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==Overview==
==Overview==
There are a variety of clinical subsets of angina that are described here<ref>{{cite book |last= Braunwald |first= Eugene |coauthors= Lee Goldman |title= [[Primary Cardiology]] |publisher= [[Saunders]] |year= 2003 |isbn= 0-7216-9444-6}}</ref>.
There are a variety of clinical subsets of angina that are described here<ref>{{cite book |last= Braunwald |first= Eugene |coauthors= Lee Goldman |title= [[Primary Cardiology]] |publisher= [[Saunders]] |year= 2003 |isbn= 0-7216-9444-6}}</ref>.


==Walk through angina pectoris==
==Walk through angina pectoris==
In the majority of patients with obstructive [[coronary artery disease]], the intensity of angina is associated with the intensity of the physical activity.  However, a subset of patients have so called "walk through angina". These patients experience angina early in the course of physical activity (e.g. walking, gardening, climbing, and short running) but the angina then disappears despite continuation of the activity. The precise underlying mechanism of walk though angina remains unclear.  It has been speculated that this may be due to an initial increase in coronary vascular tone with a consequent  reduction in [[coronary blood flow]] at the beginning of the exercise.  It has also been speculated that recruitment of [[collaterals]] may also play a role in the phenomenon.
In the majority of patients with obstructive [[coronary artery disease]], the intensity of angina is associated with the intensity of the physical activity.  However, a subset of patients have so called "walk through angina". These patients experience angina early in the course of physical activity (e.g. walking, gardening, climbing, and short running) but the angina then disappears despite continuation of the activity. The precise underlying mechanism of walk though angina remains unclear.  It has been speculated that this may be due to an initial increase in coronary vascular tone with a consequent  reduction in [[coronary blood flow]] at the beginning of the exercise.  It has also been speculated that recruitment of [[collaterals]] may also play a role in the phenomenon.


==Mixed (Variable Threshold) Angina Pectoris==
==Mixed (Variable Threshold) Angina Pectoris==
The essential clinical feature of mixed angina is a substantial variation in the degree of physical activity that induces angina. These group of patients may also experience rest or nocturnal angina on certain occasions. Angina may also occur on exposure to cold, during emotional stress, or after meals. Dynamic vasoconstriction which superimposed on fixed atherosclerotic coronary artery obstructions has been postulated as the mechanism for the variable exercise threshold.
The essential clinical feature of mixed angina is a substantial variation in the degree of physical activity that induces angina. These group of patients may also experience rest or nocturnal angina on certain occasions. Angina may also occur on exposure to cold, during emotional stress, or after meals. Dynamic vasoconstriction which superimposed on fixed atherosclerotic coronary artery obstructions has been postulated as the mechanism for the variable exercise threshold.


==Nocturnal Angina Pectoris==
==Nocturnal Angina Pectoris==
In clinical practice, two types of nocturnal angina are observed. Some patients experience angina within an hour or two after sleeping. The mechanism of angina in this group of patients is likely to be an increase in venous return and hence increased intra cardiac volume with a resulting increase in myocardial oxygen requirements. Other group of patients with nocturnal angina experience chest discomfort much later, in the early hours of the morning. In this group of patients, a primary reduction in coronary blood flow owing to increased coronary vascular tone, more likely related to different stages of sleep, has been postulated as the potential underlying mechanism.
In clinical practice, two types of nocturnal angina are observed. Some patients experience angina within an hour or two after sleeping. The mechanism of angina in this group of patients is likely to be an increase in venous return and hence increased intra cardiac volume with a resulting increase in myocardial oxygen requirements. Other group of patients with nocturnal angina experience chest discomfort much later, in the early hours of the morning. In this group of patients, a primary reduction in coronary blood flow owing to increased coronary vascular tone, more likely related to different stages of sleep, has been postulated as the potential underlying mechanism.


