Background Acute myocardial infarction is believed to be causedby rupture of an unstable coronary-artery plaque that appearsas a single lesion on angiography. However, plaque instabilitymight be caused by pathophysiologic processes, such as inflammation,that exert adverse effects throughout the coronary vasculatureand that therefore result in multiple unstable lesions.
Methods To document the presence of multiple unstable plaquesin patients with acute myocardial infarction and determine theirinfluence on outcome, we analyzed angiograms from 253 patientsfor complex coronary plaques characterized by thrombus, ulceration,plaque irregularity, and impaired flow.
Results Single complex coronary plaques were identified in 153patients (60.5 percent) and multiple complex plaques in theother 100 patients (39.5 percent). As compared with patientswith single complex plaques, those with multiple complex plaqueswere less likely to undergo primary angioplasty (86.0 percentvs. 94.8 percent, P=0.03) and more commonly required urgentbypass surgery (27.0 percent vs. 5.2 percent, P0.001). Duringthe year after myocardial infarction, the presence of multiplecomplex plaques was associated with an increased incidence ofrecurrent acute coronary syndromes (19.0 percent vs. 2.6 percent,P0.001); repeated angioplasty (32.0 percent vs. 12.4 percent,P0.001), particularly of non–infarct-related lesions (17.0percent vs. 4.6 percent, P0.001); and coronary-artery bypassgraft surgery (35.0 percent vs. 11.1 percent, P0.001).
Conclusions Patients with acute myocardial infarction may harbormultiple complex coronary plaques that are associated with adverseclinical outcomes. Plaque instability may be due to a widespreadprocess throughout the coronary vessels, which may have implicationsfor the management of acute ischemic heart disease.
Rupture of coronary-artery plaques, resulting in thromboticocclusion, is implicated in the pathogenesis of acute myocardialinfarction.1,2,3,4,5,6 Plaque disruption is thought to be afunction of the interplay between factors intrinsic to the plaqueand extrinsic forces.3,4,5 However, the specific mechanismsmediating plaque instability have not been fully delineated.
Plaque rupture is thought to reflect local plaque instabilityattributable to spontaneous or triggered disruption of a vulnerableplaque that is manifested angiographically or pathologicallyas a single complex lesion. However, the pathophysiologic factorsthat are believed to precipitate plaque rupture — whetheras a result of primary weakening of the fibrous cap attributableto inflammation3,4,7,8,9 or as a result of the extrinsic influencesof intraluminal mechanical forces modulated by sympathic toneand catecholamines10,11 — might reasonably be expectedto exert their effects in a widespread pattern throughout thecoronary vasculature. Given the potentially widespread effectof these factors that adversely influence plaques, togetherwith the typically diffuse nature of coronary atherosclerosis,12plaque instability might be expected to develop in a multifocalpattern, resulting in multiple complex, unstable plaques inanatomically remote locations; any one of these lesions mightprogress to total occlusion of a vessel and emerge as the causeof an infarct.
This angiographic study was designed to document the incidenceof multiple complex plaques in patients with acute transmuralmyocardial infarction and to determine their influence on clinicaloutcome.
Methods
Study Design
We analyzed angiograms from 253 consecutive patients with acutetransmural myocardial infarction. All the patients were treatedwith aspirin (325 mg orally), heparin (10,000 units by intravenousbolus), intravenous nitroglycerin, and beta-blockers, unlesscontraindicated. Coronary angiography, left ventricular cineangiography,and angioplasty were performed by standard techniques.13 Thestudy protocol was approved by the hospital's institutionalreview board.
Angiographic Analysis
Coronary angiograms were analyzed as previously described, withsubstantial lesions (those that narrowed the diameter of thevessel by 50 percent or more) measured by quantitative analysis.13Complex coronary plaques were identified according to previouslyused criteria14,15,16: an intraluminal filling defect consistentwith thrombus, defined as abrupt vessel cutoff with persistenceof contrast, or an intraluminal filling defect in a patent vesselwithin or adjacent to a stenotic region with surrounding homogeneouscontrast opacification; plaque ulceration, defined by the presenceof contrast and hazy contour beyond the vessel lumen; plaqueirregularity, defined by irregular margins or overhanging edges;and impaired flow.13 Lesions were considered complex if theycaused at least 50 percent stenosis and had two or more of thesemorphologic features. Care was taken to exclude lesions characteristicof chronic total occlusion, which were identified as taperinglesions with multiple fine collaterals.
The location of the infarct-related plaque was determined bycorrelating the presence of a complex plaque with electrocardiographicand wall-motion abnormalities. For each patient, the coronaryvasculature was reviewed to identify anatomically remote complexplaques. An anatomically remote plaque was defined as one ina different artery from the artery containing the infarct-relatedplaque; in the same artery as that containing the infarct-relatedplaque, but in a different branch; or in the same artery andbranch as the infarct-related plaque, but at least 5 cm fromthe infarct-related plaque, with an intervening segment of disease-freevessel. As in previous studies,14 the angiograms were analyzedby two independent angiographers, the results were compared,and when there was disagreement, a final decision was made byconsensus.
Clinical Outcomes
The patients' records and the hospital data base were reviewedto analyze clinical variables, in-hospital outcomes, and theclinical course over the 12 months after myocardial infarction.The clinical information that was analyzed included the useor nonuse of aspirin, smoking status, and the presence or absenceof diabetes, hypertension, and hypercholesterolemia. Informationwas obtained about the initial revascularization strategy; recurrentacute coronary syndromes, including unstable angina and myocardialinfarction; repeated catheterization; repeated revascularization;and death. Data from patients who required a second percutaneousrevascularization procedure were analyzed to determine whetherthe later intervention was performed on the index culprit lesionor, if it was performed on a remote plaque, whether this subsequenttarget had been previously designated as complex.
Statistical Analysis
Patients were divided into two groups according to whether theyhad single or multiple complex coronary plaques. Base-line demographiccharacteristics, angiographic variables, clinical variables,and outcomes were compared between these two groups. A separateanalysis of patients with multivessel disease was performed,in which the same variables were compared in patients with singlecomplex plaques and those with multiple complex plaques. Numericalvariables are reported as means ±SD. Frequencies andpercentages are given for categorical variables. These variableswere compared by chi-square test when applicable and otherwiseby Fisher's exact test. For continuous variables, statisticalcomparisons were made with use of the two-tailed t-test, anda P value of less than 0.05 was considered to indicate statisticalsignificance.
To examine whether the presence of multiple complex coronaryplaques was independently predictive of clinical events, multivariateanalyses were completed for one-year outcomes, including recurrentacute coronary syndromes, repeated catheterization, repeatedangioplasty, and coronary bypass surgery, as well as the combinedoutcome of multiple adverse cardiac events, defined as the occurrenceof one or more of the preceding events or of death from cardiaccauses. The covariates included were the presence or absenceof multiple complex plaques, age, and sex.
A step-down multivariate analysis was then completed for eachof these five outcomes. The covariates included were the presenceor absence of multiple complex plaques, age, sex, presence orabsence of a history of hyperlipidemia, presence or absenceof diabetes, left ventricular ejection fraction, and smokingstatus. All covariates were included initially. The least significantvariable was then dropped from the model at each step untilthe final model included only variables with a P value of lessthan 0.05.
Results
A single complex coronary plaque was identified angiographicallyin 153 patients (60.5 percent), and multiple complex plaqueswere identified in the 100 remaining patients (39.5 percent)(Table 1). The observers initially disagreed about the classificationof 25 of 370 lesions (6.8 percent). Patients with single andmultiple complex plaques did not differ significantly in meanage (63±12 vs. 64±11 years, respectively), sexratio (67 percent vs. 69 percent male), or the frequency ofcoronary risk factors, including current smoking, diabetes mellitus,and hypercholesterolemia. There were no differences betweenthe groups in the proportion with a history of infarction orangina.
