Chronic stable angina pathophysiology
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Chronic stable angina Microchapters | ||
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Classification | ||
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Differentiating Chronic Stable Angina from Acute Coronary Syndromes | ||
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Diagnosis | ||
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Alternative Therapies for Refractory Angina | ||
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Discharge Care | ||
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Guidelines for Asymptomatic Patients | ||
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Case Studies | ||
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Chronic stable angina pathophysiology On the Web | ||
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Risk calculators and risk factors for Chronic stable angina pathophysiology | ||
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor-In-Chief: Cafer Zorkun, M.D., Ph.D. [2]
Overview
The primary causes of myocardial ischemia in chronic stable angina are:
1. Fixed Epicardial Stenosis: Most commonly, chronic stable angina is due to fixed obstructive disease or atherosclerosis which narrows the coronary arteries.
- This results in inadequate supply of blood and oxygen to meet the demands of myocardial metabolism. This supply / demand mismatch activates a molecular cascade of events that causes the release of molecules such as bradykinin and adenosine which in turn stimulate the sympathetic and vagal afferent fibers, causing the anginal pain.
- Certain conditions can increase the myocardial oxygen demand secondary to an increase in cardiac output and can exacerbate chronic stable angina. These conditions include but are not limited to fever, thyrotoxicosis, anemia, emotional stress, and tachyarrythmias. This increase in cardiac demand is often treated with beta blockers or relief of the underlying condition.
2. Spasm of the Epicardial Artery: While fixed obstructive epicardial disease is the most common cause of chronic stable angina, vasospasm of the epicardial artery can also cause angina. Angina due to spasm of an epicardial artery is known as Prinzmetal's angina or variant angina. Prinzmetal's angina or variant anginais often treated with calcium channel blockers to relieve the spasm.
3. Microvascular Disease: Chronic stable angina can also result from microvascular disease as well. This is known as microvascular angina or Syndrome X. Microvascular angina is often treated with calcium channel blockers to relieve the spasm.
These causes are not mutually exclusive and two or more causes may coexist in the same patient.
The Neural Basis or Mediators of Angina Pectoris
The aforemetnioned causes of myocardial ischemia lead to the activation of the chemo and mechanoreceptors and the release of substances like bradykinin and adenosine which in turn stimulate both sympathetic and vagal afferent fibers. Sympathetic afferent impulses converge with somatic sensory fibers from thoracic structures and travel to the thalamus and frontal cortex. Sympathetic activation is responsible for the perception of referred cardiac pain. Vagal afferent fibers synapse in the medulla and innervate the upper cervical spinothalamic tract, which gives rise to the pain in the neck and jaw.
Myocardial ischemia, whether silent or symptomatic, results from an imbalance between myocardial oxygen demand (consumption) and myocardial oxygen supply.
Angina Due to Increased Myocardial Oxygen Requirements: Demand Angina
Angina precipitated by increased myocardial oxygen requirements is sometimes referred to as demand angina or fixed threshold angina. In demand angina, evidence of increased cardiac oxygen requirements can be suspected in the following situations:
- The factors mentioned below may trigger the release of norepinephrine, which increases myocardial oxygen requirements:
- Physiological responses to physical exertion, mental or emotional stresses,
- In the presence of fever, hypoglycemia, and conditions like sustained tachyarrhythmias, signs of hyperthyroidism and thyrotoxicosis,
- Markedly elevated blood pressure such as a hypertensive crisis
- Another cause of increased myocardial oxygen demand is arteriovenous fistula (AVF) in patients receiving dialysis.
- Acute exacerbation of chronic obstructive pulmonary disease (COPD) (with or without superimposed infection) can dramatically lower oxygen saturation levels and aggravates ischemia related symptoms in patients with coronary artery disease.
Demand angina has few dynamic (i.e. vasoconstrictor effects) components, and the amount of physical activity required to precipitate angina remains relatively constant.
Angina Due to Decreased Myocardial Oxygen Supply: Supply Angina
Angina that occurs secondary to a decrease in oxygen supply is sometimes referred to as supply angina or variable threshold angina.
- Major determinants of myocardial oxygen consumption are:
- Ventricular wall tension: intraventricular systolic pressure, ventricular volume, and ventricular wall thickness are the major determinants of left ventricular wall tension.
- Heart rate: All kind of tachycardias and tachyarrhythmias also increase myocardial oxygen consumption and reduce myocardial perfusion by decreasing the duration of diastole. Therefore, reduction of heart rate is associated with a decrease in myocardial oxygen demand and improved left ventricular perfusion.
- Myocardial contractility: adrenergic stimulation of the heart and tachycardia are the major determinants of contractility.
- Myocardial oxygen extraction is almost at maximal level at rest and arterial oxygen content is usually stable, but anemia or marked hypoxia is an exception. Therefore, myocardial oxygen supply is mainly determined by coronary blood flow.
- Coronary blood flow is a function of myocardial perfusion pressure (the difference between the diastolic pressure in aortic root and the right atrium). The duration of diastole has an inverse relation with the coronary vascular resistance. Coronary vascular resistance, in turn, is determined by the severity of epicardial coronary artery stenosis, the changes in epicardial coronary artery tone and by coronary arteriolar resistance; the latter is regulated by metabolic, neural, humoral, and autonomic activity.
- Increased myocardial oxygen demand occurs during physical exertion. In normal physical conditions, this reduces coronary arteriolar resistance, which causes coronary blood flow to rise (autoregulatory reserve). This autoregulatory reserve progressively diminishes in order and parallel to increased severity of epicardial coronary artery stenosis. When coronary artery stenosis reaches about 90% of the luminal diameter, dilatation in coronary arteriolar bed arises to its maximum level and coronary blood flow becomes more dependent on perfusion pressure. Under these conditions, reduction of arterial pressure may increase in myocardial oxygen demand and induce myocardial ischemia.