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Title: iscgemia


1
  • ISCHEMIC HEART DISEASE/CORONARY ARTERY DISEASE

Dr.W.C.Lwabby (MMed, MD)Lecturer Int. Med. Dpt
2
Introduction
  • Ischemic heart disease (IHD)/CORONARY ARTERY
    DISEASE(CAD)
  • Is a condition in which
  • there is an inadequate supply of blood and
    oxygen to a portion of the myocardium.
  • Occurs when there is an imbalance between
    myocardial oxygen supply and demand.
  • Common cause of myocardial ischemia is
    atherosclerotic disease of a coronary artery,
  • sufficient to cause a regional reduction in
    myocardial blood flow.

3
Introduction
  • Disease of the coronary arteries is almost always
    due to
  • atheroma and its complications, particularly
    thrombosis.
  • Occasionally, the coronary arteries are involved
    in other disorders such as
  • Aortitis
  • Polyarteritis
  • Other connective tissue disorders.

4
Introduction
  • Patients with IHD fall into two large groups
  • Chronic CAD (stable angina)
  • Acute coronary syndromes (ACSs)
  • Is a term that encompasses both unstable angina
    and myocardial infarction (MI).

5
Anatomy of the coronary vessels
  • Two main coronary arteries, branches of ascending
    aorta.
  • Left coronary arteries
  • supply  LA, LV and the anterior wall of the RV.
  • Right coronary arteries
  • supply RA,  RV as well as the SA node.

6
Anatomy of coronary arteries
7
EPIDEMIOLOGY
  • gt 60 of the global burden of IHD occurs in
    Developing countries.
  • It increases with age.
  • Men gt women, but CAD is the leading cause of
    death in both men and women

8
RISK FACTORS OF IHD
  • Generally include
  • Hypertension
  • Elevated LDL /VLDL cholesterol
  • Reduced HDL cholesterol
  • Oxidant stress caused by cigarette smoking
  • Excess angiotensin II
  • Obesity
  • Insulin resistance
  • Diabetes mellitus

9
PATHOPHYSIOLOGY
  • The underlying pathophysiological mechanisms for
    IHD begin with the process of atherosclerosis,
  • In ACS
  • Atherosclerosis can be described as a low-grade
    inflammatory state of the intima of medium-sized
    arteries.
  • It develops and progresses for decades prior to
    the acute event.
  • This is accelerated by the risk factors, such as
  • Hypertension, Hyperlipidemia, smoking,
    diabetes, and genetics.

10
PATHOPHYSIOLOGY..
  • This slow progression leads to the gradual
    thickening of the intima,
  • which may over time narrow the lumen of the
    artery to various degrees.

11
Stable angina
  • Angina pectoris
  • Is the symptom complex caused by transient
    myocardial ischaemia
  • It constitutes a clinical syndrome rather than a
    disease.
  • It may occur whenever there is an imbalance
    between myocardial oxygen supply and demand.
  • Coronary atheroma is by far the most common
    cause.
  • Coronary perfusion is impaired by fixed or stable
    atheroma of the coronary arteries.

12
Clinical features
  • Stable angina is characterized by
  • Central chest pain (retro-sternal chest pain)
  • Discomfort
  • Radiating to left( right) shoulder/arm/ neck/jaw
  • Precipitated by exertion or other forms of stress
  • Promptly relieved by rest or Nitrates.
  • Brief duration, lasting lt10-15 min
  • Associated with breathlessness, diaphoresis,
    nausea, anxiety

13
Clinical features
  • Physical examination
  • Is frequently unremarkable.
  • Should include a careful search for evidence of
  • Valve heart disease (particularly aortic)
  • Important risk factors (e.g. hypertension,
    diabetes mellitus)
  • Left ventricular dysfunction (cardiomegaly,
    gallop rhythm)
  • Other manifestations of arterial disease (carotid
    bruits, peripheral vascular disease)
  • Unrelated conditions that may exacerbate angina
    (anaemia, thyrotoxicosis).

14
Diagnosis
  • The history is the most important factor in
    making the diagnosis.
  • Investigations
  • The ECG may show evidence of previous MI but is
    often normal
  • Coronary arteriography
  • This provides detailed anatomical information
    about the extent and nature of coronary artery
    disease.

15
Treatment
  • Specific Treatment
  • Antiplatelet therapy
  • Aspirin -Low-dose (75 mg)
  • Reduces the risk of adverse events such as MI.
  • Clopidogrel (75 mg daily)
  • Is an equally effective antiplatelet agent.
  • Can be prescribed if aspirin causes troublesome
    dyspepsia.