Table 1. Clinical Outcomes of Patients with Acute Myocardial Infarction and Single or Multiple Complex Coronary Plaques.
Angiographic Results
The prevalence of multivessel coronary disease was lower inpatients with single complex coronary plaques than in thosewith multiple complex coronary plaques (74.5 percent vs. 91.0percent, P0.001). Patients with multiple complex plaques hada lower left ventricular ejection fraction at base line (38±14percent vs. 45±14 percent, P=0.003). The culprit lesionresponsible for acute myocardial infarction was clearly delineatedin all patients with a single complex plaque. Among those withmultiple complex plaques, 83 patients (83.0 percent) had twocomplex plaques (Figure 1 and Figure 2), and 17 others (17.0percent) had three or more complex plaques.
Figure 1. Angiograms from a Patient with Acute Posterolateral Myocardial Infarction.
The left-hand panel shows a culprit lesion in the circumflex artery, characterized by a long, scalloped, ulcerated, tight stenosis with haziness and ulceration (solid arrows) and with a total occlusion located just distally (open arrow). The right-hand panel shows a cranial view of the left anterior descending coronary artery in the same patient, demonstrating a complex ulcerated stenosis with overhanging edges (arrows), anatomically remote from the culprit occlusion in the circumflex artery.
Figure 2. Angiograms from a Patient with Acute Inferior–Posterior Myocardial Infarction.
Angiography of the left coronary artery (left-hand panel) shows acute occlusion of the circumflex artery (solid arrows), with haziness, a filling defect, and impaired flow consistent with the presence of an acute thrombotic occlusion. Collateral filling of the distal right coronary artery is evident (open arrows). Angiography of the right coronary artery in the same patient (right-hand panel) demonstrates near-total distal occlusion (arrows), with abrupt cutoff, haziness, and a filling defect consistent with acute thrombosis.
The complex plaque responsible for the acute myocardial infarctionwas clearly identified in 98 patients with multiple complexplaques (98.0 percent); in the other 2 patients (2.0 percent),it was not possible to determine which plaque was responsible.In one of the latter two patients, who had acute inferior myocardialinfarction and angiographic evidence of complete thromboticocclusion in both the circumflex and right coronary arteries(Figure 2), angioscopy documented the presence of thrombus superimposedon ulcerated plaques in both vessels.
There were no differences between the groups in the angiographicappearance of the infarct-related plaque with respect to theinitial percentage of stenosis, flow grade, or presence of intracoronarythrombus. In those with multiple complex plaques, the degreeof stenosis of the non–infarct-related plaque tended tobe less than that of the infarct-related plaque (82±14percent vs. 95±7 percent, P<0.003). However, the non–infarct-relatedplaque was associated with impaired flow in 27.0 percent ofcases and with total occlusion in 10.0 percent.
In-Hospital Outcomes
Primary angioplasty of the infarct-related artery was performedin 145 (94.8 percent) of the patients with single complex plaques;it was not performed in the other 8 patients (5.2 percent) becauseof the presence of technically unsuitable vessels. Angioplastywas successful in 97.9 percent of the patients in whom it wasperformed. Urgent bypass surgery was performed because of severemultivessel disease in eight (5.2 percent) of the patients withsingle complex plaques. No patients with single complex plaquesunderwent initial multivessel angioplasty, but 15 patients withsingle complex plaques (9.8 percent) underwent planned stagedpercutaneous interventions for lesions in vessels other thanthe primary infarct-related artery.
In contrast, patients with multiple complex plaques were lesslikely than those with single complex plaques to undergo initialangioplasty of the infarct-related lesion (86.0 percent vs.94.8 percent, P=0.03) (Table 1). Not surprisingly, such patientsrequired urgent bypass surgery more frequently than those withsingle complex plaques (27.0 percent vs. 5.2 percent, P0.001).Patients with multiple complex plaques more commonly underwentinitial emergency multivessel percutaneous interventions (13.0percent vs. 0 percent, P=0.003), as well as planned staged angioplasty(20.0 percent vs. 9.8 percent, P=0.03). However, the successof primary angioplasty was not significantly different in patientswith single and those with multiple complex plaques. In-hospitalmortality was slightly higher among those with multiple complexplaques (11.0 percent vs. 7.8 percent, P=0.30).
Outcome within One Year
Ninety-three percent of all patients were followed for one yearafter myocardial infarction (95 percent of those with singleand 90 percent of those with multiple complex plaques, P notsignificant). Among those with single complex plaques, recurrentischemia requiring repeated catheterization developed in 22patients (14.4 percent) within 6 months and in 37 patients (24.2percent) within 12 months, with recurrent acute coronary syndromesin 4 patients (2.6 percent) (Table 1 and Figure 3). Nineteenpatients (12.4 percent) underwent repeated angioplasty: 12 (7.8percent) in the infarct-related lesion and 7 (4.6 percent) inanother lesion. Coronary bypass surgery was necessary in 17patients (11.1 percent).
Figure 3. Outcomes within One Year after Myocardial Infarction in Patients with Multiple Complex Plaques or Single Complex Plaques.
PTCA denotes percutaneous transluminal coronary angioplasty, and CABG coronary-artery bypass grafting. P0.001 for all comparisons between groups.
As compared with patients with single complex plaques, thosewith multiple complex plaques were more likely to have recurrentischemia requiring repeated catheterization by six months (39.0percent vs. 14.4 percent, P0.001) and by one year (54.0 percentvs. 24.2 percent, P0.001) and also had a higher incidence ofrecurrent acute coronary syndromes (19.0 percent vs. 2.6 percent,P0.001) (Table 1 and Table 2 and Figure 3). Within one yearof the original myocardial infarction, patients with multiplecomplex plaques were more likely than those with single complexplaques to require repeated angioplasty of any lesion (32.0percent vs. 12.4 percent, P0.001) or of a lesion other thanthe infarct-related plaque (17.0 percent vs. 4.6 percent, P0.001).Repeated angioplasty was performed on a previously documentedcomplex plaque in 15 of the 17 patients with multiple complexplaques who underwent angioplasty on a non–infarct-relatedlesion (88.2 percent); 13 of these 17 patients (76.5 percent)presented with recurrent acute coronary syndromes. Furthermore,patients with multiple complex plaques were more likely to requirecoronary bypass surgery than those with single complex plaques(35.0 percent vs. 11.1 percent, P0.001). Those with multiplecomplex plaques had a slightly higher mortality rate duringthe year after infarction (17.0 percent vs. 12.4 percent, P=0.32).
Table 2. Step-Down Multivariate Analysis of Outcomes within One Year after Acute Myocardial Infarction.
Multivariate analysis showed that the presence of multiple complexplaques was independently predictive of adverse outcomes (Table 2).For recurrent acute coronary syndromes, repeated catheterization,or bypass surgery within one year, only the presence of multiplecomplex plaques was found to be a significant predictor. Forrepeated angioplasty, the presence of multiple complex plaquesand an age of 70 years or more were significant predictors.The presence of multiple complex plaques was a significant predictorof multiple adverse cardiac events, as was a lower left ventricularejection fraction.
