patients underwent PCI for progressive symptoms at a median of 11.5 (interquartiles: 4.5-18.5) months postsurgery. Of 30 patients, 16 (53%) had nonobstructive CAD preoperatively (group 1) with a stenosis that increased from 17 +/- 6% to 91 +/- 2% (P < 0.01) and 14 (47%) had severe CAD at the culprit site preoperatively (group 2), with a stenosis that increased 89 +/- 2% (P = 0.15). The only biomarker that was an identifier of early coronary artery lesion formation in group 1 compared with group 2 patients was a higher baseline homocysteine level (14.6 +/- 1.4 vs. 10.6 +/- 0.7 mg/dL; P = 0.02). Culprit coronary artery lesions requiring PCI after an elective vascular operation often arise from in-stent restenosis. Therapies that either stabilize existing plaques or prevent restenosis, particularly among patients with elevated homocysteine levels, have the greatest promise for improving postoperative outcomes.

The value of the ECG for decision-making at first medical contact in the patient with acute chest pain.

Background/Objectives. Rapid risk stratification of the patient with acute chest pain is essential to select the best management. We investigated the value of the ECG at first medical contact to determine size of the ischaemic myocardial area and thereby severity of risk.Methods. In 386 patients with acute chest pain, ECG findings were correlated with the coronary angiogram. Using ST-segment deviation patterns the location of the coronary culprit lesion was predicted and thereby size of the area at risk. Four groups of patients were present. Those with a narrow QRS and a total 12-lead ST-segment deviation score of >/=5 mm (group 1) or </=4 mm (group 2); a QRS width of >/=120 ms (group 3), and patients with previous coronary bypass grafting (CABG) or percutaneous coronary intervention (PCI) (group 4).Results. Correct coronary culprit lesion localisation was possible in 84% of the 185 patients in group 1, 40% of the total cohort. Accurate prediction was not possible in most patients in groups 2, 3 and 4, in spite of extensive coronary artery disease in group 3 and 4. Conclusions. Using the 12-lead ECG the size of the myocardial area at risk can be accurately predicted when the total ST-segment deviation score is >/=5 mm, allowing identification of those in need of a PCI. In most patients with bundle branch block, previous CABG or PCI, the ECG can not localise the culprit lesion. This approach simplifies and accelerates decision-making at first medical contact. (Neth Heart J 2010;18:301-6.).

Clinical significance of papillary muscle late enhancement detected via cardiac magnetic resonance imaging in patients with single old myocardial infarction

Contrast-enhanced cardiac magnetic resonance imaging (MRI) can depict papillary muscle (PM) necrosis or fibrosis by late enhancement (LE) of PM, but its clinical significance in old myocardial infarction (OMI) has been little understood. Myocardial LE and PM-LE were detected with contrast imaging in 60 patients with OMI caused by a single culprit coronary artery lesion. Left ventricular (LV) morphology and function, mitral valve geometry, and severity of mitral regurgitation were also evaluated by cine imaging. Sphericity index was calculated for the assessment of LV remodeling. PM-LE was detected in 32 of 60 (53.3%) OMI patients. Unilateral PM-LE was detected in 22 patients and bilateral PM-LE in 10 patients. Patients with bilateral PM-LE demonstrated more severe LV remodeling and functional mitral regurgitation than those with unilateral or no PM-LE (sphericity index; bilateral PM-LE, 1.60±0.15, unilateral PM-LE, 1.71±0.29, no PM-LE, 1.85±0.27, p≤0.05) (mitral regurgitation; bilateral PM-LE, 1.10±0.57, unilateral PM-LE, 0.41±0.73, no PM-LE, 0.54±0.84, p≤0.05). In cases of unilateral PM-LE, posteromedial PM-LE resulting from right coronary artery-related OMI was accompanied by less severe mitral regurgitation, while anterolateral PM-LE resulting from left coronary artery-related OMI was not associated with severity of mitral regurgitation. More than half of patients with OMI showed unilateral or bilateral PM-LE, and bilateral PM-LE was closely related to more severe LV remodeling and functional mitral regurgitation.

Relation Between Aortic Knob Calcium Observed by Simple Chest X-Ray or Fluoroscopy and Plaque Components in Patients With Diabetes Mellitus

We used virtual histology and intravascular ultrasound (VH-IVUS) to evaluate the relation between aortic knob calcium (AKC) and plaque components in diabetic patients. The presence of AKC was assessed by posteroanterior view of chest x-ray or fluoroscopy at the time of coronary angiography. A total of 137 de novo coronary culprit lesions in 137 consecutive diabetic patients were studied and coronary plaque components were analyzed using VH-IVUS according to the presence (n = 45) or absence (n = 92) of AKC. Patients with AKC were significantly older (68 +/- 8 vs 62 +/- 9 years, p <0.001) and had significantly higher high-sensitivity C-reactive protein levels (1.97 +/- 1.33 vs 0.48 +/- 1.35 mg/dl, p = 0.005) compared to patients without AKC. Absolute and percent necrotic core (NC) volumes (30 +/- 26 vs 20 +/- 19 mm(3), p = 0.003; 23.4 +/- 10.3% vs 17.4 +/- 8.9%, p = 0.005, respectively) and absolute and percent dense calcium (DC) volumes (17 +/- 12 vs 11 +/- 12 mm(3), p = 0.010; 13.3 +/- 7.3% vs 9.6 +/- 7.9%, p = 0.011, respectively) were significantly greater in lesions with AKC compared to those without AKC. Multivariable analysis showed that age (odds ratio [OR] 1.233, 95% confidence interval [CI] 1.121 to 1.355, p <0.001), high-sensitivity C-reactive protein (OR 1.871, 95% CI 1.090 to 2.943, p = 0.007), absolute DC volume (OR 1.020, 95% CI 1.050 to 1.178, p = 0.003), and absolute NC volume (OR 1.026, 95% CI 1.057 to 1.199, p <0.001) were independent predictors of AKC. In conclusion, diabetic patients with AKC were older, had greater NC- and DC-containing plaques, and higher inflammatory status compared to diabetic patients without AKC.