Atherosclerotic vascular disease

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Atherosclerotic vascular disease

• AVD may manifest as
• Coronary artery disease.
• Cerebrovascular disease.
• Peripheral vascular disease.
• Pathophysiology
• Early atherosclerosis
• Fatty streaks develop when inflammatory cells
• predominantly monocytes migrate into the
• intima,takeup oxidized LDL from the plasma and
• become lipid laden foam cells or macrophages,
  when
• these cells die and release their contents extra
• cellular lipid pools appear. Smooth muscle cells
  then
• migrate from the media into the intima in
  response to
• cytokines growth factors produced by activated
  macrophages.

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• The lipid core will be covered by smooth muscle
  cells and matrix, producing a stable
  atherosclerotic plaque which is asymptomatic
  until it becomes large enough to obstruct
  arterial flow.
• Advanced atherosclerosis
• In an established atherosclerotic plaque
  macrophages mediate inflammation smooth muscle
  cells promote repair, if inflammation
  predominates, the plaque becomes active or
  unstable may be complicated by ulceration
  superadded thrombosis. Cytokines such as
  interleukin-1, tumour necrosis-alpha, interferon
  gamma, platelet derived growth factors, and
  matrix metalloprotinases are released by
  activated macrophages may cause the initial
  smooth muscle

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• Cells overlying the plaque to become senescent
  resulting in thinning of the protective fibrous
  cap, may lead to erosion, fissuring or rupture of
  the plaque surface, exposing its content to
  circulating blood, may trigger platelet
  aggregation thrombosis, may cause partial or
  complete obstruction resulting in infarction or
  ischemia of the affected organ.

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Risk Factors

• A. Fixed R. F
• Age
• Male sex
• Family history.
• B. Modifiable R.F
• Smoking - Sedentary lifestyle
• Hypertension - Obesity
• Lipid disoder. - Diet
• D.M
• Haemostatic variables

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• Primary Prevention
• Population advice to prevent coronary disease
• Do not smoke.
• Take regular exercise (minimum of 20 minutes
  three times a week).
• Maintain ideal body weight .
• Eat a mixed diet rich in fresh fruit
  vegetables.
• Aim to get no more than 30 of energy intake from
  saturated fat.

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• Secondary prevention
• Patients who already have evidence of
  atheromatous vascular disease e.g M.I, are at
  high risk of another vascular event, can be
  offered a variety of treatment and measures to
  improve their outlook (secondary prevention).
• Correction of risk factors
• Aspirin
• Beta blockers
• ACE Inhibitors

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Coronary Heart Disease

• It is the most common form of heart disease.
• Most important cause of premature death.
• In UK 1 in 3 men 1 in 4 women die of CHD.
• Clinical manifestation
• Stable angina.
• Unstable angina.
• M.I
• Heart failure.
• Arrhythmia.
• Sudden death.

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Stable angina

• Angina pectoris is caused by transient myocardial
  ischemia.
• It may occur whenever there is an imbalance
  between myocardial oxygen supply demand.
• Coronary atheroma is the most common cause.
• Other causes include aortic valve disease
  hypertrophic cardiomyopathy.

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• Clinical features
• The history is the most important factor in
  making the diagnosis.
• Central chest pain, discomfort or breathlessness
  that is precipitated by exertion or other forms
  of stress, (heavy meal, cold exposure, intense
  emotion, lying flat/ decubitus, vivid dreams/
  nocturnal angina), and relieved by rest.
• Start up angina the pain comes when they start
  walking that later it dose not return despite
  greater effort.
• Physical examination is frequently negative, but
  should include
• Evidence of valve disease, important risk
  factors, left ventricular dysfunction, features
  of arterial disease e.g carotid bruits and
  untreated conditions that may exacerbate angina
  e.g anemia, thyrotoxicosis.

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• Investigations
• Resting ECG
• Evidence of previous M.I, but may be normal.
• Occasionally T wave flattening or inversion.
• The most important ECG changes is reversible ST
  segment depression or elevation with or without T
  wave inversion at the time the patient is
  experiencing symptoms.
• Exercise ECG
• Standard treadmill or bicycle ergometer protocol,
  planar or down-sloping ST-segment depression of 1
  mm or more is indicative of ischemia, up-sloping
  is less specific often occurs in normal
  individuals.
• Exercise ECG is used to diagnose angina, assess
  severity identifying high- risk individuals.
• False ve Digoxin, LVH, LBBB, WPW syndrome, the
  accuracy is lower in women than men.

