Coronary Plaque Morphology Research Articles

Impact of coronary artery remodeling on clinical presentation of coronary artery disease: an intravascular ultrasound study

OBJECTIVESWe examined the association between the features of the culprit lesion in coronary artery disease (CAD) and clinical presentation as shown by intravascular ultrasound (IVUS).BACKGROUNDThe association between coronary remodeling pattern and clinical presentation of CAD is unclear.METHODSWe analyzed 125 selected patients who underwent preintervention IVUS. Acute myocardial infarction (AMI) and unstable angina pectoris (UAP) were categorized as an acute coronary syndrome (ACS), and stable angina pectoris (SAP) and old myocardial infarction (OMI) as stable CAD. Coronary remodeling patterns and plaque morphology of the culprit lesion obtained by IVUS were analyzed in terms of their association with clinical presentation or angiographic morphology.RESULTSAngiographically complex lesions were associated with ACS and OMI. In patients with a complex lesion, positive remodeling was observed more frequently than in those with a simple lesion. In AMI and UAP, positive remodeling was observed more frequently than in SAP and OMI (82% vs. 78% vs. 33% vs. 40%, respectively, p < 0.0001). The remodeling ratio was greater in AMI and UAP than in SAP and OMI (1.26 ± 0.15 vs. 1.11 ± 0.10 vs. 0.94 ± 0.11 vs. 0.96 ± 0.13, respectively, p < 0.0001). Furthermore, within ACS, the remodeling ratio was greater in AMI than in UAP (1.26 ± 0.15 vs. 1.11 ± 0.10, respectively, p < 0.05), whereas the frequency of positive remodeling was not different.CONCLUSIONSPositive remodeling was more frequently observed in ACS than in stable CAD. Moreover, the degree of positive remodeling was greater in AMI than in UAP. These results may reflect the impact of remodeling types and its degree in the culprit lesion of CAD on clinical presentation.

Assessment of coronary plaque with optical coherence tomography and high-frequency ultrasound

This study compares the ability of intravascular optical coherence tomography (OCT) and high-frequency intravascular ultrasound (IVUS) to image highly stenotic human coronary arteries in vitro. Current imaging modalities have insufficient resolution to perform risk stratification based on coronary plaque morphology. OCT is a new technology capable of imaging at a resolution of 5 to 20 μm, which has demonstrated the potential for coronary arterial imaging in prior experiments. Human postmortem coronary arteries with severely stenotic segments were imaged with catheter-based OCT and IVUS. The OCT system had an axial resolution of 20 μm and a transverse resolution of 30 μm. OCT was able to penetrate and image near-occlusive coronary plaques. Compared with IVUS, these OCT images demonstrated superior delineation of vessel layers and lack of ring-down artifact, leading to clearer visualization of the vessel plaque and intima. Histology confirmed the accuracy and high contrast of vessel layer boundaries seen on OCT images. Thus, catheter-based OCT systems are able to image near-occlusive coronary plaques with higher resolution than that of IVUS.

Morphology of vulnerable coronary plaque: insights from follow-up of patients examined by intravascular ultrasound before an acute coronary syndrome

