DOCSLIB.ORG

Pathology of Vulnerable Plaque

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Pathology of Vulnerable Plaque PathologyPathology ofof VulnerableVulnerable PlaquePlaque AngioplastyAngioplasty SummitSummit 20052005 TCTTCT AsiaAsia Pacific,Pacific, Seoul,Seoul, AprilApril 2828--30,30, 20052005 Renu Virmani, MD CVPath, A Research Service of the International Registry of Pathology Gaithersburg, MD Plaque Morphology of Thrombi in SCD Plaque Rupture 55 - 60% th th Plaque Erosion th 30 - 35% th Calcified Nodule 2 -7 % th ClinicalClinical andand MorphologicMorphologic DifferenceDifference inin PlaquesPlaques AssociatedAssociated withwith LuminalLuminal ThrombiThrombi Plaque rupture Plaque erosion Calcified nodule Lumen Lumen Th Th Th Necrotic core 45-55% thrombi in 35-40% thrombi in 4-7% thrombi in SCD SCD SCD, calcified plates M>F, Older, Ca++ M=F, younger M>F, older, mid Eccentric = Usually eccentric RCA concentric Lesser % stenosis Usually eccentric Greater % stenosis SMC rich, Stenosis variable Macs, T cells,HLADr proteoglycans Nodules of bone A NC Gross and Light Microscopic Th Features of Plaque Rupture 60% of Thrombi in Sudden Coronary Death Are form Plaque Rupture B NC D F Th SMCs T cells C E G NC Th MΦ HLA-DR Fig 3-1 Plaque erosion in a 33 year-old female complaining of chest pain for two-weeks and discharged from the emergency room with a diagnoses of anxiety. A B C NC SMCs MΦ D E F T-cells PLT Fibrin Development of Human Coronary Atherosclerosis Pathologic Intimal Intimal intimal Fibrous Thin-cap thickening xanthoma thickening cap atheroma Fibroatheroma NC LP NC FC Smooth muscle cells Calcified plaque Macrophage foam cells Hemorrhage Extracellular lipid Thrombus Cholesterol clefts Healed thrombus Necrotic core Collagen What is a Vulnerable Plaque? • Plaque morphology underlying luminal thrombi represents a vulnerable plaque – Thin-cap Fibroatheroma – Plaque rupture – Pathologic intimal thickening Plaque – Fibroatheroma Erosion – Calcified plates with bone formation – Calcified nodule - surface thrombus Thin cap Fibroatheroma is a Precursor lesions of Plaque Rupture TCFA Plaque Rupture *Ruptured cap Th Thin fibrous nc cap ? th * nc Thin-Cap Atheroma (Vulnerable Plaque) Components • Necrotic core • Thin fibrous cap (< 65 µm) • Cap infiltrated by macrophages and lymphocytes • Cap composition – type 1 collagen and few smooth muscle cells A Non-Hemodynamically Limiting Thin-cap Fibroatheroma A B C NC NC Movat H&E D E Fig 2-2 MΦ SMCs Morphologic Characteristics of Plaque Rupture and Thin-cap Fibroatheromas Necrotic Fibrous cap MΦs SMCs T- Calcification Plaque type Core (%) Thickness (µm) (%) (%) lymph Score Rupture 34±17 23±19 26±20 0.002±0.004 4.9±4.3 1.53±1.03 Thin-cap Fibroatheroma 23±17 <65µm 14±10 6.6±10.4 6.6±10.4 0.97±1.1 P value 0.01 0.005 ns ns 0.014 Mean values are represented ± standard deviation. Abbreviations: MΦs= macrophages, SMCs= smooth muscle cells, T-lymph= T-lymphocytes Kolodgie