Chronic stable angina pathophysiology
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Overview
Microvascular dysfunction, flow limiting stenosis, occlusive spasm and dynamic stenosis, thrombosis and extra coronary cardiac and non-cardiac causes of ischemia are the main causes of the myocardial 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, while 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; 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 may trigger the release of norepinephrine, which increases myocardial oxygen requirements.
Another cause of increased myocardial oxygen demand is arteriovenous fistula (AVF) in patients receiving dialysis.
Acute exacerbation of (COPD) chronic obstructive pulmonary disease (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
In supply angina, similar to unstable angina, dynamic stenosis can further decrease myocardial oxygen supply in the presence of a fixed organic stenosis; platelets and leukocytes can elaborate vasoconstrictors like Thromboxane A2 (TxA2) and serotonin, which along with the already damaged endothelium and decreased NO (nitric oxide) production secondary to atherosclerotic coronary artery disease, will lead to vasoconstriction.
Other features of supply angina include a circadian variation, in which angina occurs more often in the morning, as well as cold temperature induced coronary vasoconstriction. High carbohydrate diet might redistribute coronary blood flow away from stenotic vessels supplying area and precipitate postprandial angina.
Myocardial ischemia, whether silent or symptomatic, results from an imbalance between myocardial oxygen demand (consumption) and myocardial oxygen supply. Ventricular wall tension, heart rate, and myocardial contractility are the major determinants of myocardial oxygen consumption. Intraventricular systolic pressure, ventricular volume, and ventricular wall thickness are the major determinants of left ventricular wall tension. Adrenergic stimulation of the heart and tachycardia are the major determinants of contractility.
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 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.
External links
- The MD TV: Comments on Hot Topics, State of the Art Presentations in Cardiovascular Medicine, Expert Reviews on Cardiovascular Research
- Clinical Trial Results: An up to dated resource of Cardiovascular Research
Acknowledgement and Attribution Regarding Sources of Content
Some of the initial content on this page may be incorporated in part from copyleft sources in the public domain including wikis such as Wikipedia and AskDrWiki. Drug information for patients came from the The National Library of Medicine. Infectious disease information may have come from the Centers for Disease Control (CDC). Differential Diagnoses are drawn from clinicians as well as an amalgamation of 3 sources: 1.The Disease Database; 2. Kahan, Scott, Smith, Ellen G. In A Page: Signs and Symptoms. Malden, Massachusetts: Blackwell Publishing, 2004:3; 3. Sailer, Christian, Wasner, Susanne. Differential Diagnosis Pocket. Hermosa Beach, CA: Borm Bruckmeir Publishing LLC, 2002:7 .