16
  • Anti-anginal drug treatment
  • Five groups of drug are used to relieve or
    prevent the symptoms of angina
  • Nitrates
  • ß-blockers
  • Calcium antagonists
  • Potassium channel activators
  • an If channel antagonist.

17
  • Nitrates
  • Act directly on vascular smooth muscle to produce
    venous and arteriolar dilatation.
  • Their beneficial effects are due to
  • Reduction in myocardial oxygen demand (lower
    preload and afterload)
  • Increase in myocardial oxygen supply (coronary
    vasodilatation).
  • Sublingual glyceryl trinitrate (GTN)
  • Administered from
  • a metered-dose aerosol (400 µg per spray) or
  • as a tablet (300 or 500 µg), will relieve an
    attack of angina in 23 minutes.
  • Side-effects include headache, hypotension,
    syncope.
  • Other nitrates (isosorbide dinitrate , isosorbide
    mononitrate )

18
  • Beta-blockers
  • These lower myocardial oxygen demand by
  • reducing heart rate, BP and myocardial
    contractility
  • They may provoke bronchospasm in patients with
    asthma.
  • Non- cardioselective ß-blockers may aggravate
    coronary vasospasm by
  • blocking the coronary artery ß2adrenoceptors.
  • so a once-daily cardioselective preparation is
    used (e.g. metoprolol 50200 mg daily, bisoprolol
    515 mg daily).

19
  • Calcium channel antagonists
  • They lower myocardial oxygen demand by
  • reducing BP and myocardial contractility.
  • Dihydropyridine calcium antagonists, (nifedipine
    and nicardipine), often cause a reflex
    tachycardia.
  • This may be counterproductive and it is best to
    use them in combination with a ß-blocker.
  • Verapamil and diltiazem
  • Are suitable for patients who are not receiving
    a ß-blocker (e.g. those with airways obstruction)
    because
  • Slow SA node firing
  • Inhibit conduction through the AV node
  • Tend to cause a bradycardia.

20
  • Invasive treatment
  • Percutaneous coronary intervention (PCI)
  • Is performed by passing a fine guidewire across a
    coronary stenosis under radiographic control.
  • using it to position a balloon, which is then
    inflated to dilate the stenosis.
  • Coronary artery bypass grafting
  • The internal mammary arteries
  • radial arteries or
  • reversed segments of the patients own saphenous
    vein can be used to bypass coronary artery
    stenoses

21
Acute coronary syndrome (ACS)
  • Is a term that encompasses both
  • Unstable angina(UA)
  • Myocardial infarction (MI) -(NSTEMI, and STEMI).
  • It is characterized by
  • New-onset or rapidly worsening angina (crescendo
    angina) or,
  • Angina on minimal exertion or,
  • Angina at rest in the absence of myocardial
    damage.

22
Introduction..
  • An ACS may present as a new phenomenon or against
    a background of chronic stable angina.
  • The culprit lesion is usually a complex ulcerated
    or fissured atheromatous plaque with
  • Adherent platelet-rich thrombus
  • Local coronary artery spasm.
  • This is a dynamic process whereby the degree of
    obstruction may either
  • Increase, leading to complete vessel occlusion,
    or
  • Regress due to the effects of platelet
    disaggregation and endogenous fibrinolysis.

23
Myocardial infarction
  • Myocardial infarction (MI) occurs when
  • Symptoms occur at rest.
  • There is evidence of myocardial necrosis, as
    demonstrated by an elevation in cardiac
    biomarkers (troponin or CK-MB isoenzyme).
  • STEMI occurs when
  • Coronary blood flow decreases abruptly after a
    total thrombotic occlusion of a coronary artery,
    previously affected by atherosclerosis.
  • A coronary artery thrombus develops rapidly at a
    site of vascular injury resulting into STEMI.
  • The injury is produced or facilitated by factors
    such as cigarette smoking, hypertension, and
    lipid accumulation.

24
Myocardial infarction..
  • The diagnosis of NSTEMI, is established if a
    patient with the clinical features of UA
    develops
  • Evidence of myocardial necrosis, as reflected in
    elevated cardiac biomarkers (CKMB / Troponin).
  • NSTEMI is caused by
  • a reduction in oxygen supply and/or
  • an increase in myocardial oxygen demand
    superimposed on a lesion that causes partial
    coronary arterial obstruction, usually an
    atherothrombotic coronary plaque.

