Courses

Ischaemic Heart Disease

Angina

Epidemiology

  • In the UK, the incidence of ischaemic heart disease (IHD) is approximately 21,000 cases per year; stable angina accounts for a significant proportion.
  • In people older than 55 years, prevalence is about 12% in men and 5% in women.
  • In the US, IHD is the leading cause of death.
  • Incidence increases with age.

Aetiology

  • Angina (a clinical manifestation of myocardial ischaemia) usually arises from atherosclerosis of the coronary arteries.
    • Luminal narrowing reduces blood flow, particularly during increased demand.
  • In stable angina, stenosis (>70% in some cases) typically limits blood flow during exertion but may be sufficient at rest.

Risk Factors

  • Modifiable: Smoking, hypertension, hypercholesterolaemia, diabetes
  • Non-modifiable: Age, positive family history (first-degree relative with premature coronary artery disease < 65 years)
  • These risk factors are similar to those for atherosclerosis.

Symptoms

  • Chest pain:
    • Typically heavy or crushing, felt centrally or retrosternally
    • Often radiates to the left arm, neck, or jaw
    • Usually precipitated by exertion, emotional stress, cold weather, or large meals
    • Relieved by rest or glyceryl trinitrate (usually within 10–20 minutes)
  • Dyspnoea: May occur if left ventricular systolic function is impaired, leading to increased pulmonary pressures.

Additional Angina Classifications

  • Stable Angina: Occurs on exertion/stress, relieved by rest or nitroglycerin, associated with ST-segment depression during episodes (subendocardial ischaemia).
  • Unstable Angina: Can occur at rest; often involves rupture of an atherosclerotic plaque with incomplete occlusion. High risk for progression to myocardial infarction.
  • Prinzmetal Angina: Episodic chest pain caused by coronary artery vasospasm, with ST-segment elevation due to transmural ischaemia.

Diagnosis

  • Electrocardiography (ECG):
    • Often normal at rest in stable angina unless there is prior infarction or LV hypertrophy.
    • During ischaemia, ST-segment depression may appear (subendocardial ischaemia).
  • Functional Tests (e.g., exercise ECG, stress echocardiography, perfusion imaging):
    • Used to detect inducible ischaemia by exercise or pharmacological stress.
  • Coronary Angiography (including CT angiography and invasive angiography):
    • Assesses the burden of disease and severity of luminal narrowing, guiding potential interventions.

Immediate Management

  • Pain relief and symptom control with rest or short-acting nitrates (e.g., glyceryl trinitrate).
  • Worsening severity, decreased threshold for pain, or rest pain suggests unstable angina or an acute coronary syndrome and warrants urgent evaluation.

Long-Term Management

  1. Lifestyle and Risk Factor Modification
    • Smoking cessation
    • Control of hypertension and diabetes
    • Regular exercise
    • Mediterranean-style diet (rich in fresh fruit and vegetables)
  2. Medical Therapy
    • Symptomatic Therapies:
      • Nitrates (short-acting glyceryl trinitrate, long-acting isosorbide mononitrate)
      • Calcium channel antagonists (e.g., amlodipine)
      • Potassium channel activators (e.g., nicorandil)
    • Prognostic Therapies:
      • Beta-blockers (e.g., atenolol) to reduce myocardial workload
      • Antiplatelet agents (e.g., aspirin)
      • Statins (e.g., simvastatin) to stabilize plaques by lowering cholesterol
  3. Revascularization
    • Percutaneous Coronary Intervention (PCI) (angioplasty with stent) for patients whose anginal symptoms are not controlled by medical therapy.
    • Coronary Artery Bypass Graft (CABG) for severe or extensive disease (e.g., triple-vessel or left main stem involvement) or if PCI is not suitable.

Acute Coronary Syndrome

1. Epidemiology

  • Age: ACS is rare in individuals under 35 years.
  • Prevalence (England): ~0.6% in people aged 35–74 years; ~2.3% in those ≥75 years.
  • Incidence (England): ~233,600 new ACS cases annually; majority are unstable angina or NSTEMI.
  • STEMI: Affects ~5 in 1000 people per year in the UK; its relative frequency is decreasing compared to NSTEMI.