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• Risk stratification in stable
  angina.
• High Risk post infarct angina, poor effort
  tolerance, ischemia at low workload, left main
  or three vessel disease, poor LV function.
• Low Risk
• Predictable exertional angina, good effort
  tolerance, ischemia only at high workload,
  single-vessel or minor two-vessel disease, good
  LV function.
• Other forms of stress testing
• Myocardial perfusion scanning useful when
  exercise test is not diagnostic, or patient can
  not exercise, its accuracy is higher than
  exercise test.
• The technique involve obtaining scintiscans of
  the myocardium at rest and during stress after
  administration of an i.v radioactive isotope e.g
  thallium201, it is taken up by viable myocardium.
  

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• A perfusion defect present during stress but not
  rest indicates reversible myocardial ischemia,
  whereas persistent perfusion defect indicates
  previous M.I
• Stress echocardiography
• It is alternative to perfusion scanning with
  similar accuracy.
• Uses transthoracic echo to identify ischemic
  segments of myocardium area of infarction, the
  latter do not contract at rest or during stress.
• Coronary arteriography
• Shows the extent nature of coronary artery
  disease, it may be indicated when other
  investigations fail to diagnose the cause of
  atypical chest pain.

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• Management
• Assessment of the extent severity of arterial
  disease.
• Identification control of significant risk
  factors
• Measures to control symptoms.
• Identification of high risk patients
  application of treatment to improve life
  expectancy.
• Antiplatelet therapy
• Aspirin 75-150 mg reduce the risk of MI,
  Clopidogrel 75 mg daily equally effective but
  more expensive can be used if the patient has
  dyspepsia.

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• Anti-anginal drugs
• Nitrates produces venous arteriolar dilatation
• Decrease myocardial oxygen demand (lower preload
  afterload) increase myocardial oxygen supply.
• Sublingual glyceryl trinitrate (GTN), as aerosol
  400 microgm or tablet 300-500 micro-gm
  sublingually usually relieve angina in 2-3
  minutes, side- effects include headache,
  symptomatic hypotension syncope, the tablet
  should be replaced 8 weeks after
• the bottle has been opened.
• Nitrates can be used prophylactically before
  exercise.
• GTN is subject to extensive first pass metabolism
  in the liver, its ineffeective when swallowed.
• Nitrate free period of 6-8 hr. every day to avoid
  tolerance.

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• Preparation Peak action
  Duration
• Sublingual GTN 4-8
  mins 10-30 mins
• Buccal GTN 4-10
  mins 30-300 mins
• Transdermal GTN 1-3 hrs
  up to 24 hrs
• Oral isosorbide dinitrate 45-120 mins
  2-6 hrs
• Oral isosorbide mononitrate 45-120 mins
  6-10 hrs

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• Beta-blockers
• Reduce myocardial oxygen demand by reducing heart
  rate, BP, and myocardial contractility.
• Non-selective BB may exacerbate coronary spasm by
  blocking Beta 2 coronary adrenoceptors.
• Give once daily cardioselective preparation,
  atenolol 50-100 mg daily, slow release metoprolol
  200 mg daily, bisoprolol 5-10 mg daily.
• ?ß should not be withdrawn suddenly as this may
  cause arrhythmia, more angina or MI.(ßß
  withdrawal syndrome).
• Calcium antagonists
• lower myocardial oxygen demand by reducing blood
  pressure and myocardial contractility.
• Dihydropyridine calcium antagonists, such as
  nifedipine and nicardipine, often cause a reflex
  tachycardia it is often best to use these drugs
  in combination with a ß-blocker.
• In contrast, verapamil and diltiazem are
  particularly suitable for patients who are not
  receiving a ß-blocker because they inhibit
  conduction through the AV node and tend to cause
  a bradycardia or even atrioventricular block in
  susceptible individuals.