25
UNSTABLE ANGINA(UA)
  • Is caused by
  • dynamic (partial) obstruction of a coronary
    artery due to plaque rupture with superimposed
    coronary thrombosis and spasm.
  • Occurs even at rest or with minimal exertion
  • More severe and lasts longer than stable angina,
    may be as long as 30 minutes
  • May not disappear with rest or use of angina
    medication
  • May lead to complete occlusion of vessel causing
    MI.

26
Clinical features of ACS
  • Chest Pain
  • Is the cardinal symptom of an ACS.
  • Occurs in the same sites as angina but is usually
    more severe and lasts longer
  • it is often described as a tightness, heaviness
    or constriction in the chest.
  • In acute MI
  • the pain can be excruciating
  • Breathlessness, vomiting and collapse
  • Are common features.
  • Most patients are breathless and in some, this is
    the only symptom.

27
Clinical features of AClinical features of
ACSCS cont
  • Vomiting and sinus bradycardia
  • are often due to vagal stimulation and are
    particularly common in patients with inferior MI.
  • Nausea and vomiting may also be caused or
    aggravated by opiates given for pain relief.
  • Syncope
  • If syncope occurs, it is usually due to an
    arrhythmia or profound hypotension.

28

Clinical features of ACS
  • Painless or silent MI
  • Indeed, MI may pass unrecognized.
  • Is particularly common in older patients or those
    with diabetes mellitus.
  • Sudden death
  • From ventricular fibrillation or asystole
  • May occur immediately and often within the first
    hour.
  • The development of cardiac failure reflects the
    extent of myocardial ischaemia.
  • Cardiac failure is the major cause of death in
    those who survive the first few hours.

29
  • Physical Exam (in large area of myocardial
    ischemia)
  • Diaphoresis
  • Pale
  • Cool skin
  • Sinus tachycardia
  • Hypotension
  • a third and/or fourth heart sound basilar rales

30
Diagnosis
  • The assessment of ACS depends heavily on
  • Analysis of the character of the chest pain and
    its associated features.
  • Evaluation of the ECG.
  • Serial measurements of biochemical markers of
    cardiac damage.

31
Investigations
  • Electrocardiography(ECG)
  • Is central to confirming the diagnosis.
  • The earliest ECG change is usually ST-segment
    elevation.
  • With proximal occlusion of a major coronary
    artery
  • ST-segment elevation (or new bundle branch block)
    is seen initially
  • later diminution in the size of the R wave
  • In Transmural (full-thickness) infarction
  • There is development of a Q wave.
  • Subsequently, the T wave becomes inverted because
    of a change in ventricular repolarisation.

32

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34
  • Electrocardiography(ECG).
  • In NST segement elevation there is
  • Partial occlusion of a major vessel
  • Complete occlusion of a minor vessel
  • This causing unstable angina or partial-thickness
    (subendocardial) MI.
  • This is usually associated with ST-segment
    depression and T-wave changes.
  • In the presence of infarction
  • this may be accompanied by some loss of R waves
    in the absence of Q waves.

35
  • Plasma cardiac biomarkers
  • These biochemical markers are
  • Creatine kinase (CK), a more sensitive and
    cardio-specific isoform of this enzyme is
    -CK-MB.
  • Troponins T and I -the cardio-specific proteins.
  • In unstable angina (UA)
  • There is no detectable rise in cardiac biomarkers
    or enzymes.
  • The initial diagnosis is made from the clinical
    history and ECG only.
  • In contrast MI
  • causes a rise in the plasma cardiac biomarkers or
    enzymes, that are normally concentrated within
    cardiac cells.
  • The change in plasma concentrations of these
    markers confirms the diagnosis of MI.

36
  • CK
  • Starts to rise at 46 hours
  • Peaks at about 12 hours and falls to normal
    within 4872 hours.
  • Is also present in skeletal muscle
  • a modest rise in CK (but not CK-MB) may
    sometimes be due to
  • An intramuscular injection
  • Vigorous physical exercise
  • The most sensitive markers of myocardial cell
    damage are the troponins T and I
  • These are released within 46 hours and remain
    elevated for up to 2 weeks.

37
  • Chest X-ray
  • This may demonstrate pulmonary oedema that is not
    evident on clinical examination.
  • The heart size is often normal, but there may be
    cardiomegaly due to pre-existing myocardial
    damage.
  • Echocardiography
  • Is useful for assessing ventricular function and
    for detecting important complications, such as
  • Mural thrombus
  • Cardiac rupture
  • Ventricular septal defect
  • Mitral regurgitation and
  • Pericardial effusion.

