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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Overview

Definition

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.

Epidemiology

  • 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.

Etiology

  • 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

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.

Pathophysiology

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

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

References

  1. Kannam, J., Aroesty, J., Gersh, B. (2021). Chronic coronary syndrome: Overview of care. In Cannon, C. (Ed.). UpToDate. Retrieved March 28, 2021, from https://www.uptodate.com/contents/chronic-coronary-syndrome-overview-of-care
  2. Ford, T.J., Corcoran, D., Berry C. (2018). Stable coronary syndromes: Pathophysiology, diagnostic advances and therapeutic need. Heart. 104(4), 284–292. https://pubmed.ncbi.nlm.nih.gov/29030424/
  3. Fihn, S.D., et al. (2014). 2014 ACC/AHA/AATS/PCNA/SCAI/STS focused update of the guideline for the diagnosis and management of patients with stable ischemic heart disease: A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines, and the American Association for Thoracic Surgery, Preventive Cardiovascular Nurses Association, Society for Cardiovascular Angiography and Interventions, and Society of Thoracic Surgeons. J Am Coll Cardiol. 64(18), 1929–1949. https://pubmed.ncbi.nlm.nih.gov/25077860/
  4. Cannon, C., Hoekstra, J., Jaffe, A. (2021). Diagnosis of acute myocardial infarction. In Saperia, G. (Ed.). UpToDate. Retrieved March 28, 2021, from https://www.uptodate.com/contents/diagnosis-of-acute-myocardial-infarction
  5. Fang, J., Aranki, S., (2021). Ischemic cardiomyopathy: Treatment and prognosis. In Dardas, T. (Ed.). UpToDate. Retrieved March 28, 2021, from https://www.uptodate.com/contents/ischemic-cardiomyopathy-treatment-and-prognosis
  6. Maron, B.J., et al. (2006). Contemporary definitions and classification of the cardiomyopathies: An American Heart Association Scientific Statement from the Council on Clinical Cardiology, Heart Failure and Transplantation Committee; Quality of Care and Outcomes Research and Functional Genomics and Translational Biology Interdisciplinary Working Groups; and Council on Epidemiology and Prevention. Circulation. 113(14), 1807–1816. https://pubmed.ncbi.nlm.nih.gov/16567565/

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