F, et al. Current Opinion in Cardiology 2001;16:285 Morphological Variants of the Thin-Cap Fibroatheroma Insignificant Large eccentric Large concentric Healed Plaque burden necrotic core necrotic core Rupture(s) NC NC NC NC NC NC NC Kolodgie F, et al. Current Opinion in Cardiology 2001;16:285 Vulnerable Plaque Characteristics AB Type of plaque 90 50 80 45 70 40 35 60 30 50 25 40 20 30 15 % thin cap atheroma % thin 20 10 10 5 0 0 90 % cross sectional area luminal narrowing ≥ <50% 75-89 50-74% rupture thin cap healed rupture healed hemorrhage Cross sectional luminal narrowing fibrous atheroma Mean % x-sectional area 80% of thin cap atheromas occur in arteries For TCFA is 60% with < 75% x-sectional area luminal narrowing (<50% diameter reduction) Distribution of Ruptures and Thin-Cap Atheromas by Plaque Area or Lipid Core Size A B 73 ± 13%* 45 45 40 40 77 ± 16%* ± 35 77 15%* 35 30 79 ± 13%* 30 71 ± 13%* 25 25 20 20 81 ± 9%* 78 ± 12%* (n= 90) 15 82 ± 9%* (n= 90) 15 10 10 5 Plaque Ruptures (%) 5 0 Plaque Ruptures (%) 0 % <10 %10-25 %25-50 >50% area<1 area 1-3 area 3-5 area > 5 Lipid core as % plaque area Cross sectional lipid core area, mm2 C D 45 65 ± 15%* 45 71 ± 17%* 40 40 ± 35 74 15%* 35 30 30 65 ± 17%* 25 25 ± 77 9%* n= 106) n= 106) 20 20 76 ± 14%* 78 ± 12%* 15 ± 15 77 13%* 10 10 5 5 0 0 Thin-Cap Fibroatheromas (%) Thin-Cap Fibroatheromas (%) % <10 %10-25 %25-50 >50% area<1 area 1-3 area 3-5 area > 5 Fig 2-8 * = mean cross sectional area luminal narrowing DoDo TCFAsTCFAs leadlead toto plaqueplaque progressionprogression ?? Movat pentachrome Sirius red Sirius red with polarized light Mean % Stenosis Increases with Number of Prior Rupture Sites but the Increase with Each New Rupture is Small (<20%) 90 Healed Rupture Sites Acute Rupture Sites 100 80 90 70 80 60 70 50 60 40 50 30 40 30 Mean % stenosis Mean % stenosis 20 20 10 10 0 0 1 2 3 4 A 0 1 2 3 4 Number of prior ruptures, B Number of prior ruptures, healed rupture sites acute rupture sites Burke, A P et al. Circulation 2001;103:9364-940 PercentagePercentage ofof CrossCross--SectionalSectional--AreaArea NarrowingNarrowing byby PlaquePlaque MorphologyMorphology A B P= 0.05 Thin Acute Healed cap rupture rupture 100 50 46 80 45 43 60 38 40 36 35 37 N=12 N=19 40 35 30 27 20 25 22 X-SCA Narrowing (%) Occlusive Non-Occlusive 0 20 18 Thrombus 15 C 10 45 Total Sections (%) 5 40 0 35 30 < 50 < 50 < 50 25 50- 74 50- 74 50- 74 75-100 75-100 75-100 20 15 Cross-Sectional-Area Narrowing (% ) 10 5 0 Fig 2-6 -New lumen lumen (%) Old 1234 No. Healed Ruptures Necrotic core size, sum mm2, independent of plaque area, morphometrically determined, at maximal luminal narrowing of 3 major epicardial arteries P=0.01 2 6 P=0.03 5 4 3 2 1 0 Mean necrotic core area mm Normal TC/HDL-C TC/HDL-C > 7 TC/HDL-C >5, <7 Relationship ofFibrousCapThickness to Cell Mean for % Kp-1 0 1 2 3 4 5 6 Macrophage Infiltration Less than 65 µm P =0.06 66 - 200 µm P =0.03 201 - 300 µm More than 300 µm Correlation