Coronary artery disease

Coronary Circulation

  • The coronary system is responsible for the blood supply to the myocardium.

  • Myocardial oxygen demand is consistently high, even at rest, with a significant increase observed during exercise.

  • The heart, which constitutes only 0.3% of body weight, accounts for 7% of the body's resting oxygen consumption.

Myocardial Ischaemia

  • Definition: Myocardial ischaemia occurs when the metabolic demand of the myocardium is not met, creating an imbalance between myocardial perfusion and the cardiac demand for oxygenated blood.

  • Most cases of myocardial ischaemia are due to coronary atherosclerosis.

Common Causes of Myocardial Ischaemia

  • Chronic, progressive atherosclerosis: Narrows the coronary arteries.

  • Plaque rupture with thrombus formation: This can further obstruct blood flow.

  • Vasospasm or endothelial dysfunction: Temporary constriction of the coronary arteries leads to reduced blood flow.

  • Fixed atherosclerosis: Results in an ongoing supply-demand imbalance.

  • Supply-demand imbalance alone: Even without fixed lesions, increased demand can lead to symptoms.

Consequences of Myocardial Ischaemia

  • Angina Pectoris: Chest pain resulting from ischaemia.

  • Myocardial Infarction (Heart Attack): Can cause irreversible damage to heart tissue.

  • Sudden Cardiac Death: Acute events leading to unexpected death.

  • Chronic Ischaemic Heart Disease: Long-term ischaemia may lead to heart failure.

Types of Angina Pectoris

  • Stable Angina: Predictable episodes occurring with exertion, relieved by rest.

  • Unstable Angina: More unpredictable and occurs at rest, may indicate serious heart issues.

  • Prinzmetal (Variant) Angina: Caused by vasospasm, distinct from the classic angina types.

  • William Heberden: A historical figure often referred to as the 'father of clinical observations' regarding angina.

  • Myron Prinzmetal: Recognized for describing variant angina.

Asymptomatic Atherosclerotic Stenosis

  • Stenosis may remain asymptomatic until occlusion of about 80-90%.

  • Significant coronary artery disease can still allow for adequate perfusion at rest, but increased myocardial demand (e.g., exercise or stress) can lead to symptoms like angina.

  • An imbalance becomes evident at about 50% stenosis when the metabolic demand exceeds perfusion capability.

Clinical Presentation of Angina Pectoris

  • Characteristics: Paroxysmal attacks of chest discomfort, often substernal or precordial.

  • Duration: Typically lasts from 15 seconds to 15 minutes without inducing necrosis.

  • Symptoms: Dull pain that may radiate to the arm or jaw, can be associated with shortness of breath, sweating, nausea, vomiting, but is generally not exacerbated by changing breath depth.

Mechanisms Behind Angina Pectoris

  • Angina arises due to decreased perfusion (ischaemia) leading to reduced oxygen supply (hypoxia) and subsequent reduced ATP production.

  • Adenosine Role: Infusion of adenosine can reproduce anginal symptoms even without ischaemia, as it stimulates pain receptors and causes vasodilation; however, transplanted hearts lack nerve connections and therefore do not exhibit angina symptoms despite severe ischaemia.

ECG Changes in Myocardial Ischaemia

  • Different signs indicate myocardial ischaemia, such as:
      - ST segment depression
      - T wave inversion

  • Acute Myocardial Infarction (AMI): ST elevation indicates myocardial necrosis.

Acute Myocardial Infarction

  • AMI is an ischaemic necrosis of myocardium that may occur at any age with increased frequency in older demographics.

  • Pathogenesis: Most commonly due to acute plaque changes including intraplaque hemorrhage and subsequent platelet aggregation.

Time Course and Effects of Myocardial Ischaemia

  • Within 60 seconds of coronary artery occlusion, oxygen tension in cells drops to zero.

  • ATP reserves are depleted rapidly, leading to a switch to anaerobic metabolism and lactic acid production.

  • If blood flow is not restored within 40-60 minutes, it leads to irreversible injury.

Transition of Necrosis in AMI

  • The necrotic area typically progresses outward, engulfing the entire thickness of the ventricular wall within approximately 6 hours, leading to transmural necrosis.

Clinical Diagnosis of AMI

  • Diagnosis requires prompt recognition of clinical features, ECG abnormalities, and laboratory tests identifying myocardial proteins in plasma (e.g., cardiac-specific troponins and creatine kinase).

  • Symptoms of AMI often include prolonged chest pain (beyond 30 min), a feeling of impending doom, rapid and weak pulse, profuse sweating, nausea, and dyspnoea.

  • AMI can be asymptomatic in around 25% of patients.

Complications of AMI

  • Potential post-MI complications include:
      - Death
      - Arrhythmias
      - Rupture of necrotic tissue
      - Heart failure
      - Valve disease
      - Ventricular aneurysm
      - Dressler syndrome (post-myocardial infarction pericarditis)
      - Thromboembolism
      - Recurrence.