Analysis of Patients with Multivessel Disease
Since the initial revascularization strategies and the ratesof recurrent ischemia and revascularization over time mightbe expected to differ between patients with multivessel diseaseand those with single-vessel disease, independently of the presenceor absence of multiple complex plaques, a separate analysisof patients with multivessel disease was performed. Multivesseldisease was common in patients with single complex plaques (74.5percent); not surprisingly, it was even more prevalent in thosewith multiple complex plaques (91.0 percent, P0.001). Patientswith multivessel disease and multiple complex plaques were lesslikely than those with multivessel disease and single complexplaques to undergo initial primary angioplasty (86.0 percentvs. 93.2 percent, P=0.03) and more commonly required urgentprimary coronary bypass surgery initially (25.0 percent vs.4.1 percent, P0.001). Within a year after infarction, as comparedwith patients with single complex plaques, patients with multiplecomplex plaques had a higher incidence of recurrent ischemiarequiring repeated catheterization (56.0 percent vs. 25.6 percent,P 0.001), recurrent acute coronary syndromes (1.3 percent vs.19.0 percent, P0.001), subsequent revascularization (32.0 percentvs. 14.4 percent [P=0.002] for any angioplasty; 16.0 percentvs. 6.3 percent [P=0.02] for angioplasty of a lesion other thanthe initial culprit lesion), and coronary bypass surgery (33.0percent vs. 11.7 percent, P0.001). There was no significantdifference in mortality at one year (16.0 percent vs. 14.3 percent,P not significant).
Discussion
The results of this study demonstrate that patients with acutemyocardial infarction may harbor multiple complex coronary plaques,which are associated with adverse clinical outcomes. These observationssupport the concept that plaque instability is not merely alocal vascular accident but probably reflects more generalizedpathophysiologic processes with the potential to destabilizeatherosclerotic plaques throughout the coronary tree.
In the present study, two fifths of the patients had angiographicevidence of multiple complex coronary plaques, which were associatedwith a less favorable in-hospital course. Patients with multiplecomplex plaques were less likely to undergo primary angioplasty,were more likely to require early coronary-artery bypass surgeryor staged multivessel angioplasty, and had greater depressionof left ventricular function than those with single complexplaques. The presence of multiple complex plaques was independentlypredictive of clinical events. Patients with multiple complexplaques had a more complicated course during the year aftermyocardial infarction. They had a higher incidence of recurrentangina and acute coronary syndromes. They were more likely torequire repeated angioplasty, which could be directed not onlyat the initial culprit plaque but also at non–infarct-relatedplaques previously identified as complex. They were also morelikely to require coronary-artery bypass surgery.
Our angiographic findings document the presence of multiplecomplex coronary plaques and their influence on outcome in patientswith acute transmural myocardial infarction. However, similarmultifocal plaque instability is evident in previous pathologicalstudies of patients with acute ischemic heart disease.1,2,16,17,18,19,20Multiple coronary thrombi were identified in an autopsy studyof 100 patients who died within six hours of acute myocardialinfarction, with 115 separate thrombi found in 74 patients.2Multiple coronary thrombi and multicentric plaque rupture havebeen found in other autopsy studies of fatal acute ischemicheart disease.1,16,17,18,19,20
The presence of coronary plaques with complex morphologic featuresis the angiographic hallmark of unstable coronary syndromes14,15,21,22,23,24,25,26,27,28,29,30,31,32and correlates with pathologic plaque rupture and thrombus.21,23,24Progression of stenosis and clinical instability are characteristicof such lesions.24,25,26,27,28,29,30,31 As in the present study,multiple complex plaques have been documented by angiographyin patients with unstable angina (at an average of 2.6 complexplaques per patient)32 and in patients with nontransmural infarction(423 complex lesions in 274 patients).33 The concept of multifocalplaque instability is also supported by angiographic natural-historystudies in patients with acute myocardial infarction,22 in whomrapid progression of both culprit and nonculprit lesions overa period of one month has been documented. Angiographic natural-historystudies in patients with unstable angina similarly demonstraterapid progression not only of the initial culprit lesion, butalso of nonculprit complex lesions.24,25 As in the present study,prior reports demonstrate that stenoses caused by angiographicallydetectable complex plaques are associated with a poor prognosis,23,24with a striking association between complex morphologic featuresand clinical instability.22,23,24,25,26,27,28,29,30,31 However,in some cases, complex plaques may remain stable over time.34
The present findings may have implications regarding the pathophysiologyof plaque instability. Weakening and disruption of its protectivefibrous cap appear to be the critical events triggering plaqueinstability.3,4,5 Autopsy and atherectomy specimens documentthat, as compared with stable plaques in the same patient, unstableplaques are characterized by active inflammation of the fibrouscap, concentrated at the point of plaque disruption.8,9 Inflammatorycells may activate matrix metalloproteinases that degrade theextracellular matrix and thereby weaken the fibrous cap.35,36Inflammation of the fibrous cap, whether related to the toxiceffects of oxidized low-density lipoproteins, viral triggers,or other factors,1,2,3,4,5 may arise from systemic processesand thereby affect the atherosclerotic coronary vasculaturein a more diffuse pattern.
Intrinsic plaque instability may develop owing to the expansionof intraplaque contents (e.g., lipid-pool swelling),1,2,3,4,5,6which may also reflect systemic derangements in lipid metabolism.Intraluminal mechanical forces implicated as extrinsic triggersof plaque rupture are also fundamentally influenced by determinantsthat exert effects throughout the coronary tree.10,11 Systemicalterations in platelet aggregability and clotting factors implicatedin triggering acute myocardial infarction37 would also be expectedto increase the thrombogenic potential of vulnerable erodedplaques throughout the coronary vessels.
Clinical observations support the concept that systemic processesinfluence plaque instability. Patients with acute myocardialinfarction have evidence of systemic inflammation, as reflectedby elevated levels of C-reactive and amyloid proteins.38,39,40Elevation of serologic markers of macrophage activity has beencorrelated with the presence of multiple complex plaques inpatients with unstable angina.32 The cardioprotective benefitsof aspirin against recurrent myocardial infarction may be mediatedin part by its systemic antiinflammatory effects.39 The reductionin recurrent myocardial infarction produced by systemic lipid-loweringinterventions designed to stabilize plaques adds further supportto the notion that unstable coronary artery disease is a multifocalprocess influenced by systemic factors.40 In aggregate, thesepathological, angiographic, and clinical observations supportthe concept that, at least in some patients, acute coronaryartery disease reflects a diffuse pathophysiologic process thatmay lead to multifocal plaque instability and rapid plaque progressionassociated with clinical instability.
It is important to emphasize the limitations of this study.The retrospective nature of the analysis could have influencedthe results. Angiography has a limited ability to delineatethe severity and complexity of coronary disease and to determinewhether a given complex lesion is acute or chronic. Complex-lesionmorphology may in some cases reflect more chronic occlusions;conversely, subtler plaque ulcerations may not be angiographicallyapparent. Although angiographically determined complexity correlatesclosely with plaque instability pathologically,21 and althoughcomplex plaques are associated with angiographic progressionand clinical instability,24,25,26,27,28,29,30,31 such plaquesmay remain stable over time34; therefore angiographic evidenceof complexity does not by itself necessarily determine the destinyof a plaque.
The present observations may have implications regarding thenatural history and management of acute coronary syndromes.Our results demonstrate that the presence of multiple complexcoronary plaques on angiography identifies a subgroup of patientsat increased risk for recurrent ischemia, even after successfulinitial acute percutaneous interventions. The next step willbe to determine whether strategies designed to stabilize plaquesby pharmacologic interventions (e.g., by aggressive lipid loweringor the use of antiinflammatory drugs) or multilesion revascularizationby percutaneous or surgical methods would be beneficial in patientswith multiple complex coronary plaques.
Source Information
From the Division of Cardiology, William Beaumont Hospital, Royal Oak, Mich. Presented in part in abstract form at the Scientific Sessions of the American Heart Association, Atlanta, November 7–10, 1999.
Address reprint requests to Dr. Goldstein at the Division of Cardiology, William Beaumont Hospital, 3601 W. 13 Mile Rd., Royal Oak, MI 48073-6769, or at jgoldstein{at}beaumont.edu.
