Ischemic Heart Disease

Overview
  • Ischemic Heart Disease (IHD) is the result of ischemia, or deficient blood supply, to a portion of the myocardium. Ischemic Heart Disease is generally the result of a mismatch between myocardial oxygen supply and demand. Clinically, IHD has a variable clinical manifestation along a wide clinical spectrum depending on the degree and anatomical location of the mismatch.
Etiology
  • By far the most common cause of IHD is narrowing or sudden occlusion of coronary arteries suffering from atherosclerotic disease. The notable exception is prinzmetal angina which is a variant of IHD caused by deranged vasoconstriction of coronary arteries and appears unrelated to atherosclerotic disease.
Pathogenesis
  • Overview
    • In most cases, IHD is caused by a mismatch between cardiac oxygen demand and the cardiac blood flow (Review these pages). In general, mismatch is caused by inappropriate narrowing or occlusion of coronary arteries which reduces or completely ablates cardiac blood flow to a portion of the myocardium. Depending on the degree of mismatch and the length of time such a mismatch lasts, a wide range of myocardial dysfunction and damage can occur. Reversible dysfunction usually results from narrowing of coronary arteries, whereas irreversible damage results from long periods of complete or nearly complete coronary arterial occlusion. Below we chart the rough range of myocardial dysfunction and damage which can result from instances of increasingly severe mismatch between myocardial oxygen demand and supply.
  • Brief Functional Derangements
    • Cardiomyocyte contraction and relaxation are both affected by brief periods of mild ischemia. Defects in contraction may result in a transient drop in cardiac output leading to reductions in systemic arterial pressure that may activate mechanisms Systemic Arterial Pressure - Short-term Regulation. Defects in relaxation may result in backup of blood into the pulmonary circulation, leading to an episode of mild pulmonary edema and thus symptoms of dyspnea. The local buildup of cardiomyocyte metabolites may also trigger the sensation of anginal chest pain.
  • Sustained Functional Derangements
    • More sustained and intense periods of ischemia can affect cardiomyocyte contraction for long periods of time. Such sections of myocardium are referred to as "stunned" or "hibernating" and may display prolonged contractile dysfunction. However, such damage appears to be reversible and sections of stunned of hibernating myocardium can regain functionality over time if their coronary blood flow is restored.
  • Irreversible Damage
    • Complete or nearly complete occlusion of coronary arteries resulting in severe deficiencies of coronary blood flow often result in irreversible ischemic necrosis of sections of myocardium. Clearly, these sections cannot generate any contractile force and undergo significant inflammation and remodeling as discussed further in Myocardial Infarction.
Epidemiology
  • Overview
    • IHD is the most common cause of mortality in developed countries although incidence is rising around the world. Risk factors for IHD roughly overlap with those for development of atherosclerosis, indicating the intimate relationship between these disease processes.
  • Risk Factors
    • Hyperlipidemia with high levels of LDL and low levels of HDL are important risk factors. Consumption of a high-cholesterol diet and smoking increase risk
    • Presence of chronic hypertension or diabetes adds to risk
    • Men tend to have a higher risk earlier in life although the elderly of both genders are particularly prone to IHD.
Clinical Syndromes
  • Overview
    • As mentioned, IHD manifests along a wide clinical spectrum reflecting the severity and duration of mismatch between myocardial oxygen demand and supply. Stable Angina and Prinzmetal Angina result from brief periods of reversible narrowing of coronary arteries. In contrast, Myocardial Infarctions result from complete or nearly complete occlusion of the coronary arteries
  • Syndromes