OBJECTIVESTo determine the morphologic features of coronary plaques associated with acute coronary syndrome, we prospectively followed patients with atherosclerotic disease identified by intravascular ultrasound (IVUS).BACKGROUNDAlthough clinical evaluation of the vulnerable atherosclerotic plaque is important, few data exist regarding the morphology of the vulnerable plaque in clinical settings.METHODSWe examined 114 coronary sites without significant stenosis by angiography (<50% diameter stenosis) in 106 patients. All the sites exhibited atherosclerotic lesions by IVUS. These lesions consisted of 22 concentric and 92 eccentric plaques with a percent plaque area averaging 59 ± 12%.RESULTSDuring the follow-up period of 21.8 ± 6.4 months (range 1 to 24), 12 patients had an acute coronary event at a previously examined coronary site at an average of 4.0 ± 3.4 months after the initial IVUS study. All the preexisting plaques related to the acute events exhibited an eccentric pattern and the mean percent plaque area was 67 ± 9%, which was greater than plaque area in the other 90 patients without acute events (57 ± 12%, p < 0.05). There was no statistically significant difference in lumen area between two patient groups (6.7 ± 3.0 vs. 7.5 ± 3.7 mm2). Among 12 coronary sites with an acute occlusion, 10 sites contained the echolucent zones, eight of these shallow and two deep, likely representing a lipid-rich core. In 90 sites without acute events, an echolucent zone in the shallow portion was seen at only four sites (p < 0.05).CONCLUSIONSLarge eccentric plaque containing an echolucent zone by IVUS can be at increased risk for instability even though the lumen area is preserved at the time of initial study. Compensatory enlargement of vessel wall due to remodeling may contribute to the relatively small degree of stenosis by angiography.

Insertion/Deletion Polymorphism of the Angiotensin I-Converting Enzyme Gene Is Associated With Coronary Artery Plaque Calcification As Assessed by Intravascular Ultrasound

Objectives. We evaluated the influence of the insertion/deletion (I/D) polymorphism of the angiotensin I-converting enzyme (ACE) gene on coronary plaque morphology and calcification in patients with angiographically documented coronary artery disease (CAD).Background. The ACE I/D polymorphism has been associated with an increased risk of myocardial infarction in patients with the DD genotype but not with the presence of native CAD.Methods. We studied 146 patients undergoing percutaneous transluminal coronary angioplasty for stable angina pectoris by means of preinterventional intravascular ultrasound (IVUS). Qualitative and quantitative criteria were used to classify the target lesions as poorly or highly echoreflective or as calcified. Genomic deoxyribonucleic acid was analyzed by polymerase chain reaction (PCR) to identify the I/D polymorphism, with a second insertion-specific PCR in DD genotypes to prevent mistyping.Results. The ACE genotype groups (DD 46, ID 68, II 32) were well matched for the basic characteristics. Patients with the DD genotype had significantly more calcified lesions (DD 80%, ID 57%, II 66%; unadjusted odds ratio [OR] 2.88, 95% confidence interval [CI] 1.30 to 6.92, p = 0.008) and more calcifications >180° of the vessel circumference (DD 22%, ID 10%, II 6%; OR 2.80, 95% CI 1.05 to 7.63, p = 0.03). The prevalence of myocardial infarction was not significantly associated with coronary calcification (OR 1.44, 95% CI 0.72 to 2.88, p = 0.31).Conclusions. Patients with CAD and the ACE DD genotype have a significantly higher incidence and greater extent of coronary lesion calcification, as determined by IVUS. This finding indicates that the ACE I/D gene polymorphism is related to the development or progression of atherosclerotic plaque calcification.

Age-related development of atherosclerotic plaque stress: a population-based finite-element analysis.

In order to identify those age-related factors in the development of coronary atherosclerosis that would affect the stability of the plaque system, we have developed idealized, finite-element, cross-sectional models of the arterial wall and associated lesions, derived from population-based data. The physical development and morphology of coronary plaques was documented in the Pathobiological Determinants of Atherosclerosis in Youth histological study. Using this database, finite-element analysis models were created for five age groups (15-19, 20-24, 25-29 and 30-34 years) and for the 25 largest lesions. Cosmos (Structural Research, Inc., Los Angeles, California, USA) was used to create and analyze the models. The area of greatest stress shifted from the intima opposite the lesion in the 15-19 years age group to the edge of the cap and adjacent healthy tissue in the later age groups. Increasing age had a strong positive correlation with the shoulder stress level (r = 0.95) and the per cent stenosis correlated well with shoulder stress (r = 0.99, P < 0.002). Increasing the cap stiffness from a soft cap to a fibrous cap in the 30-34 year age group model resulted in a localized increase in shoulder surface stress by 10%. A calcified cap increased this shoulder surface stress by 30%. This finite-element analysis of the population-based data shows that the increase in stress appears to be closely related to the impaired load-bearing capability of the lipid pool that develops with age. The shoulder area of the lesion has been shown to be the location of most of the plaque fractures.