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• The calcium antagonists may reduce myocardial
  contractility and can aggravate or precipitate
  heart failure. Other unwanted effects include
  peripheral oedema, flushing, headache and
  dizziness.
• Potassium channel activators
• This class of drug has arterial and venous
  dilating properties but does not exhibit the
  tolerance seen with nitrates. Nicorandil (10-30
  mg 12-hourly orally) is the only drug in this
  class currently available for clinical use.
• it is conventional to start therapy with low-dose
  aspirin, sublingual GTN and a ß-blocker, and then
  add a calcium channel antagonist or a long-acting
  nitrate later, if necessary.

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• The goal is the control of angina with minimum
  side-effects and the simplest possible drug
  regimen. There is little or no evidence that
  prescribing multiple anti-anginal drugs is of
  benefit, and revascularisation should be
  considered if an appropriate combination of two
  drugs fails to achieve a symptomatic response.
• Invasive treatment The most widely used invasive
  options for the treatment of ischaemic heart
  disease include percutaneous coronary
  intervention (PCI including percutaneous
  transluminal coronary angioplasty, PTCA) and
  coronary artery bypass graft (CABG) surgery.

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• UNSTABLE ANGINA
• is a clinical syndrome that is characterised by
  new-onset or rapidly worsening angina (crescendo
  angina), angina on minimal exertion or angina at
  rest.
• The condition shares common pathophysiological
  mechanisms with acute myocardial infarction,
• the term 'acute coronary syndrome' is used to
  describe these disorders collectively.
• These entities comprise a spectrum of disease
  that encompasses ischaemia with no myocardial
  damage, ischaemia with minimal myocardial damage,
  partial thickness (non-Q wave) myocardial
  infarction, and full thickness (Q wave)
  myocardial infarction .

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• An acute coronary syndrome 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 and local coronary artery
  spasm .
• Diagnosis and risk stratification
• The assessment of acute chest pain depends
  heavily on an analysis of the character of the
  pain and its associated features, evaluation of
  the ECG, and serial measurements of biochemical
  markers of cardiac damage, such as troponin I and
  T.

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• A 12-lead ECG is mandatory and is the most useful
  method of initial triage.
• Evolving transmural infarction is characterised
  by persistent ST elevation, new Q waves or new
  left bundle branch block
• In patients with unstable angina or partial
  thickness (non-Q wave or non-ST elevation)
  myocardial infarction, the ECG may show ST/T wave
  changes including ST depression, transient ST
  elevation and T-wave inversion the T-wave
  changes are sometimes prolonged.
• Approximately 12 of patients with
  well-characterised unstable angina or non-ST
  segment elevation myocardial infarction progress
  to acute infarction or death, and almost
  one-third will suffer a recurrence of severe
  ischaemic pain, within 6 months of the index
  event.

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• The risk markers that are indicative of an
  adverse prognosis include
• recurrent ischaemia,
• extensive ECG changes at rest or during pain,
• the release of biochemical markers (creatine
  kinase or troponin),
• arrhythmias and haemodynamic complications (e.g.
  hypotension, mitral regurgitation) during
  episodes of ischaemia
• those who experience unstable angina following
  acute myocardial infarction are also at increased
  risk.

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• Risk stratification is important because it
  guides the use of more complex pharmacological
  and interventional treatment .

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• High risk
• Clinical
• Post-infarct anginaRecurrent pain at restHeart
  failure
• ECG
• ArrhythmiaST depressionTransient ST
  elevationPersistent deep T-wave inversion
• BiochemistryTroponin T gt 0.1 µg/l

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• Low risk
• Clinical
• No history of MI
• Rapid resolution of symptoms
• ECG
• Minor or no ECG changes
• Biochemistry
• Troponin T lt 0.1 microgm/ l

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• The initial treatment should include
• bed rest,
• antiplatelet therapy (aspirin 300 mg followed by
  75-325 mg daily long-term and clopidogrel 300 mg
  followed by 75 mg daily for 12 months,
• anticoagulant therapy (e.g. unfractionated or
  fractionated heparin)
• ß-blocker (e.g. atenolol 50-100 mg daily or
  metoprolol 50-100 mg 12-hourly
• A dihydropyridine calcium antagonist (e.g.
  nifedipine or amlodipine) can be added to the
  ß-blocker, but may cause an unwanted tachycardia
  if used alone verapamil or diltiazem is
  therefore the calcium antagonist of choice if a
  ß-blocker is contraindicated

