Chronic stable angina pathophysiology: Difference between revisions
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__NOTOC__ | |||
{{ | {{Chronic stable angina}} | ||
{{CMG}} | {{CMG}}; '''Associate Editor-In-Chief:''' {{CZ}} | ||
'''Associate Editor-In-Chief:''' {{CZ}} | |||
==Overview== | ==Overview== | ||
The main causes of [[myocardial ischemia]] are: | |||
*Microvascular dysfunction, | |||
*Flow limiting stenosis, | |||
*Occlusive spasm and dynamic stenosis, | |||
*[[Thrombosis]] and | |||
*Extra coronary cardiac and non-cardiac causes of [[ischemia]] | |||
These causes are not mutually exclusive and some patients may have two or more causes. | |||
==Effects of exercise on angina== | |||
=====Molecular effects:===== | |||
=====Molecular effects===== | |||
*Increase in eNOS expression and activation | *Increase in eNOS expression and activation | ||
*Decrease in NAD (P) H expression and activity | *Decrease in NAD (P) H expression and activity | ||
*Decrease in AT1 receptor expression | *Decrease in AT1 receptor expression | ||
*Increase in SOD expression | *Increase in SOD expression | ||
=====Functional effects===== | |||
*Vascular Structure | =====Functional effects:===== | ||
*Vascular Structure: | |||
::*Increase in endothelial function | |||
::*Increase in peripheral tone | |||
::*Increase in [[plasma volume]] | |||
*Myocardium | ::*Decrease in [[blood pressure]] | ||
*Myocardium: | |||
::*Increase in [[vagal tone]] | |||
::*Decrease in [[heart rate]] | |||
*Thrombosis | ::*Decrease in oxygen demand | ||
::*Increase in preconditioning | |||
=====Other effects===== | |||
*Decrease in | *Thrombosis: | ||
::*Increase in [[fibrinolytic]] balance | |||
=====Other effects:===== | |||
*Decrease in intimal thickness | |||
*Decrease in P selectin | *Decrease in P selectin | ||
*Decrease in VCAM-1 | *Decrease in VCAM-1 | ||
*Decrease in MCP-1 | *Decrease in MCP-1 | ||
*Decrease in | *Decrease in calcium in VSMC | ||
The causes of myocardial ischemia lead to the activation of the chemo and mechanoreceptors and the release of substances like [[bradykinin]] and [[adenosine]] which stimulate both sympathetic and vagal afferent fibers. Sympathetic afferent impulses converge with somatic sensory fibers from thoracic structures and travels 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. | ==Neuromechanisms of Angina Pectoris== | ||
*The causes of [[myocardial ischemia]] lead to the activation of the chemo and mechanoreceptors and the release of substances like [[bradykinin]] and [[adenosine]] which stimulate both sympathetic and vagal afferent fibers. Sympathetic afferent impulses converge with somatic sensory fibers from thoracic structures and travels 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. | |||
Both of increased myocardial oxygen requirements and decreased myocardial oxygen supply may cause [[myocardial ischemia]]. Angina precipitated by increased myocardial oxygen requirements is sometimes termed as demand angina or fixed threshold angina, | *Both of increased myocardial oxygen requirements and decreased myocardial oxygen supply may cause [[myocardial ischemia]]. | ||
:*Angina precipitated by increased myocardial oxygen requirements is sometimes termed as demand angina or fixed threshold angina, and | |||
:*Angina occurs secondary to a temporary decreased oxygen supply is sometimes termed as supply angina or variable threshold angina. | |||
In demand angina, evidence of increased cardiac oxygen requirements can be suspected in following situations | ====Angina Due to Increased Myocardial Oxygen Requirements: Demand Angina==== | ||
In demand angina, evidence of increased cardiac oxygen requirements can be suspected in 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]] | |||
Another cause of increased myocardial oxygen demand is arteriovenous fistula (AVF) in patients receiving dialysis. | *Another cause of increased myocardial oxygen demand is [[arteriovenous fistula]] (AVF) in patients receiving [[dialysis]]. | ||
Acute exacerbation of | *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, but the amount of physical activity to precipitate angina remains relatively constant. | Demand angina has few dynamic (i.e. vasoconstrictor effects) components, but the amount of physical activity to precipitate angina remains relatively constant. | ||
====Angina Due to Decreased Myocardial Oxygen Supply: Supply Angina==== | |||
[[Myocardial ischemia]], whether silent or symptomatic, results from an imbalance between myocardial oxygen demand (consumption) and myocardial oxygen supply. | |||
*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 [[tachycardia]]s and [[tachyarrhythmia]]s 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. | *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 (diastolic pressure in aortic root). 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. | *Coronary blood flow is a function of [[myocardial perfusion pressure]] (diastolic pressure in aortic root). 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). | *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. | 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. | ||
==References== | |||
{{reflist|2}} | |||
[[Category:Disease state]] | |||
[[Category:Ischemic heart diseases]] | |||
[[Category:Cardiology]] | |||
[[Category:Emergency medicine]] | |||
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Revision as of 21:14, 15 July 2011
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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 main causes of myocardial ischemia are:
- Microvascular dysfunction,
- Flow limiting stenosis,
- Occlusive spasm and dynamic stenosis,
- Thrombosis and
- Extra coronary cardiac and non-cardiac causes of ischemia
These causes are not mutually exclusive and some patients may have two or more causes.
Effects of exercise on angina
Molecular effects:
- Increase in eNOS expression and activation
- Decrease in NAD (P) H expression and activity
- Decrease in AT1 receptor expression
- Increase in SOD expression
Functional effects:
- Vascular Structure:
- Increase in endothelial function
- Increase in peripheral tone
- Increase in plasma volume
- Decrease in blood pressure
- Myocardium:
- Increase in vagal tone
- Decrease in heart rate
- Decrease in oxygen demand
- Increase in preconditioning
- Thrombosis:
- Increase in fibrinolytic balance
Other effects:
- Decrease in intimal thickness
- Decrease in P selectin
- Decrease in VCAM-1
- Decrease in MCP-1
- Decrease in calcium in VSMC
Neuromechanisms of Angina Pectoris
- The causes of myocardial ischemia lead to the activation of the chemo and mechanoreceptors and the release of substances like bradykinin and adenosine which stimulate both sympathetic and vagal afferent fibers. Sympathetic afferent impulses converge with somatic sensory fibers from thoracic structures and travels 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.
- Both of increased myocardial oxygen requirements and decreased myocardial oxygen supply may cause myocardial ischemia.
- Angina precipitated by increased myocardial oxygen requirements is sometimes termed as demand angina or fixed threshold angina, and
- Angina occurs secondary to a temporary decreased oxygen supply is sometimes termed as supply angina or variable threshold angina.
Angina Due to Increased Myocardial Oxygen Requirements: Demand Angina
In demand angina, evidence of increased cardiac oxygen requirements can be suspected in 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
- 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, but the amount of physical activity to precipitate angina remains relatively constant.
Angina Due to Decreased Myocardial Oxygen Supply: Supply Angina
Myocardial ischemia, whether silent or symptomatic, results from an imbalance between myocardial oxygen demand (consumption) and myocardial oxygen supply.
- 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 (diastolic pressure in aortic root). 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.