of Fibrous Cap Thickness and Macrophage Infiltration 16 R2 = .117 14 P = <0.001 12 10 8 % kp-1 6 4 2 0 -2 -100 0 100 200 300 400 500 600 Fibrous cap thickness mm Relationship ofFibrousCapThickness to % Necrotic Core Underlying PercentNecrotic Core 10 15 20 25 30 35 40 0 5 Less than 65 µm 66 - 200 µm 201 - 300 µm More than 300 µm Correlation of X-Ray Calcification with Plaque type A B Speckled LM RCA LAD C Fragmented D Diffuse CalcifiedCalcified MatrixMatrix DeterminedDetermined HistologicallyHistologically Severe Coronary Artery Disease, n=36, 64+14 yrs Coronary Arteries Serially Sectioned 3 2.5 2 1.5 1 Mean calcification score calcification Mean .5 0 erosion rupture Thin cap fibroatheroma healed rupture thickening Pathologic intimal Proportion and types of “unstable” plaques, by approximate distance from ostium 60 proximal 50 n mid o i t distal u 40 b i r t s i 30 d % 20 10 0 Fibro- hemorrhage thin cap acute healed atheroma into plaque rupture rupture Frequency and Location of Unstable Lesions: Thin-cap Atheromas, Acute and Healed Ruptures in the Coronary Circulation Thin-cap Fibroatheroma Acute Plaque Rupture 50 50 45 45 31 56 40 40 35 Total Lesions= 131 35 Total Lesions= 68 30 30 25 25 17 26 15 20 23 20 Frequency (%) 15 15 11 Frequency (%) 10 ‘Plaque Rupture’ 10 ‘Thin-Cap Fibroatheroma’ 5 5 6 5 22 1 2 11 0 0 Healed Plaque Rupture 50 pLAD 61 45 pRC 40 pLCx 35 LM 30 Total Lesions= 136 LOM 25 dRC 20 23 23 dLAD 15 dLCx Frequency (%) 12 ‘Healed Rupture’ 10 6 5 6 Kolodgie F, et al. Current Opinion 4 1 0 in Cardiology 2001;16:285 P=0.009 A. P=0.01 4 P=0.04 3.5 P=0.05 3 2.5 Frequency of Thin-Cap 2 Fibroatheromas 1.5 1 by Decades .5 Mean Number of TCFAs 0 30’s 40’s 50’s 60’s 70’s B. 6 No acute MI 5 With acute MI 4 3 2 1 Mean Number of TCFAs Fig 2-7 0 30’s 40’s 50’s 60’s 70’s Number of Thin-Cap Atheromas in Various Coronary Syndromes in Males and Females 4 Male 3.5 Female 3 2.5 2 1.5 1 Mean Number of Thin-Cap Atheromas .5 0 MI SCD Incidental Erosion Fig 2-11 Frequency of thin cap atheroma, by mechanism of death 3 2.5 2 1.5 1 .5 Number of thin cap atheromas 0 erosion noncoronary stable plaque acute rupture healed rupture LCx Plaque rupture A nc RCA LCx C nc E Thin cap Fibro- atheroma F nc th nc B G Thin cap fibroatheroma nc D LAD nc E F 43-year old WM collapsed at work and could not be resuscitated. Fig. 11 Comparison of the Length, Necrotic Core Area and % Necrotic core/plaque Area Dimensions Fibroatheroma Thin-cap Plaque Atheroma Rupture Length, mm, 6 mm (range 8 mm (range 9 mm (range mean/Range 1-18 mm) 2-16 mm) 2.5-22 mm) Necrotic core 1.2 ± 2.2 1.7 ± 1.1 3.8 ± 5.5 area mm2 % necrotic 15 ± 20 % 23 ± 17 % 34 ± 17 % core/plaque area Serial Sections of a Thin-Cap Fibroatheroma Cut 250 mm apart ABCD EFGH Fig 2-16 Serial Coronary Sections (mm) Demonstrating Multiple Vulnerable Plaques and Rupture Sites Proximal LCx A B C D 0.2 0.5 1.1 1.7 E F G H 1.9 2.22.5 2.7 Distal I J K L 3.0 3.3 3.6 3.9 IEL-Expected IEL (mm2) A.