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• An intravenous infusion of unfractionated heparin
  (with dose adjusted according to the activated
  partial thromboplastin time) or weight-adjusted
  subcutaneous low molecular weight heparin (e.g.
  enoxaparin 1 mg/kg 12-hourly) should be given
• If pain persists or recurs, infusions of
  intravenous nitrates (e.g. GTN 0.6-1.2 mg/hr or
  isosorbide dinitrate 1-2 mg/hr) or buccal
  nitrates may help, but such patients should also
  be considered for early revascularisation.
• Refractory cases or those with haemodynamic
  compromise should be considered for a
  glycoprotein IIb/IIIa receptor antagonist (e.g.
  abciximab, tirofiban or eptifibatide),
  intra-aortic balloon pump or emergency coronary
  angiography .

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• Most low-risk patients stabilise with aspirin,
  clopidogrel, heparin and anti-anginal therapy,
  and can be gradually mobilised. If there are no
  contraindications,
• exercise testing may be performed prior to or
  shortly following discharge.
• Coronary angiography should be considered with a
  view to revascularisation in all patients at
  moderate or high risk, including those who fail
  to settle on medical therapy, those with
  extensive ECG changes, those with an elevated
  plasma troponin and those with severe
  pre-existing stable angina.
• This often reveals disease that is amenable to
  PCI however, if the lesions are not suitable
  for PCI the patient should be considered for
  urgent CABG.

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• MYOCARDIAL INFARCTION
• Myocardial infarction (MI) is almost always due
  to the formation of occlusive thrombus at the
  site of rupture or erosion of an atheromatous
  plaque in a coronary artery.
• The thrombus often undergoes spontaneous lysis
  over the course of the next few days, although by
  this time irreversible myocardial damage has
  occurred.
• Without treatment the infarct-related artery
  remains permanently occluded in 30 of patients.
• The process of infarction progresses over several
  hours and therefore most patients present when it
  is still possible to salvage myocardium and
  improve outcome.

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• CLINICAL FEATURES
• Pain is the cardinal symptom of MI, but
  breathlessness, vomiting, and collapse or syncope
  are common features.
• The pain 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. At its worst, the
  pain is one of the most severe which can be
  experienced and the patient's expression and
  pallor may vividly convey the seriousness of the
  situation
• Most patients are breathless and in some this is
  the only symptom. Indeed, some myocardial
  infarcts pass unrecognised.

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• Painless or 'silent' myocardial infarction is
  particularly common in older or diabetic
  patients.
• If syncope occurs, it is usually due to an
  arrhythmia or profound hypotension. 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.
• Sometimes infarction occurs in the absence of
  physical signs.
• Sudden death, from ventricular fibrillation or
  asystole, may occur immediately, and many deaths
  occur within the first hour.

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• If the patient survives this most critical stage,
  the liability to dangerous arrhythmias remains,
  but diminishes as each hour goes by.
• The development of cardiac failure reflects the
  extent of myocardial damage and is the major
  cause of death in those who survive the first few
  hours of infarction.

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• Physical signs
• Signs of sympathetic activation
• Pallor, sweating, tachycardia
• Signs of vagal activation
• Vomiting, bradycardia
• Signs of impaired myocardial function
• Hypotension, oliguria, cold peripheries
• Narrow pulse pressure
• Raised jugular venous pressure
• Third heart sound
• Quiet first heart sound
• Diffuse apical impulse
• Lung crepitations
• Signs of tissue damage
• Fever
• Signs of complications, e.g. mitral
  regurgitation, pericarditis

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• INVESTIGATIONS
• Electrocardiography The ECG is usually helpful in
  confirming the diagnosis however, it may be
  difficult to interpret if there is bundle branch
  block or evidence of previous MI.
• Only rarely is the initial ECG entirely normal,
  but in up to one-third of cases the initial ECG
  changes may not be diagnostic.
• The earliest ECG change is usually ST elevation
  later on there is diminution in the size of the R
  wave, and in transmural (full thickness)
  infarction a Q wave begins to develop.
• Subsequently, the T wave becomes inverted, this
  change persists after the ST segment has returned
  to normal.

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• In contrast to transmural lesions, partial
  thickness or subendocardial infarction causes
  ST/T wave changes, without Q waves or prominent
  ST elevation this is often accompanied by some
  loss of the R waves in the leads facing the
  infarct and is also known as non-Q wave or non-ST
  elevation myocardial infarction.
• The ECG changes are best seen in the leads that
  'face' the infarcted area.
• When there has been anteroseptal infarction,
  abnormalities are found in one or more leads from
  V1 to V4
• while anterolateral infarction produces changes
  from V4 to V6, in aVL and in lead I.