Coronary Risk Factors and Plaque Morphology in Men with Coronary Disease Who Died Suddenly

Cigarette smoking and abnormal serum cholesterol concentrations are risk factors for acute coronary syndromes, but the underlying mechanisms are poorly understood. We studied whether cigarette smoking and abnormal cholesterol values may precipitate acute coronary thrombosis and sudden death resulting from either rupture of vulnerable coronary plaques or erosion of plaques. We examined the hearts of 113 men with coronary disease who had died suddenly and also analyzed their coronary risk factors. We found an acute coronary thrombus in each of 59 men, and severe narrowing of the coronary artery by an atherosclerotic plaque without acute thrombosis (stable plaque) in 54. Cases of acute thrombosis were divided into two groups: 41 resulting from rupture of a vulnerable plaque (a thin fibrous cap overlying a lipid-rich core), and 18 resulting from the erosion of a fibrous plaque rich in smooth-muscle cells and proteoglycans. Vulnerable plaques that had not ruptured were counted in each heart. Cigarette smoking was a risk factor in 44 (75 percent) of the men with acute thrombosis, as compared with 22 (41 percent) of the men with stable plaques (P<0.001). The mean (+/-SD) ratio of serum total cholesterol to high-density lipoprotein (HDL) cholesterol was markedly elevated in the men who died of acute thrombosis with plaque rupture (mean, 8.5+/-4.0) but only mildly elevated in the men without acute thrombosis (5.5+/-2.4; P<0.001) and in the men with thrombi overlying eroded plaques (5.0+/-1.8; P<0.001). Multivariate analysis showed an association between an elevated ratio of serum total cholesterol to HDL cholesterol and the presence of vulnerable plaques (P<0.001). Among men with coronary disease who die suddenly, abnormal serum cholesterol concentrations - particularly elevated ratios of total cholesterol to HDL cholesterol - predispose patients to rupture of vulnerable plaques, whereas cigarette smoking predisposes patients to acute thrombosis.

New concept in coronary angioplasty: Dilatation with a helical balloon that allows simultaneous autoperfusion

These preclinical studies investigate a new concept in coronary angioplasty and balloon catheter technology (the P100 catheter). The study sought to evaluate the morphology of experimental coronary arterial plaques dilated with the P100 in comparison to standard balloons, to determine the in vitro flow rates occurring during the inflation of the P100 in comparison to available perfusion catheters, and to assess the in vivo coronary flow velocity and the presence of ischemia during prolonged inflations with the P100. The development of myocardial ischemia is a major limitation of standard balloon angioplasty. To limit ischemia, autoperfusion catheters have been developed, in which blood flows through the balloon in the central catheter shaft. However, as the flow lumen profile is reduced to enhance the performance of these devices, so is the accompanying flow. An angioplasty catheter was designed to evaluate the feasibility of continuous autoperfusion around the dilatation balloon. The balloon surface was engineered to develop a helical trough for blood flow to occur during inflation. Arterial plaque morphology following angioplasty with the P100 (n = 8) and with standard balloons (n = 8) was evaluated in a swine model. In vitro flow rates during inflation of the P100 and available perfusion catheters were determined using 33% glycerol solution. In vivo coronary flow velocity was determined with a Doppler-tipped wire during 60-min continuous inflations with the P100, and 15-sec inflations with a standard balloon in 12 vessel segments in 7 dogs; using 3.0–3.5-mm-diameter balloons. All lesions were successfully dilated (<50% luminal diameter stenosis) with the P100 and standard balloons. There were no morphologic differences in plaques dilated with P100 compared to standard balloons. In vitro flow rates with conventional 3.0-mm balloon perfusion catheters ranged from 27.1 ± 2.1 ml/min (RX Flowtrack™) to 38.7 ± 0.9 ml/min (Stack Perfusion™), P < .05. Flow with the P100 ranged from 54.8 ± 4.3 ml/min (2.5-mm balloon) to 103.2 ± 4.5 ml/min (3.5-mm balloon), P <.05. Distal average peak coronary flow velocity during prolonged P100 inflations varied from 69 ± 7% of baseline at 5 min to 83 ± 8% of baseline at 40 min, with an upward trend in velocity the longer the balloon was inflated. Hemodynamics remained stable. Experimental plaques are successfully dilated with a helical balloon by a mechanism that appears similar to the dilatation mechanism of standard balloons. These preclinical studies show that angioplasty and autoperfusion can be accomplished by a balloon that does not have complete surface area contact with the vessel wall. A gap created by the helix can thus provide a conduit for blood flow. Clinical studies will determine whether this innovation, which alters the tubular geometry of current angioplasty balloons, will provide autoperfusion and equivalent dilatation effects in humans. Cathet Cardiovasc Diagn 40:109–116, 1997. © 1997 Wiley-Liss, Inc.