Load more

Recommended publications
  • Association of Coronary Stenosis and Plaque Morphology with Fractional Flow Reserve and Outcomes
    Clinical Review & Education Review Association of Coronary Stenosis and Plaque Morphology With Fractional Flow Reserve and Outcomes Amir Ahmadi, MD; Gregg W. Stone, MD; Jonathon Leipsic, MD; Patrick W. Serruys, MD, PhD; Leslee Shaw, PhD; Harvey Hecht, MD; Graham Wong, MD; Bjarne Linde Nørgaard, MD, PhD; Patrick T. O’Gara, MD; Y. Chandrashekhar, MD; Jagat Narula, MD, PhD, MACC CME Quiz at jamanetworkcme.com and IMPORTANCE Obstructive coronary lesions with reduced luminal dimensions may result in CME Questions page 372 abnormal regional myocardial blood flow as assessed by stress-induced myocardial perfusion imaging or a significant fall in distal perfusion pressure with hyperemia-induced vasodilatation (fractional flow reserve [FFR] Յ0.80). An abnormal FFR has been demonstrated to identify high-risk lesions benefitting from percutaneous coronary Author Affiliations: Division of intervention while safely allowing revascularization to be deferred in low-risk lesions, Cardiology, Icahn School of Medicine resulting in a decrease in the number of revascularization procedures as well as substantially at Mount Sinai, New York, New York reduced death and myocardial infarction. While FFR identifies hemodynamically significant (Ahmadi, Hecht, Narula); Division of Cardiology and Radiology, University lesions likely to produce ischemia-related symptoms, it remains less clear as to why it might of British Columbia, Vancouver, predict the risk of acute coronary syndromes, which are usually due to plaque rupture and Canada (Ahmadi, Leipsic, Wong); coronary
    [Show full text]
  • Finding the Vulnerable Plaque
    Editorial Finding the Vulnerable Plaque By C. Richard Conti, MD, MACC, Editor-in-Chief At a recent Transcatheter Therapeutics meeting in San Francisco the PROSPECT Trial was presented by Dr. Greg Stone. Prospect stands for Providing Regional Observations to Study Predictors of Events in the Coronary Tree. This was a natural history study of atherosclerosis using multi-modality intracoronary imaging to prospectively identify vulnerable plaque. More on this later. Plaque Disruption and Risk Factors to me that intracoronary ultrasound might be useful to In 1993, I wrote an editorial titled, ‘‘Vascular Events investigate the composition of less severe stenoses and Responsible for Thrombotic Occlusion of a Blood Vessel.’’1 might eventually lead to plaque rupture and coronary In that editorial, I commented on the relationship of thrombosis. So, in another editorial in 1996, I predicted plaque disruption to the usual risk factors (smoking, that intracoronary ultrasound will evolve to a highly hyperlipidemia, hypertension) and potential triggers (cat- sophisticated level and will be used in the future to identify echolamines, myocardial contractility, heart rate), but noth- intracoronary plaques prone to rupture.4 ing was known at that time about identifying the plaque that is prone to rupture (vulnerable plaque) prospec- Virtual Histology Intravascular Ultrasound (VH-IVUS) tively. I ended the editorial by saying that current and At the 2009 Trans Catheter Therapeutics meeting (TCT), future research should be directed at identifying vulnera- the PROSPECT investigators presented imaging data of ble plaques in the individual patient, so that measures can non-culprit arteries of 700 patients with acute coronary be taken to prevent plaque rupture.
    [Show full text]
  • The Relationship Between Serum CXCL16 Level and Carotid Vulnerable Plaque in Patients with Ischemic Stroke
    European Review for Medical and Pharmacological Sciences 2017; 21: 3911-3915 The relationship between serum CXCL16 level and carotid vulnerable plaque in patients with ischemic stroke G. JIN Department of Laboratory Medicine, Brain Hospital, Siping, Jilin Province, China Abstract. – OBJECTIVE: We investigated the CONCLUSIONS: The levels of serum CXCL16 relationship between the serum macrophage are not related to high-risk factors for acute chemokine ligand 16 (CXCL16) levels and the vul- stroke and closely related to characteristics of nerable carotid plaque in patients with ischemic atherosclerotic plaque, micro-embolic signals stroke. and stroke subtypes. PATIENTS AND METHODS: We successively selected 118 cases of patients with an initial di- agnosis of acute ischemic stroke (time of onset Key Words: < 72 h), recorded risk factors, including gender, Ischemic stroke, Serum CXCL16, Vulnerable plaque, age, family history, smoking, body mass index, High-risk factors, Micro-embolic signal. blood glucose levels, blood lipid levels, average systolic pressure and diastolic blood pressure (DBP) and homocysteine levels. ELISA was used to detect the levels of serum CXCL16. GE-3000 Introduction color Doppler ultrasound diagnostic instrument was applied for the detection of the cervical ar- Ischemic stroke accounts for 60-80% of all ce- tery (including a bilateral common carotid ar- rebral vascular diseases with high disability and tery, internal carotid artery and external carot- mortality, and has become a major threat to hu- id artery) intima-media thickness (IMT), plaque man health1. Pathology and clinical studies con- number, size, nature (stable and vulnerable) and 2 luminal stenosis rate. Delica EMS-9EBx2P type firm that the formation of atherosclerotic plaques transcranial Doppler ultrasound (TCD) was used is an important mechanism of stroke, and that to detect micro-arterial micro-embolic signals the rupture and loss of vulnerable plaques are (MES).