References
Falk E. Plaque rupture with severe pre-existing stenosis precipitating coronary thrombosis: characteristics of coronary atherosclerotic plaques underlying fatal occlusive thrombi. Br Heart J 1983;50:127-134. [Free Full Text]
Davies MJ, Thomas A. Thrombosis and acute coronary-artery lesions in sudden cardiac ischemic death. N Engl J Med 1984;310:1137-1140. [Abstract]
Falk E, Shah PK, Fuster V. Coronary plaque disruption. Circulation 1995;92:657-671. [Free Full Text]
Libby P. Molecular bases of the acute coronary syndromes. Circulation 1995;91:2844-2850. [Free Full Text]
Davies MJ. A macro and micro view of coronary vascular insult in ischemic heart disease. Circulation 1990;82:Suppl II:II-38.
Farb A, Burke AP, Tang AL, et al. Coronary plaque erosion without rupture into a lipid core: a frequent cause of coronary thrombosis in sudden coronary death. Circulation 1996;93:1354-1363. [Free Full Text]
Moreno PR, Falk E, Palacios IF, Newell JB, Fuster V, Fallon JT. Macrophage infiltration in acute coronary syndromes: implications for plaque rupture. Circulation 1994;90:775-778. [Free Full Text]
van der Wal AC, Becker AE, van der Loos CM, Das PK. Site of intimal rupture or erosion of thrombosed coronary atherosclerotic plaques is characterized by an inflammatory process irrespective of the dominant plaque morphology. Circulation 1994;89:36-44. [Free Full Text]
Kovanen PT, Kaartinen M, Paavonen T. Infiltrates of activated mast cells at the site of coronary atheromatous erosion or rupture in myocardial infarction. Circulation 1995;92:1084-1088. [Free Full Text]
Gertz SD, Roberts WC. Hemodynamic shear force in rupture of coronary arterial atherosclerotic plaques. Am J Cardiol 1990;66:1368-1372. [CrossRef][Medline]
Muller JE, Stone PH, Turi ZG, et al. Circadian variation in the frequency of onset of acute myocardial infarction. N Engl J Med 1985;313:1315-1322. [Abstract]
Warnes CA, Roberts WC. Sudden coronary death: relation of amount and distribution of coronary narrowing at necropsy to previous symptoms of myocardial ischemia, left ventricular scarring and heart weight. Am J Cardiol 1984;54:65-73. [CrossRef][Medline]
Grines CL, Browne KF, Marco J, et al. A comparison of immediate angioplasty with thrombolytic therapy for acute myocardial infarction. N Engl J Med 1993;328:673-679. [Free Full Text]
Ambrose JA, Winters SL, Stern A, et al. Angiographic morphology and the pathogenesis of unstable angina pectoris. J Am Coll Cardiol 1985;5:609-616. [Abstract]
Rehr R, Disciascio G, Vetrovec G, Cowley M. Angiographic morphology of coronary artery stenoses in prolonged rest angina: evidence of intracoronary thrombosis. J Am Coll Cardiol 1989;14:1429-1437. [Abstract]
Qiao JH, Fishbein MC. The severity of coronary atherosclerosis at sites of plaque rupture with occlusive thrombosis. J Am Coll Cardiol 1991;17:1138-1142. [Abstract]
Chapman I. Morphogenesis of occluding coronary artery thrombosis. Arch Pathol 1965;80:256-261. [Medline]
Roberts WC, Buja LM. The frequency and significance of coronary arterial thrombi and other observations in fatal acute myocardial infarction: a study of 107 necropsy patients. Am J Med 1972;52:425-443. [CrossRef][Medline]
Falk E. Unstable angina with fatal outcome: dynamic coronary thrombosis leading to infarction and/or sudden death: autopsy evidence of recurrent mural thrombosis with peripheral embolization culminating in total vascular occlusion. Circulation 1985;71:699-708. [Free Full Text]
Frink RJ. Chronic ulcerated plaques: new insights into the pathogenesis of acute coronary disease. J Invasive Cardiol 1994;6:173-185. [Medline]
Levin DC, Fallon JT. Significance of the angiographic morphology of localized coronary stenoses: histopathologic correlations. Circulation 1982;66:316-320. [Free Full Text]
Guazzi MD, Bussotti M, Grancini L, et al. Evidence of multifocal activity of coronary disease in patients with acute myocardial infarction. Circulation 1997;96:1145-1151. [Free Full Text]
Ambrose JA. Prognostic implications of lesion irregularity on coronary angiography. J Am Coll Cardiol 1991;18:675-676. [Medline]
Theroux P. Angiographic and clinical progression in unstable angina: from clinical observations to clinical trials. Circulation 1995;91:2295-2298. [Free Full Text]
Moise A, Théroux P, Taeymans Y, et al. Unstable angina and progression of coronary atherosclerosis. N Engl J Med 1983;309:685-689. [Abstract]
Chen L, Chester MR, Redwood S, Huang J, Leatham E, Kaski JC. Angiographic stenosis progression and coronary events in patients with `stabilized' unstable angina. Circulation 1995;91:2319-2324. [Free Full Text]
Chester MR, Chen L, Kaski JC. The natural history of unheralded complex coronary plaques. J Am Coll Cardiol 1996;28:604-608. [Abstract]
Chen L, Chester MR, Crook R, Kaski JC. Differential progression of complex culprit stenoses in patients with stable and unstable angina pectoris. J Am Coll Cardiol 1996;28:597-603. [Abstract]
Kaski JC, Chester MR, Chen L, Katritsis D. Rapid angiographic progression of coronary artery disease in patients with angina pectoris: the role of complex stenosis morphology. Circulation 1995;92:2058-2065. [Free Full Text]
Freeman MR, Williams AE, Chisholm RJ, Armstrong PW. Intracoronary thrombus and complex morphology in unstable angina: relation to timing of angiography and in-hospital cardiac events. Circulation 1989;80:17-23. [Free Full Text]
Davies SW, Marchant B, Lyons JP, et al. Irregular coronary lesion morphology after thrombolysis predicts early clinical instability. J Am Coll Cardiol 1991;18:669-674. [Abstract]
Garcia-Moll X, Coccolo F, Cole D, Kaski JC. Serum neopterin and complex stenosis morphology in patients with unstable angina. J Am Coll Cardiol 2000;35:956-962. [Free Full Text]
Boden WE, Kerensky RA, Bertolet BD, Deedwania P, Chow BK, Pepine CJ. Coronary angiographic findings after non-Q-wave myocardial infarction: an analysis from the VANQWISH trial. Eur Heart J 1997;18:Suppl:123-123.abstract
Haft JI, al-Zarka AM. The origin and fate of complex coronary lesions. Am Heart J 1991;121:1050-1061. [CrossRef][Medline]
Galis ZS, Sukhova GK, Lark MW, Libby P. Increased expression of matrix metalloproteinases and matrix degrading activity in vulnerable regions of human atherosclerotic plaques. J Clin Invest 1994;94:2493-2503.
Shukhova GK, Schonbeck U, Rabkin E, et al. Evidence for increased collagenolysis by interstitial collagenases-1 and -3 in vulnerable human atheromatous plaques. Circulation 1999;99:2503-2509. [Free Full Text]
Thompson SG, Kienast J, Pyke SDM, Haverkate F, van de Loo JCW. Hemostatic factors and the risk of myocardial infarction or sudden death in patients with angina pectoris. N Engl J Med 1995;332:635-641. [Free Full Text]
Liuzzo G, Biasucci LM, Gallimore JR, et al. The prognostic value of C-reactive protein and serum amyloid A protein in severe unstable angina. N Engl J Med 1994;331:417-424. [Free Full Text]
Ridker PM, Cushman M, Stampfer MJ, Tracy RP, Hennekens CH. Inflammation, aspirin, and the risk of cardiovascular disease in apparently healthy men. N Engl J Med 1997;336:973-979. [Erratum, N Engl J Med 1997;337:356.] [Free Full Text]
Ridker PM, Rifai N, Pfeffer MA, et al. Inflammation, pravastatin, and the risk of coronary events after myocardial infarction in patients with average cholesterol levels. Circulation 1998;98:839-844. [Free Full Text]
Pundziute, G., Schuijf, J. D., Jukema, J. W., Decramer, I., Sarno, G., Vanhoenacker, P. K., Boersma, E., Reiber, J. H.C., Schalij, M. J., Wijns, W., Bax, J. J.