2. Aetiology

  • Primary Mechanism: Rupture of an atherosclerotic plaque with thrombosis, partially or completely occluding a coronary artery.
    • If blood flow is critically reduced or fully obstructed and not restored quickly (within ~10 minutes), myocardial necrosis (infarction) ensues.
  • Other Causes:
    • Coronary artery vasospasm (Prinzmetal angina, cocaine use)
    • Emboli
    • Vasculitis (e.g., Kawasaki disease)
Key Subtypes of ACS:
  1. Unstable Angina: Plaque rupture with incomplete occlusion but no myocardial necrosis (normal cardiac biomarkers).
  2. NSTEMI: Subtotal occlusion causing myocardial necrosis (elevated cardiac biomarkers), often with ST-segment depression or T-wave changes on ECG.
  3. STEMI: Complete occlusion of a major coronary artery, leading to transmural infarction (ST-segment elevation on ECG).

3. Risk Factors

  • Overlap with general atherosclerosis risk factors:
    • Smoking
    • Hypercholesterolaemia
    • Hypertension
    • Diabetes mellitus
  • Additional considerations: Managing and stabilizing existing plaques (e.g., via cholesterol reduction and antiplatelet therapy) helps prevent ACS progression.

4. Symptoms

  • Chest Pain:
    • Severe, crushing, tight, or ‘band-like’ across the chest
    • Often radiates to the left arm, neck, or jaw
    • In MI, typically lasts >20 minutes and is not relieved by nitroglycerin (unlike stable angina)
  • Dyspnoea: Can result from left ventricular systolic impairment.
  • Other Signs:
    • Patients may appear pale or clammy (sympathetic activation).
    • Arrhythmias or heart failure signs may be evident if ischaemia is severe.
    • Unstable angina/NSTEMI often present with persistent or worsening chest discomfort, whereas STEMI is typically more severe and acute.

5. Diagnosis

  1. Clinical History: Characteristic chest pain is central to suspicion of ACS.
  2. Electrocardiography (ECG)
    • Unstable Angina/NSTEMI: May show ST-segment depression or T-wave changes without ST elevation.
    • STEMI: Defined by ST-segment elevation in contiguous leads, reflecting transmural infarction.
  3. Cardiac Biomarkers
    • Troponin I or T: Gold standard for detecting myocardial injury; rises 2–4 hours post-infarction, peaks ~24 hours, normal by 7–10 days.
    • CK-MB: Rises 4–6 hours post-infarction, peaks ~24 hours, normal by 72 hours; useful for detecting reinfarction.
    • Elevated markers distinguish MI (NSTEMI or STEMI) from unstable angina (normal markers).
  4. Additional Tests
    • Chest X-ray: To exclude other pathologies (e.g., pulmonary oedema, aortic dissection).
    • Coronary Angiography: Defines the location and extent of stenoses or occlusions, guiding revascularization.

6. Immediate Management

General Measures for All ACS Presentations

  • Antiplatelet Therapy:
    • Aspirin (300 mg initially) plus a second agent (e.g., clopidogrel, ticagrelor, or prasugrel).
  • Analgesia and Anti-Ischaemic Therapy:
    • IV nitrates for pain control and coronary vasodilation
    • Opiates (with antiemetics) if pain is severe
  • Anticoagulation:
    • Low-molecular-weight heparin or factor Xa inhibitor (e.g., fondaparinux), unless urgent catheterization is planned.
  • Adjuncts:
    • β-blockers to reduce myocardial O₂ demand and arrhythmic risk
    • ACE inhibitors to limit LV dilation and aid recovery
    • Supplemental oxygen if hypoxic

Specific Subtype Management

  • Unstable Angina:
    • Worsening anginal symptoms without elevated cardiac biomarkers
    • Requires hospital admission, dual antiplatelet therapy, anticoagulation, and close monitoring for progression to MI.
    • Evaluate for coronary angiography once stabilized.
  • NSTEMI:
    • Similar medication regimen to unstable angina, but with elevated cardiac enzymes.
    • Often more severe presentation than unstable angina but less than STEMI.
    • Coronary angiography typically performed within 72 hours.
  • STEMI:
    • Complete arterial occlusion with ST-segment elevation and significant myocardial damage risk.
    • Primary Percutaneous Coronary Intervention (PPCI) is the treatment of choice (ideally within 120 minutes of presentation).
    • Thrombolysis (fibrinolysis) is used only when timely PPCI is unavailable (<12 hours from onset of pain if no contraindications).
    • Post-infarction management includes dual antiplatelet therapy (aspirin lifelong, plus another agent for ≥1 year), statins, β-blockers, and ACE inhibitors.