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• Inferior infarction is best shown in leads II,
  III and aVF, while at the same time leads I, aVL
  and the anterior chest leads may show
  'reciprocal' changes of ST depression
• Infarction of the posterior wall of the left
  ventricle does not cause ST elevation or Q waves
  in the standard leads, but can be diagnosed by
  the presence of reciprocal changes (ST depression
  and a tall R wave in leads V1-V4).
• Some infarctions (especially inferior) also
  involve the right ventricle this may be
  identified by recording from additional leads
  placed over the right precordium.

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• The serial evolution of ECG changes in full
  thickness myocardial infarction. A. Normal ECG
  complex. B. Acute ST elevation ('the current
  of injury'). C. Progressive loss of the R
  wave, developing Q wave, resolution
  of the ST elevation and terminal T wave
  inversion. D. Deep Q wave and T wave
  inversion. E. Old infarction

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• Plasma biochemical markers
• The biochemical markers that are most widely used
  in the detection of MI are creatine kinase (CK),
  a more sensitive and cardiospecific isoform of
  this enzyme (CK-MB), and the cardiospecific
  proteins, troponins T and I
• The troponins are also released, to a minor
  degree, in unstable angina with minimal
  myocardial damage Serial (usually daily)
  estimations are particularly helpful because it
  is the change in plasma concentrations of these
  markers that is of diagnostic value.

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• CK starts to rise at 4-6 hours, peaks at about 12
  hours and falls to normal within 48-72 hours.
• CK is also present in skeletal muscle, and a
  modest rise in CK (but not CK-MB) may sometimes
  be due to an intramuscular injection, vigorous
  physical exercise or, in old people particularly,
  a fall.
• Defibrillation causes significant release of CK
  but not CK-MB or troponins. The most sensitive
  markers of myocardial cell damage are the cardiac
  troponins T and I, which are released within 4-6
  hours and remain elevated for up to 2 weeks.
• Other blood tests A leucocytosis is usual,
  reaching a peak on the first day. The erythrocyte
  sedimentation rate (ESR) becomes raised and may
  remain so for several days. C-reactive protein
  (CRP) is also elevated in acute MI.

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• 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
• This can be performed at the bedside and is a
  very useful technique for assessing left and
  right ventricular function and for detecting
  important complications such as mural thrombus,
  cardiac rupture, ventricular septal defect,
  mitral regurgitation and pericardial effusion.

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• EARLY MANAGEMENT OF ACUTE MYOCARDIAL INFARCTION
• Provide facilities for defibrillation
• Immediate measures
• High-flow oxygen
• I.v. access
• ECG monitoring
• 12-lead ECG
• I.v. analgesia (opiates) and antiemetic
• Aspirin 300 mg

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• Reperfusion
• Primary PCI or thrombolysis
• Detect and manage acute complications
• Arrhythmias
• Ischaemia
• Heart failure
• Patients are usually managed in a dedicated
  cardiac unit because this offers a convenient way
  of concentrating the necessary expertise,
  monitoring and resuscitation facilities.
• If there are no complications, the patient can
  be mobilised from the second day and discharged
  from hospital on the fifth or sixth day.

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• Analgesia
• Adequate analgesia is essential not only to
  relieve severe distress, but also to lower
  adrenergic drive and thereby reduce pulmonary and
  systemic vascular resistance and susceptibility
  to ventricular arrhythmias.
• Intravenous opiates (initially morphine sulphate
  5-10 mg or diamorphine 2.5-5 mg) and antiemetics
  (initially metoclopramide 10 mg) should be
  administered through an intravenous cannula.

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• Acute reperfusion therapy
• Thrombolysis
• Coronary thrombolysis helps restore coronary
  patency, preserves left ventricular function and
  improves survival.
• Successful thrombolysis leads to reperfusion with
  relief of pain, resolution of acute ST elevation
  and sometimes transient arrhythmias (e.g.
  idioventricular rhythm).
• The sooner the patient is treated, the better the
  results will be any delay will only increase the
  extent of myocardial damage-'minutes mean
  muscle'.