(2008). Evaluation of plaque characteristics in acute coronary syndromes: non-invasive assessment with multi-slice computed tomography and invasive evaluation with intravascular ultrasound radiofrequency data analysis. Eur Heart J
0: ehn356v1-9
[Abstract][Full Text]
Dodd, J. D., Rieber, J., Pomerantsev, E., Chaithiraphan, V., Achenbach, S., Moreiras, J. M., Abbara, S., Hoffmann, U., Brady, T. J., Cury, R. C.
(2008). Quantification of Nonculprit Coronary Lesions: Comparison of Cardiac 64-MDCT and Invasive Coronary Angiography. Am. J. Roentgenol.
191: 432-438
[Abstract][Full Text]
Duerinckx, A. J.
(2008). The Nonculprit Coronary Lesion as Seen by Coronary CT Angiography: What Should We Be Looking For?. Am. J. Roentgenol.
191: 439-440
[Full Text]
Foglieni, C., Maisano, F., Dreas, L., Giazzon, A., Ruotolo, G., Ferrero, E., Li Volsi, L., Coli, S., Sinagra, G., Zingone, B., Alfieri, O., Becker, A. E., Maseri, A.
(2008). Mild inflammatory activation of mammary arteries in patients with acute coronary syndromes. Am. J. Physiol. Heart Circ. Physiol.
294: H2831-H2837
[Abstract][Full Text]
Caymaz, H. O., Yuksel, G.
(2008). Fate of Incidental, Asymptomatic Lesions Discovered During Percutaneous Coronary Intervention. ANGIOLOGY
59: 193-197
[Abstract]
Bunch, T. J., Rihal, C. S., Gumina, R. J., Cooper, L., Caplice, N. M.
(2008). Progression of Nonculprit Plaque Stenosis Following Successful Percutaneous Intervention. ANGIOLOGY
59: 236-239
[Abstract]
Biasucci, L. M., Leo, M., De Maria, G. L.
(2008). Local and Systemic Mechanisms of Plaque Rupture. ANGIOLOGY
59: 73S-76S
[Abstract]
Spagnoli, L. G., Bonanno, E., Sangiorgi, G., Mauriello, A.
(2007). Role of Inflammation in Atherosclerosis. JNM
48: 1800-1815
[Abstract][Full Text]
Sabeti, S., Schlager, O., Exner, M., Mlekusch, W., Amighi, J., Dick, P., Maurer, G., Huber, K., Koppensteiner, R., Wagner, O., Minar, E., Schillinger, M.
(2007). Progression of Carotid Stenosis Detected by Duplex Ultrasonography Predicts Adverse Outcomes in Cardiovascular High-Risk Patients. Stroke
38: 2887-2894
[Abstract][Full Text]
Kubo, T., Imanishi, T., Takarada, S., Kuroi, A., Ueno, S., Yamano, T., Tanimoto, T., Matsuo, Y., Masho, T., Kitabata, H., Tsuda, K., Tomobuchi, Y., Akasaka, T.
(2007). Assessment of Culprit Lesion Morphology in Acute Myocardial Infarction: Ability of Optical Coherence Tomography Compared With Intravascular Ultrasound and Coronary Angioscopy. J Am Coll Cardiol
50: 933-939
[Abstract][Full Text]
Serruys, P. W., Garcia-Garcia, H. M., Regar, E.
(2007). From Postmortem Characterization to the In Vivo Detection of Thin-Capped Fibroatheromas: The Missing Link Toward Percutaneous Treatment: What If Diogenes Would Have Found What He Was Looking For?. J Am Coll Cardiol
50: 950-952
[Full Text]
Cheruvu, P. K., Finn, A. V., Gardner, C., Caplan, J., Goldstein, J., Stone, G. W., Virmani, R., Muller, J. E.
(2007). Frequency and Distribution of Thin-Cap Fibroatheroma and Ruptured Plaques in Human Coronary Arteries: A Pathologic Study. J Am Coll Cardiol
50: 940-949
[Abstract][Full Text]
Sorajja, P., Gersh, B. J., Cox, D. A., McLaughlin, M. G., Zimetbaum, P., Costantini, C., Stuckey, T., Tcheng, J. E., Mehran, R., Lansky, A. J., Grines, C. L., Stone, G. W.
(2007). Impact of multivessel disease on reperfusion success and clinical outcomes in patients undergoing primary percutaneous coronary intervention for acute myocardial infarction. Eur Heart J
28: 1709-1716
[Abstract][Full Text]
Saam, T., Hatsukami, T. S., Takaya, N., Chu, B., Underhill, H., Kerwin, W. S., Cai, J., Ferguson, M. S., Yuan, C.
(2007). The Vulnerable, or High-Risk, Atherosclerotic Plaque: Noninvasive MR Imaging for Characterization and Assessment. Radiology
244: 64-77
[Abstract][Full Text]
Grad, E., Golomb, M., Mor-Yosef, I., Koroukhov, N., Lotan, C., Edelman, E. R., Danenberg, H. D.
(2007). Transgenic expression of human C-reactive protein suppresses endothelial nitric oxide synthase expression and bioactivity after vascular injury. Am. J. Physiol. Heart Circ. Physiol.
293: H489-H495
[Abstract][Full Text]
Spagnoli, L. G., Pucci, S., Bonanno, E., Cassone, A., Sesti, F., Ciervo, A., Mauriello, A.
(2007). Persistent Chlamydia pneumoniae Infection of Cardiomyocytes Is Correlated with Fatal Myocardial Infarction. Am. J. Pathol.
170: 33-42
[Abstract][Full Text]
Mazzadi, A. N., Andre-Fouet, X., Costes, N., Croisille, P., Revel, D., Janier, M. F.
(2006). Mechanisms leading to reversible mechanical dysfunction in severe CAD: alternatives to myocardial stunning. Am. J. Physiol. Heart Circ. Physiol.
291: H2570-H2582
[Abstract][Full Text]
Waxman, S., Ishibashi, F., Muller, J. E.
(2006). Detection and Treatment of Vulnerable Plaques and Vulnerable Patients: Novel Approaches to Prevention of Coronary Events. Circulation
114: 2390-2411
[Full Text]
Boushra, N. N., Muntazar, M.
(2006). Review article: The role of statins in reducing perioperative cardiac risk: physiologic and clinical perspectives: [Le role des statines dans la reduction du risque cardiaque perioperatoire : perspectives physiologiques et cliniques].. Canadian J. Anesthesia
53: 1126-1147
[Abstract][Full Text]
Van De Graaff, E., Dutta, M., Das, P., Shry, E. A., Frederick, P. D., Blaney, M., Pasta, D. J., Steinhubl, S. R.
(2006). Early Coronary Revascularization Diminishes the Risk of Ischemic Stroke With Acute Myocardial Infarction. Stroke
37: 2546-2551
[Abstract][Full Text]
Hofmann, R., Niessner, A., Kypta, A., Steinwender, C., Kammler, J., Kerschner, K., Grund, M., Leisch, F., Huber, K.
(2006). Risk Score for Peri-Interventional Complications of Carotid Artery Stenting. Stroke
37: 2557-2561
[Abstract][Full Text]
Burke, A. P., Joner, M., Virmani, R.
