Coronary Heart Disease

Coronary heart disease (CHD), or ischemic heart disease, describes a situation in which an inadequate supply of blood to the myocardium exists due to a stenosis of the coronary arteries, typically from atherosclerosis. The myocardium becomes ischemic when oxygen supply does not meet oxygen demand. Diagnosis is based on history and ECG findings; cardiac stress tests and catheterizations may also be needed. Treatment is primarily based on reducing the heart’s oxygen demand and increasing the delivery of oxygen.

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Coronary heart disease (CHD) is the manifestation of atherosclerosis in the coronary arteries such that there is an imbalance between oxygen supply and myocardial demands resulting in ischemia to a portion of the myocardium.


  • Most common cause of death in the world
  • Most common cardiovascular disease in the world
  • Incidence rate: 0.6% per year
  • Incidence increases with age.
  • More common in men
  • 90% of CHD occurs in individuals with at least 1 risk factor.


  • Underlying mechanism is atherosclerosis.
  • Modifiable risk factors:
    • Diabetes
    • Smoking
    • Lack of exercise
    • Obesity, especially abdominal
    • Alcohol consumption: in excess of 2 drinks per day
    • Hypertension: both systolic and diastolic
    • Hyperlipidemia: 
      • Elevated LDL cholesterol
      • Decreased HDL cholesterol
  • Fixed risk factors:
    • Age
    • Male sex
    • Family history of premature disease in 1st-degree relative:
      •  < 55-year-old man
      •  < 65-year-old woman
Coronary heart disease pathophysiology

Image demonstrating pathophysiology of coronary heart disease

Image: “Coronary heart disease-atherosclerosis” by National Heart, Lung and Blood Institute. License: Public Domain, edited by Lecturio.


Pathogenesis of coronary atherosclerosis

  • Initiating event is a disruption of the endothelium of a coronary artery due to factors such as:
    • Hypertension
    • Smoking
    • Diabetes
    • Elevated LDL (“bad” cholesterol)
  • Platelets adhere to sites of endothelial injury.
  • Lipids (LDL) gain access to the arterial sub-endothelial area.
  • Chronic inflammation develops:
    • Additional LDL accumulates secondary to inflammation.
    • More inflammation results from additional LDL accumulation.
    • Feedback cycle ensues.
  • Vessel wall changes develop due to inflammation:
    • Infiltration by macrophages and lymphocytes: 
      • Ingestion of oxidized LDL (by macrophages)
      • Formation of foam cells (LDL-loaded macrophages)
    • Increased release of cytokines and growth factors
    • Migration of smooth muscle cells
    • Calcification

Effects on myocardium

  • Narrowing of arterial lumen (stenosis): 
    • Reduces myocardial blood supply
    • Symptoms appear if the stenosis is ≥ 70% (greater stenosis produces higher resistance to flow).
  • Inability to meet oxygen demand with increased exertion then develops.
  • Symptoms are induced by decreased oxygen delivery or increased demand.
Composition of the atherosclerotic plaque

Composition of the atherosclerotic plaque

Image: “Neovascularization of coronary tunica intima (DIT) is the cause of coronary atherosclerosis. Lipoproteins invade coronary intima via neovascularization from adventitial vasa vasorum, but not from the arterial lumen: a hypothesis” by Subbotin, VM/ Encyclopeadia Britannica. License: CC BY 2.0

Clinical Spectrum

Coronary heart disease has a spectrum of clinical presentations.

Angina pectoris

General characteristics:

  • Condition marked by severe pain in the chest, often also spreading to the shoulders, arms, and neck, caused by an inadequate blood supply to the heart
  • Typical symptoms/manifestations: 
    • Chest pain (retrosternal dull, squeezing/pressure-like pain)
    • Pain radiating to left arm/shoulder, jaw
    • Pain is not pleuritic or positional.
    • Dyspnea on exertion
    • Orthopnea
    • Pallor
    • Blurry vision
    • Confusion
    • Dizziness
    • Nausea/vomiting
    • Anxiety
    • Symptoms can get worse with meals (mimics indigestion/GERD).
    • Syncope
  • Classical angina characteristics: 
    • The typical quality of pain: retrosternal location, dull/squeezing
    • Provoked by physical/emotional stress
    • Relieved with nitroglycerin/rest
  • Atypical angina characteristics: 
    • Chest pain
    • ⅔ classic features
  • Non-anginal chest pain: 0–1 classic angina characteristics

Stable angina:

  • Triggers:
    • Physical stressors
    • Emotional stressors
    • Increased oxygen demand
  • Predictable triggers and timing
  • Relieved by:
    • Rest
    • Nitrates
  • ECG is typically normal.
  • Cardiac enzymes are normal.
  • Does not involve cell death

Unstable angina:

  • Occurs at rest
  • No predictable pattern
  • Not relieved by:
    • Rest
    • Nitrates
  • ECG shows nonspecific ST segment changes: 
    • ST depression/transient elevation
    • T wave inversions
    • Changes are reversible.
  • Cardiac enzymes are normal.
  • Does not involve cell death

Myocardial infarction

General characteristics:

  • Pathologic event in the setting of myocardial ischemia in which there is evidence of myocardial injury or necrosis (cell death)
  • Acute cessation of blood flow to an area of myocardium
  • Medical emergency
  • Symptoms:
    • Chest pain:
      •  Most common symptom
      •  More severe and prolonged than angina
      •  Does not resolve
    • Diaphoresis
    • Anxiety
  • Atypical symptoms and ECG findings can be seen in:
    • Women
    • People with diabetes
    • Older individuals
  • Rise of cardiac biomarkers: 
    • Troponin
    • Released from myocardial cells when they are dying

ECG changes (irreversible):

  • ST segment changes:
    • STEMI or new left bundle branch block (LBBB):
      • Most severe form
      • Coronary artery completely blocked
      • Typically large areas of myocardium at risk of cell death
      • Cardiac enzymes significantly elevated
    • NSTEMI:
      • ST depressions and/or T wave inversions without ST segment elevations or pathologic Q waves
      • Cardiac enzymes are typically not as elevated as STEMI.
      • Typically smaller area at risk of myocardium
  • Q waves (absence of electrical activity in “scarred” myocardium):
    • Non-Q wave MI:
      • No Q waves on ECG
      • Less severe form, less myocardial injury than Q wave MI
      • More common than Q wave MI
      • Predominantly seen with NSTEMI but can be seen in some STEMIs
    • Q wave MI:
      • Q waves present on ECG.
      • More severe form, more myocardial injury than non-Q wave MI
      • Less common than non-Q wave MI
      • Seen more often in STEMIs but can be seen in some NSTEMIs

Ischemic cardiomyopathy

  • Significantly impaired left ventricular function (left ventricular ejection fraction (LVEF) < 40%) that is the result of coronary artery disease
  • Results from:
    • Irreversible loss of myocardium due to prior myocardial infarction OR
    • Reversible loss of contractility due to chronically ischemic but still viable myocardium


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