percutaneous coronary intervention by hossein

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  • HOSSEIN EFTEKHARI,MDVULNERABLE PLAQUEANIMAL MODELSPERCUTANEOUS CORONARY INTERVENTION

  • AT THE BEGINNING OF 20thCENTRY,CVD ACCOUNTED FOR LESS THAN 10 PERCENT OF ALL DEATHS WORLD WIDE.AT ITS END,CVD ACCOUNTED FOR NEARLY HALF OF ALL DEATH IN DEVELOPED COUNTRIES.BY 2020,CVD WILL CLAIM 25 MILLION DEATHS ANNUALLY AND WILL SURPASS INFECTIOUS DISEASE AS THE WORLDS NUMBER ONE CAUSE OF DEATH AND DISABILITES.

  • THREE COMPLEMENTARY STRATEGIES TO REDUCE MORBIDITY AND MORTALITY FROM CVD:Lowering overall burden of CVD risk factors in the entire population through population-wide public health measures (national campaign).Identifying and targeting high-risk subgroup of population who may benefit from preventive intervention.Resources can be allocated to acute and chronic treatment and secondary prevention.

  • VULNERABLE Ps

    Vulnerable populationVulnerable patientVulnerable plaque

  • Vulnerable plaques, vulnerable myocardium, and hypercoagulable state of the blood lead to

    sudden cardiac death and acute myocardial infarction.

  • What causes heart attack?

  • Mostly it is secondary to acute thrombosis over an underlying vulnerable plaque.

  • lipid-rich core

    thrombus

    cap

    cap

  • The vast majority of plaque of disruptions are self-contained and clinically silent.So plaque disruption leading to ACS is not a rule but an exception in a -symptomatic patients with non-obstructing atherosclerosis but contributes to plaque progression and luminal narrowing.

  • Culprit Plaque; a retrospective terminology

    Vulnerable Plaque; a prospective terminology

    Vulnerable Plaque = Future Culprit Plaque

    Clarification of Terminologies

  • Vulnerable Plaque

    The short answer is:

  • What are

    vulnerable plaques?

  • Dangerous forms of atherosclerotic plaques that can rupture or induce thrombosis and lead to critical disruption of blood flow.

    The short answer is:

  • Proposed Histopathological and Clinical Criteria for Definition of Vulnerable Plaque

    Major Criteria:

    Active Inflammation (monocyte/ macrophage infiltration)

    Thin Cap with Large Lipid Core

    Endothelial Denudation with Superficial Platelet Aggregation

    Fissured / Wounded Plaque

  • Proposed Histopathological and Clinical Criteria for Definition of Vulnerable Plaque

    Minor Criteria:

    Superficial Calcified nodule

    Glistening Yellow

    Intraplaque Hemorrhage

    Critical Stenosis

    Positive Remodeling?

  • Plaque Rupture: Definition

    Structural failure of the fibrocellular cap1 that separates an atheromatous core2 from the lumen of an atherosclerotic artery (ie, lumen core).

    1 cap defect/gaprupture, fissure, break, tear

    not just missing endothelium

    2 lipid-richGreek athere, gruel (soft)

    Propensity to rupture

    lipid-rich core+ +++

    no core no cap-

  • Plaque Rupture

  • Ruptured Plaques (~70%)

    1.Stenotic (~20%)

    2. Non-stenotic (~50%)

    Non-ruptured Plaques (~ 30%)

    1.Erosion (~20%)

    2.Calcified Nodule (~5%)

    3.Others / Unknown (~5%)

    Plaque Pathology Responsible for Coronary Thrombotic Death

    In summary:

  • Vulnerable Plaque and Vulnerable Patient, The Challenge of Cardiovascular Medicine in 21st Century

    An introductory tutorial from

    VP.org

    In conjunction with

    The Center for Vulnerable Plaque Research

    University of Texas Houston and

    Texas Heart Institute

  • Ideal method for screening vulnerable plaque/patient

    Non-invasive

    Inexpensive

    Accurate

    Widely Reproducible

  • Emerging Techniques for Detection of Vulnerable Plaque

  • Emerging Diagnostic Techniques

    A. Invasive Techniques

    Angioscopy

    Intravascular Ultrasound (IVUS)

    Intravascular Thermography

    Intravascular Optical Coherence Tomography (OCT)