    [Show full text]
  • Imaging Atherosclerosis and Vulnerable Plaque
    Imaging Atherosclerosis and Vulnerable Plaque Mehran M. Sadeghi1, David K. Glover2, Gregory M. Lanza3, Zahi A. Fayad4, and Lynne L. Johnson5 1Yale University School of Medicine, New Haven, Connecticut, and Veterans Administration Connecticut Healthcare System, West Haven, Connecticut; 2University of Virginia, Charlottesville, Virginia; 3Washington University in St. Louis, St. Louis, Missouri; 4Mount Sinai School of Medicine, New York, New York; and 5Columbia University, New York, New York Identifying patients at high risk for an acute cardiovascular event with lipids, producing large lipid-filled cores. To accom- such as myocardial infarction or stroke and assessing the total modate plaque growth, the extracellular matrix remodels by atherosclerotic burden are clinically important. Currently avail- enzymatic degradation and apoptosis. Inflammation is able imaging modalities can delineate vascular wall anatomy and, with novel probes, target biologic processes important in a prominent feature of this process. plaque evolution and plaque stability. Expansion of the vessel All of the stages along the way to advanced vascular wall involving remodeling of the extracellular matrix can be im- disease involve biologic processes that can be targeted for aged, as can angiogenesis of the vasa vasorum, plaque inflam- imaging. Several imaging platforms are available for mation, and fibrin deposits on early nonocclusive vascular targeted vascular imaging and include nuclear, CT, MRI, thrombosis. Several imaging platforms are available for targeted and optical. This section will discuss the first 3 of these vascular imaging to acquire information on both anatomy and platforms. The described imaging modalities acquire in- pathobiology in the same imaging session using either hybrid technology (nuclear combined with CT) or MRI combined with formation on both anatomy and pathobiology at the same novel probes targeting processes identified by molecular biology time.
    [Show full text]
  • Personalized Assessment of the Coronary Atherosclerotic Arteries by Intravascular Ultrasound Imaging: Hunting the Vulnerable Plaque
    Journal of Personalized Medicine Review Personalized Assessment of the Coronary Atherosclerotic Arteries by Intravascular Ultrasound Imaging: Hunting the Vulnerable Plaque Theodore G. Papaioannou 1,*,†,‡, Charalampos Kalantzis 1,†, Efstratios Katsianos 1, Despina Sanoudou 2, Manolis Vavuranakis 3 and Dimitrios Tousoulis 1 1 Biomedical Engineering Unit, First Department of Cardiology, Hippokration Hospital, Medical School, National and Kapodistrian University of Athens, 11527 Athens, Greece; [email protected] (C.K.); [email protected] (E.K.); [email protected] (D.T.) 2 Fourth Department of Internal Medicine, “Attikon” Hospital, Medical School, National and Kapodistrian University of Athens, 12462 Athens, Greece; [email protected] 3 Third Department of Cardiology, Medical School, National and Kapodistrian University of Athens, 11527 Athens, Greece; [email protected] * Correspondence: [email protected]; Tel.: +30-213-2088286; Fax: +30-213-2088676 † Equal first authorship. ‡ Current address: Biomedical Engineering Unit, First University Department of Cardiology, Hippokration Hospital, 114 Vas. Sophias ave., 11527 Athens, Greece. Received: 25 November 2018; Accepted: 21 January 2019; Published: 24 January 2019 Abstract: The term “vulnerable plaque” is commonly used to refer to an atherosclerotic plaque that is prone to rupture and the formation of thrombosis, which can lead to several cardiovascular and cerebrovascular events. Coronary artery atherosclerosis has a wide variety of different phenotypes among patients who may have a substantially variable risk for plaque rupture and cardiovascular events. Mounting evidence has proposed three distinctive histopathological mechanisms: plaque rupture, plaque erosion and calcified nodules. Studies have demonstrated the characteristics of plaques with high vulnerability such as the presence of a thin fibrous cap, a necrotic lipid-rich core, abundant infiltrating macrophages and neovascularization.
