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IHD & Angina Dika 671

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    Ischemic heart disease &

    Angina pectoris

    By

    Onyedika

    MD5

    #671

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    Content

    Definition

    Epidemiology

    Pathogenesis (Acute plaque change, Inflammation,thrombus, vasoconstriction)

    Angina pectoris

    Myocardial infarctionChronic IHD

    SCD

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    Ischaemic heart disease

    DefinitionAn imbalance between the supplyofoxygenandthe myocardialdemandresulting in myocardialischaemia.

    Anginapectoris

    symptom not a disease

    chest discomfort associated with abnormalmyocardial function in the absence of myocardialnecrosis

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    Determinants of myocardial

    oxygen demandThe major determinants of myocardial oxygen

    demand are heart rate, myocardial contractility,

    and myocardial wall tension.

    An adequate supply of oxygen to the myocardium

    requires a satisfactory level of oxygen-carrying

    capacity of the blood and an adequate level of

    coronary blood flow.

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    Epidemiology

    Leading cause of death in US and industrialized

    nations

    Incidence rises progressively with increasing age.

    M>F. Women are protected against MI duringtheir reproductive years

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    Pathogenesis

    Acute plaque change

    Inflammation

    Thrombus

    Vasoconstriction

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    Acute plaque changes

    In most patients, unstable angina, infarction, andmany cases of SCD occur because of abrupt

    plaque change followed by thrombosis, hence the

    term acute coronary syndrome.

    Vulnerable plaques

    Plaques containing large a areas of foam cells and

    extracellular lipid

    Thin fibrous cap, contain few smooth muscle cells

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    Role of Inflammation

    Endothelial cells release CAMs, selectins

    T-cells release TNF, IL-6, IFN-gamma tostimulate and activate endothelial cells and

    macrophages

    CRP predicts the risk of damage in coronary heart

    disease

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    Role of Thrombus

    Total or partial vascular occlusion by a newly

    formed thrombus on a disrupted

    atherosclerotic plaque lead to unstableangina or sudden death.

    Organizing thrombi produce potent activators

    of smooth muscle proliferation, which can

    contribute to the growth of atherosclerotic

    lesions.

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    Role of Vasoconstriction

    Vasoconstriction directly compromises lumendiameter and potentiate plaque disruption.

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    Classification s of IHD

    Myocardial infarction (MI)

    Sudden cardiac death

    Angina pectoris

    Chronic IHD with heart failure

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    Angina Pectoris

    Stable = 75% vessel block, transient ( 15 min.), not relived by rest, VD, Pre-infarctionAngina

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    Microvascular Angina

    (syndrome x)It may be due to spasm in the tiny blood

    vessels of the heart, arms, and legs.

    It is not characterized by arterial blockages,

    so harder to diagnose but its prognosis is

    excellent.

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    Angina - Chest Pain

    Site - Jaw to navel, retrosternal, left submammary

    Radiation - Left chest, left arm, jaw, mandible,teeth, palate, back

    Quality/severity - Tightness, heaviness,compressionclenched fists

    Precipitating - physical exertion, cold windy

    weather, emotion

    Relieving factors -Rest, sublingual nitrates, aspirin

    Autonomic symptoms - Sweating, pallor,

    peripheral vasoconstriction.

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    Chest Pain

    Differential diagnosisCardiac pathology

    Pericarditis, aortic dissection

    Pulmonary pathology

    Pulmonary embolus, pneumothorax, pneumonia

    Gastrointestinal pathology

    Peptic ulcer disease, reflux, pancreatitis, cafcoronary

    Musculoskeletal pathology

    Trauma, TietzesSyndrome

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    Myocardial Infarction

    It is necrosis of heart muscle resulting from ischemia.Chest pain

    EKG ST-segment elevation (minutes to hours)

    Q-wave and T-wave inversion (hours to days)

    Lab. Evaluation: CK-MB gold standard,

    Troponin- specific

    CRP predicts risk of AMI in angina patients

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    Chronic IHD

    Also called ischemic cardiomyopathy

    Patients - Post heart transplant receipts, previous

    MI or CABG pts

    Cause - Compromised ventricular function

    Morphology - Vacuoles, Myocyte Hypertrophy

    Diagnosis is by exclusion

    Dr. Krishna Tadepalli, MD, www.mletips.com19

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    Sudden cardiac death

    It is unexpected death in one hour due to cardiac

    causes with or without clinical symptoms

    CauseAtherosclerosis ( 90%), others (10%)

    Romano- Ward syndrome (KCNEgenes)

    Long Q-T syndrome ( K+, Na+ channel

    defects)

    Mechanism- Most likely due to arrhythmias ( VF)

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    Management

    Pharmaceuticals:Beta Blockers

    Ca++ Blockers

    Nitrates - Vasculature vasodilationAnti-Hypercholesterolemia

    HMG CoA Reductase Inhibitors

    Antiplatelet MedicationClopidogrel (Plavix)

    Aspirin

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    Surgical Treatment

    Stenting

    Angioplasty (balloon)

    Coronary Artery Bypass Graft

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    Acute coronary syndrome

    Syndrome Stenoses

    Plaque

    Disruption

    Plaque-Associated

    Thrombus

    Stable angina >75% No NoUnstable

    angina

    Variable Frequent Non-occlusive

    Transmural

    MI

    Variable Frequent Occlusive

    Subendocard

    ial MI

    Variable Variable Widely variable

    Sudden

    death

    severe Frequent Often small

    Summary

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    References

    Kumar, V., & Robbins, S. L. 1. (2007). Robbins basic

    pathology(8th ed.). Philadelphia, PA: Saunders/Elsevier.

    P.Kumar and M.Clark: Kumar & Clarks Clinical Medicine

    Lindenfeld J, et al. HFSA 2010 Comprehensive Heart FaailureGuidline.

    Dr Chris Gale Clinical Research Fellow Medical Research Council -

    University of Leeds

    Dr.KrishnaTadepalli,MD. www.mletips.com


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