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• Clinical trials have shown that the appropriate
  use of these drugs can reduce the hospital
  mortality of myocardial infarction by 25-50 and
  follow-up studies have demonstrated that this
  survival advantage is maintained for at least 10
  years.
• The benefit is greatest in those patients who
  receive treatment within the first few hours, and
  choice of agent is less important than speed of
  treatment.
• Streptokinase, 1.5 million U in 100 ml of saline
  given as an intravenous infusion over 1 hour, is
  a widely used regimen. Streptokinase is antigenic
  and occasionally causes serious allergic
  manifestations. It may also cause hypotension,
  which can often be managed by stopping the
  infusion and restarting at

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• slower rate.
• Circulating neutralising antibodies are formed
  following treatment with streptokinase and may
  persist for 5 years or more.
• These antibodies can render subsequent infusions
  of streptokinase ineffective so it is advisable
  to use another non-antigenic agent if the patient
  requires further thrombolysis in the future.
• Alteplase (human tissue plasminogen activator or
  tPA) is a genetically engineered drug that is not
  antigenic and seldom causes hypotension. The
  standard regimen is given over 90 minutes (bolus
  dose of 15 mg, followed by 0.75 mg/kg body
  weight, but not exceeding 50 mg, over 30 minutes
  and then 0.5 mg/kg

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• body weight, but not exceeding 35 mg, over 60
  minutes).
• There is evidence that tPA may produce better
  survival rates than streptokinase, particularly
  among high-risk patients (e.g. large anterior
  infarct), but with a slightly higher risk of
  intracerebral bleeding (10 per 1000 increased
  survival, but 1 per 1000 more non-fatal stroke).
• Newer-generation analogues of tPA have been
  generated that have a longer plasma half-life and
  can be given as an intravenous bolus. Large-scale
  trial data have demonstrated that tenecteplase
  (TNK) is as effective as alteplase at reducing
  death and MI whilst conferring similar
  intracerebral bleeding risks.

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• Reteplase (rPA) is administered as a double bolus
  and trial data indicate a similar outcome to that
  achieved with alteplase, although some of the
  bleeding risks appear slightly higher. The double
  bolus administration may provide practical
  advantages over the infusion of alteplase.
• An overview of all the large randomised trials
  confirms that thrombolytic therapy significantly
  reduces short-term mortality in patients with
  suspected MI if it is given within 12 hours of
  the onset of symptoms and the ECG shows bundle
  branch block or characteristic ST segment
  elevation of greater than 1 mm in the limb leads
  or 2 mm in the chest leads.

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• Thrombolysis appears to be of little net benefit,
  and may be harmful in other patient groups,
  specifically those who present more than 12 hours
  after the onset of symptoms and those with a
  normal ECG or ST depression.
• The major hazard of thrombolytic therapy is
  bleeding.

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• RELATIVE CONTRAINDICATIONS TO THROMBOLYTIC
  THERAPY (POTENTIAL CANDIDATES FOR PRIMARY
  ANGIOPLASTY)
• Active internal bleeding
• Previous subarachnoid or intracerebral
  haemorrhage
• Uncontrolled hypertension
• Recent surgery (within 1 month)
• Recent trauma (including traumatic resuscitation)
  
• High probability of active peptic ulcer
• Pregnancy

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• Primary percutaneous coronary intervention (PCI)
• In institutions that are able to offer rapid
  access (within 3 hours) to a 24-hour catheter
  laboratory service, percutaneous coronary
  intervention is the treatment of choice.
• In comparison to thrombolytic therapy, it is
  associated with a 50 greater reduction in the
  risk of death, recurrent myocardial infarction or
  stroke.

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• The widespread use of PCI has been limited by the
  availability of the resources necessary to
  achieve this highly specialized emergency
  service.
• As a consequence, intravenous thrombolytic
  therapy remains the first-line reperfusion
  treatment in many hospitals.
• For some patients, thrombolytic therapy is
  contraindicated or fails to achieve coronary
  arterial reperfusion. Early emergency PCI (within
  6 hours of symptom onset) may be considered under
  such circumstances, particularly where there is
  evidence of cardiogenic shock.

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• Acute right
• Coronary art.
• Occlusion.

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• Initial angio Filling defect

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• Complete resolution of flow following insertion
  of stent