    [Show full text]
  • Imaging of High-Risk Carotid Artery Plaques: Current Status and Future Directions
    Neurosurg Focus 36 (1):E1, 2014 ©AANS, 2014 Imaging of high-risk carotid artery plaques: current status and future directions J. KEVIN DEMARCO, M.D.,1 AND JOHN HUSTON III, M.D.2 1Department of Radiology, Michigan State University, East Lansing, Michigan; and 2Department of Radiology, Mayo Clinic, Rochester, Minnesota In this paper, the authors review the definition of high-risk plaque as developed by experienced researchers in atherosclerosis, including pathologists, clinicians, molecular biologists, and imaging scientists. Current concepts of vulnerable plaque are based on histological studies of coronary and carotid artery plaque as well as natural history studies and include the presence of a lipid-rich necrotic core with an overlying thin fibrous cap, plaque inflammation, fissured plaque, and intraplaque hemorrhage. The extension of these histologically identified high-risk carotid plaque features to human in vivo MRI is reviewed as well. The authors also assess the ability of in vivo MRI to depict these vulnerable carotid plaque features. Next, the ability of these MRI-demonstrated high-risk carotid plaque features to predict the risk of ipsilateral carotid thromboembolic events is reviewed and compared with the risk assessment pro- vided by simple carotid artery stenosis measurements. Lastly, future directions of high-risk carotid plaque MRI are discussed, including the potential for increased clinical availability and more automated analysis of carotid plaque MRI. The ultimate goal of high-risk plaque imaging is to design and run future multicenter trials using carotid plaque MRI to guide individual patient selection and decisions about optimal atherosclerotic treatment strategies. (http://thejns.org/doi/abs/10.3171/2013.10.FOCUS13384) KEY WORDS • carotid stenosis • stroke • carotid plaque • MRI TROKE remains a leading cause of morbidity and current medical intervention alone is now best for stroke mortality.
    [Show full text]
  • Understanding Vulnerable Plaques: Current Status and Future Directions
    Korean Circ J. 2019 Dec;49(12):1115-1122 https://doi.org/10.4070/kcj.2019.0211 pISSN 1738-5520·eISSN 1738-5555 Review Article Understanding Vulnerable Plaques: Current Status and Future Directions Kwan Yong Lee , MD, PhD1 and Kiyuk Chang , MD, PhD2 1Cardiovascular Center and Cardiology Division, Incheon St. Mary's Hospital, College of Medicine, The Catholic University of Korea, Seoul, Korea 2Cardiovascular Center and Cardiology Division, Seoul St. Mary's Hospital, College of Medicine, The Catholic University of Korea, Seoul, Korea Received: Jul 3, 2019 ABSTRACT Revised: Sep 30, 2019 Accepted: Oct 7, 2019 The main cause of acute myocardial infarction is plaque rupture accompanied by Correspondence to superimposed coronary thrombosis. Thin-cap fibroatheromas (TCFAs) have been suggested Kiyuk Chang, MD, PhD as a type of lesion with a vulnerability that can cause plaque rupture. However, not only Cardiovascular Center and Cardiology Division, Seoul St. Mary's Hospital, College of Medicine, the existence of a TCFA but also the fine and complex interactions of other anatomical The Catholic University of Korea, 222, Banpo- and hemodynamic factors, such as microcalcification in the fibrous cap, cholesterol daero, Seocho-gu, Seoul 06591, Korea. crystal-induced inflammasome activation, the apoptosis of intraplaque macrophages, and E-mail: [email protected] endothelial shear stress distribution should precede a clinical event caused by plaque rupture. Recent studies are being conducted to identify these mechanisms through molecular imaging Copyright © 2019. The Korean Society of Cardiology and hemodynamic assessment using computational fluid dynamics, which will result in This is an Open Access article distributed better clinical results through selective coronary interventions.