    Intravascular Elastography

    Intravascular and Transesophageal MRI

    Intravascular Nuclear Imaging

    Intravascular Electrical Impedance Imaging

    Intravascular Tissue Doppler

    Intravascular Shear Stress Imaging

    Intravascular (Photonic) Spectroscopy

  • -Raman Spectroscopy

    -Near-Infrared Diffuse Reflectance Spectroscopy

    -Fibrousis and lipid measurement

    -pH and lactate measurement

    - Fluorescence Emission Spectroscopy

    - Spectroscopy with contrast media

    Invasive Techniques

    Intravascular (Photonic) Spectroscopy

    Intra-coronary assessment of endothelial function

    Intra-coronary measurement of MMPs and cytokines

  • Emerging Diagnostic Techniques

    B. Non-Invasive Techniques:

    A. MRI

    1- MRI without contrast media

    2- MRI with contrast media: Gadolinium-DPTA

    2- MR Imaging of Inflammation: Super Paramagnetic Iron Oxide (SPIO and USPIO)

    3- MR Imaging of Thrombosis using monoclonal Ab

    B. Electron Beam Tomography (EBT)

    C. Multi-Slice Fast Spiral / Helical Computed Tomography

    Nuclear Imaging (18-FDG, MCP-1, Annexin V, CD40)

  • Emerging Diagnostic Techniques

    C. Blood Tests / Serum Markers

    - CRP

    - ICAM-1, VCAM, p-Selectin, sCD40-L

    - Proinflamatory cytokines

    - Lp-PLA2

    - Ox-LDL Ab

    - PAPP-A

    D. Endothelial Function Test

    -Intra coronary acethylcholine test

    -Noninvasive flow mediated dilatation of brachial artery

    - Anti-body against endothelial cells

  • CONCLUSIONIt is well established that composition and size of lipid core,composition and thickness of fibrous cap, inflammatory process,and the quantity of SMCs within a plaque are predictors of plaque rupture.

  • ANIMAL MODELS FOR EXPERIMENTAL STUDIES

  • THE IMPORTANCE OF ANIMAL MODELAnimal models are important to research directed toward better understanding of human atherosclerosis.For this reason much effort has been expended to identify and characterize species suitable as animal model.

  • Criteria needed for choosing animal modelSusceptibility under standard system of husbandry Ready availability at reasonable cost Ready trainability and size adequate for all project lab procedureRecognition that behavior responses to experimental situations may determine result

  • The ideal animal model of human atherosclrosis:

    *Should be easy to acquire and maintain at reasonable cost*Easy to handle *Proper in size*Should be reproducible in lab*Should have well-defined genetic characteristics*Should share with human the most important aspect of disease process

  • THE CHICKEN AS A MODEL*The chicken is good animal model for atherosclerosis study because it is:OmnivorousSmall and suitable for prolonged lab investigationAble to develop spontaneous atherosclerosisCapable of producing atherosclerosis after cholesterol feeding Plasma level of cholesterol and triglyceride are similar to those in humanLipid composition of LDL , HDL and chylomicron resemble those in humanThere is no essential difference between vascular lesion in chicken on high cholesterol diet and that of human

  • DISADVANTAGES OF CHICKENNonmammalsLesion site inconsistentComplication uncommonIntramyocardial coronary involvementChicken herpes virus can be the sources of variability

  • THE PIG AS A MODEL* Some similarities between man and pig in atherosclerosis:Atherosclerosis in man and pigs develops most frequently in aorta,coronary and intracranial arteriesThe age at which lesion originate and the rate of progression in any lesion is independent of otherThe origin and distribution of coronary artery in man and pig corresponds closelyThe histological change of growth and aging that leads to atherosclerosis of aorta and coronary artery are closely similarAccording to the mean age of death and its relation to morphological character and size of lesion,the sequel of atherosclerosis in man and pig also correspond closely

  • MOUSE AS A MODEL*As a species the mouse is highly resistant to atherosclerosis.But through induced mutation lines of mice have been developed to be susceptible to atherosclerosis,such as:Mice that are deficient in apoEMice that are deficient in LDL receptorTransgenic mice that express human apoETransgenic mice with transdominant mutant form of apoE

  • pathology Comparison of atherosclerosis

    ApoE-deficient mouse HumanFatty streak with MAC and Tcells yes yesFibrous plaque with SMC yes yesLesion calcification yes yes Oxidized apitopes present yes yesLesions at branches and sites with disturbed flow yes yesDiet responsiveness yes yesAneurysms observed yes yesPlaque rupture observed no yes

  • NO PLAQUE RUPTURE IN ANIMAL MODELAtherosclerosis plaque rupture is the main cause of coronary thrombosis and MI but currently,there is no animal model of plaque disruption ?

  • THE POTENTIAL CAUSE OF LACK OF PLAQUE RUPTURE IN MICEMay be due to small diameter of mice aorta (
  • RABBIT AS AN ANIMAL MODELAdvantages:Lesion well characterizedLesion inducible with dietary cholesterol Reproduce rapidlyRelatively inexpensive

  • RABBIT AS AN ANIMAL MODELDisadvantages:Whole body cholesterol is different from humanLesions dont duplicate many important features of humanLesions usually occur in aortic arch and thoracic aortaDistribution of coronary artery lesion is different from human(proximal portions a

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