(2006). IVUS-VH: a predictor of plaque morphology?. Eur Heart J
27: 1889-1890
[Full Text]
Suzuki, M., Saito, M., Nagai, T., Saeki, H., Kazatani, Y.
(2006). Systemic Versus Coronary Levels of Inflammation in Acute Coronary Syndromes. ANGIOLOGY
57: 459-463
[Abstract]
Bloomgarden, Z. T.
(2006). Third Annual World Congress on the Insulin Resistance Syndrome: Atherothrombotic disease. Diabetes Care
29: 1973-1980
[Full Text]
Elesber, A. A., Conover, C. A., Denktas, A. E., Lennon, R. J., Holmes, D. R. Jr, Overgaard, M. T., Christiansen, M., Oxvig, C., Lerman, L. O., Lerman, A.
(2006). Prognostic value of circulating pregnancy-associated plasma protein levels in patients with chronic stable angina. Eur Heart J
27: 1678-1684
[Abstract][Full Text]
Ohtani, T., Ueda, Y., Mizote, I., Oyabu, J., Okada, K., Hirayama, A., Kodama, K.
(2006). Number of Yellow Plaques Detected in a Coronary Artery Is Associated With Future Risk of Acute Coronary Syndrome: Detection of Vulnerable Patients by Angioscopy. J Am Coll Cardiol
47: 2194-2200
[Abstract][Full Text]
Hoffmann, U., Moselewski, F., Nieman, K., Jang, I.-K., Ferencik, M., Rahman, A. M., Cury, R. C., Abbara, S., Joneidi-Jafari, H., Achenbach, S., Brady, T. J.
(2006). Noninvasive Assessment of Plaque Morphology and Composition in Culprit and Stable Lesions in Acute Coronary Syndrome and Stable Lesions in Stable Angina by Multidetector Computed Tomography. J Am Coll Cardiol
47: 1655-1662
[Abstract][Full Text]
DeMaria, A. N., Narula, J., Mahmud, E., Tsimikas, S.
(2006). Imaging vulnerable plaque by ultrasound.. J Am Coll Cardiol
47: C32-C39
[Abstract][Full Text]
Stamper, D., Weissman, N. J., Brezinski, M.
(2006). Plaque Characterization With Optical Coherence Tomography.. J Am Coll Cardiol
47: C69-C79
[Abstract][Full Text]
Escolar, E., Weigold, G., Fuisz, A., Weissman, N. J.
(2006). New imaging techniques for diagnosing coronary artery disease.. CMAJ
174: 487-495
[Abstract][Full Text]
De Palma, R., Del Galdo, F., Abbate, G., Chiariello, M., Calabro, R., Forte, L., Cimmino, G., Papa, M. F., Russo, M. G., Ambrosio, G., Giombolini, C., Tritto, I., Notaristefano, S., Berrino, L., Rossi, F., Golino, P.
(2006). Patients With Acute Coronary Syndrome Show Oligoclonal T-Cell Recruitment Within Unstable Plaque: Evidence for a Local, Intracoronary Immunologic Mechanism. Circulation
113: 640-646
[Abstract][Full Text]
Toutouzas, K., Drakopoulou, M., Mitropoulos, J., Tsiamis, E., Vaina, S., Vavuranakis, M., Markou, V., Bosinakou, E., Stefanadis, C.
(2006). Elevated Plaque Temperature in Non-Culprit De Novo Atheromatous Lesions of Patients With Acute Coronary Syndromes. J Am Coll Cardiol
47: 301-306
[Abstract][Full Text]
Sdringola, S., Loghin, C., Boccalandro, F., Gould, K. L.
(2006). Mechanisms of Progression and Regression of Coronary Artery Disease by PET Related to Treatment Intensity and Clinical Events at Long-Term Follow-up. JNM
47: 59-67
[Abstract][Full Text]
Rodriguez-Granillo, G. A., Garcia-Garcia, H. M., Mc Fadden, E. P., Valgimigli, M., Aoki, J., de Feyter, P., Serruys, P. W.
(2005). In Vivo Intravascular Ultrasound-Derived Thin-Cap Fibroatheroma Detection Using Ultrasound Radiofrequency Data Analysis. J Am Coll Cardiol
46: 2038-2042
[Abstract][Full Text]
Smith, E J, Mathur, A, Rothman, M T
(2005). Recent advances in primary percutaneous intervention for acute myocardial infarction. Heart
91: 1533-1536
[Full Text]
Ince, H., Petzsch, M., Kleine, H. D., Schmidt, H., Rehders, T., Korber, T., Schumichen, C., Freund, M., Nienaber, C. A.
(2005). Preservation From Left Ventricular Remodeling by Front-Integrated Revascularization and Stem Cell Liberation in Evolving Acute Myocardial Infarction by Use of Granulocyte-Colony-Stimulating Factor (FIRSTLINE-AMI). Circulation
112: 3097-3106
[Abstract][Full Text]
Zimarino, M., Calafiore, A. M., De Caterina, R.
(2005). Complete myocardial revascularization: between myth and reality. Eur Heart J
26: 1824-1830
[Abstract][Full Text]
Biasucci, L M, Giubilato, G, Graziani, F, Piro, M
(2005). CRP is or is not a reliable marker of ischaemic heart disease?. Lupus
14: 752-755
[Abstract]
Zimarino, M., De Caterina, R.
(2005). Complete myocardial revascularization: between myth and reality: reply. Eur Heart J
26: 1810-1811
[Full Text]
Valgimigli, M., Agostoni, P., Biondi Zoccai, G. G.L.
(2005). Complete myocardial revascularization: between myth and reality. Eur Heart J
26: 1809-1810
[Full Text]
Figueras, J, Pena, C, Soler-Soler, J
(2005). Thirty day prognosis of patients with acute pulmonary oedema complicating acute coronary syndromes. Heart
91: 889-893
[Abstract][Full Text]
Libby, P., Theroux, P.
(2005). Pathophysiology of Coronary Artery Disease. Circulation
111: 3481-3488
[Abstract][Full Text]
Mauriello, A., Sangiorgi, G., Fratoni, S., Palmieri, G., Bonanno, E., Anemona, L., Schwartz, R. S., Spagnoli, L. G.
(2005). Diffuse and Active Inflammation Occurs in Both Vulnerable and Stable Plaques of the Entire Coronary Tree: A Histopathologic Study of Patients Dying of Acute Myocardial Infarction. J Am Coll Cardiol
45: 1585-1593
[Abstract][Full Text]
Tanaka, A., Shimada, K., Sano, T., Namba, M., Sakamoto, T., Nishida, Y., Kawarabayashi, T., Fukuda, D., Yoshikawa, J.
(2005). Multiple Plaque Rupture and C-Reactive Protein in Acute Myocardial Infarction. J Am Coll Cardiol
45: 1594-1599
[Abstract][Full Text]
Libby, P.
(2005). Act Local, Act Global: Inflammation and the Multiplicity of "Vulnerable" Coronary Plaques. J Am Coll Cardiol
45: 1600-1602
[Full Text]
Schillinger, M., Exner, M., Mlekusch, W., Sabeti, S., Amighi, J., Nikowitsch, R., Timmel, E., Kickinger, B., Minar, C., Pones, M., Lalouschek, W., Rumpold, H., Maurer, G., Wagner, O., Minar, E.
(2005). Inflammation and Carotid Artery--Risk for Atherosclerosis Study (ICARAS). Circulation
111: 2203-2209
[Abstract][Full Text]
Takano, M., Inami, S., Ishibashi, F., Okamatsu, K., Seimiya, K., Ohba, T., Sakai, S., Mizuno, K.
(2005). Angioscopic follow-up study of coronary ruptured plaques in nonculprit lesions. J Am Coll Cardiol
45: 652-658
[Abstract][Full Text]
Ambrose, J. A., D'Agate, D. J.