    [Show full text]
  • Download PDF File
    INTERVENTIONAL CARDIOLOGY Cardiology Journal XXXX, Vol. XX, No. X, X–X DOI: 10.5603/CJ.a2019.0126 Copyright © 2019 Via Medica ORIGINAL ARTICLE ISSN 1897–5593 The influence of high-density lipoprotein cholesterol on maximal lipid core burden indexing thin cap fibrous atheroma lesions as assessed by near infrared spectroscopy Magdalena M. Dobrolińska1, Paweł Gąsior1, Wojciech Wańha1, Przemysław Pietraszewski2, Elżbieta Pociask3, Grzegorz Smolka1, Wojciech Wojakowski1, Tomasz Roleder4 1Division of Cardiology and Structural Heart Diseases, Medical University of Silesia in Katowice, Poland 2Department of Sports Theory, Jerzy Kukuczka Academy of Physical Education in Katowice, Poland 3Department of Biocybernetics and Biomedical Engineering, AGH University of Science and Technology, Krakow, Poland 4Regional Specialist Hospital, Research and Development Center, Wroclaw, Poland Abstract Background: Previous studies suggest that higher plasma concentrations of several lipid molecules are associated with higher lipid core burden index (LCBI) near infrared spectroscopy (NIRS) imag- ing. The aim of this study was to investigate whether an association between plasma lipids depends on plaque morphology (thin cap fibrous atheroma [TCFA] vs. non-TFCA) as measured by near-infrared spectroscopy–intravascular ultrasound (NIRS-IVUS). Methods: Sixty-four patients retrospectively enrolled were diagnosed with stable coronary artery dis- ease or acute coronary syndrome who underwent NIRS-IVUS imaging. Before percutaneous coronary intervention, blood samples were collected for measurement of serum levels of total cholesterol (TC), low- density lipoprotein cholesterol (HDL-C), high-density lipoprotein cholesterol (HDL-C) and triglycerides (TG). Patients were divided into two groups based on maxLCBI4mm and IVUS imaging. Those with maxLCBI4mm ≥ 323 were included into TCFA group (n = 35) while others were assigned to the non-TCFA group (n = 29).
    [Show full text]
  • Coronary Angiography, Too Far to Be a Gold Standard Technique for Identifying a Vulnerable Plaque
    & Experim l e ca n i t in a l l C C Minana et al. J Clinic Experiment Cardiol 2011, 2:4 f a Journal of Clinical & Experimental o r d l DOI: 10.4172/2155-9880.1000132 i a o n l o r g u y o J Cardiology ISSN: 2155-9880 Case Report Open Access Coronary Angiography, Too Far to be a Gold Standard Technique for Identifying a Vulnerable Plaque Gema Minana*, Julio Nunez and Juan Sanchis Servicio de Cardiologia, Hospital Clínico Universitario de Valencia, Valencia, Spain Abstract A 79 year-old woman with symptomatic heart failure and severe aortic stenosis was referred to a routine diagnostic coronary angiography previous to surgical aortic valve replacement. Coronary angiography showed severe stenosis in the left circumflex artery and in the ostium of the posterior descending artery. Four days later the patient presented an inferior ST-segment elevation acute coronary syndrome with cardiogenic shock. A rescue angioplasty was performed after failed thrombolysis. Coronary angiography revealed no changes in left coronary artery and a total acute occlusion in the middle segment of the right coronary artery, where only a mild lesion was observed four days before. A rescue angioplasty with a bare-metal stent implantation was performed with an optimal angiographic result. This case highlights the low ability of the conventional x-ray coronary angiography to identify vulnerable plaques. Even knowing the coronary anatomy four days before, we were unable to predict the culprit lesion. Introduction Four days later, patient experienced severe, retrosternal chest pain associated with nausea and dizziness and a blood pressure of This case illustrates the low diagnostic accuracy of the conventional 60/40 mmHg.
    [Show full text]
  • Circulating Biomarkers Reflecting Destabilization Mechanisms Of
    biomolecules Review Circulating Biomarkers Reflecting Destabilization Mechanisms of Coronary Artery Plaques: Are We Looking for the Impossible? Marko Kumric 1, Josip A. Borovac 1,2 , Dinko Martinovic 1 , Tina Ticinovic Kurir 1,3 and Josko Bozic 1,* 1 Department of Pathophysiology, University of Split School of Medicine, 21000 Split, Croatia; [email protected] (M.K.); [email protected] (J.A.B.); [email protected] (D.M.); [email protected] (T.T.K.) 2 Clinic for Cardiovascular Diseases, University Hospital of Split, 21000 Split, Croatia 3 Department of Endocrinology, University Hospital of Split, 21000 Split, Croatia * Correspondence: [email protected] Abstract: Despite significant strides to mitigate the complications of acute coronary syndrome (ACS), this clinical entity still represents a major global health burden. It has so far been well-established that most of the plaques leading to ACS are not a result of gradual narrowing of the vessel lumen, but rather a result of sudden disruption of vulnerable atherosclerotic plaques. As most of the developed imaging modalities for vulnerable plaque detection are invasive, multiple biomarkers were proposed to identify their presence. Owing to the pivotal role of lipids and inflammation in the pathophysiology of atherosclerosis, most of the biomarkers originated from one of those processes, whereas recent Citation: Kumric, M.; Borovac, J.A.; advancements in molecular sciences shed light on the use of microRNAs. Yet, at present there are no Martinovic, D.; Ticinovic Kurir, T.; clinically implemented biomarkers or any other method for that matter that could non-invasively, Bozic, J. Circulating Biomarkers yet reliably, diagnose the vulnerable plaque.