7. Long-Term Management (Where Relevant)

  • Secondary Prevention:
    • Smoking cessation
    • Optimised control of hypertension, diabetes, and hyperlipidaemia (statin therapy)
    • Lifelong aspirin (75 mg daily) unless contraindicated
    • Additional antiplatelet (e.g., clopidogrel or ticagrelor) usually continued for at least 1 year post-MI
  • Revascularisation Follow-up:
    • If PCI was limited to the culprit lesion, further assessment and angiography may be required to address other significant lesions.
  • Monitoring for Complications:
    • Arrhythmias, heart failure, and mechanical complications can occur post-MI and may be related to the stage of myocardial necrosis and repair.
Complications of MI

1. Epidemiology

  • Heart failure is the most prevalent complication following MI.
  • Other post-MI complications, though less common, can be life-threatening and often occur in the early period after infarction if not promptly recognised and managed.

2. Aetiology

  • All complications arise from myocardial necrosis and the subsequent pathological changes in cardiac muscle and structures.
  • Extensive ‘full-thickness’ infarcts (particularly without prompt revascularisation) are more prone to rupture and other severe complications.

3. Risk Factors

  • Large or anterior MI: Raises the risk for arrhythmias, ventricular thrombus, and certain mechanical complications (e.g., septal rupture).
  • Inadequate reperfusion: Less successful or delayed revascularisation can increase the likelihood of complications.
  • Impaired left ventricular function (LVEF <40%): Increases risk of sudden arrhythmic events and may necessitate additional intervention (e.g., defibrillator placement).

4. Symptoms

Arrhythmias

  • May be asymptomatic or present with palpitations, light-headedness, syncope, or hypotension.
  • Tachycardia, bradycardia, or signs of reduced cardiac output can be noted.

Myocardial Structural Rupture

  • Ventricular free wall rupture: Acute shock, collapse, and often pulseless electrical activity; usually rapidly fatal.
  • Ventricular septal defect (VSD): Acute heart failure signs (dyspnoea, hypotension) and a new pansystolic murmur.
  • Papillary muscle rupture: Sudden severe mitral regurgitation, presenting with acute pulmonary oedema and a new pansystolic murmur.

Ongoing Ischaemia or Recurrent MI

  • Chest pain suggestive of recurrent infarction or unstable angina.
  • Potential ST elevation in the same territory if acute stent thrombosis occurs.

Left Ventricular Thrombus

  • Often asymptomatic until an embolic event (e.g., stroke).
  • More common in anterior infarctions.

Pericarditis

  • Chest pain of a pleuritic nature, distinct from the original MI pain.
  • A pericardial rub may be heard on auscultation.

5. Diagnosis

  1. Continuous Monitoring
    • ECG rhythm monitoring in a coronary care unit to detect arrhythmias promptly.
  2. Transthoracic Echocardiography
    • Identifies mechanical complications (ventricular rupture, septal defect, papillary muscle dysfunction, pericardial effusion).
    • Detects left ventricular thrombus.
  3. Repeat ECGs
    • Assesses for ongoing ischaemia (new ST changes) or recurrent STEMI in the same leads.

6. Immediate Management

Arrhythmias

  • Coronary Care Unit monitoring is crucial.
  • Asymptomatic or short-lived arrhythmias typically resolve within 48 hours.
  • Cardiac arrest: Immediate CPR and defibrillation.
  • Ventricular fibrillation (VF) or sustained VT: Often prevented or reduced by beta-blockers. Post-48 h recurrence, or if LVEF <40%, consider implantable defibrillator.
  • AV block:
    • In inferior MI: Usually transient and may resolve spontaneously (up to 10 days).
    • In anterior MI: Indicates extensive damage; may require urgent pacing.

Rupture of Myocardial Structures

  • Suspected free wall rupture, VSD, or papillary muscle rupture: Immediate echocardiography and urgent surgical referral. Prognosis is often poor without rapid intervention.

