T1 L10: Ischaemic Heart disease and acute coronary syndromes

• What are the Three main categories of cardiovascular disease CVD?

  1. Coronary heart disease
  2. cerebrovascular disease
  3. peripheral vascular disease
• What is the Framingham Heart Study?


  • ongoing study in 5000+ healthy men and women aged 30-62 yrs in Framingham, MA, USA
  • begun in 1948 and now in 3rd generation of participants
  • origin of the term 'risk factor'
  • in order established these factors as risk factors to CHD: high cholesterol and high BP, smoking, obesity and inactivity, diabetes
• What are the controllable risk factors for CHD?

  • cigarette smoking
  • diabetes
  • high blood pressure
  • high cholesterol
  • obesity
• What are the Non-controllable risk factors for CHD?

  • age
  • family history of premature coronary disease
  • previous heart attack
• What is Atherosclerosis?

  • clinical manifestation of CHD
  • development of fatty streak, lipid deposition, intimal fibrosis
  • 'hardening of arteries"

  
• What is Ischaemic Heart Disease (IHD) / Myocardial Ischaemia?

  • occurs due to atherosclerotic plaque build up within coronary arteries, obstructing myocardial blood flow
  • leads to imbalance between myocardial oxygen supply and demand
• What are the 4 categories of clinical manifestations of IHD?

  1. Asymptomatic (silent ischaemia)
  2. Stable angina
  3. Acute coronary syndromes (unstable angina, heart attacks)
  4. Long-term (heart failure, arrhythmias, sudden death)
• What is the Management of stable angina?

  1st line of treatment:

  • short-acting nitrates (dilate arteries, increasing blood flow)
  • beta blockers (decrease heart rate, reducing myocardial oxygen demand)

  2nd line of treatment:

  • long-acting nitrates
  • ivabradine
  • consider angiogram, PCI, stenting or CABG

  Event prevention:

  • lifestyle management
  • Control of risk factors
  • educate patient
• What is Acute coronary syndromes (ACS)?

  includes two groups:

  1. unstable angina
  2. acute myocardial infarction (STEMIs (ST elevation myocardial infarction) and NSTEMIs (non-ST elevation myocardial infarction)

  STEMIs and NSTEMIs differentiated by specific pattern of abnormality on the ECG

  • all patients with an acute MI have a rise in troponin (cardiac enzyme) - measured on a blood test
• What is the Pathology of STEMI(ST elevated myocardial infarction)?


  ST elevation on ECG

  marker of complete coronary occlusion

  
• What is the Pathology of UA (Unstable angina) / NSTEMI (Non-ST elevated myocardial infarction)?


  ST depression, variable T wave abnormalities or normal ECG

  associated with incomplete occlusion

  
• What is the pathological correlation to stable angina?

  ischaemia due to fixed atheromatous stenosis of one or more coronary arteries
• What is the pathological correlation to unstable angina?

  ischaemia caused by dynamic obstruction of a coronary artery

  due to plaque rupture

  with superimposed thrombosis and spasm
• What is the pathological correlation to myocardial infarction?

  myocardial necrosis caused by acute occlusion of a coronary artery

  due to plaque rupture

  with superimposed thrombosis and spasm
• What is the pathological correlation to heart failure?

  myocardial dysfunction due to infarction or ischaemia
• What is the pathological correlation to arrhythmia?

  altered conduction

  due to ischaemia or infarction
• What is the pathological correlation to sudden death?

  ventricular arrhythmia, asystole or massive myocardial infarction
• How is chest pain classified?

  Typical angina (definite): meets ALL 3 of the following characteristics:

  1. substernal chest discomfort of characteristic quality and duration;
  2. provoked by exertion or emotional stress;
  3. relieved by rest and/or nitrates within minutes.

  Atypical angina (probable): meets two of these characteristics

  Non-anginal chest pain: lacks or meets only one or none of these characteristics.
• Troponin levels are elevated in acute MI but NOT in unstable angina.
• What is ACS (Acute Coronary Syndromes) characterised by?

  development of a thrombosis

  at the site of acute disruption of an atherosclerotic plaque

  within the wall of the coronary artery

  
• Following plaque disruption, what does thrombus result from?

  • Adherence, activation and aggregation of platelets
  • Thrombin and fibrin production via the coagulation cascade (and thrombin release from platelets)
  • Vasoactive molecules released from platelets which cause vasoconstriction

  
• What are the classical symptoms of ACS at presentation?

  • Discomfort/pain in the centre of the chest that lasts for more than a few minutes or recurs
  • Discomfort/pain radiating to other areas, e.g. left arm/jaw/back
  • Can occur at rest and/or with exertion
  • Not relieved immediately with sublingual GTN
• What do elderly or diabetic patients with ACS often present with?

  • Breathlessness
  • Nausea or vomiting
  • Sweating and clamminess
• What is the Immediate assessment of patients with suspected ACS?

  First:

  • patient history
  • ECG
  • physical examination

  Then/in parallel:

  • risk stratification (assign risk level to patients)
  • cardiac biomarkers (troponin)
• How to take patients history for suspected ACS?

  Take a detailed clinical history including:

  • Nature and site of pain
  • Time of onset of pain and duration
  • History of cardiovascular disease/risk factors
• What are the therapeutic goals in ACS?

  Restore coronary artery patency (STEMI)

  Limit myocardial necrosis (STEMI)

  Control symptoms
• What is the medical management of ACS?

  Anti-platelet therapy

  Anti-ischaemic therapy

  Secondary prevention therapy
• What are examples of Anti-platelet therapy?

  Aspirin

  Clopidogrel / Prasugrel / Ticagrelor
• What does anti-ischaemic therapy consist of?

  nitrates
• What does secondary prevention therapy include?

  statin

  ACE inhibitors

  beta blockers

  smoking cessation

  lifestyle modification
• What is the importance of time for management of STEMI?

  1. Timely diagnosis of STEMI is the key to successful management
  2. The most critical time is the very early phase when the patient is liable to cardiac arrest
  3. Minimising delays to treatment is associated with improved clinical outcome
• What are the guidelines for rapid treatment of STEMI?

  • morphine and/or nitrates for pain relief
  • antiplatelet agents (Aspirin + Clopidogrel)

  AND:

  • emergency primary angioplasty (balloons, stents) to mechanically reopen artery & restore blood flow
  • 'Clot-busting' drugs (thrombolysis): pharmacologically break up clots, restoring blood flow (when no access to primary angioplasty)
• What is 'angina at rest' relating to unstable angina?

  > 20 mins
• What is 'new onset' relating to unstable angina?

  < 2 months exertional angina
• What is 'recent' acceleration / progression of angina symptoms relating to unstable angina?

  < 2 months
• What is the definition of NSTEMI?

  absence of ST elevation on ECG, but with angina symptoms and elevated cardiac biomarkers (troponin)
• What else could positive troponin be an indication of?

  NOT synonymous with NSTEMI

  could also be:

  • pneumonia
  • pulmonary embolism
  • pericarditis
  • sepsis
  • heart failure
  • uncontrolled tachycardia
• What kinds of patients are high-risk for ACS?

  • elevated troponin levels
  • renal impairment
  • recurrent chest pain
  • dynamic ST depression / T wave changes on ECG
  • haemodynamic instability
  • major arrhythmias
  • heart failure
  • elderly
• What is the management of UA/NSTEMI?

  • analgesia
  • anti-platelet therapy
  • anti-ischaemic therapy
  • statins
  • early coronary angiography with a view of revascularisation (stenting / CABG)