New concept in coronary angioplasty: dilatation with a helical balloon that allows simultaneous autoperfusion.

These preclinical studies investigate a new concept in coronary angioplasty and balloon catheter technology (the P100 catheter). The study sought to evaluate the morphology of experimental coronary arterial plaques dilated with the P100 in comparison to standard balloons, to determine the in vitro flow rates occurring during the inflation of the P100 in comparison to available perfusion catheters, and to assess the in vivo coronary flow velocity and the presence of ischemia during prolonged inflations with the P100. The development of myocardial ischemia is a major limitation of standard balloon angioplasty. To limit ischemia, autoperfusion catheters have been developed, in which blood flows through the balloon in the central catheter shaft. However, as the flow lumen profile is reduced to enhance the performance of these devices, so is the accompanying flow. An angioplasty catheter was designed to evaluate the feasibility of continuous autoperfusion around the dilatation balloon. The balloon surface was engineered to develop a helical trough for blood flow to occur during inflation. Arterial plaque morphology following angioplasty with the P100 (n = 8) and with standard balloons (n = 8) was evaluated in a swine model. In vitro flow rates during inflation of the P100 and available perfusion catheters were determined using 33% glycerol solution. In vivo coronary flow velocity was determined with a Doppler-tipped wire during 60-min continuous inflations with the P100, and 15-sec inflations with a standard balloon in 12 vessel segments in 7 dogs; using 3.0-3.5-mm-diameter balloons. All lesions were successfully dilated (< 50% luminal diameter stenosis) with the P100 and standard balloons. There were no morphologic differences in plaques dilated with P100 compared to standard balloons. In vitro flow rates with conventional 3.0-mm balloon perfusion catheters ranged from 27.1 +/- 2.1 ml/min (RX Flowtrack) to 38.7 +/- 0.9 ml/min (Stack Perfusion), P < .05. Flow with the P100 ranged from 54.8 +/- 4.3 ml/min (2.5-mm balloon) to 103.2 +/- 4.5 ml/min (3.5-mm balloon), P < .05. Distal average peak coronary flow velocity during prolonged P100 inflations varied from 69 +/- 7% of baseline at 5 min to 83 +/- 8% of baseline at 40 min, with an upward trend in velocity the longer the balloon was inflated. Hemodynamics remained stable. Experimental plaques are successfully dilated with a helical balloon by a mechanism that appears similar to the dilatation mechanism of standard balloons. These preclinical studies show that angioplasty and autoperfusion can be accomplished by a balloon that does not have complete surface area contact with the vessel wall. A gap created by the helix can thus provide a conduit for blood flow. Clinical studies will determine whether this innovation, which alters the tubular geometry of current angioplasty balloons, will provide autoperfusion and equivalent dilatation effects in human.