38
Treatment
  • Immediate treatment
  • Analgesia
  • Is essential, not only to relieve distress but
    also to lower adrenergic drive and there by
    reduce
  • vascular resistance,
  • BP
  • Infarct size and
  • Susceptibility to ventricular arrhythmias.
  • Intravenous opiates ( morphine sulphate 510 mg
    or diamorphine 2.55 mg)
  • OXYGEN THERAPY

39
  • Antithrombotic therapy
  • Antiplatelet therapy
  • Aspirin
  • Oral administration of 75325 mg aspirin daily
  • improves survival, with a 25 relative risk
    reduction in mortality.
  • The first tablet (300 mg) should be given orally
    within the first 12 hours.
  • Clopidogrel
  • In combination with aspirin
  • The early (within 12 hours) use of Clopidogrel
    (600 mg, followed by 150 mg daily for 1 week and
    75 mg daily thereafter)
  • This confers a further reduction in ischaemic
    events.

40
  • Anticoagulants
  • Reduces the risk of thromboembolic complications
  • Prevents re-infarction in the absence of
    reperfusion therapy or after successful
    thrombolysis.
  • Can be achieved using
  • Unfractionated heparin
  • Fractioned (low-molecularweight) heparin

41
  • Anti-anginal therapy
  • Nitrates
  • Sublingual glyceryl trinitrate (300500 µg)
  • Is a valuable first-aid measure in UA or
    threatened infarction
  • I/V nitrates (glyceryl trinitrate 0.61.2 mg/hr
    or isosorbide dinitrate 12 mg/hr)
  • are useful for the treatment of LV failure and
    the relief of recurrent or persistent ischaemic
    pain.

42
  • ß-blockers
  • I/V ß-blockers (e.g. atenolol 510 mg or
    metoprolol 515 mg given over 5 mins)
  • Relieve pain
  • Reduce arrhythmias
  • Improve short-term mortality in patients who
    present within 12 hours of the onset of symptoms.
  • They should be avoided if there is
  • HF (pulmonary oedema)
  • Hypotension (systolic BP lt 105 mmHg)
  • Bradycardia (heart rate lt 65/min).

43
  • Calcium channel antagonist
  • A dihydropyridine calcium channel antagonist
    (e.g. nifedipine or amlodipine)
  • This can be added to the ß-blocker if there is
    persistent chest discomfort but may cause
    tachycardia if used alone.
  • verapamil and diltiazem
  • Because of their rate-limiting action, these are
    the calcium channel antagonists of choice if a
    ß-blocker is contraindicated

44
  • Fibrinolysis
  • Fibrinolytic therapy should ideally be initiated
    within 30 min of presentation.
  • The principal goal prompt restoration of full
    coronary arterial patency.
  • The approved fibrinolytics
  • Tissue plasminogen activator (tPA),
    streptokinase, tenecteplase (TNK), and reteplase
    (rPA)
  • Promote the conversion of plasminogen to plasmin,
    which subsequently lyses fibrin thrombi.

45
  • Interventional Cardiology
  • Percutaneous coronary intervetion (PCI)
  • Is a procedure that's used to open a blocked or
    narrowed coronary arteries.
  • Improve blood flow to heart, relieve chest pain,
    and possibly prevent a heart attack.
  • Sometimes a small mesh tube (stent) is placed in
    the artery to keep it open after the procedure.
  • Antiplatelet admin. post stent
  • Aspirin for life
  • Clopidogrel for at least 6wks for metal stent

46
  • Coronary artery by pass grafting (CABG)
  • To improve blood flow to the myocardial tissue
    that are at risk for
  • Ischemia
  • Infarction as a result of the occluded artery.
  • Arteries or veins from elsewhere in the patient's
    body are grafted to the coronary arteries to
    bypass atherosclerotic narrowings
  • This improves the blood supply to the coronary
    circulation supplying the myocardium.

47
Long-term Treatment
  • Risk factor modification eg. cessation of
    smoking
  • Lipid lowering drugs ( e.g. statins,fibrates)
  • ACE inhibitors are recommended for long-term
    plaque stabilization.
  • Antiplatelet therapy,
  • Now recommended to be the combination of
    aspirin and clopidogrel for at least 912 months,
    then continue with aspirin to prevent rupture of
    plaque.

48
References
  • Brian R,Walker N,Stuart H. Davdsons Principle
    and Practice of Medicine 22nd Edition.CORONARY
    ARTERY DISEASE,Pg 583-600.
  • KASPER F,HAUSER LONGO. HARRISONS PRINCIPLES OF
    INTERNAL MEDICINE 19th Edition. Ischemic Heart
    Disease pg 1998-2004.

49
  • THANK YOU
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