==Postprandial Angina Pectoris==
==Postprandial Angina Pectoris==
Angina can occur after meals without any ordinary physical activity because of increased coronary vascular tone and a primary decrease in [[coronary blood flow]]. However, postprandial angina may occur only during physical activity after meals because of an associated increase in myocardial oxygen demand. Postprandial angina is almost always associated with significant atherosclerotic [[coronary artery disease]].
Angina can occur after meals without any ordinary physical activity because of increased coronary vascular tone and a primary decrease in [[coronary blood flow]]. However, postprandial angina may occur only during physical activity after meals because of an associated increase in myocardial oxygen demand. Postprandial angina is almost always associated with significant atherosclerotic [[coronary artery disease]].


==Syndrome X==  
==Syndrome X==  
Syndrome X is defined as the presence of typical anginal chest pain with angiographically normal coronary arteries.  Although the syndrome originally referred to patients in whom the chest pain was due to non coronary causes, the current, stricter definition limits it to those patients who appear to have true [[myocardial ischemia]] despite epicardial coronary arteries that are normal or nearly so on coronary angiography.
Syndrome X is defined as the presence of typical anginal chest pain with angiographically normal coronary arteries.  Although the syndrome originally referred to patients in whom the chest pain was due to non coronary causes, the current, stricter definition limits it to those patients who appear to have true [[myocardial ischemia]] despite epicardial coronary arteries that are normal or nearly so on coronary angiography.


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Latest revision as of 19:36, 9 December 2011

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor-In-Chief: Cafer Zorkun, M.D., Ph.D. [2]

Overview

There are a variety of clinical subsets of angina that are described here[1].

Walk through angina pectoris

In the majority of patients with obstructive coronary artery disease, the intensity of angina is associated with the intensity of the physical activity. However, a subset of patients have so called "walk through angina". These patients experience angina early in the course of physical activity (e.g. walking, gardening, climbing, and short running) but the angina then disappears despite continuation of the activity. The precise underlying mechanism of walk though angina remains unclear. It has been speculated that this may be due to an initial increase in coronary vascular tone with a consequent reduction in coronary blood flow at the beginning of the exercise. It has also been speculated that recruitment of collaterals may also play a role in the phenomenon.

Mixed (Variable Threshold) Angina Pectoris

The essential clinical feature of mixed angina is a substantial variation in the degree of physical activity that induces angina. These group of patients may also experience rest or nocturnal angina on certain occasions. Angina may also occur on exposure to cold, during emotional stress, or after meals. Dynamic vasoconstriction which superimposed on fixed atherosclerotic coronary artery obstructions has been postulated as the mechanism for the variable exercise threshold.

Nocturnal Angina Pectoris

In clinical practice, two types of nocturnal angina are observed. Some patients experience angina within an hour or two after sleeping. The mechanism of angina in this group of patients is likely to be an increase in venous return and hence increased intra cardiac volume with a resulting increase in myocardial oxygen requirements. Other group of patients with nocturnal angina experience chest discomfort much later, in the early hours of the morning. In this group of patients, a primary reduction in coronary blood flow owing to increased coronary vascular tone, more likely related to different stages of sleep, has been postulated as the potential underlying mechanism.

Postprandial Angina Pectoris

Angina can occur after meals without any ordinary physical activity because of increased coronary vascular tone and a primary decrease in coronary blood flow. However, postprandial angina may occur only during physical activity after meals because of an associated increase in myocardial oxygen demand. Postprandial angina is almost always associated with significant atherosclerotic coronary artery disease.

Syndrome X

Syndrome X is defined as the presence of typical anginal chest pain with angiographically normal coronary arteries. Although the syndrome originally referred to patients in whom the chest pain was due to non coronary causes, the current, stricter definition limits it to those patients who appear to have true myocardial ischemia despite epicardial coronary arteries that are normal or nearly so on coronary angiography.

To establish the diagnosis, patients must have evidence of myocardial ischemia by exercise ECG, stress scintigraphy, or stress echocardiography in conjunction with anginal chest discomfort. Some of these patients have documented reductions in coronary vasodilator reserve presumably due to abnormalities in the coronary microcirculation and can be shown to have true ischemia because their myocardium produces rather than removes lactate during stress.

The syndrome may be more common in patients with hypertrophied myocardium secondary to any cause. The prognosis in terms of major coronary events appears to be benign.

References

  1. Braunwald, Eugene (2003). Primary Cardiology. Saunders. ISBN 0-7216-9444-6. Unknown parameter |coauthors= ignored (help)

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