Ongoing Ischaemia or Recurrent MI

  • Recurrent chest pain or ST elevation (e.g., stent thrombosis): Urgent coronary angiography and, if needed, repeat PCI.
  • Supportive therapies (nitrates, analgesia) as appropriate.

Left Ventricular Thrombus

  • Suspected with anterior MI or echo findings of thrombus formation.
  • Immediate anticoagulation to reduce stroke risk.

Pericarditis

  • Treat with high-dose aspirin or colchicine.
  • Follow-up echocardiography (at diagnosis and ~7 days) to evaluate for pericardial effusion.

7. Long-Term Management

  • Lifestyle and Medical Therapy to address underlying atherosclerosis (smoking cessation, statins, etc.), as per standard post-MI secondary prevention guidelines.
  • Heart Failure monitoring and therapy as needed (e.g., ACE inhibitors, beta-blockers, diuretics).
  • Defibrillator placement if high arrhythmic risk persists (low ejection fraction, recurrent arrhythmias beyond 48 hours).
  • Anticoagulation for left ventricular thrombus (often long-term, given persistent wall motion abnormality).
  • Surveillance echocardiography to monitor ventricle function, rule out mechanical defects, and check resolution or progression of effusions.
Other: Sudden Cardiac Death & Chronic Ischaemic Heart Disease

Sudden Cardiac Death

Epidemiology

  • Occurs unexpectedly due to cardiac disease.
  • IHD (ischaemic heart disease) is the leading cause of death in the US; sudden cardiac death can be a presentation of severe underlying coronary atherosclerosis.

Aetiology

  • Most often caused by a fatal ventricular arrhythmia.
  • Commonly triggered by acute ischaemia (90% of patients have pre-existing severe atherosclerosis).

Risk Factors

  • Severe coronary artery atherosclerosis.
  • Less common causes include:
    • Mitral valve prolapse
    • Cardiomyopathy
    • Cocaine abuse

Symptoms

  • Unexpected death without prior symptoms, or death occurring within 1 hour of symptom onset.

Diagnosis

  • Largely retrospective once the event has occurred; recognized as a sudden, unexpected death due to cardiac causes.

Immediate Management

  • In a witnessed arrest scenario, immediate resuscitation and defibrillation (if shockable rhythm) are critical; however, by definition, sudden cardiac death often occurs too rapidly for intervention.

Long-Term Management

  • By definition, sudden cardiac death often occurs too rapidly for intervention.
  • If patient does survive, treatment would focus on managing symptoms related to cardiac damade (e.g. arrythmia, heart failure)

Chronic Ischaemic Heart Disease

Epidemiology

  • IHD is a major cause of morbidity and mortality:
    • Chronic ischaemic heart disease is part of this spectrum, leading to progressive cardiac dysfunction.

Aetiology

  • Chronic myocardial ischaemia resulting from long-standing coronary artery disease (with or without past infarction).

Risk Factors

  • Same as for atherosclerosis and general IHD:
    • Smoking
    • Hypercholesterolaemia
    • Hypertension
    • Diabetes
    • Positive family history

Symptoms

  • Progressive decline in myocardial function, often manifesting as symptoms of congestive heart failure (e.g., exertional dyspnoea, fatigue).

Diagnosis

  • Typically identified through clinical evaluation of cardiac function (e.g., echocardiography, history of coronary artery disease), alongside tests indicating reduced myocardial performance.

Immediate Management

  • Acute exacerbations may be managed similarly to heart failure decompensation (e.g., diuretics, oxygen, and support).

Long-Term Management

  • Control and modification of risk factors (smoking cessation, blood pressure and glycaemic control, lipid management).
  • Medical therapy for IHD (e.g., beta-blockers, antiplatelets, statins) and for heart failure if present (e.g., ACE inhibitors, diuretics).
  • Revascularisation procedures (PCI or CABG) may be considered if there is significant ongoing ischaemia amenable to intervention.
Written by Dr Ahmed Kazie MD, MSc
  • References
    1. Morris P, Warriner D, Morton A. Eureka: Cardiovascular Medicine. Scion Publishing Ltd; 2015.
    2. Sattar HA. Fundamentals of pathology : medical course and step 1 review. Chicago, Illinois: Pathoma.com; 2024.

Last Updated: January 2025