Effect of Hypertension and Cardiac Hypertrophy on Coronary Artery Morphology in Sudden Cardiac Death

Epidemiological studies have shown that hypertension and left ventricular hypertrophy (LVH) increase the risk of sudden cardiac death (SCD) in patients with severe coronary artery disease (CAD). However, autopsy studies comparing the morphological substrates for SCD in normotensives and hypertensives are lacking. Heart weight and coronary plaque morphology were prospectively compared in SCD in 36 hypertensive and 63 normotensive individuals. The frequency of CAD was similar in hypertensives (69%, n = 25) and normotensives (73%, n = 46). In 71 hearts with CAD, acute coronary thrombi were present in 76% of normotensives versus 36% of hypertensives (P = .002), LVH was present in 64% of hypertensives versus 33% of normotensives (P = .01) and in 72% of hypertensives with one-vessel disease versus 17% of normotensives with one-vessel disease (P = .0005), and a healed or acute infarct without acute thrombus was present in 36% of hypertensives versus 9% of normotensives (P = .007). Heart weight was higher in all cases of plaque rupture (519 +/- 109 g) than eroded plaque (381 +/- 92 g, P = .0002). In contrast to hypertensives, normotensive hearts with severe CAD showed a stepwise increase in heart weight with one-, two-, and three-vessel disease (P = .01). Severe CAD is present in most SCD in hypertensive and normotensive individuals, but acute thrombi are more common in normotensives. LVH is an important contributing mechanism of SCD in hypertensives, especially in cases of one-vessel disease. LVH is associated with plaque rupture and extent of disease in SCD in normotensives with severe CAD.

Quantitative assessment of coronary atherosclerotic plaque profile by morphometric analysis of angiographic images.

Coronary plaque morphology (simple or complex) has a recognized clinical, pathophysiologic, and prognostic importance, but its routine use is hampered by the subjective and qualitative nature of the assessment. The aim of this study was to assess the feasibility and accuracy of mathematical, objective, operator-independent assessment of plaque morphology, by means of algorithms based on vector and fractal analysis, previously developed for describing continuous curves. Twenty coronary angiograms were analyzed: 10 with "simple-type" stenosis (defined according to Ambrose type I pattern, Group I) and 10 with "complex-type" stenosis (Ambrose type II pattern, Group II). Five morphometric parameters effectively separated simple and complex-type stenosis: peaks/cm (Group I = 0.24 +/- 0.31 vs Group II = 2.46 +/- 1.83, P < .01); summed maximum error/cm (I = 0.94 +/- 1.19 vs II = 4.53 +/- 0.56, P < .01); integrated error/cm (I = 0.22 +/- 0.27 vs II = 2.25 +/- 1.68, P < .01); number of features/cm (I = 0.02 +/- 0.05 vs II = 1.19 +/- 0.65, P < .01); standard deviation curvature (I = 0.07 +/- 0.01 vs II = 0.22 +/- 0.21, P = 0.06). The scaled edge-length ratio-the only parameter based on fractal analysis-was not different between the two groups (I = 1.03 +/- 0.01 vs II = 1.13 +/- 0.10, P = ns). Hence, a quantitative description of plaque morphology is feasible and allows an effective discrimination of simple and complex plaque profiles with morphometric parameters based on vector analysis.

Coronary plaque morphology affects stent deployment: Assessment by intracoronary ultrasound

Coronary plaque morphology affects stent deployment: Assessment by intracoronary ultrasound

Coronary plaque morphology affects stent deployment: assessment by intracoronary ultrasound.