(2005). Plaque rupture and intracoronary thrombus in nonculprit vessels: An eyewitness account. J Am Coll Cardiol
45: 659-660
[Full Text]
Lerman, A., Zeiher, A. M.
(2005). Endothelial Function: Cardiac Events. Circulation
111: 363-368
[Full Text]
Monaco, C., Rossi, E., Milazzo, D., Citterio, F., Ginnetti, F., D'Onofrio, G., Cianflone, D., Crea, F., Biasucci, L. M., Maseri, A.
(2005). Persistent systemic inflammation in unstable angina is largely unrelated to the atherothrombotic burden. J Am Coll Cardiol
45: 238-243
[Abstract][Full Text]
Vetrovec, G. W.
(2005). Optimizing Percutaneous Coronary Intervention Outcomes: The Next Steps. Circulation
111: 125-126
[Full Text]
Glaser, R., Selzer, F., Faxon, D. P., Laskey, W. K., Cohen, H. A., Slater, J., Detre, K. M., Wilensky, R. L.
(2005). Clinical Progression of Incidental, Asymptomatic Lesions Discovered During Culprit Vessel Coronary Intervention. Circulation
111: 143-149
[Abstract][Full Text]
Rioufol, G., Gilard, M., Finet, G., Ginon, I., Boschat, J., Andre-Fouet, X.
(2004). Evolution of Spontaneous Atherosclerotic Plaque Rupture With Medical Therapy: Long-Term Follow-Up With Intravascular Ultrasound. Circulation
110: 2875-2880
[Abstract][Full Text]
Madjid, M., Zarrabi, A., Litovsky, S., Willerson, J. T., Casscells, W.
(2004). Finding Vulnerable Atherosclerotic Plaques: Is It Worth the Effort?. Arterioscler. Thromb. Vasc. Bio.
24: 1775-1782
[Abstract][Full Text]
Fernandez-Aviles, F., San Roman, J. A., Garcia-Frade, J., Fernandez, M. E., Penarrubia, M. J., de la Fuente, L., Gomez-Bueno, M., Cantalapiedra, A., Fernandez, J., Gutierrez, O., Sanchez, P. L., Hernandez, C., Sanz, R., Garcia-Sancho, J., Sanchez, A.
(2004). Experimental and Clinical Regenerative Capability of Human Bone Marrow Cells After Myocardial Infarction. Circ. Res.
95: 742-748
[Abstract][Full Text]
Zouridakis, E., Avanzas, P., Arroyo-Espliguero, R., Fredericks, S., Kaski, J. C.
(2004). Markers of Inflammation and Rapid Coronary Artery Disease Progression in Patients With Stable Angina Pectoris. Circulation
110: 1747-1753
[Abstract][Full Text]
Okazaki, S., Yokoyama, T., Miyauchi, K., Shimada, K., Kurata, T., Sato, H., Daida, H.
(2004). Early Statin Treatment in Patients With Acute Coronary Syndrome: Demonstration of the Beneficial Effect on Atherosclerotic Lesions by Serial Volumetric Intravascular Ultrasound Analysis During Half a Year After Coronary Event: The ESTABLISH Study. Circulation
110: 1061-1068
[Abstract][Full Text]
Hong, M.-K., Mintz, G. S., Lee, C. W., Kim, Y.-H., Lee, S.-W., Song, J.-M., Han, K.-H., Kang, D.-H., Song, J.-K., Kim, J.-J., Park, S.-W., Park, S.-J.
(2004). Comparison of Coronary Plaque Rupture Between Stable Angina and Acute Myocardial Infarction: A Three-Vessel Intravascular Ultrasound Study in 235 Patients. Circulation
110: 928-933
[Abstract][Full Text]
Avanzas, P, Arroyo-Espliguero, R, Cosin-Sales, J, Aldama, G, Pizzi, C, Quiles, J, Kaski, J C
(2004). Markers of inflammation and multiple complex stenoses (pancoronary plaque vulnerability) in patients with non-ST segment elevation acute coronary syndromes. Heart
90: 847-852
[Abstract][Full Text]
Abbate, A., Bonanno, E., Mauriello, A., Bussani, R., Biondi-Zoccai, G. G.L., Liuzzo, G., Leone, A. M., Silvestri, F., Dobrina, A., Baldi, F., Pandolfi, F., Biasucci, L. M., Baldi, A., Spagnoli, L. G., Crea, F.
(2004). Widespread Myocardial Inflammation and Infarct-Related Artery Patency. Circulation
110: 46-50
[Abstract][Full Text]
Priebe, H.-J.
(2004). Triggers of perioperative myocardial ischaemia and infarction. Br J Anaesth
93: 9-20
[Abstract][Full Text]
Gibson, C. M., Schomig, A.
(2004). Coronary and Myocardial Angiography: Angiographic Assessment of Both Epicardial and Myocardial Perfusion. Circulation
109: 3096-3105
[Full Text]
Lombardo, A., Biasucci, L. M., Lanza, G. A., Coli, S., Silvestri, P., Cianflone, D., Liuzzo, G., Burzotta, F., Crea, F., Maseri, A.
(2004). Inflammation as a Possible Link Between Coronary and Carotid Plaque Instability. Circulation
109: 3158-3163
[Abstract][Full Text]
Luft, F. C.
(2004). Cardiac Angiotensin Is Upregulated in the Hearts of Unstable Angina Patients. Circ. Res.
94: 1530-1532
[Full Text]
Neri Serneri, G. G., Boddi, M., Modesti, P. A., Coppo, M., Cecioni, I., Toscano, T., Papa, M. L., Bandinelli, M., Lisi, G. F., Chiavarelli, M.
(2004). Cardiac Angiotensin II Participates in Coronary Microvessel Inflammation of Unstable Angina and Strengthens the Immunomediated Component. Circ. Res.
94: 1630-1637
[Abstract][Full Text]
Langheinrich, A. C., Bohle, R. M., Greschus, S., Hackstein, N., Walker, G., von Gerlach, S., Rau, W. S., Holschermann, H.
(2004). Atherosclerotic Lesions at Micro CT: Feasibility for Analysis of Coronary Artery Wall in Autopsy Specimens. Radiology
231: 675-681
[Abstract][Full Text]
Cannon, C. P., Braunwald, E., McCabe, C. H., Rader, D. J., Rouleau, J. L., Belder, R., Joyal, S. V., Hill, K. A., Pfeffer, M. A., Skene, A. M., the Pravastatin or Atorvastatin Evaluation and Inf,
(2004). Intensive versus Moderate Lipid Lowering with Statins after Acute Coronary Syndromes. NEJM
350: 1495-1504
[Abstract][Full Text]
Honda, O., Sugiyama, S., Kugiyama, K., Fukushima, H., Nakamura, S., Koide, S., Kojima, S., Hirai, N., Kawano, H., Soejima, H., Sakamoto, T., Yoshimura, M., Ogawa, H.
(2004). Echolucent carotid plaques predict future coronary events in patients with coronary artery disease. J Am Coll Cardiol
43: 1177-1184
[Abstract][Full Text]
Leber, A. W., Knez, A., Becker, A., Becker, C., von Ziegler, F., Nikolaou, K., Rist, C., Reiser, M., White, C., Steinbeck, G., Boekstegers, P.
(2004). Accuracy of multidetector spiral computed tomography in identifying and differentiating the composition of coronary atherosclerotic plaques: A comparative study with intracoronary ultrasound. J Am Coll Cardiol
43: 1241-1247
[Abstract][Full Text]
Arroyo-Espliguero, R., Avanzas, P., Cosin-Sales, J., Aldama, G., Pizzi, C., Kaski, J. C.
