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ACUTE ISCHAEMIC EVENT
                                                  05/07/2010

Learning Objectives
• Pathogenesis of atherosclerosis
• Pathophysiology of myocardial ischaemia
• Prevalence and interaction of risk factors for vascular disease
• Presentations of acute myocardial infarction
• Treatment principles of acute myocardial infarction
• Potential complications of acute myocardial infarction
• Long term therapy following acute myocardial infarction

Pathogenesis of Atherosclerosis




    1. Intimal accumulation of lipoprotein particles. Lipoprotein modification (oxidised) depicted by darker
       colour
    2. Local cytokine production.
    3. Increase expression of adhesion and chemoattractant molecules.
    4. Blood monocytes, enter artery wall, augmented scavenger receptor expression.
    5. Uptake of modified lipoprotein particles leads to development of foam cells. Produce further
       cytokines and effector molecules (e.g. hypochlorous acid, superoxide anion (O2-), and matrix
       metalloproteinases.
    6. Smooth muscle cell migration from media.
    7. Proliferation and elaboration of extracellular matrix. The fatty streak evolves into a fibrofatty lesion.
    8. Later, calcification may occur (not depicted) and fibrosis continues. Smooth muscle cell death
       (including apoptosis) may occur producing a relatively acellular fibrous capsule surrounding a lipid-
       rich core that may contain dying or dead cells and their detritus.
Pathophysiology of Myocardial Ischaemia / Angina

Angina/MI occurs when the Oxygen demand outweigh the oxygen supply. So, this imbalance might be
contributed by increased requirement or reduced supply compared to normal conditions.

Factors affecting the oxygen requirement include :
        Heart rate
        Contractility
        Wall tension (Systolic pressure and volume)
Factors affecting the oxygen supply, thus coronary blood flow include :
        Muscle spasm
        Diastolic Time > Heart Rate
        Aortic Pressure- Left Ventricular End-Diastolic Pressure Gradient
        Local autoregulation




* In relieving angina pectoris, nitrates exert favorable effects by reducing O2 requirements and increasing
supply. Although a reflex increase in heart rate would tend to reduce the time for coronary flow, dilation of
collaterals and enhancement of the pressure gradient for flow to occur as the left ventricular end-diastolic
pressure (LVEDP) falls tend to increase coronary flow.

Presentation of AMI
       Sudden death
       Resuscitated collapse
       Pain/ Discomfort :
           o S        : Central chest , Below Maxilla, Above Umbilicus
           o O        : Gradual onset
o C         : Indigestion , Squeezing, chest discomfort
           o R         : Left Arm, Left side of Neck
           o A         :
           o T         : Often last <12h (myocardium dead afterwards)
           o E         :
           o S         :
       Shortness of Breath (Dysponea) /Pulmonary Oedema
       Shock
       Arrhythmia
       Palpitation (Sense of impending doom)
       Nausea and Vomiting
       Dizziness/Lightheadedness/Weakness
       Sweating
       Anxiety
       Shock
       None/Incidental

DDx of Acute Chest Pain
System           Syndrome                        Clinical
Cardiac          Stable Angina                   Retrosternal chest pressure, burning/heaviness, radiating
                                                 to the neck/jaw/epigastrium/shoulder/left arm
                  Unstable Angina                Same as angina but more severe
                  AMI                            Same as angina but more severe

                  Pericarditis                   Sharp, pleuritic pain aggrevated by changes in position,
                                                 duration variable
Vascular          Aortic dissection              Excruciating, ripping pain of sudden onset of anterior
                                                 chest pain radiating to the back
                  Pulmonary embolism             Sudden onset of SOB/dysponea and pain, pleuritic with
                                                 pulmonary infarct
                  Pulmonary hypertension         Substernal chest pressure exarcebated by exertion
Pulmonary         Pleuritis +/- pneumonia        Pleuritic pain, usually brief, localized area of lung involved
                  Tracheobrochitis               Burning discomfort of midline
                  Spontaneous pneumothorax       Spontaenous unilateral pleuritic pain + dysponea
GIT               GORD                           Burning substernal and epigastric discomfort, 10-60min
                                                 duration
                Peptic ulcer                     Prolonged epigastric and substernal pain
                Gallbladder disease              Prolonged epigastric / RUQ pain
                Pancreatitis                     Prolonged intense epigastric and substernal pain
Musculoskeletal Costochondritis
                Cervical Disc Disease
Infectious      Herpes Zoster                    Prolonged burning pain in dermatome distribution
Psychological   Panic disorder                   Chest tightness/aching, accompanied by SOB, duration >
                                                 30min, unrelated to exertion/movement