The purpose of this study was to evaluate the changes in arterial wall morphology induced by coronary stent implantation and the influence of plaque morphology on stent expansion by intravascular ultrasound. Intravascular ultrasound imaging was performed in 25 lesions before and after Palmaz-Schatz stent implantation. In the 25 lesions with ultrasound images before and after stent deployment angiographic percent diameter stenosis decreased from 71% +/- 11% to 6% +/- 14%. By ultrasound there was a gain in luminal area from 2.0 mm2 +/- 1.5 mm2 to 6.6 mm2 +/- 2.1 mm2 owing to gain in external elastic membrane area of 2.5 mm2 +/- 1.7 mm2 and reduction of plaque area of 2.1 mm2 +/- 1.7 mm2. Calcified lesions (n = 8) showed significantly less relative luminal gain (218% +/- 128% vs. 421% +/- 276%, P = .01), and stent expansion was significantly less symmetric (minimal/maximal stent diameter 0.8 +/- 0.1 vs. 0.9 +/- 0.1, P = .002) as compared to non-calcified lesions (n = 17). The difference in lumen area within the stent between the previously stenotic area and the ends of the stent was significantly larger in calcified lesions as compared to non-calcified lesions (29 +/- 28% vs. 8 +/- 23%, P = .03). Both vessel stretch and plaque reduction contribute to the luminal gain after coronary stenting. Calcified lesions interfere with optimal stent expansion.

Sudden coronary death. Frequency of active coronary lesions, inactive coronary lesions, and myocardial infarction.

The reported frequency of active coronary lesions (plaque rupture and coronary thrombosis) in sudden death due to coronary artery atherosclerosis (sudden coronary death) has varied from < 20% to > 80% of cases in previous series. In hearts lacking an active coronary lesion, sudden death has usually been attributed to a healed myocardial infarction. The purpose of the present study was to determine the frequency of active and inactive coronary lesions and myocardial infarction in individuals with sudden coronary death. The hearts of persons who died as a result of sudden coronary death underwent perfusion-fixation and postmortem angiography. An active coronary lesion was defined as a disrupted plaque, luminal fibrin/platelet thrombus, or both. We defined an inactive lesion as having a cross-sectional luminal stenosis of > or = 75% with neither plaque disruption nor luminal thrombus. Ninety hearts were examined (from 72 men and 18 women; mean age at the time of death, 51 +/- 10 years). Acute myocardial infarction was present in 19 (21% [acute myocardial infarction only in 9, both acute and healed myocardial infarction in 10]), healed myocardial infarction only in 37 (41%), and no myocardial infarction in 34 (38%). Active coronary lesions were identified in 51 (57%): acute thrombi plus disrupted plaques in 27, acute thrombi only in 21, and disrupted plaques only in 3. In hearts with acute myocardial infarction, active coronary lesions were significantly more prevalent than in hearts with only healed myocardial infarction or hearts lacking an acute or a healed myocardial infarction (89%, 46%, and 50%, respectively; P < .005). Hearts without acute or healed myocardial infarction and without active lesions were similar to hearts with active lesions with respect to heart weight and severity of epicardial coronary disease. Acute changes in coronary plaque morphology (thrombus, plaque disruption, or both) were found in 57% of cases of sudden coronary death. In hearts with myocardial scars and no acute infarction, active coronary lesions were identified in 46% of cases. Neither myocardial infarction (acute or healed) nor an active coronary lesion was present in 19% of hearts.

Coronary artery plaque morphology in stable angina and subsets of unstable angina: an in vivo intracoronary ultrasound study.

Little information is available regarding the in vivo composition of angina producing culprit atherosclerotic lesions in various anginal syndromes. In this study we used intracoronary ultrasound to determine the composition of culprit lesions in various subsets of anginal syndromes and correlated this composition with the patient's clinical presentation. One hundred and forty six patients referred for angioplasty or atherectomy were classified as having either chronic stable angina (angina which was clinically unchanged for > 2 months), crescendo angina (an accelerating pattern of frequent or prolonged anginal episodes), severe rest angina (abrupt onset of prolonged angina) or post-infarction angina (angina within 2 weeks of acute myocardial infarction). Intracoronary ultrasound imaging of the culprit lesion was performed before intervention. Lesions were classified as soft, mixed fibrous without calcium, mixed fibrous with calcium or calcified. Analysis of the ultrasound images revealed that the majority of culprit lesions were soft in severe rest (71%) and post-infarction angina (73%) whereas, the majority of culprit lesions were mixed fibrous or calcified in chronic stable (69%) and crescendo (53%) angina (X2 = 22.73, p = 0.007). In addition, the frequency of intralesional calcium in chronic stable or crescendo angina was significantly higher than that in severe rest or stable angina. We conclude that the composition of culprit lesions in various anginal subsets are different. The lesion morphology in crescendo angina frequently resembles that in chronic stable angina; while those in severe rest and post-infarction angina are frequently similar. These findings may have implications for medical or interventional treatment of patients with angina.