    [Show full text]
  • Pathogenesis of Vulnerable Plaque
    Pathogenesis of vulnerable plaque Andrew Newby Wei-chun Huang, Nick Jenkins, Sarah George, Jason Johnson, Karina di Gregoli, Buket Reel, Rebecca Salter, Graciela Sala-Newby Questions • What is a vulnerable plaque? • What effect does it have in patients? • What are the mechanisms? • Is there an animal model? • What can we do about it? Atherosclerotic plaque is a highly prevalent, slowly developing cause of angina pectoris and a risk factor for MI and stroke 0 10 20 40+ years I Type II Type III Type IV Stary HC An Atlas of Atherosclerosis Stroke and MI (heart attack) are mainly caused by plaque rupture or endothelial erosion Plaque rupture Surface erosion – 85% of male MI - 40% of female MI Davies, MJ Heart 2000; 83:361-6 - smokers Vulnerable plaque - definitions and assumptions • Plaque with a high probability to rupture or erode hence provoke thrombosis • Predictor of MI and stroke • Similar structural characteristics as plaques with recent thrombus • Formed by similar mechanisms as other plaques only more so! Are these assumptions valid? Does Vulnerable Plaque predict MI In 697 STEMI patients, thin-cap fibroatheromas were more likely to give rise to MACE in next 3 years. However, most MACE were new episodes of angina MI was too infrequent for statistical power Vulnerable plaque was a good predictor of subsequent MACE but the situation for MI is still unclear. Stone, NEJM;364:226 Transient ischaemic attacks predicts stroke – carotid endarterectomy Ulcerated plaque with thrombus What features of VP are predictive? In 818 carotid plaques from AtheroExpress • Haemorrhage and micro-vessels were predictors of MACE • Lipid core size, macrophages, smooth muscle cells and collagen were not predictive Hellings, Circulation 2010;121:1941 Why does plaque rupture occur? Davies MJ Plaque rupture like bridge collapse Circulation results from the chance interplay of Heart 2000; 83:361-6 intrinsic weakness and external forces Factors that influence MI and stroke Cap weakening Haemodynamics Reduced endothelial i.e.
    [Show full text]
  • Nuclear Cardiac Stress Testing in the Era of Molecular Medicine*
    CONTINUING EDUCATION Nuclear Cardiac Stress Testing in the Era of Molecular Medicine* Mark R. Vesely and Vasken Dilsizian infarction and preoperative states. However, acute coronary The objective of cardiac stress testing is to detect coronary syndrome (ACS), with its associated high morbidity and artery disease (CAD) and to prevent future adverse events, mortality, is a common initial presentation of CAD and has such as myocardial infarction or death. The progression from been difficult to predict and prevent. Therefore, detection of electrocardiographically based stress testing to current SPECT CAD in the subclinical setting or during symptomatic presen- and PET technologies has brought improvements in diagnostic efficacy and resolution. Myocardial perfusion imaging facilitates tation as ACS should be a foremost goal of cardiac stress management of CAD in elective and acute settings by providing testing in the future. Stress testing will accordingly allow valuable diagnostic and prognostic information. Hybrid PET/CT tailored management in both additional diagnostic and ther- and SPECT/CT systems impart complementary information of apeutic procedures as well as adjustment of medical therapies. coronary anatomy and its physiologic significance on blood flow re- serve. In the current era, diagnosis and treatment of cardiovascu- PHYSIOLOGY OF FLOW-LIMITING CORONARY lar disease is increasingly defined by underlying molecular and ARTERY LESIONS genomic aberrations rather than by clinical signs and symptoms Exercise serves as a cardiac stress by increasing myo- alone. Nuclear imaging is uniquely primed to exploit the targeting of expressed cell-surface molecules and intracellular processes cardial demand through increased heart rate, contractility, of cardiovascular disease and to foster the development of inno- and blood pressure.
    [Show full text]