Treatment principles of acute myocardial infarction

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Acute ischaemic event

  • 1. ACUTE ISCHAEMIC EVENT 05/07/2010 Learning Objectives • Pathogenesis of atherosclerosis • Pathophysiology of myocardial ischaemia • Prevalence and interaction of risk factors for vascular disease • Presentations of acute myocardial infarction • Treatment principles of acute myocardial infarction • Potential complications of acute myocardial infarction • Long term therapy following acute myocardial infarction Pathogenesis of Atherosclerosis 1. Intimal accumulation of lipoprotein particles. Lipoprotein modification (oxidised) depicted by darker colour 2. Local cytokine production. 3. Increase expression of adhesion and chemoattractant molecules. 4. Blood monocytes, enter artery wall, augmented scavenger receptor expression. 5. Uptake of modified lipoprotein particles leads to development of foam cells. Produce further cytokines and effector molecules (e.g. hypochlorous acid, superoxide anion (O2-), and matrix metalloproteinases. 6. Smooth muscle cell migration from media. 7. Proliferation and elaboration of extracellular matrix. The fatty streak evolves into a fibrofatty lesion. 8. Later, calcification may occur (not depicted) and fibrosis continues. Smooth muscle cell death (including apoptosis) may occur producing a relatively acellular fibrous capsule surrounding a lipid- rich core that may contain dying or dead cells and their detritus.
  • 2. Pathophysiology of Myocardial Ischaemia / Angina Angina/MI occurs when the Oxygen demand outweigh the oxygen supply. So, this imbalance might be contributed by increased requirement or reduced supply compared to normal conditions. Factors affecting the oxygen requirement include : Heart rate Contractility Wall tension (Systolic pressure and volume) Factors affecting the oxygen supply, thus coronary blood flow include : Muscle spasm Diastolic Time > Heart Rate Aortic Pressure- Left Ventricular End-Diastolic Pressure Gradient Local autoregulation * In relieving angina pectoris, nitrates exert favorable effects by reducing O2 requirements and increasing supply. Although a reflex increase in heart rate would tend to reduce the time for coronary flow, dilation of collaterals and enhancement of the pressure gradient for flow to occur as the left ventricular end-diastolic pressure (LVEDP) falls tend to increase coronary flow. Presentation of AMI Sudden death Resuscitated collapse Pain/ Discomfort : o S : Central chest , Below Maxilla, Above Umbilicus o O : Gradual onset
  • 3. o C : Indigestion , Squeezing, chest discomfort o R : Left Arm, Left side of Neck o A : o T : Often last <12h (myocardium dead afterwards) o E : o S : Shortness of Breath (Dysponea) /Pulmonary Oedema Shock Arrhythmia Palpitation (Sense of impending doom) Nausea and Vomiting Dizziness/Lightheadedness/Weakness Sweating Anxiety Shock None/Incidental DDx of Acute Chest Pain System Syndrome Clinical Cardiac Stable Angina Retrosternal chest pressure, burning/heaviness, radiating to the neck/jaw/epigastrium/shoulder/left arm Unstable Angina Same as angina but more severe AMI Same as angina but more severe Pericarditis Sharp, pleuritic pain aggrevated by changes in position, duration variable Vascular Aortic dissection Excruciating, ripping pain of sudden onset of anterior chest pain radiating to the back Pulmonary embolism Sudden onset of SOB/dysponea and pain, pleuritic with pulmonary infarct Pulmonary hypertension Substernal chest pressure exarcebated by exertion Pulmonary Pleuritis +/- pneumonia Pleuritic pain, usually brief, localized area of lung involved Tracheobrochitis Burning discomfort of midline Spontaneous pneumothorax Spontaenous unilateral pleuritic pain + dysponea GIT GORD Burning substernal and epigastric discomfort, 10-60min duration Peptic ulcer Prolonged epigastric and substernal pain Gallbladder disease Prolonged epigastric / RUQ pain Pancreatitis Prolonged intense epigastric and substernal pain Musculoskeletal Costochondritis Cervical Disc Disease Infectious Herpes Zoster Prolonged burning pain in dermatome distribution Psychological Panic disorder Chest tightness/aching, accompanied by SOB, duration > 30min, unrelated to exertion/movement Treatment principles of acute myocardial infarction