Morphometric analysis of the composition of coronary arterial plaques in isolated unstable angina pectoris with pain at rest

Coronary artery plaque morphology was studied in 354 five-mm segments of the 4 major (left main, left anterior descending, left circumflex and right) epicardial coronary arteries in 10 patients with isolated unstable angina pectoris with pain at rest. The 4 major coronary arteries were sectioned at 5mm intervals and a drawing of each of the resulting 354 Movat-stained histologic sections was analyzed using a computerized morphometry system. The major component of plaque was a combination of dense acellular and cellular fibrous tissue with much smaller portions of plaque being composed of pultaceous debris, calcium, foam cells with and without inflammatory infiltrates and inflammatory infiltrates without foam cells. There were no differences in plaque composition among any of the 4 major epicardial coronary arteries. Plaque composition varied as a function of the degree of luminal narrowing. Linear increases were observed in the mean percent of dense fibrous tissue (from 5 to 50%), calcific deposits (from 1 to 10%), pultaceous debris (from 0 to 10%) and inflammatory infiltrates without significant numbers of foam cells (from 0 to 5%), and a linear decrease was observed in the mean percent of cellular fibrous tissue (from 94 to 22%) in sections narrowed up to 25% to more than 95% in cross-sectional area. Multiluminal channels were seen in all 10 patients (28 [19%] of the 146 sections narrowed >75% in cross-sectional area and in 36 [10%] of all 354 segments); occlusive thrombi in no patient; nonocclusive thrombi in 2 patients (1 section each of 2 arteries); plaque rupture in 2 patients (4 segments from 2 arteries); and plaque hemorrhages in 6 patients (11 sections from 10 arteries).

Doctors and Overtime Pay

<h3>Background</h3> Myeloperoxidase (MPO) is a leucocyte enzyme that catalyses the formation of a number of reactive oxidant species. <h3>Objective</h3> The purpose of this study is to evaluate the relationship between angiographic coronary plaque morphology in patients with unstable angina pectoris (UAP) or stable angina pectoris (SAP) and MPO levels. <h3>Patients and design</h3> Plasma MPO levels on admission were measured in 236 patients with UAP, 146 with SAP and 85 control subjects using an ELISA kit. The angiographic morphology of the culprit lesion was classified into two types, simple or complex, based on the Ambrose classification. In addition, 61 atherectomy specimens obtained from a different cohort of patients with UAP and SAP were studied immunohistochemically for MPO. <h3>Results</h3> Median (IQR) plasma MPO levels in patients with UAP with a complex lesion were significantly higher than in patients with a simple lesion (41.9 (21.7–73.7) ng/ml vs 20.5 (15.9–27.9) ng/ml, p&lt;0.0001), but there was no significant difference between the two groups in patients with SAP. On multivariate analysis, raised plasma MPO levels and Braunwald class III were independent factors for angiographically-detected complex lesions (adjusted OR 12.49, 95% CI 3.24 to 48.17, p=0.0002). In the atherectomy specimens the number of MPO-positive cells in patients with UAP with complex lesions was significantly higher (p&lt;0.0005) than in patients with simple lesions. Moreover, in this cohort, plasma MPO levels were positively correlated with the number of MPO-positive cells in atherectomy specimens (R=0.42, p=0.024). <h3>Conclusions</h3> This study shows that increased expression and plasma MPO levels are closely related to the presence of angiographically-detected complex lesion morphology in patients with UAP.