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Angina Ihd

Date post: 07-Apr-2018
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    ISCHAEMIC HEART DISEASE

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    Magnitude of the problem

    USA 13.2 Million CAD , angina 6.8 million

    CAD 54% of all CVD deaths(2001 US data)

    Global deaths,CAD 7.1 to 11.1 million by2020

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    A pain, vaguely described as:A heaviness

    Pressure

    Squeezing sensationConstriction

    Aching burning pain

    DiscomfortBreathlessness

    Fauci et al. Harrison 1998; 1: 59-60.

    Angina a typeof temporarychest painpressure ordiscomfort

    Narrowedartery

    IschemiaHeart muscle is not

    receiving enoughoxygen due to anarrowed coronaryartery

    DEFINITION

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    Typical: Substernal region (center of the chest)Radiation:

    Interscapular region(back of the chest)

    ArmsShoulders

    Teeth

    AbdomenBack of neck

    SITE

    Braunwald et al. Harrison 1998; 1: 1365-80.

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    Develops gradually during exertion

    Appears after heavy meals

    Associated with anger, excitement, frustration and otheremotional states

    Resolves within 5-30 minutes

    Braunwald et al. Harrison 1998; 1: 1365-80.

    TYPICAL ANGINA

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    CAD

    Stable Angina

    Unstable angina

    Prinzmetal angina

    Acute MI

    Silent ischemia

    Heart failure

    arrhythmia

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    STABLE ANGINA

    Classification

    Exertional

    Anginal Equivalent Syndrome

    Prinzmetals (Variant) Angina

    Syndrome-X

    Silent Ischemia

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    ACS- clinical presentation

    Ebers papyrus 2600BCIf you find a man with

    heart discomfort,with pain in arms , at the

    side of his heart,death is near

    1. Occurring at rest lasting > 20 min

    2. New onset severe angina < 1 month3. Crescendo angina

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    Unstable angina -classification

    Severity

    Cl I New onset of severe/crescendo angina, no rest pain

    Cl II Angina at rest within in one month but not < 48hrs

    Cl III Angina at rest within 48 hrs

    Clinical circumstances

    A (secondary) extra cardiac condition

    B (primary) absence of extra cardiac condition

    C (post MI) within 2 weeks of MITIMI III registry , AJC 90:821,2002

    Contd

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    Unstable angina -classification

    Intensity of treatment

    1. In the absence of Rx for SAP

    2. During Rx of SAP

    3. Despite maximal medication for SAP

    ECG Changes

    With ECG changes

    Without ECG changes

    TIMI III registry , AJC 90:821,2002

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    ACS-patho physiology

    1. The development of unstable plaque

    2. Acute ischemic event

    3. Long term risk of recurrent coronary events

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    Non occlusive thrombus

    Thrombosis

    Platelet activation & aggregation

    Secondary haemostasis

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    Angina-Dx tests

    ECG

    Chest X Ray

    Resting echo

    Exercise echo

    Exercise ECG

    Stress nuclear scan

    Ambulatory ECG

    CORONARY ANGIO

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    RISK STRATIFICATION

    History

    Clinical class

    ECG

    Cardiac markers

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    History

    Advanced Age > 70 y

    Diabetes mellitus

    Post MI angina

    Prior PAD

    Prior CVA

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    Angina - physical

    Xanthelasma, HTN,PVD

    LV dysfunction

    Split S2

    AS,HOCM, MVP Precipitating factors

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    Clinical Presentation

    Braunwald Cl II /III ( acute /sub acute)

    Braunwald Cl B (sec)

    Heart failure / hypotension

    Ventricular arrhythmias

    ECG changes

    ST changes > 0.05 mV

    T inversion

    LBBB

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    Cardiac markers

    Increased TROP T /I ,CKMB

    Increased CRP or WBC count

    Increased BNP

    Elevated CD40 ligand

    Elevated glucose /HBA1 C Elevated s-creatinine

    Angiogram

    1. Thrombus

    2. Triple vessel disease

    3. Reduced LVEF

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    Coronary Angio

    TACTICS TIMI 18

    34% TRIPLE VESSEL DISEASE

    28% TWO VESSEL DISEASE

    26% ONE VESSEL DISEASE

    5-10% LMCD

    13% NO CORONARY DISEASE

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    Medical therapy

    Anti thrombotic Rx

    Anti ischemic Rx

    Prevention of events

    revascularization

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    Anti thrombotic Rx

    Aspirin

    Clopidogrel,ticlopedine Heparin

    Direct thrombin inhibitors

    Anticoagulants Gp IIb /IIIa inhibitors

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    Medical management

    1. Identification &treatment of Ppt factors

    2. Reduction of coronary risk factors

    3. General methods-life style modification

    4. Drugs

    5. Revascularization- PCI , CABG

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    Rx associated diseases

    Anemia

    Obesity

    Occult thyrotoxicosis

    Fever

    Infection

    anxiety

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    Coronary risk factors

    Hypertension

    Smoking

    Dyslipidemia

    Diabetes

    Inflammation- ACEI,Statins

    Aspirin, clopidogrel

    Beta blockers

    Anti oxidents -no role

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    Anti anginal drugs- Nitrates

    Vasodilator action

    Reduce ventricular preload, after load Redistribution of blood flow normal>ischemia

    Anti thrombotic effect

    Oral, sublingual, transdermal, IV

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    Anti anginal drugs- Beta blockers

    Anti ischemic, reduce oxygen demand Anti hypertensive

    Anti arrhythmic

    Reduce mortality in post MI

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    Beta blocker

    Ideal candidates

    1. Physical activity

    2. Coexistent HTN3. SVT, vent arrhythmias

    4. Old MI

    5. LVEF reduced6. Anxiety

    Poor candidates

    1. Asthma, COPD

    2. Severe LVF

    3. Severe Depression

    4. Raynaud phenomenon

    5. PVD

    6. Severe bradycardia

    7. Brittle diabetes

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    Anti angina drugs- CCB

    Reduce oxygen demand

    Increase oxygen supply

    Anti atherogenic

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    Other therapies

    Nicorndil-IONA study

    Spinal cord stimulation

    EECP

    Chelation- no role

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    PCI in angina

    Medically refractory pts

    Severe myocardial ischemia

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    CABG- angina

    Medically refractory Angina

    LMCD, triple vessel disease

    Diabetes with triple vessel disease

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