(2004). C-reactive protein elevation and disease activity in patients with coronary artery disease. Eur Heart J
25: 401-408
[Abstract][Full Text]
Chandra, H. R., Goldstein, J. A., Choudhary, N., O'Neill, C. S., George, P. B., Gangasani, S. R., Cronin, L., Marcovitz, P. A., Hauser, A. M., O'Neill, W. W.
(2004). Adverse outcome in aortic sclerosis is associated with coronary artery disease and inflammation. J Am Coll Cardiol
43: 169-175
[Abstract][Full Text]
Lutgens, E., van Suylen, R.-J., Faber, B. C., Gijbels, M. J., Eurlings, P. M., Bijnens, A.-P., Cleutjens, K. B., Heeneman, S., Daemen, M. J.A.P.
(2003). Atherosclerotic Plaque Rupture: Local or Systemic Process?. Arterioscler. Thromb. Vasc. Bio.
23: 2123-2130
[Abstract][Full Text]
Fujii, K., Kobayashi, Y., Mintz, G. S., Takebayashi, H., Dangas, G., Moussa, I., Mehran, R., Lansky, A. J., Kreps, E., Collins, M., Colombo, A., Stone, G. W., Leon, M. B., Moses, J. W.
(2003). Intravascular Ultrasound Assessment of Ulcerated Ruptured Plaques: A Comparison of Culprit and Nonculprit Lesions of Patients With Acute Coronary Syndromes and Lesions in Patients Without Acute Coronary Syndromes. Circulation
108: 2473-2478
[Abstract][Full Text]
Naghavi, M., Libby, P., Falk, E., Casscells, S. W., Litovsky, S., Rumberger, J., Badimon, J. J., Stefanadis, C., Moreno, P., Pasterkamp, G., Fayad, Z., Stone, P. H., Waxman, S., Raggi, P., Madjid, M., Zarrabi, A., Burke, A., Yuan, C., Fitzgerald, P. J., Siscovick, D. S., de Korte, C. L., Aikawa, M., Juhani Airaksinen, K.E., Assmann, G., Becker, C. R., Chesebro, J. H., Farb, A., Galis, Z. S., Jackson, C., Jang, I.-K., Koenig, W., Lodder, R. A., March, K., Demirovic, J., Navab, M., Priori, S. G., Rekhter, M. D., Bahr, R., Grundy, S. M., Mehran, R., Colombo, A., Boerwinkle, E., Ballantyne, C., Insull, W. Jr, Schwartz, R. S., Vogel, R., Serruys, P. W., Hansson, G. K., Faxon, D. P., Kaul, S., Drexler, H., Greenland, P., Muller, J. E., Virmani, R., Ridker, P. M, Zipes, D. P., Shah, P. K., Willerson, J. T.
(2003). From Vulnerable Plaque to Vulnerable Patient: A Call for New Definitions and Risk Assessment Strategies: Part I. Circulation
108: 1664-1672
[Abstract][Full Text]
Schoenhagen, P., Stone, G. W., Nissen, S. E., Grines, C. L., Griffin, J., Clemson, B. S., Vince, D. G., Ziada, K., Crowe, T., Apperson-Hanson, C., Kapadia, S. R., Tuzcu, E. M.
(2003). Coronary Plaque Morphology and Frequency of Ulceration Distant From Culprit Lesions in Patients With Unstable and Stable Presentation. Arterioscler. Thromb. Vasc. Bio.
23: 1895-1900
[Abstract][Full Text]
Kato, M., Dote, K., Habara, S., Takemoto, H., Goto, K., Nakaoka, K.
(2003). Clinical implications of carotid artery remodeling in acute coronary syndrome: Ultrasonographic assessment of positive remodeling. J Am Coll Cardiol
42: 1026-1032
[Abstract][Full Text]
Tuzcu, E. M., Schoenhagen, P.
(2003). Acute coronary syndromes, plaque vulnerability,and carotid artery disease: The changing role ofatherosclerosis imaging. J Am Coll Cardiol
42: 1033-1036
[Full Text]
Forrester, J. S., Price, M. J., Makkar, R. R.
(2003). Stem Cell Repair of Infarcted Myocardium: An Overview for Clinicians. Circulation
108: 1139-1145
[Full Text]
Erbel, R
(2003). Spontaneous and interventional coronary microembolisation. Heart
89: 986-989
[Full Text]
Neri Serneri, G. G., Boddi, M., Modesti, P. A., Cecioni, I., Coppo, M., Papa, M. L., Toscano, T., Marullo, A., Chiavarelli, M.
(2003). Immunomediated and Ischemia-Independent Inflammation of Coronary Microvessels in Unstable Angina. Circ. Res.
92: 1359-1366
[Abstract][Full Text]
Kotani, J.-i., Mintz, G. S., Castagna, M. T., Pinnow, E., Berzingi, C. O., Bui, A. B., Pichard, A. D., Satler, L. F., Suddath, W. O., Waksman, R., Laird, J. R. Jr, Kent, K. M., Weissman, N. J.
(2003). Intravascular Ultrasound Analysis of Infarct-Related and Non-Infarct-Related Arteries in Patients Who Presented With an Acute Myocardial Infarction. Circulation
107: 2889-2893
[Abstract][Full Text]
Maseri, A., Fuster, V.
(2003). Is There a Vulnerable Plaque?. Circulation
107: 2068-2071
[Full Text]
Casscells, W., Naghavi, M., Willerson, J. T.
(2003). Vulnerable Atherosclerotic Plaque: A Multifocal Disease. Circulation
107: 2072-2075
[Full Text]
Poldermans, D., Bax, J. J., Kertai, M. D., Krenning, B., Westerhout, C. M., Schinkel, A. F.L., Thomson, I. R., Lansberg, P. J., Fleisher, L. A., Klein, J., van Urk, H., Roelandt, J. R.T.C., Boersma, E.
(2003). Statins Are Associated With a Reduced Incidence of Perioperative Mortality in Patients Undergoing Major Noncardiac Vascular Surgery. Circulation
107: 1848-1851
[Abstract][Full Text]
Haft, J. I., Rioufol, G., Finet, G., Ginon, I., Andre-Fouet, X., Rossi, R., Vialle, E., Desjoyaux, E., Convert, G., Huret, J.-F., Tabib, A.
(2003). Multiple Atherosclerotic Plaque Rupture in Acute Coronary Syndrome * Response. Circulation
107
: e65-e66
[Full Text]
Shah, P. K.
(2003). Mechanisms of plaque vulnerability and rupture. J Am Coll Cardiol
41: 15S-22S
[Abstract][Full Text]
Mehta, S. R., Yusuf, S.
(2003). Short- and long-term oral antiplatelet therapy in acute coronary syndromes and percutaneous coronary intervention. J Am Coll Cardiol
41: 79S-88S
[Abstract][Full Text]
McKay, R. G.
(2003). "Ischemia-guided" versus "early invasive" strategies in the management of acute coronary syndrome/non-ST-segment elevation myocardial infarction: The interventionalist's perspective. J Am Coll Cardiol
41: 96S-102S
[Abstract][Full Text]
Nissen, S. E.
(2003). Pathobiology, not angiography, should guide managementin acute coronary syndrome/non-ST-segment elevation myocardial infarction: The non-interventionist's perspective. J Am Coll Cardiol
41: 103S-112S
[Abstract][Full Text]
Tsimikas, S., Bergmark, C., Beyer, R. W., Patel, R., Pattison, J., Miller, E., Juliano, J., Witztum, J. L.
(2003). Temporal increases in plasma markers of oxidized low-density lipoprotein strongly reflect the presence of acute coronary syndromes. J Am Coll Cardiol
41: 360-370
[Abstract][Full Text]
0.001). During the year after myocardial infarction, the presence of multiple complex plaques was associated with an increased incidence of recurrent acute coronary syndromes (19.0 percent vs. 2.6 percent, P
Previous
